NARKETPALLY SYNDROME CBBLE; PARTICIPATORY MEDICAL COGNITION WEB 2.0-3.0, APRIL 2025
01/04/2025, 10:19 - cm: This book was on integrating medical education and practice in the times of Web 2.0
The next book will be about integrating medical education and practice in the current Web 3.0 era that's growing exponentially by leaps and bounds and may not remain bound by paper volumes!
01/04/2025, 11:02 - cm: Appears to be very little changes in the last few days unlike what one would expect in a STEMI! Was this pericarditis after all or STEMI (the ECG did evolve in the beginning) with pericarditis? @huai85 @huai46@huai2
01/04/2025, 13:46 - pajr.in CEO, NHS Endocrinologist: Addisons!
01/04/2025, 14:29 - huai85: Another differential etiology of myocardial injury due to supply demand mismatch needs to be considered sir...
01/04/2025, 15:22 - cm: EHR:
01/04/2025, 16:53 - cm: Just a simple minor road traffic injury getting this much complicated! Can happen any day to any of us or is there an individual genetic HLA mediated immune susceptibility involved here? @huai4 @huai13 @huai14 can check out this patient today in the AMC
01/04/2025, 17:10 - Kolkata Medical College Intern: hand hyperpigmented palmar creases, which might suggest a metabolic or endocrine disorder.
• posible diagnosis - Addison’s disease. marfanoid habitus and the Narketpally sign variant, Marfan syndrome, Ehlers-Danlos syndrome (EDS).
01/04/2025, 17:12 - Kolkata Medical College Intern: • connective tissue disorders like Marfan syndrome or Ehlers-Danlos syndrome (EDS).
01/04/2025, 19:30 - cm: I guess one needs to palpate those palms to really know what it is!
01/04/2025, 19:32 - huai61: It indeed looks like a STEMI sir
Was this patient discharged?
01/04/2025, 19:34 - cm: Not sure where he went! @huai100 may know
01/04/2025, 19:34 - huai61: Pericarditis usually you’ll have global st elevations
01/04/2025, 19:35 - huai61: And any echo video sir?
01/04/2025, 19:35 - huai61: Okay
01/04/2025, 19:36 - Kolkata Medical College Intern: Palpation is key to assess texture, thickness, and any hidden abnormalities.
01/04/2025, 19:37 - PI Portal Hypertension Project 2022: Patient went to NIMS for CRRT sir as he was having refractory Hypotension and there was further drop in Blood pressure during hemodialysis
01/04/2025, 19:59 - cm: The issue here is around what is known to explain persistence of ST elevation and:
"an association was found between persistent ST elevation and anterior infarction, larger microvascular damage.
Anterior myocardial infarcts have less frequently adequate collateral flow and more frequently a high amount of ischaemic tissue and higher wall stress;"
Unquote
02/04/2025, 12:06 - cm: OPD now:
[02/04, 11:53]: Reviewing this patient in the OPD right now after many years!
She was more or less okay from 2021 when her cutaneous vasculopathy and cerebral neurological deficits recovered after the first episode.
Since 2nd June last year 2024 she is on the medications attached
https://chat.whatsapp.com/IVsV2JINwLSAjzTO8A1RTL
[02/04, 11:59]: @huai104 shared this another case report of her which mentions that all her problems started after the covid vaccine! Reminds me of our pediatric PG who also had a stroke that hasn't yet recovered while this patient was lucky to have recovered in one day!
[02/04, 12:03] cm: Had bicytopenia in the first admission and ever since then the hemogram is normal. On MMF 360 bid reduced from 500 bid
02/04/2025, 15:56 - cm: Today's update. Urine output yesterday's 24 hours is 50 ml and input 5.7 liters. 1st hemo dialysis done at midnight yesterday and ultrafiltrate removed was 500 ml
04/04/2025, 12:38 - huai102: International Carrot Day, celebrated annually on April 4th, pays homage to the humble carrot—a versatile and nutritious vegetable loved by many around the world. Falling on the same date each year, this day invites us to appreciate the culinary and nutritional value of carrots while exploring their rich history and cultural significance.
Originating in Sweden, International Carrot Day has grown into a global celebration, with enthusiasts coming together to share their love for this vibrant root vegetable. Whether enjoyed raw as a crunchy snack, roasted to caramelized perfection, or incorporated into soups, salads, and desserts, carrots offer endless possibilities for delicious and healthy dishes.
04/04/2025, 12:38 -huai102: Carrots are a good source of vitamin A (beta-carotene), fiber, and other nutrients, offering health benefits like improved vision, digestion, and immune function.
Here's a breakdown of the nutritional value of carrots:
Key Nutrients:
Vitamin A (Beta-Carotene):
Carrots are rich in beta-carotene, which the body converts into vitamin A, essential for vision, immune function, and skin health.
Fiber:
Carrots provide dietary fiber, which aids digestion, promotes satiety, and helps regulate blood sugar levels.
Vitamins:
Carrots also contain Vitamin C, Vitamin K, and B vitamins like niacin and B6.
Minerals:
Carrots contain potassium, calcium, and other minerals.
Antioxidants:
Carrots are a source of antioxidants, which help protect the body against damage from free radicals.
04/04/2025, 12:55 - cm: We need both carrot and stick!?
04/04/2025, 12:57 -cm: 👆 answer to quiz for those who couldn't palpate this hand. It's bilateral dupytrens contracture!
04/04/2025, 13:19 - Nri Med: Simplified wonderfully👌🏻
04/04/2025, 15:32 -cm: This Wildebeest model of EBM values is inspired by Trisha's commentary on EBM values!👇
The most difficult aspect of the EBM definition which states that it "combines the best available evidence with clinical expertise and patient values in order to provide the best care for the individual patient," is the part about how to combine patient values.
04/04/2025, 16:53 - cm: Afternoon PaJR:
05/04/2025, 17:02 - cm: One click PaJR registration into WhatsApp 👇
https://theappsoul.com/pajr/
05/04/2025, 18:42 - pajr.in CEO, NHS Endocrinologist: Beautiful picket fence. What's the story of this fever?
06/04/2025, 11:47 - cm: @huai47 can you share the story or at least the intern's EMR summary?
06/04/2025, 11:49 - cm: Long distance patient admitted yesterday in the ward:
https://chat.whatsapp.com/FjPbCJMVBBZCQvJJLNyiyA
Below is the history shared by admitting PGY1.
50y old male came with
c/o greasy stools since 4-5 months
c/o cough since 2 months
c/o pain in epigastrium since 1 month
history of red colored stools 8-9 months back followed by tarry colored stools which subsided 4 months back with medication
now patient had greasy stools
on and off
cough since 2 months insidious onset associated with feeling of something stuck in the throat
h/o frothing of urine since 8 months
patient had previous history of blood transfusions
k/c/o chronic kidney disease since 9 months
k/c/o hiatus hernia
k/c/o hypertension since 9 months on tab cilnidipine 20mg po/od (non compliance to medication )
chronic alcoholic daily stopped 8 yrs back
chronic tabacco chewing stopped now
06/04/2025, 21:03 - cm: Three long distance patients arriving for admission tomorrow @huai40
Please ask the respective unit PGs to join their PaJR groups below 👇
https://chat.whatsapp.com/JFs7cRDs27uGtVHie0bA0g
https://chat.whatsapp.com/CzBgFtclZaMBGcQky9B88f
06/04/2025, 21:05 - cm: @huai40
https://chat.whatsapp.com/CmoIDQPWmsI5xLEp9VmxAT
06/04/2025, 21:05 - Medical Student CBBLE: Okay sir
06/04/2025, 21:10 - cm: @huai40 we'll need to get his 24 hour urine protein and creatinine <This message was edited>
06/04/2025, 21:10 - Medical Student CBBLE: already instructed the patient regarding it sir from tomorrow morning he will collect urine
07/04/2025, 07:04 - cm: https://pajr.in/
08/04/2025, 08:32 - cm: Residency welcome note from a final year student:
"Over these years, these young men and women will be challenged working long hours, bearing witness to how the title “resident” originated.
They will be doused by every type of bodily fluid. Through study and direct experience, they will confront the nuances, surprises, and tragedies of human illness.
They will meet patients who will leave a mark on their soul. Through it all and with time, the young resident fundamentally changes into a different type of person altogether. Residency training is a journey of a thousand miles, with the very first step taken on that fateful first day of joining!
And how could this process be anything less than transformational? It is, after all, the most profound vulnerability of the human condition that medicine seeks to address — that of injury, disease, and death. In the grip of such vulnerability, patients seek trustworthy advocates that they can turn to for help. And while learning is life-long, it is in residency training that the aspiring clinician first acquires the techne of medical practice.
They will feel something that cannot be explained in technical language, and in many ways it will remind them of what drove them to pursue medicine in the first place.
Unfortunately, residency training brings with it distractions—prioritization of efficiency, the so-called “hidden curriculum”, and systemic barriers—all of which can obfuscate the true focus of the physician’s practice, the patient. This has been described in the literature as moral injury or moral erosion. Therefore intentional practice, guided by mentors whom one wishes to emulate, is of paramount importance.
Enjoy the journey
The adage that “the days are long, but the years are short” is true. The road will be tough, but set aside moments to reflect and commend yourself on how far you’ve come. In training as physicians we have the privilege of joining a beautiful tradition, refined over millennia, and experience humanity in a way that very few people do
08/04/2025, 14:39 - cm: Please attend the presentation of our current work on PaJR tomorrow 👇
*IMP: Mark your 🗓️ on April 09 2025 ⏰ 8.30 PM to 9.30 PM IST
We are fortunate to have 2 speakers address us on the coming Wed:
1. Ms. Ishiyetaa Sani, founder of Tequity will take us through what it takes to make the right 'UX for Healthcare' with interesting examples from their work and best practices for healthcare apps.
2. In his session titled - 'PaJR - Patient Journals for Patient Outcomes' Dr. Aditya will be taking us through the use of PaJR https://pajr.in/ with anonymized real patient journeys on a blog and explain how this simple technique proves useful for improving patient outcomes.
Everyone, please do not miss this double opportunity!!
Please sign up on the pinned message to participate in the upcoming Wednesday session.
Topic: Ms Ishiyetaa Sani - UX for Healthcare and Dr. Aditya - PaJR
Time: Apr 9, 2025 08:30 PM Mumbai, Kolkata, New Delhi
Join Zoom Meeting:
https://us06web.zoom.us/j/84015710264?pwd=sCeRQSLP5IvbSlbzikp0vmMYkpMpae.1
Meeting ID: 840 1571 0264
Passcode: 533193
#Ishiyetaa Sani #UX for Healthcare #Tequity #PaJR #huai2 #NHS #UK
09/04/2025, 14:51 - cm: 👆@huai47 's thesis
09/04/2025, 16:54 - Kolkata Medical College Intern: Unstable Angina/NSTEMI (Non-ST Elevation Myocardial Infarction)
•• features suggestive of evolving anterior ischemia, possibly Wellens' Syndrome
Symptoms- Intermittent epigastric pain (often anginal equivalent in older females).
ECG progression 7–9 April
09/04/2025, 18:58 - cm: Which LLM?
10/04/2025, 11:10 - cm: 👆step 1 of toddy tree climbing and prominent latissimi
10/04/2025, 11:10 - cm: 👆Step 2 of toddy tree climbing and prominent latissimi
10/04/2025, 11:19 - Kolkata Medical College Intern: Evolving Inferior Wall Myocardial Infarction (MI)
Involving the Right Coronary Artery (RCA) territory — Type 1 MI (spontaneous atherosclerotic plaque rupture or erosion with thrombus formation).
10/04/2025, 11:34 - Kolkata Medical College Intern: 1. Acute Pulmonary Thromboembolism
2. Left Pyelonephritis
3. Urinary Tract Infection (UTI)
4. Prominent Left Latissimus Dorsi (likely due to toddy tree climbing)
10/04/2025, 11:57 - cm: @huai47 any follow up of this patient? Did it reach @huai41 ?
10/04/2025, 12:10 - Pushed Communicator 1N22: Yesterday evening after discharge they went to Hrudaya hospitals ,nalgonda.
They advised angiogram but due to affordability issues they went to Gandhi finally and was admitted in MICU
As per the attender repeat ecg and echo were done and currently the patient is under observation
Sir
10/04/2025, 12:31 - cm: Thanks for that update.
Can call them back here once Gandhi discharges them
10/04/2025, 12:37 - Pushed Communicator 1N22: Okay sir
10/04/2025, 13:42 - cm: Last patient in the morning OPD:
This was a quick outpatient consultation for a 55 year old woman with anxiety primarily because her daughter was suffering from panic attacks with alkalotic tetany and her daughter was suffering these because she was very emotionally attached to a14 year old girl in her neighbourhood living next door who was suffering from an inoperable brain tumor and doctors had given up on her!
10/04/2025, 16:07 - cm: Afternoon session:
10/04/2025, 16:22 - cm: Afternoon session:
10/04/2025, 22:17 - Nri Med: Anxiety is contagious
10/04/2025, 22:35 - Nri Med: Naked eye stool Examination still relevant...a good tool for bedside.
The clinical scenario very much suggestive of Tuberculosis...
So many coming AFB negative in RNTCP too,but clinical improvement with ATT remarkable.
EBM at crossroads sometimes.
10/04/2025, 22:44 - pajr.in CEO, NHS Endocrinologist: Can almost see the MR turbulence without and color there!
11/04/2025, 08:09 - Rakesh Biswas: Thanks for the pointer! Will need to recheck today again this afternoon with colour @916302536191
11/04/2025, 09:01 - K Naveen Kims 2024 Pg: Ok sir i will inform patient once
11/04/2025, 12:10 - You added Dr.Abdulsalam Med Ed Leads
11/04/2025, 12:10 - You added Patient Advocate Diabetes 75F WB
11/04/2025, 12:28 - Rakesh Biswas: @918074725352 same patient's PaJR here: https://chat.whatsapp.com/I2uXMK4gDSr8phUbeXCRYq
11/04/2025, 12:38 - Rakesh Biswas: Additional interesting findings in this patient @918074725352 👇
https://youtu.be/M8_HVkbixb0?feature=shared
11/04/2025, 12:49 - pajr.in CEO, NHS Endocrinologist: Yes been long I've seen the insides of that lecture hall as well 😅
11/04/2025, 15:57 - Dr.Abdulsalam Med Ed Leads: This image appears to be a bedside ultrasound using color Doppler, likely focused on the abdominal aorta or another major abdominal vessel. The patient is a 69-year-old male, and based on the context and the image characteristics, here are a few points to consider:
1. Color Doppler Usage: The presence of blue and red colors indicates blood flow. Red typically denotes flow towards the probe, and blue away from it (depending on the Doppler settings).
2. Anatomical Focus: The vessel shown looks like it could be the abdominal aorta with possible flow assessment for aneurysm or stenosis, or maybe renal artery evaluation. The grayscale background shows typical longitudinal abdominal structures.
3. Clinical Relevance: In older patients, this kind of imaging is often performed to evaluate for:
Abdominal aortic aneurysm (AAA)
Renal artery stenosis
Vascular compromise or occlusion
Or to assess for volume status through IVC assessment.
4. Next Steps: It would be helpful to know the clinical context—symptoms like abdominal pain, pulsatile mass, hypotension, or renal function abnormalities—to correlate with this image.
Would you like help interpreting this image further in a specific clinical scenario, or turning this into a teaching discussion for your students?
11/04/2025, 16:01 - Dr.Abdulsalam Med Ed Leads: The clinical description in the image points toward "Anton’s syndrome", a rare condition of denial of blindness or anosognosia, but in this specific context—where a hemiparetic patient is unaware of their body position and insists they are sitting when they are actually lying down—it aligns more closely with a form of asomatognosia or body schema distortion.
A more accurate and likely diagnosis here would be "Pusher syndrome" (also known as contraversive pushing). It’s a post-stroke condition, commonly associated with right hemispheric (especially posterior thalamic) lesions, where patients:
Are unaware of their body orientation.
Actively push away from the non-hemiparetic side, leading to loss of balance.
Have impaired perception of verticality and position.
However, in your case, if the patient has left hemiparesis and thinks he's sitting upright while already lying down, it suggests a disturbance in body awareness and position sense, possibly involving parietal lobe dysfunction, particularly the right parietal lobe.
So in summary:
Most consistent term: Pusher syndrome.
Possible underlying mechanism: Parietal lobe dysfunction leading to impaired body schema and anosognosia. <This message was edited>
11/04/2025, 16:05 - Rajesh Menon: Is there any posture in which he feels is lying down? With his eyes closed if possible..
11/04/2025, 16:10 - Dr.Abdulsalam Med Ed Leads: That's a brilliant clinical thought—you're probing body schema and proprioceptive integration, especially independent of visual cues.
If the patient believes he's sitting when he’s actually lying, it suggests his internal representation of posture is distorted, likely due to right parietal lobe dysfunction. Testing different positions with eyes closed can help isolate the sensory inputs contributing to the illusion.
Here’s how you could approach it:
1. Change his head/neck angle slightly (like propping up the headrest) while keeping the body flat—ask if he feels more "lying down" now.
2. Try lateral decubitus position (lying on his right or left side) and ask again how he perceives his posture.
3. Have him close his eyes, gently raise his legs or back—does that match his internal feeling of "lying"?
4. Ask him to describe what lying down feels like—this may expose how distorted his internal body map is.
If he never feels like he’s lying down in any position, even with eyes closed, it reinforces a central deficit in body position awareness—not just a visual/vestibular mismatch.
11/04/2025, 16:14 - Rakesh Biswas: Excellent Inputs 👏👏
@919347505324 @916302536191 please try 2-4 asap and let us know.
We tried making him lie flat to which he initially said yes now he's lying down but after sometime he again went back to the previous perception of being in a sitting position and insisted that he needs to lie down!
11/04/2025, 16:15 - Rakesh Biswas: Is it the same LLM as the first input?
11/04/2025, 16:15 - Dr.Abdulsalam Med Ed Leads: Yes, it is
11/04/2025, 16:17 - Dr.Abdulsalam Med Ed Leads: Yes, it enhances personalized learning and management
11/04/2025, 16:18 - Dr.Abdulsalam Med Ed Leads: Scholar ChatGPT <This message was edited>
11/04/2025, 16:27 - Dr.Abdulsalam Med Ed Leads: it reinforces a central deficit in body position awareness—not just a visual/vestibular mismatch.
11/04/2025, 16:27 - Rakesh Biswas: @916302536191 please share his MRI findings in images
11/04/2025, 17:00 - Rakesh Biswas: @919347505324 is this the second case for mortality discussion tomorrow? Can you pm me his IP number?👇
https://pajrcasereporter.blogspot.com/2025/03/70m-with-metabolic-syn-left-hemiparesis.html?m=1
@918074725352 I guess I shall need to remind Saidulu to send me his EMR summary short of which the case report above looks incomplete?
11/04/2025, 17:02 - Rakesh Biswas: https://youtu.be/qGWAc7kN_do?feature=shared
11/04/2025, 17:04 - Dr.Abdulsalam Med Ed Leads: His MRI images, if possible.
11/04/2025, 17:09 - Dr.Abdulsalam Med Ed Leads: Summary
The video outlines the cardiac evaluation of a 69-year-old man from West Bengal who is experiencing symptoms such as palpitations and shortness of breath. His medical examination reveals a complete assessment of his cardiac condition using echocardiography. The key findings include significant dilation of the left atrium, indicative of possible increased left ventricular diastolic pressure (LVDP) or valvular issues. Observations within the heart chambers indicate that both the left atrium and left ventricle are mildly dilated. The left atrium’s irregular contractions suggest the presence of ectopic contractions. Detailed analysis of the mitral and aortic valves shows signs of mitral regurgitation (MR) categorized as mild to moderate, alongside mild aortic regurgitation (AR). The assessment concludes with a portrayal of the heart’s structure and functionality, underscoring the need for further examination and monitoring due to the evident abnormalities.
Highlights
🩺 69-year-old man presents with palpitations and shortness of breath.
🔍 Echocardiography reveals dilation of heart chambers.
💔 Left atrium shows signs of increased LVDP or valvular issues.
⚡ Irregular contractions possibly indicate ectopic beats.
💧 Mild to moderate mitral regurgitation detected.
🌪️ Mild aortic regurgitation also noted during evaluation.
📉 Heart function metrics suggest need for further monitoring.
Key Insights
🕵️♂️ Age-Related Cardiac Risks: The 69-year-old patient exemplifies how age increases susceptibility to cardiovascular conditions. As individuals age, the heart undergoes structural changes like dilation and impaired contractility, leading to elevated risks for heart disease, which must be monitored closely.
❤️ Dilation of Heart Chambers: The dilation of both left atrium and ventricle signifies possible underlying issues such as hypertension, heart valve dysfunction, or cardiomyopathy. This dilation can lead to further complications like thrombus formation, thus requiring rigorous follow-up.
⚠️ Ectopic Contractions: The irregular contractions observed could be a benign finding or signal an arrhythmia that requires further assessment. This finding accentuates the importance of rhythm monitoring in patients presenting with similar symptoms.
📉 Mitral and Aortic Valves Assessments: The detection of mild to moderate MR suggests regurgitation that may not be immediately critical but indicates the need for regular follow-ups to prevent progression to more severe heart conditions or heart failure.
🩺 Importance of Doppler Imaging: The use of Doppler echocardiography provides essential insights into valvular blood flow dynamics. Identifying both MR and AR through this method highlights its critical role in the diagnosis and management of valvular heart disease.
📊 Heart Function Assessment: Investigation into chamber sizes and contractility provides valuable data for understanding overall heart function. The configuration of the heart’s structure can indicate chronicity of disease processes, necessitating more innocent and preventive interventions.
🔍 Future Monitoring Needs: Given the findings, the patient requires ongoing monitoring for further changes in heart functionality and symptoms, which speaks to the broader need for comprehensive cardiovascular care and patient education regarding potential symptoms of worsening conditions.
11/04/2025, 20:47 - Rakesh Biswas: @916302536191 please share the MR video here after deidentification and removal of patient and hospital identifiers
11/04/2025, 20:49 - Rakesh Biswas: Thanks! Amazing!
Any URL to this YouTube video summarizer?
11/04/2025, 20:53 - Dr.Abdulsalam Med Ed Leads: Yes
11/04/2025, 20:53 - K Naveen Kims 2024 Pg: Above videos are of that patient sir
11/04/2025, 20:54 - Rakesh Biswas: Thanks
11/04/2025, 20:55 - K Naveen Kims 2024 Pg: Ok sir
11/04/2025, 20:57 - Dr.Abdulsalam Med Ed Leads: This MRI image appears to be a diffusion-weighted imaging (DWI) scan of the brain, often used in the context of acute stroke evaluation. Here are some observations:
Right Hemisphere Lesion: The image on the right (DWI) shows a bright hyperintense area in the left side of the scan, which corresponds to the right cerebral hemisphere (remember that radiologic images are typically viewed in mirror image). This hyperintensity suggests restricted diffusion, a hallmark of acute ischemic stroke.
ADC Correlation: The image on the left may represent the Apparent Diffusion Coefficient (ADC) map. Although it’s not very clear, the same region appears darker, which supports the diagnosis of acute infarct (restricted diffusion on DWI corresponds to low ADC values).
Location: The lesion seems to involve the posterior cerebral territory, possibly affecting the occipital and parietal lobes.
Clinical implication: This is likely an acute ischemic infarct in the right posterior cerebral artery (PCA) territory, which might present clinically with left-sided visual field deficits (e.g., left homonymous hemianopia), sensory disturbances, or cortical blindness depending on the extent.
Would you like a more detailed breakdown or an educational note for teaching purposes?
11/04/2025, 21:00 - Rakesh Biswas: Wow! @917639986241 what do you think about the above report from the MRI video? Can you guess the LLM?
11/04/2025, 21:01 - You added TSAPI Morning Sun
11/04/2025, 21:05 - Rakesh Biswas: GPT Ux interface? Was it reading the video or just an image?
11/04/2025, 21:07 - Dr.Abdulsalam Med Ed Leads: just the image.
11/04/2025, 21:20 - Suvrankar Datta AIIMS: It’s a completely false report
11/04/2025, 21:23 - Suvrankar Datta AIIMS: Is this GPT4o latest model?
11/04/2025, 21:24 - Dr.Abdulsalam Med Ed Leads: Yes
11/04/2025, 21:27 - Dr.Abdulsalam Med Ed Leads: The content provided ("120 / 120") does not include an actual MRI image but appears to show numerical values. In the context of MRI scans, these numbers could represent:
1. **Image slices** (e.g., 120 out of 120 slices acquired, indicating a complete scan series).
2. **Signal intensity ratios** (though this would require context about the regions being compared).
3. **Scoring metrics** (e.g., a grading system for findings, though 120/120 is atypical for clinical scores).
To provide a meaningful interpretation of the MRI, the visual image itself is necessary to assess anatomical structures, abnormalities, or artifacts. Please share the actual MRI image for a detailed analysis.This is DeepSeek response.
12/04/2025, 00:09 - Dr.Abdulsalam Med Ed Leads: Kindly share the MRI report so I can inturn share it with the AI to enhance its performance next time .
12/04/2025, 00:11 - Dr.Abdulsalam Med Ed Leads: Of course after eliminating the patient and center ID
12/04/2025, 06:49 - Rakesh Biswas: @916302536191 please share the report given by our radiology department around that MRI video you shared.
Thanks @917639986241 for the adversarial stance that may help us to generate potential newer insights into AI vs human learning!
@919604701505 while it's clear that human influences had a lot to do with the term GAN generative adversarial networks, can you help us further correlate how the human adversarial learning analogy (for example healthy debates) may compare with actual mechanics behind GANs?
12/04/2025, 07:00 - K Naveen Kims 2024 Pg: This message was deleted
12/04/2025, 08:30 - Rakesh Biswas: Please remove hospital and patient identifiers and then reshare and also delete the one that you shared here
12/04/2025, 08:35 - Rakesh Biswas: Thanks
@917639986241 how much different is our radiology department's report from what the LLM ventured to gather from the video on it's own?
12/04/2025, 08:58 - Rakesh Biswas: Was going through a round of unexpected clinical auscultation around our first clinical encounter with this patient yesterday who appeared to have some additional sounds other than the S1 and S2
https://pajrcasereporter.blogspot.com/2025/04/69m-pedal-edema-abdominal-distension.html?m=1 and this was driven by a
a few final year interested students and their infectious enthusiasm when it occurred to us why not capture his sound data and visualise it graphically!
That's when we remembered @919845031486 's brilliant device which he had generously gifted to Narketpally. @919154575937 @919652955915 would you know where is the device these days after you completed your audicor project?
12/04/2025, 09:17 - Rakesh Biswas: Wow! Yes would be keen to see the visual overlay promised here by the LLM
12/04/2025, 09:55 - Sai Charan Kulkarni 2020 KIMS Pg: In icu locker sir
12/04/2025, 09:59 - PaJR Physicist: It's very interesting. I've been playing around with both Chat GPT and Gemini research to help physicians conduct a differential as quickly as possible. The goal is 'not a disease' but the possibility of co-existing ones. So begins with confounding symptoms and a 'subjective' inference from the physical examinations and office examination tools. Then capturing all these inputs onto an individual patient health record. A library of 'prompt sheets' are manually (for now) selected and posted onto the LLM Chat with specific advice that all references are to be from evidence based (including some anecdotal one from respected journals) and prepare two sets of documents - one for the clinician's guidance and one for the patient as an advisory. Referral, lifestyle, secondary preventive strategies, etc. The problem, I wanted to attend to were, (1) reduce the number of erroneous referrals (2) enhance the speed and efficiency of a primary care encounter and (3) and manage the disease(s) in the continuum using the updated practices and protocols from, say, the ESC and ACC.
12/04/2025, 11:38 - MD.AKRAM Kolkata Medical College Intern: 1) Recent (acute) stroke —
In the right parietal lobe and right occipitotemporal lobe. These regions of the brain are involved in functions such as vision, sensation, and language comprehension.
2. Old small strokes (chronic lacunar infarcts) —
Found in the right corona radiata, which is a deep part of the brain that contains important nerve fiber tracts.
3. Shrinkage or reduction in brain volume (diffuse cerebral atrophy) —
This is commonly age-related, but it can also be due to long-term illness or neurodegenerative conditions.
•• Other parts of the brain, such as the thalamus, brain stem, cerebellum, pituitary gland, appear normal.
••• No abnormal blood vessels, bleeding, or calcifications have been seen.
•• The eyes and surrounding structures are normal.
12/04/2025, 12:36 - Dr.Abdulsalam Med Ed Leads: Here is the **realistic overlay** of an **acute ischemic stroke** affecting the **right parietal** and **right occipitotemporal** regions:
### Description of the Overlay:
- **Blue Shaded Areas**:
- **Right Parietal Region (Superior Posterior)**: Often involved in spatial attention and body awareness — infarction here can cause **left-sided neglect**, especially in right-dominant brains.
- **Right Occipitotemporal Region (Inferoposterior)**: Critical for **visual association** and **object recognition**; infarction may result in **visual agnosia** or **alexia without agraphia** if connected to splenial fibers.
- **Clinical Relevance**:
- These areas are typically supplied by distal branches of the **posterior cerebral artery (PCA)** and parts of the **middle cerebral artery (MCA)**.
- Acute ischemia here may present with a combination of **visual deficits**, **visuospatial neglect**, and **higher-order processing impairments**.
Would you like me to generate **diffusion-weighted MRI style visuals**, **lesion progression maps**, or correlate this with **angiographic territories** next?
12/04/2025, 12:39 - MD.AKRAM Kolkata Medical College Intern: 1. DWI-style visuals of the stroke
2. Lesion progression maps
3. Angiographic territory overlays
12/04/2025, 12:39 - Dr.Abdulsalam Med Ed Leads: Which largely correlate with patient loss of the spacial orientation and visual and vestibular mismatch.
12/04/2025, 12:41 - Rakesh Biswas: That's our regular PaJR workflow 👏👏
12/04/2025, 12:44 - Dr.Abdulsalam Med Ed Leads: <Media omitted>
12/04/2025, 12:44 - Rakesh Biswas: The schematic diagrams are not as rejuvenating as the actual imageology that we are used to I guess
12/04/2025, 12:46 - Dr.Abdulsalam Med Ed Leads: I guess so, but you know I've to follow to it's extreme ,then I'll give it my feedback
12/04/2025, 12:47 - Dr.Abdulsalam Med Ed Leads: In the meanwhile I will try another AI
12/04/2025, 12:51 - Dr.Abdulsalam Med Ed Leads: Creating an overlay to illustrate ischemia (reduced blood flow) in the **parietal** and **occipitotemporal** regions of the brain involves highlighting specific anatomical areas. Below is a step-by-step guide to conceptualize this overlay:
---
### **1. Brain Anatomy Reference**
Start with a lateral (side) view of the left cerebral hemisphere. Key landmarks:
- **Central sulcus**: Separates the frontal and parietal lobes.
- **Parieto-occipital sulcus**: Divides the parietal and occipital lobes.
- **Lateral sulcus (Sylvian fissure)**: Separates the temporal lobe from the frontal and parietal lobes.
---
### **2. Highlighting Ischemic Regions**
Use **color coding** (e.g., blue or gray shading) to indicate areas of reduced blood flow:
#### **A. Parietal Lobe Ischemia**
- **Location**: Superior and posterior to the lateral sulcus, extending to the parieto-occipital sulcus.
- **Key structures affected**:
- **Postcentral gyrus** (primary somatosensory cortex).
- **Superior parietal lobule** (spatial awareness, sensory integration).
- **Inferior parietal lobule** (language processing, calculation).
#### **B. Occipitotemporal Region Ischemia**
- **Location**: Posterior-inferior brain, spanning the occipital lobe and ventral temporal lobe.
- **Key structures affected**:
- **Occipital lobe** (primary visual cortex, visual association areas).
- **Fusiform gyrus** (facial/object recognition).
- **Inferior temporal gyrus** (complex visual processing).
---
### **3. Overlay Design**
- Use **transparent shading** or cross-hatching to overlay ischemic zones on a brain diagram.
- **Parietal ischemia**: Highlight the area between the postcentral gyrus and the parieto-occipital sulcus.
- **Occipitotemporal ischemia**: Highlight the ventral (underside) junction of the occipital and temporal lobes.
---
### **4. Functional Implications**
Label the overlay with clinical effects of ischemia in these regions:
- **Parietal ischemia**:
- Contralateral sensory loss (numbness).
- Neglect syndrome (ignoring one side of space).
- Acalculia (difficulty with math) or agraphia (writing impairment).
- **Occipitotemporal ischemia**:
- Visual field deficits (e.g., homonymous hemianopia).
- Prosopagnosia (inability to recognize faces).
- Object agnosia (inability to recognize objects).
---
### **5. Example Visualization**
Imagine a brain diagram with:
- Blue shading over the parietal lobe (above the lateral sulcus) and the ventral occipitotemporal junction.
- Labels indicating "Parietal Ischemia" and "Occipitotemporal Ischemia."
- Arrows pointing to clinical symptoms (e.g., "Visual Field Loss" near the occipital lobe).
This overlay helps correlate anatomy with functional deficits caused by ischemic strokes or hypoperfusion. Let me know if you'd like further refinement!
12/04/2025, 12:51 - Dr.Abdulsalam Med Ed Leads: That was DeepSeek response 👆
12/04/2025, 13:25 - Suvrankar Datta AIIMS: @919121046928 Since you asked
1. The MRI is not just DWI but also shows T2 sequences
2. Infarct diagnosis is correct (which is very obvious too) but the territory is not correct
3. The left side is not an ADC
4. This does not seem to involve the cortical blindness territory (I doubt if patient would have blindness)
12/04/2025, 13:27 - Suvrankar Datta AIIMS: Ai has given a wrong vascular territory and a suspicious clinical correlation.
12/04/2025, 13:27 - Suvrankar Datta AIIMS: But that’s just because it’s a generalised model.
12/04/2025, 13:28 - Suvrankar Datta AIIMS: Generalist Medical foundational models can do much better.
12/04/2025, 13:44 - Dr.Abdulsalam Med Ed Leads: Visual vestibular mismatch
12/04/2025, 13:46 - Dr.Abdulsalam Med Ed Leads: I could only share a screenshot of the site of the suspected lesion and not the whole sequence.
12/04/2025, 13:48 - Dr.Abdulsalam Med Ed Leads: Anyone can kindly examine the patient in detail and tell us whether the clinical findings match those of the AI? <This message was edited>
12/04/2025, 14:09 - Suvrankar Datta AIIMS: That’s not cortical blindness
12/04/2025, 14:10 - Suvrankar Datta AIIMS: Correct me if I am wrong
12/04/2025, 14:11 - Suvrankar Datta AIIMS: As per the MRI video, primary visual cortex (occipital lobe) is spared
12/04/2025, 14:12 - Suvrankar Datta AIIMS: But AI thinks it’s involved
12/04/2025, 14:19 - Dr.Abdulsalam Med Ed Leads: It's the optic / visual pathway was interrupted in aWay resulting in mismatch between visual input and the intact vestibular tract this would result in that the higher cortical proces deranged in a way of disturbance of the spacial orientation to extent propotional to to extent of and cuteness of the ischemia and other comorbidies of relevance and the composation mechanisms..
12/04/2025, 14:31 - Sadhana Sharma Nri Med: This is just thrilling, i would say...I mean ,i can feel how a UG student would feel.
12/04/2025, 14:42 - Dr.Abdulsalam Med Ed Leads: Clinical implication: This is likely an acute ischemic infarct in the right posterior cerebral artery (PCA) territory, which might present clinically with left-sided visual field deficits (e.g., left homonymous hemianopia), sensory disturbances, or cortical blindness depending on the extent.
12/04/2025, 15:01 - Dr.Abdulsalam Med Ed Leads: <Media omitted>
12/04/2025, 15:46 - Dr.Abdulsalam Med Ed Leads: This case stimulated healthy discussions and debates about the topic from different perspectives.
12/04/2025, 15:47 - Dr.Abdulsalam Med Ed Leads: With the aid of the latest version of NotebookLM, this “manual was produced
12/04/2025, 16:23 - Rakesh Biswas: Agree 👏👏 thanks to Prof @9647501361306 and Dr @917639986241
It's a pleasure to introduce both to this group.
Prof Salam is a respected and busy ENT surgeon and teacher in his country and as you can see is also very tech savvy. Suvrankar is a brilliant radiology faculty from India's topmost institute and is also building an AI infrastructure for the future to support global healthcare needs. 👏👏
12/04/2025, 16:51 - Dr.Abdulsalam Med Ed Leads: It is my pleasure and honor to be among you.
12/04/2025, 17:02 - Rakesh Biswas: You deleted this message
12/04/2025, 17:03 - Rakesh Biswas: You deleted this message
12/04/2025, 17:05 - Rakesh Biswas: You deleted this message
12/04/2025, 17:19 - Rakesh Biswas: You deleted this message
12/04/2025, 17:52 - ~ Theertha left
13/04/2025, 20:37 - Rishitha Kims 2019 left
13/04/2025, 20:44 - Rakesh Biswas: A very interesting presentation about our work here by @919652955915 in a global forum this week with some of our members here @918106177663 adding value at the end. 👏
There's another interesting presentation on user interface and our presentation starts at 32 minutes here 👇
https://youtu.be/76tC-1m5nk4?feature=shared
13/04/2025, 21:48 - Rakesh Biswas: @918106096962 @918886202111 would you like to check the ICU locker tomorrow for the audicor so that we can graph and collectively hear the current admitted patient's cardiac sounds tomorrow? The same patient you saw in the OPD
13/04/2025, 21:50 - Ahana Mukherjee Kims 2021: yes sir, we'll go tomorrow.
13/04/2025, 21:50 - Braahmani Bobba 2021 Kims UG: Yes sir, we will.
13/04/2025, 21:53 - +91 93225 35788 left
14/04/2025, 00:23 - +91 81425 22041 left
14/04/2025, 08:17 - PaJR Physicist: I think you need an updated kit. Will bring it on 14th May.
14/04/2025, 08:41 - Rakesh Biswas: Wow! That would be great. Let's explore what we have in our ICU locker today @918106096962 @918886202111 @919154575937
14/04/2025, 09:40 - Rakesh Biswas: Finally the much awaited annual CPD of general medicine department, Narketpally is happening this week and the first topic by Prof @919419526285 looks quite promising and I'm looking forward to attending it.
https://medicinedepartment.blogspot.com/2025/04/2025-annual-cpd-of-general-medicine.html?m=1
Hoping to attend amidst the regular OPD and IPD workflow and wish the proceedings are recorded on zoom similar to our recent presentation here: https://youtu.be/76tC-1m5nk4?feature=shared
Kudos to the organizers @918332874734 @919550360199 @918500119292 @919818741334 @918099474777 @918008671890 and the tireless PGs who worked hard for it's success.
Met with Raveen for the first time today after weeks of his joining and he gave the impression that going out of Narketpally for a year felt like moving from the frying pan to fire and he's glad to be back into the frying pan! @919154575937 @919652955915
14/04/2025, 11:06 - Dr.Abdulsalam Med Ed Leads: This clinical scenario presents a 53-year-old male with chronic exposure to bore water, raising the suspicion of dental fluorosis, as evidenced by the characteristic yellow-brown discoloration and pitting of the teeth seen in the image. The appearance is consistent with long-term fluoride exposure, especially in areas with high groundwater fluoride levels.
Key Points:
1. Dental Fluorosis:
The patient's teeth show discoloration and possible enamel erosion, typical of moderate to severe fluorosis.
Chronic bore water consumption over 50 years strongly supports this etiology.
The absence of "Narketpally sign" (a reference to more specific fluorosis signs, possibly from regional literature or local clinical findings) doesn't rule out fluorosis.
2. Current Complaints:
Giddiness and neck pain are non-specific and may not be directly related to fluorosis.
These symptoms could point toward cervical spondylosis or vertebrobasilar insufficiency, both common in this age group.
Further workup like cervical spine X-ray and possibly MRI could be warranted.
3. Past History of Vitiligo:
The perioral depigmentation and body changes are consistent with healed or inactive vitiligo, as described.
Though not currently active, the residual depigmentation may still have psychosocial impact, and it’s important to address this if the patient has concerns.
Suggestions:
Serum and urine fluoride levels could help confirm fluorosis.
Evaluate for skeletal fluorosis if there are signs like joint stiffness, chronic bone pain, or neurological symptoms.
Consider neurological evaluation for giddiness and neck pain (e.g., vertebrobasilar insufficiency, cervical myelopathy).
Education on safe water sources and possible defluoridation techniques may benefit the community.
Would you like to draft a brief teaching case summary or discuss differential diagnoses in more detail?
14/04/2025, 11:07 - Dr.Abdulsalam Med Ed Leads: Scholar ChatGPT comment 👆
14/04/2025, 12:27 - ~ Neelam left
14/04/2025, 12:49 - Dr.Abdulsalam Med Ed Leads: Summary
In the presentation led by Ishita, co-founder and Chief Design Officer of Techquity, the focus is on how to effectively transform health tech products into user-centric solutions through UX design. Ishita, who comes from a background in UX and service design, explains her company’s mission to convert innovative ideas into practical health products. Techquity has identified three segments within the health sector, ranging from care enablers to life sciences, and emphasizes two primary growth strategies for health tech: product-led growth (PLG) and sales-led growth (SLG).
Ishita advocates for prioritizing PLG due to its benefits, such as fostering trust through user experience, reducing sales cycles, and generating valuable usage data. She elaborates on crucial components of the user journey, like clear communication, customized user experiences, and effective onboarding processes. Engaging first-time users through compelling website design is also discussed, highlighting the significance of emotional messaging and relatability.
The presentation features case studies showcasing redesigns that led to improved user engagement and conversion rates. Concerns raised during the Q&A segment underline the complexities of the B2B2C nature of health tech and the challenges of moving from SLG to PLG in enterprise environments. Ishita concludes by stressing the importance of integrating both strategies and fostering ongoing dialogue to enhance user retention.
Additionally, the presentation showcases the importance of personalized healthcare through case studies of patients with chronic diseases like diabetes. It highlights the success of a platform called “pager,” which empowers patients by helping them log daily health behaviors and their impacts. Moreover, the necessity of medical education and active student involvement in patient care is emphasized, with discussions on how to scale personalized approaches through automation. The dialogue concludes with reflections on trust in healthcare, accessibility, and the democratization of health knowledge.
Highlights
🌟 User-Centric Focus: Ishita emphasizes the importance of creating health tech products centered around user experience.
📈 Prioritizing PLG: Product-led growth is presented as a more effective strategy for user trust and data gathering.
🛠️ Improved Onboarding: Effective UX design can simplify onboarding and enhance user retention.
🎨 Compelling Design Matters: Website redesigns can significantly boost user engagement and conversion metrics.
💡 Patient Empowerment: Case studies illustrate how technology can help chronic disease patients manage their health better.
📚 Medical Education’s Role: The focus on engaging medical students to prioritize patient outcomes is crucial for improving healthcare.
🔄 Interconnected Strategies: A balance between sales and product-led growth strategies is necessary for successful health tech solutions.
Key Insights
🚀 Impact of UX Design on Growth: Prioritizing product-led growth (PLG) allows health tech companies to create products that are intuitive and user-friendly, enhancing trust and ultimately leading to shorter sales cycles. This emphasizes that a focus on user experience is not just beneficial for users but also strategically advantageous for businesses.
⚙️ Transformative Patient Experiences: By harnessing platforms like “pager” that log daily health activities, patients can gain insights into how their personal habits affect their conditions. This empowers patients by allowing them to actively partake in their health management, which can lead to improved outcomes.
📊 Value of Case Studies: Successful case studies play a vital role in demonstrating the practical benefits of well-designed health tech solutions. By analyzing user needs and experiences, companies can iterate and enhance their offerings effectively.
🎯 Challenges of Health Tech Scalability: The transition from sales-led to product-led growth can be tricky due to the inherent structures of enterprise environments. It requires thoughtful strategic planning and necessitates clear communication with multiple stakeholders involved in the healthcare process.
🔬 Role of Medical Education: Integrating a focus on patient outcomes in medical training fosters a more compassionate and engaged healthcare workforce. This progressive approach encourages healthcare professionals to prioritize personalized care strategies.
🤖 Need for Automated Solutions: Combining technology with current practices, such as automating data collection methods, can streamline the process of gathering health-related information, thereby increasing patient engagement and accuracy.
💰 Trust and Financial Models: As healthcare undergoes digital transformation, the dynamics of trust between providers and patients are shifting. Creating transparent, actionable financial models tailored to the local context can address accessibility issues while ensuring healthcare sustainability, ultimately contributing to better patient outcomes.
14/04/2025, 13:00 - Dr.Abdulsalam Med Ed Leads: Thanks for sharing the cervical spine X-rays — both the anteroposterior (AP) and lateral views are quite informative.
### 🧠 **Preliminary Impression (Not a diagnosis):**
The lateral view (right side image) clearly shows **linear calcification along the posterior aspect of the vertebral bodies**, particularly in the **cervical spine**. This appearance is **highly suggestive of ossification or calcification of the posterior longitudinal ligament (OPLL)**. You’re absolutely right — this could indeed be consistent with the features seen in **“Narketpally syndrome”**, a term used locally or informally, often linked to endemic spinal ligament ossifications, though it’s not a widely recognized term in international medical literature.
---
### 🦴 **Key Radiological Features Noted:**
- **Posterior longitudinal ligament calcification**: Seen as a radiodense line paralleling the posterior vertebral margins in the lateral view.
- **No significant vertebral body collapse**: The vertebral body heights appear preserved.
- **Disc spaces**: Reasonably maintained though slightly narrowed at some levels.
- **No gross misalignment**: No signs of dislocation or fracture.
---
### 📘 Clinical Correlation:
Calcification of the **posterior longitudinal ligament** may result in:
- **Neck stiffness**
- **Cervical radiculopathy or myelopathy**
- **Progressive motor weakness or sensory deficits** (due to spinal canal narrowing)
---
### 🔍 Suggestive Next Steps:
If not already done:
1. **MRI Cervical Spine** – To assess the degree of spinal cord compression or myelomalacia.
2. **Neurological Evaluation** – Correlation with symptoms like gait disturbance, limb weakness, etc.
3. **Bone metabolism tests** – Calcium, phosphate, Vitamin D, and PTH levels.
4. **CT Scan** (in some cases) – Offers better detail of ossified structures.
---
Would you like me to pull up some clinical papers on OPLL and any related syndromes (including possibly endemic or region-specific ones like “Narketpally syndrome”)? I can get 10–15 top scholarly references for you in one go.
---
***Handling multiple papers?***
Speed up your research with Sider! Our AI-powered sidebar features 10+ one-click tools including a more advanced Search Agent, ChatPDF, context-aware utilities and more to help you work smarter and faster.
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14/04/2025, 13:09 - Dr.Abdulsalam Med Ed Leads: Thanks for uploading the complete set of images and clinical summary. Here's a detailed breakdown of the case based on the reports and images:
---
### 👩⚕️ **Clinical Summary**
- **Patient**: 24-year-old female
- **Symptoms**: Shortness of breath, syncope episodes since December 2020
- **Incidental Finding**: Tumor posterior to stomach found on ultrasound
- **Procedure**: EUS-guided biopsy performed
- **Histopathology**: Confirmed **Solid Pseudopapillary Tumor (SPT)** of the pancreas
- **Anemia**: Hemoglobin 6.5 g/dL (significant anemia, possibly chronic disease-related)
---
### 📄 **Key Report Findings**
#### **1. Upper GI Endoscopy (UGIE) Report**
- **Stomach**: External bulging seen in the proximal part of the body and antrum, likely due to **extrinsic compression**.
- **Duodenum**: Normal mucosa, no obstruction or mass.
- **Conclusion**: **External compression suspected — referred for EUS.**
#### **2. Endoscopic Ultrasound (EUS)**
- EUS image shows a lesion posterior to the stomach — consistent with a **peripancreatic mass**.
- Biopsy taken during EUS.
#### **3. Histopathology Report**
- **Macroscopic**: 3 linear cores, largest 3.5 cm
- **Microscopic**:
- Tumor composed of **pseudopapillary structures**
- **Ovoid nuclei**, **moderate cytoplasm**
- **No mitosis**, **no atypia**, **cholesterol clefts present**
- **IHC** was suggested but **refused by patient**
- **Diagnosis**: **Solid Pseudopapillary Tumor (SPT)**
---
### 🧠 **Interpretation & Clinical Insights**
**Solid Pseudopapillary Tumor (SPT)** of the pancreas is:
- A **rare, low-grade malignant tumor**
- Typically affects **young women** (consistent with this case)
- Often presents **incidentally** or with vague symptoms (like the syncopal episodes or anemia here may not be directly related)
- **Prognosis is excellent** with complete surgical resection
---
### 🔍 **Management Considerations**
1. **Surgical Resection (Whipple or distal pancreatectomy)** is **curative in most cases**.
2. **Immunohistochemistry (IHC)** is typically used to confirm (markers like β-catenin, vimentin, CD10) — though refused here.
3. Anemia (Hb 6.5 g/dL) requires further evaluation — may be chronic disease-related or unrelated; **iron studies** and **nutritional workup** suggested.
4. **Follow-up Imaging (CT/MRI)** to assess:
- Tumor extent
- Involvement of vessels or surrounding organs
- Metastasis (rare but possible)
---
Would you like me to pull 10–15 top scholarly articles on **Solid Pseudopapillary Tumors** (SPT) — including diagnosis, pathology, treatment, and outcomes — to support further case planning?
Let me know if you're also interested in guidelines (like from ESMO or NCCN) or case series reviews.
---
***Handling multiple papers?***
Speed up your research with Sider! Our AI-powered sidebar features 10+ one-click tools including a more advanced Search Agent, ChatPDF, context-aware utilities and more to help you work smarter and faster.
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14/04/2025, 13:14 - Dr.Abdulsalam Med Ed Leads: Here's an in-depth overview of the current scholarly understanding of **Solid Pseudopapillary Tumors (SPTs)** of the pancreas, focusing on diagnosis, pathology, treatment, and clinical outcomes. SPTs are rare pancreatic neoplasms with low malignant potential, most often affecting young women. Although usually indolent, they can exhibit aggressive features in a minority of cases. Advances in radiologic imaging, immunohistochemistry, and surgical management have significantly improved detection and prognosis.
---
## 🔬 **Overview of Key Findings**
- **Diagnosis**: Imaging modalities (CT, MRI, EUS) combined with biopsy are effective in identifying SPTs. Radiologic features like well-defined margins, hemorrhagic cystic components, and capsular enhancement are common.
- **Pathology**: Characterized by solid and cystic areas with pseudopapillary architecture. Immunohistochemistry markers like β-catenin, CD10, and progesterone receptor aid in diagnosis.
- **Treatment**: Surgical resection remains the mainstay, often curative. Minimally invasive techniques like laparoscopic or robotic resection are increasingly used.
- **Outcomes**: Excellent overall survival after surgery; recurrence is rare but possible, especially in cases with capsular invasion or vascular involvement.
---
## 📚 **Top 12 Scholarly Articles on SPTs**
1. **Law, J. K., et al. (2014).**
*A systematic review of solid-pseudopapillary neoplasms: are these rare lesions?*
*Pancreas, 43(3), 331–337.*
[DOI: 10.1097/MPA.0000000000000031](https://doi.org/10.1097/MPA.0000000000000031)
► Systematic review highlighting rising incidence due to better imaging and classification; excellent prognosis with surgery.
2. **Papavramidis, T., & Papavramidis, S. (2005).**
*Solid pseudopapillary tumors of the pancreas: review of 718 patients reported in English literature.*
*J Am Coll Surg, 200(6), 965–972.*
[DOI: 10.1016/j.jamcollsurg.2005.02.011](https://doi.org/10.1016/j.jamcollsurg.2005.02.011)
► Large-scale literature review; outlines diagnostic and therapeutic patterns, gender differences.
3. **Zhang, H., et al. (2020).**
*Surgical management and outcomes of solid pseudopapillary neoplasms: a multicenter experience in China.*
*World Journal of Gastroenterology, 26(30), 4506–4518.*
[Link](https://www.wjgnet.com/1007-9327/full/v26/i30/4506.htm)
► Provides long-term outcomes across multiple centers; confirms favorable survival.
4. **Tanaka, Y., et al. (2012).**
*Clinicopathological features and immunohistochemical characterization of pancreatic solid pseudopapillary tumors.*
*Pathology International, 62(9), 485–492.*
[DOI: 10.1111/j.1440-1827.2012.02842.x](https://doi.org/10.1111/j.1440-1827.2012.02842.x)
► Focus on diagnostic markers (β-catenin, CD56, CD10); key for histological confirmation.
5. **Klimstra, D. S., et al. (2000).**
*Solid-pseudopapillary neoplasm of the pancreas: a typically cystic tumor of low malignant potential.*
*Seminars in Diagnostic Pathology, 17(1), 66–80.*
[PubMed Link](https://pubmed.ncbi.nlm.nih.gov/10721808/)
► Seminal work establishing low-grade malignancy profile and morphologic criteria.
6. **Butte, J. M., et al. (2011).**
*Laparoscopic resection for solid pseudopapillary tumor of the pancreas: single-institution experience and review of the literature.*
*J Gastrointest Surg, 15(10), 1751–1756.*
[DOI: 10.1007/s11605-011-1601-8](https://doi.org/10.1007/s11605-011-1601-8)
► Reviews safety and efficacy of laparoscopic pancreatectomy.
7. **Zhou, Y., et al. (2017).**
*Solid pseudopapillary tumor of the pancreas: a 10-year single-institution experience.*
*Surgical Today, 47(9), 1102–1109.*
[DOI: 10.1007/s00595-017-1480-z](https://doi.org/10.1007/s00595-017-1480-z)
► Clinical series detailing recurrence risks and follow-up outcomes.
8. **Choi, J. Y., et al. (2006).**
*Imaging features of solid pseudopapillary tumor of the pancreas on CT and MRI.*
*AJR Am J Roentgenol, 187(2), W333–W338.*
[DOI: 10.2214/AJR.05.1065](https://doi.org/10.2214/AJR.05.1065)
► Describes diagnostic imaging hallmarks for SPTs.
9. **Tang, L. H., et al. (2005).**
*Molecular genetics of solid pseudopapillary tumors: implications for diagnosis and prognosis.*
*Human Pathology, 36(9), 1047–1052.*
[DOI: 10.1016/j.humpath.2005.07.001](https://doi.org/10.1016/j.humpath.2005.07.001)
► Molecular studies focusing on CTNNB1 mutations and nuclear β-catenin.
10. **Sclafani, L. M., et al. (2012).**
*Solid pseudopapillary tumors of the pancreas: current state of diagnosis, management, and future directions.*
*Pancreas, 41(8), 1123–1130.*
[DOI: 10.1097/MPA.0b013e3182571f58](https://doi.org/10.1097/MPA.0b013e3182571f58)
► Comprehensive update with suggested management protocols.
11. **Reid, M. D., et al. (2018).**
*Poorly differentiated solid pseudopapillary neoplasm of the pancreas: a rare but aggressive variant.*
*American Journal of Surgical Pathology, 42(6), 822–832.*
[DOI: 10.1097/PAS.0000000000001045](https://doi.org/10.1097/PAS.0000000000001045)
► Case series on aggressive subtypes and prognostic markers.
12. **Wu, J., et al. (2021).**
*A rare pancreatic tumor in young women: clinical features and prognosis of solid pseudopapillary tumor.*
*Annals of Surgical Oncology, 28(5), 2703–2711.*
[DOI: 10.1245/s10434-020-09134-z](https://doi.org/10.1245/s10434-020-09134-z)
► Modern insights on outcomes and recurrence post-resection.
---
Would you like a **summary table** comparing key points across these studies (e.g., sample size, markers, outcomes)? I can also help build a **mind map for surgical planning** or assist with **critical reading** of a specific paper.
---
***Handling multiple papers?***
Speed up your research with Sider! Our AI-powered sidebar features 10+ one-click tools including a more advanced Search Agent, ChatPDF, context-aware utilities and more to help you work smarter and faster.
[Level up your research game here](https://bit.ly/4aSnMXa)
14/04/2025, 13:17 - Dr.Abdulsalam Med Ed Leads: Here is a **comparative summary table** of 12 key studies on Solid Pseudopapillary Tumors (SPTs), highlighting diagnostic methods, surgical outcomes, and features of aggressive behavior:
| No. | **Study** | **Focus** | **Sample Size** | **Diagnostic Markers** | **Surgical Outcomes** | **Aggressive Features** |
|-----|---------------------------------------|----------------------------|----------------------|--------------------------------------------|------------------------------------------|-------------------------------|
| 1 | Law et al. (2014) | Systematic Review | 292 cases | Imaging, β-catenin | Excellent prognosis with surgery | Rare |
| 2 | Papavramidis & Papavramidis (2005) | Literature Review | 718 cases | Histology, β-catenin | Favorable | 5–10% recurrence |
| 3 | Zhang et al. (2020) | Multicenter Study | 241 patients | Imaging, Histopathology | Very good | Low |
| 4 | Tanaka et al. (2012) | Immunohistochemistry | 28 cases | β-catenin, CD56, CD10 | Not specified | None highlighted |
| 5 | Klimstra et al. (2000) | Histopathological Review | 24 patients | Histology, β-catenin | Excellent | Minimal |
| 6 | Butte et al. (2011) | Laparoscopic Resection | 13 patients | Imaging | Safe and effective | None reported |
| 7 | Zhou et al. (2017) | 10-year Experience | 63 patients | Histopathology | Favorable | 2 recurrences |
| 8 | Choi et al. (2006) | CT & MRI Imaging | 23 patients | Imaging only | Not discussed | Not discussed |
| 9 | Tang et al. (2005) | Molecular Genetics | 19 tumors | CTNNB1 mutation, β-catenin | Not addressed | Not addressed |
| 10 | Sclafani et al. (2012) | Review & Guidelines | Narrative Review | Histology + Imaging | Excellent | Rare |
| 11 | Reid et al. (2018) | Aggressive Variants | 9 cases | Histology | Varied | High in subset |
| 12 | Wu et al. (2021) | Prognosis & Recurrence | 106 cases | Histopathology, Imaging | Excellent, some recurrence | Noted in 7% |
---
### Key Takeaways:
- **Diagnosis**: β-catenin mutation and histopathology are critical across studies. Imaging plays a pivotal role in detection.
- **Surgical Prognosis**: Outcomes are overwhelmingly positive when resection is possible.
- **Aggressive Potential**: Though rare, a minority of cases show recurrence or malignant transformation, requiring follow-up.
Would you like me to build a visual summary or assist with critical interpretation for a specific aspect (e.g., recurrence predictors or treatment guidelines)?
---
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14/04/2025, 13:19 - Rakesh Biswas: Amazing 👏👏
@919604701505 @919652955915 @919171769005 we seem to have finally moved to Web 3.0. Thanks @9647501361306 👏👏
14/04/2025, 13:19 - Dr.Abdulsalam Med Ed Leads: Here's a **visual summary** of key studies on **Solid Pseudopapillary Tumors (SPTs)**:
- **Blue bars** represent the *sample size* of each study.
- **Red line with dots** shows the *percentage of aggressive or malignant cases* reported.
- Notably, **Reid et al. (2018)** stands out with 44% aggressive cases in a small sample (n=9), suggesting variability in tumor behavior and selection bias.
This visualization helps quickly assess the consistency of findings across studies and underscores the overall low malignancy potential in most series.
Let me know if you'd like a version with annotations or tailored for presentation or publication.
---
***Handling multiple papers?***
Speed up your research with Sider! Our AI-powered sidebar features 10+ one-click tools including a more advanced Search Agent, ChatPDF, context-aware utilities and more to help you work smarter and faster.
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14/04/2025, 13:20 - Rakesh Biswas: Can't see the visual
14/04/2025, 13:37 - Dr.Abdulsalam Med Ed Leads: Great! You’ve got the **Audicor® machine**, which is used to assess **left ventricular (LV) function** through *acoustic cardiography*. It combines **heart sounds with ECG** to provide insights into **LV dysfunction, systolic/diastolic performance**, and can be helpful even in low-resource or point-of-care settings.
### 🔧 **Basic Components Identified in Your Kit:**
1. **Audicor handheld sensor** – the main auscultation/ECG device.
2. **Charging adapter and USB cable**.
3. **USB receiver/recorder** – may plug into a PC or mobile device.
4. **Chart of clinical reference values** – color-coded guide for interpreting results (green/yellow/red zones).
---
## 🧭 **How to Use the Audicor Machine** (Step-by-Step):
### 1. **Setup**
- **Charge the device** using the provided adapter.
- Install the **Audicor software or app** on a PC/tablet (if not pre-installed).
- Plug the **USB receiver** into the system to enable data syncing.
### 2. **Patient Preparation**
- Place patient in a **supine or semi-recumbent position**.
- Ensure **quiet surroundings** to minimize ambient noise during auscultation.
### 3. **Device Placement**
- Place the **sensor over the chest**, typically at:
- **V3/V4 location** (for precordial auscultation),
- Or left sternal border (to capture both heart sounds + ECG).
- The device should **make full contact with the skin**—use alcohol swabs to clean and remove oils.
### 4. **Initiate Recording**
- Press the button on the device to **begin a snapshot or monitoring session**.
- Session duration:
- **Snapshot** – quick diagnostic (10–20 seconds).
- **Monitoring** – continuous observation (30–60 seconds or longer).
### 5. **Interpreting the Data**
- The software will **automatically analyze heart sounds + ECG**, generating:
- **LV dysfunction markers (SDI)**,
- **Diastolic dysfunction** indices,
- **Systolic time intervals (EMAT, LVST)**,
- **Graphical waveforms** + *green/yellow/red flags*.
Refer to the **chart on the case lid** to interpret:
- **Green** – Normal
- **Yellow** – Borderline / Monitor
- **Red** – Referral to cardiologist suggested.
---
## 📊 **Key Parameters Displayed**
| Term | Meaning | Red Flag Values |
|------|--------|------------------|
| **SDI** (Systolic Dysfunction Index) | Reflects overall LV systolic function | >7.5 |
| **EMAT%** (Electromechanical Activation Time) | Prolonged values = LV contractility issue | >15% |
| **LVST** (LV Systolic Time) | Shortened time = poor systolic ejection | <300 ms |
| **Diastolic Dysfunction Score** | Composite diastolic markers | Above reference cutoffs |
| **Snapshot vs Monitoring** | Single-point vs Continuous data |
---
## ⚠️ **Important Reminders:**
- **Ensure good skin contact** to avoid noisy/incomplete tracings.
- **Always correlate** with clinical judgment and echocardiography.
- **Red zone readings** should prompt **referral to cardiology**.
- Store and sync data to the **Audicor database** if required.
---
Would you like a **one-page quick-start guide PDF** or a **demo walkthrough video link**? I can help with that too!
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14/04/2025, 13:40 - Dr.Abdulsalam Med Ed Leads: It looks like I'm currently unable to fetch external links or videos directly due to a system limitation. But here's how you can **quickly find a demo walkthrough video** for the **Audicor machine**:
### 🔍 Try searching on:
- **YouTube** using the query:
✅ `Audicor device how to use walkthrough demo`
✅ `Audicor PCG ECG device training`
- **Manufacturer’s site**: [https://www.inovise.com](https://www.inovise.com)
Look under the **support** or **resources** section.
- **YouTube Channel**: Look for content by *Inovise Medical*, the developer of Audicor.
---
### 🚀 Quick Use Guide (Based on Device Layout Seen):
1. **Charge device** using provided USB cable.
2. **Connect to computer** (via USB dongle) or compatible mobile device.
3. **Apply chest sensor patch** to the patient (usually 4th intercostal space mid-clavicular line).
4. **Hold or secure the sensor wand** against the chest at specified positions.
5. Launch **Audicor software** or **app** and follow on-screen guidance.
6. Device simultaneously records **ECG + heart sounds (PCG)**.
7. Results are auto-classified into categories (e.g., LV dysfunction, heart failure risk).
🔴 **Red zone readings** = refer to cardiologist (as seen in the reference chart inside the box).
Would you like me to create a **step-by-step illustrated setup guide** or printable cheat-sheet for your team?
---
***Handling multiple papers?***
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14/04/2025, 15:58 - Dr.Abdulsalam Med Ed Leads: The case shared shows a 50-year-old female presenting with coma and left-sided conjugate eye deviation. The note references hypoactive delirium, which is a form of delirium characterized by reduced motor activity, lethargy, drowsiness, and decreased responsiveness—often making it harder to recognize compared to hyperactive delirium, which presents with agitation and restlessness.
Possible clinical insights:
History of increased alcohol intake (from a quarter to a full bottle of OC per day) suggests the possibility of alcohol-related encephalopathy, hepatic encephalopathy, or alcohol withdrawal syndrome.
The progress note (by Dr. Rakesh Biswas) mentions:
Metabolic encephalopathy (possibly due to hepatic or alcoholic causes)
Hyponatremia
Alcohol dependence
Liver dysfunction (Acute hepatitis, Acute-on-chronic liver disease)
Hypoactive delirium:
It is often underdiagnosed due to its subtle presentation. It can be caused by:
Metabolic disturbances (like hyponatremia, hepatic encephalopathy)
CNS infections
Alcohol-related conditions
In this patient, alcohol dependence, possible liver dysfunction, and metabolic imbalance (likely hyponatremia) could all be contributing to a hypoactive delirium or encephalopathy state, mimicking coma.
Would you like a more detailed explanation of the CNS findings in the note or the approach to altered sensorium in alcohol-dependent patients?
14/04/2025, 16:03 - pajr.in CEO, NHS Endocrinologist: Wernickes!!
14/04/2025, 16:03 - Raveen 2020 Pg Med KIMs: Yes sir 😅
14/04/2025, 16:04 - pajr.in CEO, NHS Endocrinologist: Plenty of wasting in the lower limbs as well, I'm sure she has alcoholic polyneuroapthy too!
14/04/2025, 16:07 - Dr.Abdulsalam Med Ed Leads: Yes! Wernicke's encephalopathy is a key differential here, especially given:
Chronic alcohol use
Acute neurological deterioration
Ophthalmoplegia or conjugate eye deviation
Altered mental status (coma/hypoactive delirium)
Possibly ataxia (though hard to assess in coma)
Classic triad of Wernicke’s:
1. Ophthalmoplegia / nystagmus / conjugate gaze palsies
2. Ataxia
3. Confusion / altered mental status
Even though the full triad is only seen in a minority of patients, suspecting Wernicke's early is crucial, because thiamine deficiency (B1) is the root cause, and it's treatable but often missed.
Management tip:
Always give IV thiamine before glucose in suspected Wernicke's to avoid precipitating or worsening the encephalopathy.
Given her alcohol dependence, liver dysfunction, and current presentation—Wernicke's is a strong contender. Would you want to explore Korsakoff’s psychosis or the transition from Wernicke’s next?
14/04/2025, 21:16 - PaJR Physicist: 2.) We use 2x2025CR lithium primary cells. Not rechargeable. This pair can perform between 80-100 snapshot tests and a 24 hour. In the snapshot mode, i.e. for the 10 second recording, the device wirelessly transmits the signal to the computer that hosts the CC100 software. It's complete with the analysis part, so no need for a cloud connection. The computer has to have a reasonable computing capability with a CPU (core i3+). I now have a chest belt with pre positioned electrodes that gives good conductivity with a drop of ophthalmic saline solution. The belt is sanitised in between patients with a savlon spray and the belt can be washed after about 150-200 patients. In our accelerated testing we've seen it go for around a 150 wash cycles without loss of conductivity or elastic/velcro grip performance. You will be able to see the phonocardiographic trace as data is being acquired and once the patient is rested, just click on the 'acquire' button on screen. The report can be stored in a pdf file for more detailed features to be read, while the first page gives a comprehensive report on the overall status of the heart ( speaking to the patient).
Am happy to get on a zoom/microsoft teams meeting to demo its use.
Also, it would be kind of helpful to take a quick read on the clinical significance and scores with the reference studies published. (Enclosed).
14/04/2025, 21:18 - PaJR Physicist: <Media omitted>
14/04/2025, 21:24 - Rakesh Biswas: @918106096962 @918886202111 @919171769005 and others interested: would be great if you can take this zoom call with @919845031486 to understand how to utilise the device in mapping out the heart sounds of our patients to make them better accessible to collective cognition
14/04/2025, 21:26 - PaJR Physicist: I would definitely feel most comfortable to set the whole system up here with comp and all and ship you the pack to get you started right out of the box?
14/04/2025, 21:32 - Braahmani Bobba 2021 Kims UG: Yes sir, we would be thrilled to learn from you!
14/04/2025, 21:35 - Rakesh Biswas: Any future designs for the mobile phone interface as that would be most convenient?
14/04/2025, 21:50 - PaJR Physicist: Yes, are in process to get that through USFDA. We could probably would get it through with the USFDA designating it as a "breakthrough device". However, it would need a connectivity to the cloud, which maybe a challenge for many regions. This was designed around home use by HF patients to communicate remotely with physicians.
https://www.jacc.org/doi/abs/10.1016/j.jacbts.2022.02.007
14/04/2025, 21:52 - PaJR Physicist: Hopefully, the USFDA does not get into restructuring in the near future.
14/04/2025, 22:00 - ~Mansi MGM Indore UG Nurture Oncology: Let us know sir when can we know about this
15/04/2025, 02:27 - +91 73372 17595 left
15/04/2025, 09:09 - Dr.Abdulsalam Med Ed Leads: Your case describes a **65-year-old male** with **chronic kidney disease (CKD)** presenting acutely with:
- **Inability to close both eyes**
- **Slurred speech**
- **Absent palatal movement**
- **Absent gag reflex**
---
### **Clinical Summary & Concern**
This constellation of signs suggests involvement of **multiple cranial nerves**, especially:
- **Facial nerve (CN VII)** – bilateral inability to close eyes
- **Glossopharyngeal (CN IX)** and **Vagus (CN X)** – absent gag reflex and palatal movement
- Possibly **hypoglossal nerve (CN XII)** – contributing to slurred speech
---
### **Key Differential Diagnoses to Consider:**
| Condition | Notes |
|----------|-------|
| **Guillain-Barré Syndrome (GBS)** – *especially Miller Fisher variant or cranial polyneuritis* | Acute demyelination affecting multiple cranial nerves. Often follows infection. |
| **Brainstem Stroke** | Could cause bilateral CN involvement depending on vascular territory, but less likely without other focal deficits. |
| **Uremic encephalopathy** | In CKD, metabolic encephalopathy can cause slurred speech but usually not focal CN findings like these. |
| **Myasthenia Gravis (MG)** – *especially bulbar variant* | Can present with bilateral cranial weakness, slurred speech, ptosis, and difficulty swallowing. May mimic GBS. |
| **Botulism** | Descending paralysis, cranial nerve involvement early on. Ask about food exposure or wounds. |
| **Bilateral facial nerve palsy due to Lyme, sarcoidosis, or other inflammatory neuropathies** | Consider in endemic regions or if systemic signs present. |
---
### **Initial Investigations:**
- **Neuroimaging**: Urgent **MRI brain** to rule out brainstem lesion or stroke.
- **Nerve conduction studies / EMG**: If GBS or MG suspected.
- **Serum antibodies**: AChR & MuSK (for MG); anti-GQ1b (for Miller Fisher variant).
- **Lumbar puncture**: Look for albuminocytologic dissociation in GBS.
- **Infective panel**: HIV, Lyme, HSV, syphilis – if risk factors present.
---
### **Urgency:**
This is potentially a **neurological emergency**. Bulbar involvement increases risk of aspiration and airway compromise.
**Admit to monitored setting**, consider ICU. Secure airway if needed.
Would you like me to create a diagnostic algorithm or quick summary table for this presentation?
---
***Handling multiple papers?***
Speed up your research with Sider! Our AI-powered sidebar features 10+ one-click tools including a more advanced Search Agent, ChatPDF, context-aware utilities and more to help you work smarter and faster.
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15/04/2025, 09:16 - Dr.Abdulsalam Med Ed Leads: The 65-year-old male with CKD presenting with **bilateral facial weakness (inability to close eyes)**, **slurred speech**, **absent palatal movement**, and **absent gag reflex** likely has a **neuromuscular disorder affecting multiple cranial nerves**. The key considerations are:
### **1. Guillain-Barré Syndrome (GBS) Variant**
- **Pharyngeal-cervical-brachial variant** or **Miller Fisher syndrome** (MFS):
- Bilateral facial weakness (CN VII) and bulbar involvement (CN IX/X) align with these subtypes.
- Areflexia (absent gag reflex) is characteristic of GBS.
- Preceding infection (e.g., Campylobacter, URI) may trigger an autoimmune response.
- **Diagnosis**: Lumbar puncture (elevated CSF protein), nerve conduction studies.
- **Management**: IVIG or plasma exchange; monitor for respiratory failure.
### **2. Brainstem Stroke**
- **Medullary or pontine infarct** (e.g., basilar artery occlusion):
- Acute bilateral cranial nerve deficits (CN VII, IX/X) with possible limb weakness/ataxia.
- Requires emergent MRI/MRA to confirm.
- **Management**: Stroke unit care, thrombolysis if within window.
### **3. Myasthenia Gravis (MG) Crisis**
- Bulbar/facial weakness and dysarthria can occur in myasthenic crisis.
- **Key distinction**: Fatigable weakness, ptosis, diplopia; preserved reflexes.
- **Diagnosis**: Edrophonium test, anti-AChR/MuSK antibodies.
- **Management**: IVIG, plasmapheresis, respiratory support.
### **4. Botulism**
- Descending paralysis with cranial nerve deficits, dilated pupils, and GI symptoms.
- **Diagnosis**: Toxin assay, history of contaminated food.
- **Management**: Antitoxin, supportive care.
### **Evaluation Steps**
- **Imaging**: MRI brain (rule out stroke, brainstem lesions).
- **Labs**: Electrolytes (exclude uremia/hyperkalemia), CK, ABG, Lyme/botulism testing if indicated.
- **Neurophysiology**: Nerve conduction studies (GBS), EMG (MG).
### **CKD Considerations**
- Uremic neuropathy is less likely (typically symmetric sensorimotor deficits).
- CKD increases infection risk (trigger for GBS) and alters drug clearance (adjust IVIG/plasmapheresis).
**Most Likely Diagnosis**: **Guillain-Barré Syndrome** (pharyngeal-cervical-brachial variant). Urgent neurology consultation and respiratory monitoring are critical. DeepSeek Generated Response.
15/04/2025, 09:16 - Dr.Abdulsalam Med Ed Leads: Which response do you prefer?
15/04/2025, 09:39 - Rakesh Biswas: While both are close deep seek appears better! 👏
While the above is human in the loop Web 3.0 @919604701505 we had an interesting Web 2.0 session with the same patient in another case based platform CBBLE where we plugged in and our other students who are there such as @919171769005 @918106096962 can gather how these two different approaches stand out and they may consider adding it to the chapters under construction
15/04/2025, 09:44 - +91 93907 34510 left
15/04/2025, 10:07 - ~Mansi MGM Indore UG Nurture Oncology: Its difficult to choose either of the response.. Both of them are good!
15/04/2025, 10:08 - PaJR Physicist: <Media omitted>
15/04/2025, 10:09 - ~Mansi MGM Indore UG Nurture Oncology: What prompt did you give?
15/04/2025, 10:09 - ~Mansi MGM Indore UG Nurture Oncology: This is awesome!
15/04/2025, 10:13 - PaJR Physicist: For some reason, USFDA has gone silent. CDSCO is still trying to figure out whether EKG and Ascultation is a Class A or Class C. Class C?? Why??
15/04/2025, 10:14 - You changed the group name from "Collective medical cognition bridging bedside and bench through NMC driven E logs" to "Narketpally Collective medical cognition bridging bedside and bench"
15/04/2025, 10:22 - PaJR Physicist: Just added a line to provide a rule out strategy, I guess..
15/04/2025, 10:51 - +91 70137 56375 left
15/04/2025, 11:12 - MD.AKRAM Kolkata Medical College Intern: Multiple Seborrheic Keratoses
,autosomal dominant inheritance in some families.,Strongly supports a hereditary pattern.
15/04/2025, 11:15 - Dr.Abdulsalam Med Ed Leads: Thanks for sharing the image and clinical context. Based on the distribution, appearance, and family history, this presentation is highly suggestive of seborrheic keratoses, possibly associated with familial multiple seborrheic keratoses.
Key features supporting this:
Multiple brown to dark, waxy, verrucous lesions.
Gradual onset over decades.
Strong family history (father and brother also affected).
Lesions are benign and commonly found on the trunk.
These lesions are benign and typically do not require treatment unless for cosmetic reasons or if there's irritation. However, if any lesion shows rapid change, ulceration, or bleeding, a biopsy may be indicated to rule out malignancy.
Differentials to consider (though less likely here due to the history):
Neurofibromatosis (especially NF1 – but these lack neurofibromas or café-au-lait macules).
Epidermal nevi (more linear or localized and congenital).
Basal cell nevus syndrome (would show other systemic signs).
Would you like a template for documentation or counseling points for the patient and family?
15/04/2025, 11:27 - Dr.Abdulsalam Med Ed Leads: The presentation of a 61-year-old man with gradually erupting skin spots over decades, alongside a family history in his father and brother, strongly suggests an **autosomal dominant genodermatosis**. Below is a structured analysis of the likely differential diagnoses and recommendations:
---
### **Most Likely Diagnosis**
1. **Neurofibromatosis Type 1 (NF1)**
- **Key Features**: Café-au-lait macules (flat, pigmented spots), axillary/groin freckling, neurofibromas (benign tumors), and Lisch nodules.
- **Rationale**: NF1 is autosomal dominant and commonly presents with skin lesions that develop progressively. Neurofibromas often appear in adulthood, aligning with the timeline of "gradual eruption over decades." Family history supports this diagnosis.
- **Note**: Café-au-lait spots typically emerge in childhood, but neurofibromas may develop later. Absence of systemic features (e.g., skeletal abnormalities, optic gliomas) does not exclude NF1.
---
### **Other Considerations**
2. **Birt-Hogg-Dubé Syndrome**
- **Key Features**: Fibrofolliculomas (skin-colored papules on the face/neck), lung cysts, and renal tumors.
- **Rationale**: Autosomal dominant; lesions often appear in adulthood. Family history and gradual onset fit, but association with systemic findings (e.g., pneumothorax) should be evaluated.
3. **Familial Atypical Multiple Mole Melanoma Syndrome (FAMMM)**
- **Key Features**: Numerous atypical nevi, increased melanoma risk.
- **Rationale**: Autosomal dominant (germline CDKN2A mutation). Lesions are pigmented and may develop over time. Family history of melanoma would strengthen this diagnosis.
4. **Brooke-Spiegler Syndrome**
- **Key Features**: Trichoepitheliomas and cylindromas (skin-colored nodules on the head/neck).
- **Rationale**: Autosomal dominant; lesions may be mistaken for "spots" if small. Typically benign but can be disfiguring.
5. **Hereditary Leiomyomatosis and Renal Cell Cancer (HLRCC)**
- **Key Features**: Cutaneous leiomyomas (painful, firm papules), uterine fibroids, renal cancer.
- **Rationale**: Autosomal dominant; skin lesions may present in adulthood. Painful lesions are a key clue.
---
### **Evaluation Recommendations**
- **Clinical Examination**: Assess lesion morphology (color, texture, distribution), presence of systemic signs (e.g., Lisch nodules, mucosal involvement).
- **Skin Biopsy**: To differentiate between neurofibromas, fibrofolliculomas, or other histologic patterns.
- **Imaging/Genetic Testing**:
- **NF1**: Genetic testing for *NF1* mutation.
- **Birt-Hogg-Dubé**: Chest CT (lung cysts), renal imaging, *FLCN* gene testing.
- **FAMMM**: Dermatoscopic evaluation of nevi, *CDKN2A* testing.
- **Family Screening**: Encourage genetic counseling and evaluation of relatives.
---
### **Conclusion**
**Neurofibromatosis Type 1** is the leading diagnosis, but further evaluation is critical to exclude other familial syndromes. A multidisciplinary approach (dermatology, genetics, oncology) is recommended for comprehensive management. This is DeepSeek Response depending on the text only (could not upload the photo)
15/04/2025, 11:35 - Sadhana Sharma Nri Med: Though both are good, Deep seek appears more humanly.
15/04/2025, 16:38 - Rakesh Biswas: @919100290270 can you share the Dermatology department's impression on this patient we saw in the OPD today. The patient is currently staying as an attendant in SS ward so you or your duty colleague can just visit their ward and check what impression they have given in their ticket.
If you recall our diagnosis of this was cherry angiomas
15/04/2025, 16:39 - Rakesh Biswas: We thought these were cherry angiomas
15/04/2025, 19:46 - ~Mansi MGM Indore UG Nurture Oncology: Keep us posted sir! If you get to know the final diagnosis
15/04/2025, 19:57 - Rakesh Biswas: Hope to meet him again in the hospital tomorrow and finalize
15/04/2025, 21:27 - Dr.Abdulsalam Med Ed Leads: Yes, the lesions seen in the image are consistent with cherry angiomas. These are common benign vascular skin lesions that appear as:
Small, round to oval papules
Bright red to purple in color
Typically appear on the trunk but can occur anywhere on the body
Usually increase in number and size with age
From the image, multiple scattered reddish papules are seen on the trunk and upper arm, which supports the diagnosis.
However, it's always good practice to:
Confirm via dermatoscopic examination if there’s diagnostic uncertainty
Biopsy if there's rapid change in size, color, or bleeding, to rule out other vascular or malignant lesions
Would you like to go over differential diagnoses or management strategies for teaching purposes?
This is Scholar ChatGPT response to the question? Could it be cherry angioma and sharing the photo with trunkal lesions
15/04/2025, 21:28 - Dr.Abdulsalam Med Ed Leads: Great! Here's a concise but useful breakdown you can use for teaching 3rd-year medical students during a clinical session or PPDP.
---
Cherry Angioma – Teaching Points
1. Definition:
Cherry angiomas (aka senile angiomas or Campbell de Morgan spots) are benign capillary proliferations commonly seen in adults, especially over age 30.
---
2. Clinical Features:
---
3. Differential Diagnoses:
---
4. Dermoscopy (Optional for Clinical Sessions):
Red to reddish-blue "lagoons" (clusters of dilated capillaries)
---
5. Management:
No treatment required if asymptomatic and diagnosis is clear.
Options if removal is desired (for cosmetic or symptomatic reasons):
Electrocautery
Cryotherapy
Laser therapy (e.g., pulsed dye laser)
Shave excision for histopathological confirmation if suspicious
---
6. When to Worry:
Biopsy or referral if:
Sudden rapid increase in number or size
Irregular borders or color changes
Ulceration or spontaneous bleeding
---
Would you like this converted into a handout/slide for your next Zoom session? I can also include a quiz-style case vignette.
16/04/2025, 00:29 - Poreddy Jahnavi Kims PG 2024: Derma opinion:
Multiple erythematous sessile papules, few hypopigmented pedunculated papules noted in abdomen, back,
B/L UL , LL
Diagnosis: Cherry angiomas+ acrochordons
Advised: RBS, RFT, CXR, USG ABD AND PELVIS(reported as hemangioma of liver)
16/04/2025, 06:16 - Rakesh Biswas: Thanks
So I guess we'll take the diagnosis to be Cherry angiomas for now @919171769005
16/04/2025, 09:54 - +91 96660 84876 joined from the community
16/04/2025, 09:57 - Dr.Abdulsalam Med Ed Leads: <Media omitted>
16/04/2025, 09:57 - Rakesh Biswas: You deleted this message
16/04/2025, 09:59 - Rakesh Biswas: 👆@918074725352 hope the text above doesn't contain any patient identifiers?
16/04/2025, 10:00 - Patient Advocate 56F Migraine Hypothyroidism 2000: No
16/04/2025, 10:00 - Rakesh Biswas: Thanks!
Will YouTube this today after preparing the case report to go along with it
16/04/2025, 10:00 - Patient Advocate 56F Migraine Hypothyroidism 2000: Painful area
16/04/2025, 10:01 - Patient Advocate 56F Migraine Hypothyroidism 2000: Right hand is painful and has become pale
16/04/2025, 10:07 - Dr.Abdulsalam Med Ed Leads: The symptoms you described—pain and paleness in the right hand—could indicate reduced blood flow, which may be caused by conditions such as acute limb ischemia, Raynaud's phenomenon, or thrombosis. These are serious and require **immediate medical attention** to prevent complications like tissue damage.
### Recommended Actions:
1. **Seek emergency care immediately** to assess blood flow and rule out critical issues like a blood clot or arterial blockage.
2. Avoid using the hand until evaluated.
3. Do not ignore the symptoms, as delays can worsen outcomes.
The file details (e.g., device name, date) appear unrelated to the medical issue and may be incidental (e.g., a photo taken with a Xiaomi Redmi Note 11 Pro+ 5G with an incorrect date setting). Prioritize urgent medical evaluation. DeepSeek Response.
16/04/2025, 10:11 - Patient Advocate 56F Migraine Hypothyroidism 2000: Will inform the PA Doctor <This message was edited>
16/04/2025, 10:14 - Dr.Abdulsalam Med Ed Leads: That’s a good step. When informing the Physician Assistant (PA), ensure you clearly describe:
- **The sudden onset** of pain and paleness.
- **Duration** of symptoms (how long the hand has been pale/painful).
- Any **additional symptoms** (e.g., numbness, coldness, weakness, or color changes).
The PA will likely check for **pulses, capillary refill, and sensation** and may order urgent tests (e.g., Doppler ultrasound) to assess blood flow. Early intervention is critical—do not delay evaluation. Wishing you prompt care and relief!
16/04/2025, 11:05 - Dr.Abdulsalam Med Ed Leads: The case involves a 45-year-old male with **progressive paraplegia over one week**, **no sensory loss**, and **no bowel/bladder involvement**. Key considerations and next steps are as follows:
### **Differential Diagnosis**
1. **Compressive Myelopathy**
- **Epidural hematoma, tumor, or abscess**: Rapidly progressive motor deficits may occur with spinal compression. Thoracic lesions can spare sensory/autonomic functions initially.
- **Imaging Priority**: Urgent MRI spine (with contrast) to rule out structural lesions.
2. **Inflammatory Myelitis**
- **Transverse myelitis or NMOSD**: May present with predominant motor involvement. Atypical but possible if inflammation spares sensory tracts.
- **CSF analysis** and **autoimmune markers** (e.g., anti-AQP4 for NMOSD) required if MRI suggests inflammation.
3. **Vascular Causes**
- **Anterior spinal artery infarction**: Unlikely due to absent sensory loss (typically involves spinothalamic tracts), but small infarcts may rarely present atypically.
- **Vascular malformations (AVM, dural fistula)**: May cause venous congestion with progressive deficits. Consider MR/CT angiography.
4. **Motor Neuron Disease**
- **ALS/PLS**: Rapid progression is atypical, but upper motor neuron signs (hyperreflexia, spasticity) may suggest this. Typically chronic; exclude structural causes first.
### **Diagnostic Workup**
1. **Immediate MRI Spine**
- **Entire spinal cord** (with and without contrast) to assess for compression, myelitis, or infarction.
- **Thoracic spine focus**: Paraplegia localizes to thoracic or higher cord levels.
2. **Neurological Exam**
- Assess for **upper motor neuron signs** (hyperreflexia, Babinski) vs. **lower motor neuron signs** (flaccidity, hyporeflexia).
- Evaluate for subtle sensory or autonomic involvement missed initially.
3. **CSF Analysis**
- If MRI is negative or shows myelitis: Check for pleocytosis, oligoclonal bands, IgG index, and infectious agents.
4. **Blood Tests**
- **Inflammatory markers** (ESR, CRP), **autoimmune panels** (ANA, anti-AQP4, anti-MOG), **infectious serologies** (HIV, HTLV-1), **B12**, and **paraneoplastic antibodies**.
5. **Vascular Imaging**
- MR/CT angiography if vascular malformation or infarction is suspected.
### **Management**
- **Neurosurgical Emergency**: If MRI reveals compression (e.g., hematoma, tumor), urgent decompression is critical.
- **IV Steroids/Plasma Exchange**: For inflammatory myelitis (e.g., transverse myelitis, NMOSD).
- **Anticoagulation/Aortic Evaluation**: If spinal cord infarction is confirmed (rare without sensory loss).
- **Rehabilitation**: Early physiotherapy to preserve function, regardless of etiology.
### **Conclusion**
**Urgent spinal MRI is paramount** to exclude compressive lesions requiring surgery. If imaging is negative, inflammatory, vascular, or atypical metabolic causes should be pursued. Rapid diagnosis and intervention are crucial to preserve neurological function. [DeepSeek]
16/04/2025, 11:46 - Dr.Abdulsalam Med Ed Leads: This message was deleted
16/04/2025, 12:44 - Dr.Abdulsalam Med Ed Leads: ## Clinical Summary
A 45-year-old male presents with **progressive paraplegia over one week**, but **no sensory loss** and **no bowel or bladder involvement**.
## Differential Diagnosis Considerations
The clinical picture is notable for:
- Progressive weakness (paraplegia) affecting both legs
- Absence of sensory deficits
- No disturbance of bowel or bladder function
This constellation of findings is unusual for most spinal cord pathologies, as these often involve sensory changes and/or autonomic dysfunction (bowel/bladder involvement), especially when the motor deficit is severe and progressive.
## Key Differential Diagnoses
### 1. **Hereditary Spastic Paraplegia (HSP)**
- **Description:** HSP is a group of inherited neurodegenerative disorders characterized by progressive spasticity and weakness (paraplegia) of the lower limbs.
- **Sensory and Autonomic Involvement:** In the *pure* forms of HSP, there is typically no sensory loss and bowel/bladder function is often preserved, especially early in the disease[5]. Variable mild urinary disturbances can occur, but severe involvement is rare and usually develops late[3][5].
- **Progression:** The progression is usually slow over years, but subacute worsening can occasionally be seen.
- **Supporting Features:** The absence of sensory and autonomic involvement is a hallmark of pure HSP[5].
### 2. **Primary Lateral Sclerosis (PLS)**
- **Description:** PLS is a rare motor neuron disorder that affects upper motor neurons, leading to progressive spasticity and weakness, usually starting in the legs.
- **Sensory and Autonomic Involvement:** Sensory function and sphincter control are typically preserved.
- **Progression:** Progression is usually slow, but can be subacute in some cases.
### 3. **Structural Spinal Cord Lesions (e.g., Tumor, Abscess, Hematoma)**
- **Description:** Most compressive or infiltrative lesions (tumors, abscesses, hematomas) of the spinal cord cause both motor and sensory deficits, and often bowel/bladder dysfunction, especially if the lesion is severe enough to cause paraplegia[1][6].
- **Against Diagnosis:** The absence of sensory and autonomic involvement makes these less likely.
### 4. **Functional (Conversion) Disorder**
- **Description:** Functional neurological disorders can present with motor deficits without objective findings on examination or imaging.
- **Against Diagnosis:** Progressive course over a week is less typical.
## Diagnostic Approach
Given the rapid progression (over one week), hereditary or degenerative conditions like HSP or PLS are less likely, as they usually progress over months to years. However, rare subacute presentations have been described.
Most acquired causes of paraplegia (e.g., transverse myelitis, spinal cord infarction, trauma, compressive lesions) would almost always involve sensory changes and/or bowel/bladder dysfunction[1][6][7].
## Summary Table: Key Features
| Diagnosis | Motor | Sensory | Bowel/Bladder | Typical Course |
|---------------------------------|-------|---------|---------------|------------------|
| Hereditary Spastic Paraplegia | + | - | -/mild late | Slow, rare rapid |
| Primary Lateral Sclerosis | + | - | - | Slow |
| Spinal Cord Compression | + | + | + | Acute/subacute |
| Functional Disorder | + | - | - | Variable |
## Conclusion
**The most likely diagnosis is a pure upper motor neuron syndrome such as Hereditary Spastic Paraplegia (HSP) or Primary Lateral Sclerosis (PLS), given the absence of sensory and autonomic involvement.** However, the rapid progression over one week is atypical and warrants urgent neuroimaging to rule out a compressive or inflammatory spinal cord lesion, even if sensory and autonomic symptoms are absent[1][6]. If imaging is negative, consideration should be given to rare presentations of HSP/PLS or functional neurological disorder[5].
**Key next step:** Urgent MRI of the spine to exclude compressive or inflammatory causes. If negative, consider genetic and neurophysiological testing for HSP/PLS.
Sources
[1] Paraplegia: Definition, Causes, Symptoms, Types & Treatment https://my.clevelandclinic.org/health/symptoms/23984-paraplegia
[2] Progressive supranuclear palsy as differential diagnosis of ... - Elsevier https://www.elsevier.es/es-revista-revista-espanola-geriatria-gerontologia-124-articulo-progressive-supranuclear-palsy-as-differential-S0211139X19300721
[3] Bladder dysfunction in hereditary spastic paraplegia: a clinical and ... https://www.nature.com/articles/sc2011193
[4] Bladder dysfunction in spinal tuberculosis: clinical, urodynamic and ... https://www.nature.com/articles/sc2009199
[5] HEREDITARY SPASTIC PARAPLEGIA DUE TO NIPA1 GENE ... http://www.scielo.org.co/scielo.php?script=sci_arttext&pid=S2462-85222022000100032
[6] Traumatic Paraplegia - Physiopedia https://www.physio-pedia.com/Traumatic_Paraplegia
[7] Neurogenic Bladder: Overview, Neuroanatomy, Physiology and ... https://emedicine.medscape.com/article/453539-overview
[8] Neurogenic Bladder and Neurogenic Lower Urinary Tract Dysfunction https://www.ncbi.nlm.nih.gov/books/NBK560617/
[9] Paraplegia - an overview | ScienceDirect Topics https://www.sciencedirect.com/topics/medicine-and-dentistry/paraplegia
[10] Progressive Lower Extremity Weakness and Axonal Sensorimotor ... https://pmc.ncbi.nlm.nih.gov/articles/PMC4620279/
[11] Clinical Features and Genetic Spectrum of Patients With ... - Frontiers https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2022.872927/full
[12] Spinal Cord Injuries - StatPearls - NCBI Bookshelf https://www.ncbi.nlm.nih.gov/books/NBK560721/
[13] Spinal Cord Injury (SCI) - Bladder and Bowel Function - Wellspect https://www.wellspect.co.uk/education/articles/spinal-cord-injury/
[14] Hereditary Spastic Paraplegia Overview - GeneReviews - NCBI https://www.ncbi.nlm.nih.gov/books/NBK1509/
[15] Bladder Management in Spinal Cord Injury - Physiopedia https://www.physio-pedia.com/Bladder_Management_in_Spinal_Cord_Injury
[16] Cauda Equina Syndrome - Physiopedia https://www.physio-pedia.com/Cauda_Equina_Syndrome
[17] Spastic Paraplegia - an overview | ScienceDirect Topics https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/spastic-paraplegia
[18] Monoplegia - an overview | ScienceDirect Topics https://www.sciencedirect.com/topics/neuroscience/monoplegia
[19] Spastic Paraplegia - an overview | ScienceDirect Topics https://www.sciencedirect.com/topics/nursing-and-health-professions/spastic-paraplegia
[20] Central Cord Syndrome - Physiopedia https://www.physio-pedia.com/Central_Cord_Syndrome
(perplexity)
16/04/2025, 12:46 - Dr.Abdulsalam Med Ed Leads: Here’s one way to frame it academically:
>A 45‐year‐old male presents with a one‐week history of progressively worsening paraplegia that is confined exclusively to motor impairment, with intact sensory function and preserved bowel and bladder control.
This formulation provides a concise yet detailed clinical description suitable for academic or professional contexts.
To expand further—if you’re discussing differential diagnoses in a case discussion, for instance, you might add:
>Such a presentation suggests a selective involvement of the motor pathways, prompting consideration of diagnoses such as primary lateral sclerosis or a focal myelopathic process sparing the dorsal columns and autonomic fibers.
This additional sentence deepens the clinical reasoning and encourages further exploration of potential etiologies without overextending beyond the initial presentation.(Copilot)
16/04/2025, 12:48 - Dr.Abdulsalam Med Ed Leads: Below is an academic discussion of the differential diagnoses for a 45‐year‐old male presenting with a one‐week history of progressive paraplegia characterized by pure motor weakness without accompanying sensory or autonomic disturbances:
1. **Acute Motor Axonal Neuropathy (AMAN) Variant of Guillain‑Barré Syndrome:**
This variant represents a form of Guillain‑Barré syndrome where the immune-mediated process selectively targets motor fibers, leading to rapid-onset weakness with sparing of sensory modalities. The typical clinical course and absence of sensory loss make this an important consideration in cases of acute pure motor weakness.
2. **Spinal Cord Infarction with Selective Involvement of Motor Tracts:**
Although classical anterior spinal artery syndrome entails both motor deficits and loss of pain and temperature sensation, a more focal ischemic event that primarily affects the lateral corticospinal tracts could potentially result in an isolated motor deficit. Differentiating this entity usually requires careful neuroimaging and clinical correlation.
3. **Compressive Myelopathy (e.g., Spinal Epidural Hematoma or Intradural Tumor):**
A focal compressive lesion may preferentially impinge on the anterior aspects of the spinal cord where the corticospinal tracts reside, thereby producing predominantly motor deficits. While such lesions often generate associated pain and sometimes minor sensory alterations, early or focal compression might initially spare sensory and autonomic functions. MRI evaluation is critical for clarifying this possibility.
4. **Acute Transverse Myelitis (Motor-Predominant Variant):**
Transverse myelitis generally presents with a combination of motor, sensory, and autonomic involvement. However, rare variants may predominantly affect motor pathways. This possibility should be entertained, although the classic presentation typically includes a sensory level and bowel or bladder dysfunction.
5. **Early Onset of a Motor Neuron Disease (e.g., Primary Lateral Sclerosis):**
While primary lateral sclerosis (PLS) is generally characterized by a slow, insidious onset of upper motor neuron signs, atypical presentations with a more rapid progression cannot be entirely excluded. Nonetheless, an acute one‑week progression is uncommon in such neurodegenerative conditions.
Each of these conditions would be pursued with appropriate investigations. Neuroimaging (especially MRI) is essential for identifying structural lesions or infarction, while electrophysiological studies and cerebrospinal fluid analysis can help distinguish between demyelinating and primary neurodegenerative processes.
Considering the differential, further evaluations—including a detailed neurological exam with reflex testing, nerve conduction studies, and possibly early imaging—are crucial for reaching a definitive diagnosis.
---
Would you like to explore additional nuances regarding the diagnostic evaluations or the pathophysiological mechanisms underlying these conditions?(Copilot)
16/04/2025, 12:48 - +91 93207 64466: This message was deleted
16/04/2025, 13:07 - Dr.Abdulsalam Med Ed Leads: <Media omitted>
16/04/2025, 13:23 - Dr.Abdulsalam Med Ed Leads: <Media omitted>
16/04/2025, 16:53 - Rakesh Biswas: Adding the Web 2.0 transcripts for this same patient done this morning from the peaky healers group. Can providing this back to Web 3.0 along with the newer data points that emerge in the conversational transcripts make it generate a closer diagnosis @919604701505 :
[16/04, 10:44] cm : OPD right now: 45M with progressive paraplegia since one week. No sensory loss and bowel bladder involvement
[16/04, 10:56]HU2: What abt Reflexes, any h/o repeated URTi?
Is orientation normal or altered?
[16/04, 11:47]HU2: Any Band like sensation ?? ....
[16/04, 15:00] cm : No sensory symptoms
[16/04, 15:01]cm: What are the features visible in the video that may have arose the suspicion of GBS?
[16/04, 15:01]cm: Reflexes are absent
Slightly disoriented
[16/04, 15:04] HU 2: Wht abt Electrolyte and Vit B12 levels?
[16/04, 15:05) cm: This was an OPD evaluation done today
[16/04, 15:09]HU3: ALS ?? ... As it is a pure motor syndrome
[16/04, 15:41]cm: What would be the specific CNS signs of ALS that this patient doesn't have?
[16/04, 15:42] HU3: Bulbar palsy ?
[16/04, 16:07]cm: Yes let's say UMN involvement is necessary along with LMN to call it ALS in general isn't it?
[16/04, 16:14]HU 3: Yes sir
[16/04, 16:26] cm: Clinically on CNS examination we also found he has cerebellar signs other than his peripheral neuropathy features
16/04/2025, 16:53 - Rakesh Biswas: @919640006934 please share his deidentified MRI images and video asap
16/04/2025, 17:03 - Dr.Abdulsalam Med Ed Leads: **Updated Diagnosis & Approach Integrating New Data**
The additional clinical details and discussion from the transcripts refine the differential diagnosis and highlight critical next steps:
---
### **Key New Clinical Findings**
1. **Absent reflexes** (lower motor neuron/LMN sign).
2. **Cerebellar signs** (e.g., ataxia, dysmetria).
3. **Slight disorientation** (encephalopathy).
4. **Peripheral neuropathy features**.
5. **No sensory loss** persists.
---
### **Revised Differential Diagnosis**
#### **1. Metabolic Deficiencies**
- **B12 or Copper Deficiency**:
- Both can cause **combined CNS/PNS involvement**:
- **B12**: Subacute combined degeneration (posterior/lateral spinal cord + peripheral neuropathy), encephalopathy, rare cerebellar ataxia.
- **Copper**: Myelopathy, neuropathy, cerebellar signs.
- **Next Steps**: Urgent serum B12, methylmalonic acid, homocysteine, copper/ceruloplasmin.
#### **2. Paraneoplastic Syndrome**
- **Anti-CRMP5, Anti-Ma2, Anti-Yo antibodies**:
- May cause **encephalomyelitis, cerebellar degeneration, and peripheral neuropathy**.
- Associated with lung, breast, or testicular cancers.
- **Next Steps**: Paraneoplastic antibody panel, CT/PET for occult malignancy.
#### **3. Inflammatory/Autoimmune**
- **Acute Disseminated Encephalomyelitis (ADEM)**:
- Post-infectious autoimmune demyelination affecting brain, spinal cord, and nerves.
- **Neuromyelitis Optica Spectrum Disorder (NMOSD)**:
- Atypical if purely motor, but cerebellar signs may suggest brainstem involvement.
- **Next Steps**: MRI brain/spine, CSF analysis (oligoclonal bands, IgG index).
#### **4. Guillain-Barré Syndrome (GBS) Variants**
- **Acute Motor Axonal Neuropathy (AMAN)**:
- Pure motor involvement with areflexia.
- **Atypical features**: Cerebellar signs and encephalopathy suggest overlap with **Bickerstaff encephalitis** (GBS + brainstem involvement).
- **Next Steps**: Nerve conduction studies/EMG, anti-ganglioside antibodies (e.g., anti-GQ1b).
#### **5. Toxic/Nutritional**
- **Alcohol, Chemotherapy, or Toxins**:
- Chronic alcohol use → cerebellar degeneration + neuropathy.
- **Next Steps**: Toxicology screen, dietary history.
#### **6. Hereditary Disorders**
- **Spinocerebellar Ataxia (SCA) with neuropathy**:
- Unlikely given acute onset, but genetic testing if chronicity is unclear.
---
### **Critical Workup**
1. **Imaging**:
- **MRI Brain/Spine (with contrast)**: Assess for demyelination (ADEM, NMOSD), cerebellar lesions, or spinal cord compression.
2. **Lab Tests**:
- **Metabolic**: B12, copper/ceruloplasmin, electrolytes, LFTs.
- **Inflammatory/Infectious**: CRP, ESR, HIV, syphilis serology.
- **Autoimmune/Paraneoplastic**: ANA, anti-AQP4, anti-MOG, paraneoplastic panel.
3. **CSF Analysis**:
- Cell count, protein, IgG index, oligoclonal bands, cytology.
4. **Neurophysiology**:
- **EMG/NCS**: Confirm peripheral neuropathy vs. anterior horn cell involvement (ALS).
---
### **ALS Revisited**
- **Red flags against ALS**:
- Cerebellar signs (not part of ALS).
- Absent reflexes (suggests LMN dominance; ALS requires UMN + LMN signs).
- Acute progression (ALS typically subacute/chronic).
---
### **Immediate Management**
- **Empirical B12/Thiamine supplementation** pending lab results.
- **IVIG/Plasma Exchange**: If GBS/ADEM is suspected.
- **Steroids**: Hold until infection/neoplasm ruled out.
- **Neurosurgery Consult**: If MRI reveals compressive lesion.
---
### **Conclusion**
The combination of **cerebellar signs, LMN-predominant paraplegia, and encephalopathy** prioritizes **metabolic (B12/copper deficiency)**, **paraneoplastic**, or **inflammatory (ADEM)** etiologies. Urgent MRI and metabolic labs are critical. ALS is less likely given the atypical features.
16/04/2025, 18:05 - Rakesh Biswas: Thanks.
@919640006934 did they return back to you with the MRI report?
16/04/2025, 18:26 - ~Mansi MGM Indore UG Nurture Oncology: Sir which software is this?
16/04/2025, 18:31 - ~Mansi MGM Indore UG Nurture Oncology added ~ Harshita Agarwal, ~ Lekhana and ~ Mohammad Orooj Azmi
16/04/2025, 18:39 - ~Mansi MGM Indore UG Nurture Oncology added Yousra Nurture Oncology
16/04/2025, 18:49 - Dr.Abdulsalam Med Ed Leads: Not yet
16/04/2025, 18:50 - ~Mansi MGM Indore UG Nurture Oncology: @919123761825 @919831249909 @919113602031 @917075040647
Please don't get overwhelmed by the number of new groups 😅 but these will give you a better understanding of the PaJR and CBBLE workflow.
This system helps patients track their journeys and is uploaded on a common base accessible via blog spots and links shared by @919121046928. PaJR groups can be created by anyone, even you guys via the website.
Feel free to ask any doubts regarding the workflow. (dm me or here in the group or to @919121046928 or @919652955915 or @919604701505 sir.)
We would be documenting the workflow in the projects discussed in the book proposal group. These are also the base of the book chapters of the workshop proceedings.
16/04/2025, 18:52 - Dr.Abdulsalam Med Ed Leads: This is cherry angioma's mind map <This message was edited>
16/04/2025, 18:52 - ~Mansi MGM Indore UG Nurture Oncology: Okay, sir. Generated using?
16/04/2025, 18:52 - ~Mansi MGM Indore UG Nurture Oncology: Google collab?
16/04/2025, 18:52 - ~Mansi MGM Indore UG Nurture Oncology: Spider web?
16/04/2025, 18:52 - Dr.Abdulsalam Med Ed Leads: NotebookLM last update
16/04/2025, 18:59 - Rakesh Biswas: @919347505324 @916302536191 what's the update of this patient?
16/04/2025, 20:54 - Dr.Abdulsalam Med Ed Leads: Not yet
16/04/2025, 22:33 - Anonymous Pm: We have asked him again,in lateral decubitus position,while closing his eyes,he said he was lying down (there just seems to be momentary confusion due to head end elevation)
16/04/2025, 22:59 - Dr.Abdulsalam Med Ed Leads: Or maybe due to visual vestibular mismatch
16/04/2025, 23:28 - Dr.Abdulsalam Med Ed Leads: <Media omitted>
16/04/2025, 23:31 - Dr.Abdulsalam Med Ed Leads: spinal cord syndromes mindmaps
16/04/2025, 23:33 - MD.AKRAM Kolkata Medical College Intern: Resend please sir
16/04/2025, 23:33 - MD.AKRAM Kolkata Medical College Intern: Download forget show me.
16/04/2025, 23:33 - MD.AKRAM Kolkata Medical College Intern: Mind map.
17/04/2025, 07:09 - Rakesh Biswas: Yesterday's patient's clinical findings were suggestive of peripheral neuropathy with cerebellar involvement and in the MRI we are expecting predominantly cerebellar findings. Let's hope we shall be able to retrieve the MRI images today
17/04/2025, 07:10 - Rakesh Biswas: I meant how is he now?
17/04/2025, 07:11 - Rakesh Biswas: 👏👏
17/04/2025, 07:14 - Rakesh Biswas: From this input, one thought around the only disadvantage of current Web 3.0 tools as they are trained and modelled now is that they tend to promote over-testing and overtreatment and this is surely another medical cognition project to be addressed by retraining AI models and also speaks volumes about how current available published literature is key to promoting the over-testing and overtreatment bias?
17/04/2025, 09:13 - Dr.Abdulsalam Med Ed Leads: AI can't fabricate from it's self , it just collect data about every word in our prompt, and respond accordingly, nowadays it's in the process of responding according to hints and concepts and ignoring distracters the way human do in their practice. But there's a chance to miss some diagnoses because not all presentations fit certain patterns as we do from time to time ( as when report that as case report).
17/04/2025, 09:32 - Rakesh Biswas: Absolutely agree!
It's not a fabrication bias or a tendency to fabricate aka hallucinate that is the current issue.
It's the training data set fed to AI that is already ridden with bias towards over testing!
17/04/2025, 10:37 - Rakesh Biswas: Looking forward to @9647501361306 incorporating this Web 2.0 feedback from another CBBLE (cable) to drive and reshape the previous Web 3.0 outputs for this individual patient's overall benefits👇
https://pajrcasereporter.blogspot.com/2025/04/24f-retroperitoneal-tumor-severe-anemia.html?m=1
[17/04, 09:59]: Sir in 24/f retroperitoneal mass pt, oncology opinion for surgical resection ?
[17/04, 10:03]cm: Oncology opinion for medical management of this rare variety of pancreatic tumor. Check out the web 3.0 discussion in the Narketpally collective group for medical management.
Surgical oncology comes every Wednesday to Narketpally and has already seen the patient here yesterday! He can review her CT abdomen.
[17/04, 10:08]: But sir, surgery remains main stay
[17/04, 10:11]cm: Alright medical management also means doing nothing.
Check out what was the difference in overall outcomes between the surgical intervention group vs the non surgical intervention group by looking at any study that may have had enough patient follow up data to compare though given the rarity of the tumor its likely that there may not have been any such study? Will submit this for Web 3.0 help
17/04/2025, 10:59 - Rakesh Biswas: https://pajrcasereporter.blogspot.com/2024/09/74f-metabolic-syn-diabetes-15yrs-heart.html?m=1
17/04/2025, 11:26 - Patient Advocate 75F Metabolic Syn joined from the community
17/04/2025, 17:19 - Dr.Abdulsalam Med Ed Leads: Ist impression gasritits +colitis + oral ulceration ?eyes? Joints?
17/04/2025, 17:23 - Dr.Abdulsalam Med Ed Leads: Thanks for the update and the photo. It looks like the patient is in a monitored ICU setting with multiple infusions running and vitals monitored closely. From your notes and the progression:
Febrile illness with vomiting and diarrhea starting 5 days before admission
Developed atrial fibrillation → managed with oral metoprolol
Hypotension followed
Persistent fever spikes
Oral ulcerations post-admission; dermatologists suggest oral pemphigus
The clinical suspicion for oral pemphigus, as discussed, seems plausible especially if:
The ulcerations are extensive, painful, and non-healing
They're located in classic sites like buccal mucosa, palate, or oropharynx
There's involvement beyond the oral cavity or recurrence
Key next steps might include:
1. Biopsy and DIF (Direct Immunofluorescence) from the edge of the ulcer for diagnosis confirmation
2. Tzanck smear, though less specific, can still support diagnosis (acantholytic cells)
3. ENT examination for deeper mucosal involvement (especially oropharynx/larynx)
4. Consider systemic autoimmune markers if not already done (ANA panel, anti-desmoglein antibodies)
Let me know if you'd like help creating a simplified flow or summary slide for your students based on this case—it’s a rich clinical learning example!
17/04/2025, 17:25 - Dr.Abdulsalam Med Ed Leads: Great question. Given the clinical picture of persistent fever, diarrhea and vomiting, atrial fibrillation with hypotension, and now oral ulcerations suspected to be pemphigus, a broad differential diagnosis should consider both infectious, autoimmune, cardiac, and drug-related causes:
---
Differential Diagnosis
1. Infectious Causes
Sepsis (gastrointestinal source) – Fever, diarrhea, vomiting, hypotension; possibly leading to multi-organ involvement.
Viral illness (e.g., HSV, CMV, EBV) – Can cause oral ulcerations and systemic symptoms.
HIV – Can present with oral ulcers, persistent fever, diarrhea; immune suppression can trigger secondary autoimmune diseases like pemphigus.
Typhoid or enteric fever – Persistent fever, abdominal symptoms, relative bradycardia; occasionally associated with mucosal ulcerations.
Amoebiasis/Parasitic enteritis – Especially in endemic regions with diarrhea.
2. Autoimmune/Mucocutaneous Disorders
Pemphigus vulgaris – Painful oral ulcers (often precede skin involvement); confirmed by biopsy + DIF.
Stevens-Johnson Syndrome/TEN – If drug-related; mucosal ulceration with systemic symptoms.
Behçet’s disease – Recurrent oral/genital ulcers, uveitis, systemic symptoms.
Systemic lupus erythematosus (SLE) – May cause oral ulcers, AF (serositis), fever.
3. Cardiac-Related Complications
Atrial fibrillation secondary to sepsis or electrolyte imbalance
Myocarditis – Viral myocarditis can cause AF, fever, and hypotension.
Drug-induced hypotension – Especially with beta blockers like metoprolol in acute illness.
4. Drug Reactions
Drug-induced mucositis or pemphigus-like reaction – Check recent medications.
NSAIDs, antibiotics (e.g., penicillins, cephalosporins) can rarely trigger pemphigus or mucosal reactions.
5. Malignancy-related
Paraneoplastic pemphigus – Less common but possible in elderly with new onset severe mucosal ulceration and systemic illness.
---
Would you like a table summarizing the differential by symptoms (fever, ulcers, hypotension, etc.) for teaching purposes?
17/04/2025, 18:12 - Dr.Abdulsalam Med Ed Leads: Is it the first attack, or recurrent?
17/04/2025, 18:12 - Dr.Abdulsalam Med Ed Leads: Any skin lesions?
17/04/2025, 18:12 - Dr.Abdulsalam Med Ed Leads: Eye involvement?
17/04/2025, 18:15 - Dr.Abdulsalam Med Ed Leads: Here's a clear and concise differential diagnosis table based on the patient’s key symptoms — fever, diarrhea/vomiting, hypotension, oral ulcerations, and atrial fibrillation — useful for bedside discussion or teaching:
---
Differential Diagnosis Table
---
Let me know if you want this as a PDF/PowerPoint slide or formatted for teaching rounds. I can also help build a flowchart for oral ulcer differential, if you'd like.
18/04/2025, 00:11 - Dr.Abdulsalam Med Ed Leads: **Clinical Summary and Management Plan for 40F with Chronic Occipital Headache, Nuchal Pain, Fluorosis, and Suspected OPLL**
**Key Findings:**
1. **Chronic Symptoms:** 20-year history of occipital headaches, 1 year of nuchal (neck) pain.
2. **Environmental Exposure:** Drank borewell groundwater (high fluoride risk) for 30 years, switched to river water 10 years ago.
3. **Imaging:**
- Cervical spine X-ray suggests early **ossification of the posterior longitudinal ligament (OPLL)**.
- Dental findings suspicious for **fluorosis**.
**Pathophysiology Links:**
- **Fluorosis** from chronic fluoride exposure (borewell water) likely contributed to **skeletal fluorosis** (ligament calcification) and **dental fluorosis**.
- **OPLL** may result from skeletal fluorosis, leading to cervical spine stiffness, nerve compression, and pain.
**Diagnostic Workup:**
1. **Confirm OPLL:**
- **MRI/CT cervical spine** to evaluate spinal cord/nerve compression and ossification extent.
2. **Assess Fluorosis:**
- **Serum/urine fluoride levels** (though possibly normalized post-exposure).
- **Bone scan/X-rays** (e.g., pelvis, forearm) to check for skeletal fluorosis (rosted appearance, osteosclerosis).
3. **Rule Out Metabolic Bone Disease:**
- Check serum calcium, phosphate, ALP, PTH, vitamin D, renal function.
4. **Water Testing:** Verify current/past borewell water fluoride levels.
**Differential Diagnoses:**
- Cervical spondylosis, tension-type headache, metabolic bone disorders (e.g., hyperparathyroidism), other environmental toxins (e.g., arsenic).
**Management:**
1. **OPLL:**
- **Neurological monitoring:** If MRI shows cord compression, refer to neurosurgery for decompression.
- **Conservative care:** Physical therapy, NSAIDs, muscle relaxants, posture correction.
2. **Fluorosis:**
- **Prevent further exposure:** Confirm safe fluoride levels in current water supply.
- **Symptomatic care:** Analgesics, joint/mobility support.
3. **Dental Care:** Cosmetic or restorative treatments for fluorotic teeth.
4. **Patient Education:**
- Avoid fluoride supplements/toothpaste excess.
- Regular follow-up for spinal/neurological symptoms.
**Follow-Up:**
- Monitor for progressive OPLL (e.g., myelopathy signs: gait disturbances, hand weakness).
- Address secondary complications (e.g., restricted neck mobility, chronic pain).
**Conclusion:**
Chronic fluoride toxicity likely underpins both dental fluorosis and OPLL. Multidisciplinary care (neurology, orthopedics, dentistry) is essential to optimize outcomes.[DeepSeek]
18/04/2025, 07:13 - Rakesh Biswas: 👏👏 amazing. This Web 3.0 inclusion should get into our current write up on Narketpally syndrome! @919604701505 @13055398941 @919171769005
18/04/2025, 07:13 - You changed the group name from "Narketpally Collective medical cognition bridging bedside and bench" to "Narketpally syndrome: Collective medical cognition bridging bedside and bench"
18/04/2025, 10:50 - Rakesh Biswas: OPD now:
Reviewing this 39F with gestational portal hypertension and cirrhosis of Liver who I first met in 2016 in Bhopal and she was doing fairly well till few weeks back when she developed sudden blood vomiting due to her portal hypertensive varicieal rupture for which local doctors did an endoscopic variceal band ligation recently.
Her first tryst with her illness was when she found that her post partum abdominal size wasn't reducing and she waited from 2014 to 2016 before consulting in sskm, Kolkata when doctors there found her esophageal varices!
Currently on examination:
Liver and spleen palpable (with difficulty and soft, will review the ultrasound personally with POCUS in the afternoon.
Details available here:
https://pajrcasereporter.blogspot.com/2025/04/39f-cirrhosis-of-liver-2016-now-blood.html?m=1
Question to our Web 3.0 champion:
What may have caused her gestational portal hypertension? What can we do to help her at present?
18/04/2025, 11:09 - Rakesh Biswas: OPD now: Amazing 46M, native village from near Narketpally with amazing trunkal obesity with upper abdominal bulge possibly due to greater omental fat and very prominent parotidomegaly (@9647501361306 we need to formalize this as an important marker of metabolic syn). He says he's having this phenotype since age of 10! Any web 3.0 help to further deep dive into obesity phenotypes could be useful here.
He didn't consent to my taking his deidentified photograph!
18/04/2025, 11:10 - You added 37M Staphysagria Patient Advocate, Patient Advocate 60M DM2 and Patient Advocate 63M Metabolic Syn
18/04/2025, 11:13 - Dr.Abdulsalam Med Ed Leads: The case of this 46-year-old male with truncal obesity, upper abdominal fat distribution, and parotidomegaly since childhood raises intriguing questions about metabolic syndrome, obesity phenotypes, and potential underlying endocrine or genetic factors. Below is a structured analysis based on the search results and clinical insights:
---
### **1. Truncal Obesity and Metabolic Syndrome**
Truncal (abdominal) obesity is a hallmark of metabolic syndrome, characterized by insulin resistance, dyslipidemia, and hypertension. Key findings from the search results include:
- **Visceral Fat and Cardiometabolic Risk**: Excess omental fat is strongly linked to insulin resistance, inflammation, and cardiovascular disease due to altered adipokine secretion (e.g., reduced adiponectin, elevated leptin) and systemic inflammation.
- **Diagnostic Criteria**: Waist circumference (>35 inches in males) or waist-to-height ratio (>0.5) are better indicators of metabolic risk than BMI alone.
- **Early-Onset Obesity**: The patient’s phenotype since age 10 suggests possible genetic or developmental factors (e.g., monogenic obesity syndromes, hypothalamic dysfunction) or childhood-onset metabolic dysregulation.
---
### **2. Parotidomegaly as a Metabolic Marker**
The prominent parotid enlargement may signal **sialadenosis** (non-inflammatory salivary gland swelling), which is associated with:
- **Metabolic Disorders**: Diabetes, cirrhosis, and endocrine imbalances (e.g., hypothyroidism) can cause bilateral glandular hypertrophy.
- **Obesity-Related Mechanisms**: Chronic hyperinsulinemia and insulin resistance may promote glandular hyperplasia via growth factor pathways.
- **Clinical Relevance**: Parotidomegaly is increasingly recognized as a potential marker of metabolic dysfunction, particularly in patients with visceral adiposity.
---
### **3. Obesity Phenotypes and Precision Medicine**
The search results highlight emerging classifications of obesity phenotypes that could guide personalized interventions:
- **Metabolic Obesity Subtypes** :
- **Metabolically Healthy Obesity (MHO)**: Normal insulin sensitivity, lower visceral fat.
- **Metabolically Unhealthy Obesity (MUO)**: Insulin resistance, inflammation, and high visceral fat (likely this patient’s subtype).
- **Behavioral/Etiological Phenotypes** :
1. **Hungry Brain**: Impaired satiety signaling.
2. **Emotional Hunger**: Stress/hedonic eating.
3. **Hungry Gut**: Rapid gastric emptying.
4. **Slow Burning**: Reduced metabolic rate.
- **Genetic/Developmental Phenotypes**: Early-onset cases may involve monogenic mutations (e.g., leptin deficiency) or epigenetic changes triggered by childhood environment.
---
### **4. Investigative Pathways**
#### **A. Metabolic Workup**
- **Lab Tests**: Fasting glucose, HbA1c, lipid profile, hsCRP, adiponectin/leptin levels.
- **Endocrine Evaluation**: Cortisol (to exclude Cushing’s), thyroid function, testosterone (low levels correlate with truncal obesity).
#### **B. Imaging**
- **Visceral Fat Quantification**: CT/MRI to assess omental and hepatic fat.
- **Salivary Gland Imaging**: Ultrasound or MRI to rule out neoplasms and confirm sialadenosis.
#### **C. Genetic Testing**
- Consider panels for monogenic obesity (e.g., *LEP*, *MC4R*) or syndromes like Prader-Willi if developmental delays are present.
---
### **5. Therapeutic Considerations**
- **Lifestyle Interventions**:
- **Exercise**: Aerobic and resistance training reduce visceral fat independent of weight loss.
- **Diet**: Mediterranean or low-glycemic diets improve insulin sensitivity; limit ultra-processed foods linked to truncal fat.
- **Pharmacotherapy**:
- **GLP-1 Agonists** (e.g., semaglutide): Effective for weight loss and metabolic improvement.
- **Anti-Inflammatory Agents**: NSAIDs or statins if hsCRP is elevated.
- **Surgical Options**: Bariatric surgery for refractory cases, targeting omental fat reduction.
---
### **6. Research and Technology Integration**
- **Web 3.0 Applications**:
- **AI-Driven Phenotyping**: Platforms like [Obesity Digital Phenotyping Systems](https://example.com) could integrate genetic, metabolic, and imaging data to classify subtypes.
- **Blockchain for Data Sharing**: Securely aggregate anonymized cases to identify rare patterns (e.g., childhood-onset metabolic-parotid syndrome).
---
### **Conclusion**
This patient’s phenotype underscores the interplay between visceral adiposity, metabolic dysregulation, and atypical manifestations like parotidomegaly. A multidisciplinary approach—combining metabolic profiling, genetic screening, and personalized lifestyle/drug interventions—is critical. Early-onset cases warrant exploration of developmental or genetic drivers, while emerging obesity classifications (e.g., hungry gut vs. slow burning) may refine therapeutic targeting.
18/04/2025, 11:18 - Dr.Abdulsalam Med Ed Leads: DeepSeek 👆
18/04/2025, 11:43 - Rakesh Biswas: Thanks. Again Web 3.0 is heavy on maximalist over testing and overtreatment! How do we make these models to promote minimalist EBM? Also in the context of Groopman's books shared in the other groups
18/04/2025, 11:47 - Dr.Abdulsalam Med Ed Leads: This is because most of them are shifting from web searches into deep thinking models
18/04/2025, 11:47 - Dr.Abdulsalam Med Ed Leads: To address the challenge of aligning Web 3.0 technologies with minimalist Evidence-Based Medicine (EBM) and avoiding maximalist overtesting/overtreatment—while incorporating insights from Jerome Groopman’s work on medical decision-making—the following strategies and models could be implemented:
---
### **1. Decentralized, Patient-Centric Data Ownership**
Web 3.0’s decentralized architecture allows patients to control their health data via blockchain-secured digital wallets. This shifts power from centralized institutions (e.g., hospitals, insurers) to individuals, enabling personalized care that prioritizes patient narratives over rigid protocols.
- **Example**: Patients could share granular data selectively with providers, ensuring interventions are tailored to their unique risk profiles rather than defaulting to population-wide guidelines .
- **Groopman’s Insight**: Groopman emphasizes the importance of patient stories and individualized decision-making, warning against "one-size-fits-all" approaches driven by bureaucratic or algorithmic mandates .
---
### **2. Semantic Web for Nuanced Evidence Interpretation**
Web 3.0’s semantic modeling (RDF, OWL) can contextualize medical evidence by linking data across decentralized sources, enabling AI to interpret guidelines with flexibility.
- **Application**: AI systems could analyze patient-specific factors (e.g., comorbidities, lifestyle) to recommend minimalist interventions when supported by evidence, while flagging scenarios where maximalist testing is unnecessary .
- **Avoiding Cognitive Traps**: Groopman highlights how doctors often fall into "diagnostic momentum" or confirmation bias. Semantic AI could counter this by surfacing alternative hypotheses or conflicting evidence .
---
### **3. Smart Contracts for Dynamic Guidelines**
Blockchain-based smart contracts could encode EBM guidelines as adaptive, self-executing rules that evolve with real-world data.
- **Functionality**:
- Automate care pathways for low-risk cases (e.g., watchful waiting for stable symptoms).
- Trigger additional testing only when predefined thresholds (e.g., biomarker levels) are met, reducing overuse .
- **Groopman’s Warning**: Rigid adherence to guidelines can lead to errors. Smart contracts could integrate patient preferences (e.g., minimalist vs. maximalist inclinations) and update dynamically based on outcomes data .
---
### **4. Decentralized Autonomous Organizations (DAOs) for Guideline Governance**
DAOs—decentralized communities of patients, clinicians, and researchers—could govern EBM protocols, ensuring transparency and minimizing corporate/pharma influence.
- **Mechanism**:
- Stakeholders vote on guideline updates using tokenized governance.
- Conflicts of interest (e.g., pharmaceutical funding) are audited on-chain .
- **Alignment with Groopman**: This mirrors his critique of top-down "best practices" imposed by centralized panels, which often fail in real-world contexts .
---
### **5. AI-Driven Risk Communication and Shared Decision-Making**
Web 3.0’s AI tools can translate complex statistical risks into patient-friendly narratives, fostering shared decision-making.
- **Implementation**:
- Use natural language processing to explain probabilities (e.g., "This test has a 5% chance of a false positive").
- Integrate patient values (e.g., aversion to invasive procedures) into recommendations .
- **Groopman’s Framework**: Patients’ mindsets (e.g., naturalists vs. technologists) must inform care. AI could map these preferences to EBM options, reducing overtreatment in risk-averse individuals .
---
### **Pitfalls to Mitigate**
- **Algorithmic Bias**: Ensure AI models are trained on diverse datasets to avoid perpetuating inequities.
- **Over-Decentralization**: Balance patient autonomy with clinician expertise to prevent fragmentation.
- **Ethical DAOs**: Guard against "tyranny of the majority" in guideline governance.
---
### **Conclusion**
By leveraging Web 3.0’s decentralization, semantic intelligence, and patient empowerment, healthcare systems can shift from maximalist defaults to minimalist, evidence-based care. Groopman’s emphasis on narrative, individualized judgment, and skepticism of rigid protocols provides a critical ethical framework for this transition. The goal is not to replace human intuition but to augment it with tools that prioritize precision, transparency, and patient agency .
18/04/2025, 11:48 - Rakesh Biswas: 👏👏
18/04/2025, 11:53 - Dr.Abdulsalam Med Ed Leads: We have to accept it until we get accustomed to each other
18/04/2025, 12:04 - Rakesh Biswas: Agree! We can easily interpret the Web 3.0 outputs using CRH to promote more rational minimalist UDLCOs
18/04/2025, 12:06 - Rakesh Biswas: Meanwhile will be looking forward to your Web 3.0 inputs on these two questions <This message was edited>
18/04/2025, 12:19 - Dr.Abdulsalam Med Ed Leads: ### **1. Sensitivity and Specificity of Wood’s Lamp in Diagnosing Primary Vitiligo**
Wood’s lamp (long-wave UV light, 320–400 nm) is widely used to enhance the visibility of hypopigmented or depigmented lesions in vitiligo. Under UV light, areas of melanin loss in primary vitiligo typically fluoresce as **bright blue-white or yellow-green** due to the absence of melanin, which normally absorbs UV light. This tool helps differentiate primary vitiligo from post-inflammatory hypopigmentation (PIH), which may appear less sharply demarcated and lack fluorescence.
- **Sensitivity**: While exact sensitivity values are not explicitly stated in the literature, Wood’s lamp is particularly effective in **lighter skin tones**, where depigmented patches are more easily visualized. In darker skin, fluorescence may be less pronounced, reducing sensitivity.
- **Specificity**: The specificity is high for conditions like vitiligo when combined with clinical context. For example, coral-red fluorescence suggests erythrasma (bacterial), while blue-green indicates fungal infections (e.g., tinea capitis). However, false positives can occur due to contaminants (e.g., soap residue, cosmetics) or medications (e.g., tetracyclines).
**Limitations**:
- Recent washing or topical products may alter fluorescence, leading to false negatives/positives.
- Dermal pigmentation (e.g., melasma) may not fluoresce, limiting utility in mixed epidermal-dermal conditions.
---
### **2. Efficacy of Methotrexate vs. Placebo in Primary Vitiligo**
The evidence for methotrexate (MTX) in vitiligo is **limited but evolving**, with mixed results from clinical trials:
#### **Key Findings from RCTs**
1. **Methotrexate + Phototherapy vs. Phototherapy Alone**
- A 2023 double-blinded RCT (42 patients) compared **MTX + NB-UVB** vs. **placebo + NB-UVB** for 6 months. Both groups showed similar improvements in VASI and VIDA scores, with no statistically significant difference.
- Another 2023 study (48 patients) found that **topical MTX gel combined with NB-UVB** outperformed MTX alone, achieving 49.7% repigmentation vs. 19.3% for monotherapy. However, MTX alone was ineffective.
2. **Methotrexate Monotherapy**
- Case reports (e.g., a 10-year-old boy with concurrent psoriasis and vitiligo) describe MTX improving vitiligo over 3 years, but these are observational and lack placebo controls.
- Systemic reviews highlight that MTX’s immunomodulatory effects (e.g., reducing TNF-α and promoting IL-10) may stabilize active vitiligo, but robust RCT data supporting monotherapy are lacking.
#### **Mechanistic Rationale**
MTX inhibits T-cell activation and cytokine pathways (e.g., IL-17/23) implicated in melanocyte destruction. However, its efficacy appears **synergistic with phototherapy** rather than standalone.
#### **Clinical Implications**
- **Combination therapy** (MTX + NB-UVB) shows promise for faster repigmentation.
- MTX monotherapy is **not a first-line option** per current guidelines but may be considered in refractory or rapidly progressive cases.
---
### **Conclusion**
1. **Wood’s Lamp**: A valuable tool for distinguishing primary vitiligo from PIH, with high specificity in appropriate clinical settings. Sensitivity varies by skin tone and preparation.
2. **Methotrexate**: Limited RCT evidence supports its use in combination with phototherapy, but monotherapy efficacy remains unproven. Dermatologists may trial MTX off-label for active, widespread vitiligo, particularly with comorbid autoimmune conditions.
For this patient, close monitoring of MTX’s hematologic/hepatic side effects and repigmentation progress is advised, alongside shared decision-making regarding off-label use.
18/04/2025, 12:29 - Rakesh Biswas: @13135550002 any RCT evidence for the efficacy of Woods lamp in primary vitiligo vs post inflammatory hypopigmentation?
Please share the RCT evidence if any in a PICO format and please ensure that you share absolute numbers instead of relative percentages
18/04/2025, 12:29 - Meta AI: I'm sorry, but I couldn't find any Randomized Controlled Trial (RCT) evidence specifically comparing the efficacy of Wood's lamp in primary vitiligo versus post-inflammatory hypopigmentation. Wood's lamp examination is commonly used to aid in the diagnosis of various skin conditions, including vitiligo and post-inflammatory hypopigmentation, due to its ability to highlight differences in skin pigmentation under ultraviolet light.
For *Vitiligo*, Wood's lamp can help identify areas of depigmentation, as affected skin tends to appear bright blue or white under the lamp due to the loss of melanocytes.
For *Post-Inflammatory Hypopigmentation*, the appearance under Wood's lamp can vary depending on the underlying cause and the extent of melanocyte damage or dysfunction. However, specific RCT evidence comparing the diagnostic or therapeutic efficacy of Wood's lamp in these conditions isn't readily available in the literature I've accessed.¹
If you're looking for detailed RCT evidence, I recommend searching specialized medical databases or journals focusing on dermatology for the most current research findings.
18/04/2025, 12:29 - Meta AI: https://www.mdpi.com/2077-0383/12/3/1243
18/04/2025, 12:32 - Rakesh Biswas: @13135550002 thanks! It probably appears to be a logical patholophysiologic rationale that primary and secondary vitiligo can have similar amount of melanocyte destruction and it may not be right to try and diagnose them on the basis of woods lamp alone
18/04/2025, 12:32 - Meta AI: Exactly. The Wood's lamp examination, while useful, has its limitations in differentiating between primary vitiligo and post-inflammatory hypopigmentation due to overlapping features under UV light. Both conditions can exhibit alterations in pigmentation that might appear similar under the Wood's lamp, making differential diagnosis based solely on this tool potentially challenging.
A comprehensive diagnosis typically involves a combination of clinical history, physical examination, and sometimes additional diagnostic tests to accurately distinguish between these conditions and guide appropriate treatment. The pathophysiological rationale supports the idea that both primary and secondary causes of vitiligo or hypopigmentation can result in significant melanocyte dysfunction or loss, further complicating diagnosis based on Wood's lamp findings alone.
18/04/2025, 12:35 - Dr.Abdulsalam Med Ed Leads: any RCT evidence for the efficacy of Woods lamp in primary vitiligo vs post inflammatory hypopigmentation?
Please share the RCT evidence if any in a PICO format and please ensure that you share absolute numbers instead of relative percentages
There appears to be no randomized controlled trial (RCT) evidence directly comparing the efficacy of Wood's lamp in primary vitiligo versus post-inflammatory hypopigmentation. The available literature mainly discusses Wood's lamp as a diagnostic and assessment tool rather than a treatment modality.
**Key points from the evidence:**
- Wood's lamp is primarily used to aid diagnosis and delineate hypopigmented disorders including vitiligo and to assess disease stability and repigmentation extent after treatment or surgery[5][8].
- No RCTs were found that evaluate Wood's lamp itself as a treatment for vitiligo or post-inflammatory hypopigmentation.
- RCTs in vitiligo treatment focus on phototherapy methods such as 308-nm LED or excimer lamps and topical agents, not on Wood's lamp usage[1][2][4][7].
- Wood's lamp helps differentiate vitiligo from other hypopigmented conditions by highlighting absence of melanin with characteristic fluorescence but does not have a direct therapeutic role documented in RCTs[3][5][8].
**Summary in PICO format (based on available data):**
| PICO Element | Description |
|--------------------|-------------------------------------------------------------------------------------------------|
| Population (P) | Patients with primary vitiligo or post-inflammatory hypopigmentation |
| Intervention (I) | Use of Wood's lamp for diagnosis and assessment |
| Comparison (C) | No Wood's lamp or other diagnostic methods |
| Outcome (O) | Diagnostic accuracy, disease stability assessment, repigmentation delineation |
| RCT Evidence | No RCTs found evaluating Wood's lamp efficacy as treatment or direct comparison between conditions |
**Absolute numbers from related RCTs on vitiligo treatment (not Wood's lamp):**
- In a trial with 269 vitiligo patches, 50% or more repigmentation was achieved in 50 patches (38.17%) with 308-nm LED and 53 patches (38.41%) with 308-nm excimer lamp after 16 sessions[1].
- Another RCT showed 16 out of 25 patients (64%) treated with narrowband UVB had >50% improvement vs 9 out of 25 (36%) with PUVA therapy[4].
**Conclusion:**
No RCT evidence supports Wood's lamp efficacy as a treatment for vitiligo or post-inflammatory hypopigmentation. Its role remains diagnostic and evaluative. Treatment RCTs focus on phototherapy and topical agents with reported absolute response rates but do not involve Wood's lamp as an intervention[1][4][7][8].
Citations:
[1] Comparing the efficacy of 308-nm light-emitting diode and ... - PubMed https://pubmed.ncbi.nlm.nih.gov/38752300/
[2] Randomized controlled trial of topical corticosteroid and home ... https://academic.oup.com/bjd/article/184/5/828/6702324
[3] Wood's Light - StatPearls - NCBI Bookshelf https://www.ncbi.nlm.nih.gov/books/NBK537193/
[4] Randomized Double-blind Trial of Treatment of Vitiligo https://jamanetwork.com/journals/jamadermatology/fullarticle/412893
[5] Revealing The Unseen: A Review of Wood's Lamp in Dermatology https://jcadonline.com/review-of-woods-lamp-in-dermatology/
[6] vitiligo: Topics by Science.gov https://www.science.gov/topicpages/v/vitiligo
[7] Clinical and dermoscopic assessment of the efficacy of topical ... https://www.nature.com/articles/s41598-025-88811-w
[8] Wood's Light in Inflammatory and Autoimmune Dermatoses ... https://www.actasdermo.org/en-wood-s-light-in-inflammatory-articulo-S0001731024009955
Perplexity Response
18/04/2025, 12:47 - Rakesh Biswas: While parotidomegaly is increasingly recognised as a potential marker of metabolic syn it's not featured prominently in the protocol of metabolic syn evaluation and may not have been afforded any prognostic value in it's evaluation?
Perhaps for this we need to design a new study where we record an individual's parotidomegaly parameters and then also log their other phenotype abnormalities and then study if the outcomes are variable for different phenotypes within the metabolic syn phenotype? @13135550002 @919652955915 ?
18/04/2025, 12:47 - Meta AI: That's an interesting perspective on parotidomegaly and its potential role in metabolic syndrome (MetS) evaluation. You're right; while parotidomegaly has been linked to various metabolic disturbances, it's not a standard component of MetS assessment protocols.
Designing a study as you've outlined could provide valuable insights into the prognostic value of parotidomegaly in MetS. By correlating parotidomegaly parameters with other phenotypic abnormalities and outcomes, researchers could better understand its significance and potential utility in risk stratification.
Some key considerations for such a study would include:
1. *Standardized measurement of parotidomegaly*: Developing consistent methods for assessing parotid gland size and correlating it with metabolic parameters.
2. *Phenotypic characterization*: Accurately documenting other MetS components and phenotypic features to identify potential correlations or patterns.
3. *Longitudinal design*: Following participants over time to assess outcomes and determine if parotidomegaly adds prognostic value.
4. *Diverse population*: Ensuring the study includes a diverse population to enhance generalizability of findings.
This approach could help clarify the role of parotidomegaly in MetS and potentially inform future diagnostic and therapeutic strategies.
18/04/2025, 12:50 - Dr.Abdulsalam Med Ed Leads: AI is changing the game rules and taking the steering.
18/04/2025, 12:51 - Ganesh Joshi: If the parotid region swells in minutes, it is due to block of it's duct in the vestibule. Just do one Valsalva and it will be relieved. Courtesy my friend from Peds Dentistry🙏🏻
18/04/2025, 12:52 - Rakesh Biswas: In metabolic syn it's generally a chronic parotidomegaly but it's an interesting tip
18/04/2025, 12:53 - Ganesh Joshi: Yes, you are right. Just took an opportunity to share this gyan🤪
18/04/2025, 12:54 - Dr.Abdulsalam Med Ed Leads: Pntermittent painful swelling related to food is mostly due to a sialolithiasis and can be proved by bimanual palpation in the OP setting
18/04/2025, 12:54 - Ganesh Joshi: The relief is within minutes but repeating Valsalva many times may increase the block, please note🙏🏻
18/04/2025, 12:57 - Dr.Abdulsalam Med Ed Leads: I don't think Valsalva by any meam would relieve it ,paradoxically, it can force the stone to migrate more proximal towards the gland, making its discovery and management more difficult 🤔 <This message was edited>
18/04/2025, 12:59 - Ganesh Joshi: Not talking of sialolithiasis. It is usually some food particle stuck at the outlet. Hence specified vestibule
18/04/2025, 12:59 - Ganesh Joshi: Also doing it many time may push in and cause more trouble
18/04/2025, 13:00 - Dr.Abdulsalam Med Ed Leads: Rather we encourage milking the gland towards its drainage path
18/04/2025, 13:00 - Rakesh Biswas: We need some epidemiological data around this! How commonly is it seen in practice?
18/04/2025, 13:01 - Ganesh Joshi: How to move...
Below the zygoma...
18/04/2025, 13:06 - Dr.Abdulsalam Med Ed Leads: This message was deleted
18/04/2025, 13:12 - Dr.Abdulsalam Med Ed Leads: Never food particles have been claimed for that. Some studies raise issues against toothpaste particles as a possible nidus for developing future stones but never of acute obstruction causing problems in the clinical setting
18/04/2025, 13:14 - Dr.Abdulsalam Med Ed Leads: And these stones are common in the submandibular salivary gland duct due factors well known to every ENT specialist. <This message was edited>
18/04/2025, 13:20 - Ganesh Joshi: This message was deleted
18/04/2025, 13:21 - Ganesh Joshi: This message was deleted
18/04/2025, 13:42 - Dr.Abdulsalam Med Ed Leads: This message was deleted
18/04/2025, 14:36 - +91 63035 16964 left
18/04/2025, 15:43 - MD.AKRAM Kolkata Medical College Intern: ••• Right Upper Lobe Pulmonary Mass – Suspicious for Bronchogenic Carcinoma
1) HRCT Thorax
Bronchoscopy ± biopsy
Sputum cytology (if productive cough)
PET-CT for staging, if malignancy confirmed
18/04/2025, 16:08 - Rakesh Biswas: What is against bronchogenic carcinoma in the chest X-ray @9647501361306 ? <This message was edited>
18/04/2025, 16:09 - Dr.Abdulsalam Med Ed Leads: Lung opacities can arise from a range of conditions, and their interpretation depends on factors like patient history, clinical symptoms, and additional imaging. Here are some potential causes:
1. **Infectious Processes**
- **Pneumonia**: Consolidation due to bacterial, viral, or fungal infection.
- **Tuberculosis**: Nodular or cavitary lesions, typically in the upper lobes.
2. **Neoplastic Causes**
- **Primary Lung Cancer**: Solitary pulmonary nodules or larger masses.
- **Metastases**: Multiple round opacities from secondary cancer spread.
3. **Inflammatory and Autoimmune Conditions**
- **Sarcoidosis**: Bilateral hilar lymphadenopathy with pulmonary involvement.
- **Interstitial Lung Disease**: Fibrotic changes causing diffuse opacities.
4. **Vascular Conditions**
- **Pulmonary Edema**: Cardiogenic causes leading to diffuse haziness.
- **Pulmonary Embolism**: Hampton’s hump (wedge-shaped opacity).
5. **Benign or Congenital Conditions**
- **Rounded Atelectasis**: Commonly linked to pleural disease.
- **Congenital cystic lung disease**: Less common, but can mimic pathology.
6. **Trauma and Post-Surgical Changes**
- **Contusion**: Post-traumatic localized opacity.
- **Post-radiation fibrosis**: Dense scarring following radiotherapy.
Further imaging like CT scans and histopathological studies can refine the diagnosis. Given your expertise in medical imaging, do you have any specific considerations in mind for this case?
18/04/2025, 16:13 - Dr.Abdulsalam Med Ed Leads: The provided WhatsApp chat contains medical case discussions and a request for assistance. Below is a structured breakdown and analysis:
### **1. Patient Case Summary**
- **Demographics**: 58-year-old male (58M).
- **Chief Complaint**: Recurrent mucocutaneous ulcerations.
- **Possible Differential Diagnoses**:
- Behçet’s disease (systemic vasculitis).
- Recurrent herpes simplex virus (HSV) infection.
- Autoimmune disorders (e.g., lupus, lichen planus).
- Infectious causes (e.g., syphilis, fungal infections).
- Nutritional deficiencies (e.g., vitamin B12, iron).
- **Next Steps**:
- Detailed history (duration, ulcer locations, triggers, systemic symptoms).
- Lab tests (CBC, autoimmune panels, viral PCR, biopsy).
---
### **2. Incidental Chest X-ray Findings**
- **Context**: Findings discovered incidentally during unrelated evaluation.
- **Common Incidental Abnormalities**:
- Pulmonary nodules (evaluate for malignancy, TB, fungal infection).
- Mediastinal lymphadenopathy (consider sarcoidosis, lymphoma).
- Pleural effusion (infectious, inflammatory, or malignant causes).
- Fibrotic changes (e.g., old TB, interstitial lung disease).
- **Action**:
- Compare with prior imaging (if available).
- Further imaging (CT scan) or biopsy if suspicious lesion.
---
### **3. Web 3.0 Reference**
- Likely refers to decentralized platforms or AI tools for collaborative diagnosis.
- **Potential Applications**:
- Secure sharing of medical images via blockchain.
- Crowdsourced expert opinions through decentralized networks.
- AI-driven analysis of imaging findings.
---
### **4. Sensitive Information Note**
- The chat includes a phone number (**+91 94250 07641**) and personal names. Ensure compliance with privacy regulations (e.g., HIPAA, GDPR) before sharing further.
---
### **Key Recommendations**
- For the **ulcerations**: Rule out systemic conditions (e.g., Behçet’s) via multidisciplinary evaluation.
- For the **chest X-ray**: Obtain CT scan and involve a radiologist for precise interpretation.
- **Web 3.0 Utilization**: Explore platforms enabling secure, real-time collaboration among specialists.
Let me know if you need further clarification!
18/04/2025, 16:16 - Dr.Abdulsalam Med Ed Leads: Copilot
18/04/2025, 16:17 - Dr.Abdulsalam Med Ed Leads: DeepSeek
18/04/2025, 16:25 - Rakesh Biswas: Co pilot's pointing out that there are potential identifiers in this is pretty impressive @919652955915 @919604701505 ?
18/04/2025, 16:26 - Rakesh Biswas: What is striking is the brightness of the lymph nodes as if they are totally calcified? @917639986241
18/04/2025, 16:29 - Rakesh Biswas: Afternoon session on the same patient:
Bedside palpation of massive splenomegaly due to portal hypertension and imageology to assess the cause of her portal hypertension 👇
https://youtu.be/67aer1hkwYY?feature=shared
18/04/2025, 16:30 - Dr.Abdulsalam Med Ed Leads: ### **Answer: Relationship Between Chest X-ray Findings and Vitiligo**
#### **Direct Link**
There is **no established direct relationship** between primary vitiligo (autoimmune melanocyte destruction) and incidental chest X-ray abnormalities. Vitiligo is primarily associated with autoimmune conditions (e.g., thyroid disorders, diabetes) but not directly with pulmonary pathology.
---
#### **Indirect Considerations**
1. **Methotrexate Use**:
- Methotrexate, proposed for vitiligo treatment, carries a risk of **pulmonary toxicity** (e.g., interstitial lung disease, fibrosis).
- **Action**:
- Review the chest X-ray for signs of pre-existing lung disease (e.g., fibrosis, nodules).
- If abnormalities exist, avoid methotrexate and consider safer alternatives (e.g., JAK inhibitors like ruxolitinib cream).
2. **Underlying Systemic Disease**:
- Rarely, conditions causing **both skin hypopigmentation and chest abnormalities** include:
- **Sarcoidosis** (skin lesions + hilar lymphadenopathy/parenchymal changes).
- **Tuberous Sclerosis Complex** (ash-leaf spots + lung cysts/LAM).
- **Action**:
- Correlate clinical history, labs (e.g., ACE levels for sarcoidosis), and imaging to rule out these conditions.
---
#### **Key Recommendations**
1. **Re-evaluate the Chest X-ray**:
- Describe the specific findings (e.g., nodules, fibrosis) to guide further workup.
- Consult a radiologist or pulmonologist if abnormalities are detected.
2. **Safety Before Methotrexate**:
- Perform baseline **pulmonary function tests** (if X-ray is abnormal) and liver/kidney function tests.
3. **Alternative Diagnoses**:
- If hypopigmentation is atypical (e.g., ulcerations precede depigmentation), consider **syndromic associations** (e.g., lupus, Behçet’s disease).
---
### **Conclusion**
The chest X-ray findings are likely **incidental** and unrelated to vitiligo itself. However, they are critical for **guiding methotrexate safety** and ruling out rare systemic diseases. Further collaboration between dermatology, radiology, and pulmonology is advised.
Let me know if you need clarification! 🩺
18/04/2025, 16:35 - Rakesh Biswas: Kudos to @919505766290 who went and convinced the dermatologist to reconsider their diagnosis of primary vitiligo and made them change their mind about the methotrexate!
They had referred the patient to us for ECG abnormalities and they didn't expect we would utilise our CRH medical cognition tool to contest their dermatologic diagnosis! 👏👏
18/04/2025, 16:37 - Dr.Abdulsalam Med Ed Leads: **Interpretation of Lateral Chest X-Ray in a Patient with Vitiligo Hypopigmentation:**
1. **Technical Adequacy:**
- Confirm proper lateral positioning (e.g., adequate penetration, no rotation, scapulae clear of lung fields).
- Ensure the image includes the entire thoracic cavity (apices to costophrenic angles).
2. **Key Anatomical Review:**
- **Lungs:** Assess for consolidations, nodules, effusions, or interstitial patterns (e.g., sarcoidosis, which may associate with vitiligo in autoimmune contexts).
- **Mediastinum:** Evaluate for lymphadenopathy (e.g., hilar enlargement suggestive of sarcoidosis or tuberculosis).
- **Heart:** Check for cardiomegaly or pericardial effusion (unrelated to vitiligo but part of routine assessment).
- **Bones:** Look for rib lesions, vertebral abnormalities, or osteopenia (chronic steroid use for autoimmune conditions could cause osteoporosis).
3. **Vitiligo-Related Considerations:**
- **Autoimmune Associations:** Vitiligo may coexist with thyroid disorders (e.g., goiter) or Addison’s disease (adrenal insufficiency). These do not directly alter chest X-ray findings but warrant clinical correlation.
- **Immunosuppression:** If the patient is on systemic steroids/immunosuppressants for vitiligo, consider opportunistic infections (e.g., pneumonia, tuberculosis).
4. **Limitations:**
- Without the actual image or clinical history (e.g., symptoms, medications), findings are speculative.
- Vitiligo itself does not directly affect X-ray interpretation but may prompt evaluation for systemic associations.
**Next Steps:**
- Correlate with PA chest X-ray for comprehensive assessment.
- Clinical evaluation for autoimmune/endocrine disorders if suggestive symptoms exist.
- Further imaging (e.g., CT) if abnormalities are suspected.
**Conclusion:**
No direct link between vitiligo and chest X-ray abnormalities, but systemic associations should be considered based on clinical context.
18/04/2025, 16:40 - Dr.Abdulsalam Med Ed Leads: In fact, this is one of the powers of AI as it may attract your attention to an important concept we were not aware of ( occasionally seems far from our prompt) <This message was edited>
18/04/2025, 16:43 - Rakesh Biswas: @919171769005 point to be noted for the book!
We like to call this phenomenon:
Getting to correlate our learning outcomes with the same patient's outcomes
18/04/2025, 16:46 - Dr.Abdulsalam Med Ed Leads: Yes, to correlate AI outcomes with the impact on patients' outcomes rather than our interest outcomes
18/04/2025, 16:47 - Dr.Abdulsalam Med Ed Leads: Put our dignity aside
18/04/2025, 16:58 - Rakesh Biswas: AI driven human learning outcomes I guess?
Well at least till humans are still in the loop that is!
18/04/2025, 17:29 - Dr.Abdulsalam Med Ed Leads: It seems so for the time being
18/04/2025, 22:01 - ~Mansi MGM Indore UG Nurture Oncology: Yes sir!!
19/04/2025, 10:01 - Rakesh Biswas: In the condition of this patient where things have eventually settled down to practically following up with pharmacological therapy using propranolol:
"95 consecutive patients recruited from our prospective database. After hepatic venous pressure gradient measurement, patients received propranolol 10 mg, twice daily increased 10 mg daily until to 80 or 120 mg/day. Secondary hepatic venous pressure gradient was also measured. For nonresponders at 80 mg/day, propranolol was titrated to 120 mg/day.
Results
For 58 patients, propranolol was titrated to 80 mg/day, whereas for 37 patients, it was titrated to 120 mg/day. Hemodynamic response was similar in both groups (50 vs. 54.1%, P=0.700). Eighteen of the 29 nonresponders at propranolol 80 mg/day received a dose of 120 mg/day. Two patients achieved a hemodynamic response, but two could not tolerate the dose. Nine (15.5%) patients achieved the target dose of propranolol at 80 mg/day, whereas 16 (43.2%) patients at 120 mg/day achieved this (P=0.003). The difference in patients achieving the target dose between responders and nonresponders was not significant (14 vs. 14, P=0.642). Reduction or discontinuation was required by two (6.9%) patients using 80 mg/day propranolol and six (30%) patients using 120 mg/day propranolol (P=0.032).
Conclusion
There is no dose-dependent effect of 80–120 mg/day of propranolol on the hemodynamic response in cirrhotic patients with gastroesophageal varices. This indicates that low-dose propranolol below the target dose might lead to a considerable hemodynamic response and is much safer and well tolerated."
https://pmc.ncbi.nlm.nih.gov/articles/PMC6380447/
19/04/2025, 10:32 - Rakesh Biswas: OPD now:
70 year old with history of involuntary movements with no loss of consciousness continuously for 2 days!
The movements as enacted by the wife and even the patient is suggestive of myoclonus.
What are the Web 3.0 Inputs on this @9647501361306 @13135550002
From the differentials we reviewed again from our PGs web 3.0 devices we have already planned a MMSE and psychometric assessment today
From the differentials we reviewed
19/04/2025, 10:32 - Meta AI: Given the 70-year-old patient's presentation of involuntary movements consistent with myoclonus without loss of consciousness, here are some potential differentials to consider:
1. *Medication-induced myoclonus*: Certain medications, such as antidepressants, antipsychotics, or opioids, can cause myoclonus.
2. *Neurodegenerative disorders*: Conditions like Alzheimer's disease, Creutzfeldt-Jakob disease, or corticobasal degeneration can present with myoclonus.
3. *Metabolic disturbances*: Electrolyte imbalances, renal or hepatic dysfunction, or hypoxia can cause myoclonus.
4. *Infectious or inflammatory causes*: Encephalitis, meningitis, or autoimmune disorders like Hashimoto's encephalopathy can present with myoclonus.
5. *Toxic exposures*: Exposure to toxins like heavy metals or certain chemicals can cause myoclonus.
Given the planned MMSE and psychometric assessment, it's likely you're also considering potential cognitive or psychiatric components to the patient's presentation.
Additional assessments to consider:
1. *Detailed medication history*: Review the patient's medication list to identify potential culprits.
2. *Laboratory tests*: Electrolyte panel, liver and renal function tests, and potentially toxicology screens.
3. *Neurological examination*: Detailed examination to assess for other signs of neurodegenerative disease or focal neurological deficits.
4. *Imaging studies*: MRI or CT scans may be necessary to rule out structural causes.
The MMSE and psychometric assessment will help evaluate cognitive function and potential psychiatric contributions to the patient's symptoms.
19/04/2025, 11:14 - Dr.Abdulsalam Med Ed Leads: **Comprehensive Analysis and Management Plan for 70-Year-Old with Continuous Myoclonus**
### **Clinical Context**
- **Presentation**: Acute-onset, continuous involuntary movements (myoclonus-like) for 2 days without loss of consciousness.
- **Age**: 70 years, raising suspicion for metabolic, toxic, or neurodegenerative etiologies.
- **Web 3.0 Integration**: Leveraging AI, decentralized data, and collaborative platforms for diagnostics.
---
### **Key Differentials & Workup**
#### **1. Metabolic/Toxic Causes**
- **Labs**: Electrolytes (Na⁺, Ca²⁺), renal/hepatic function, ammonia, glucose, CK, toxicology screen (drugs, alcohol withdrawal).
- **Web 3.0 Input**: Blockchain-secured medication history to identify drug-induced causes (e.g., SSRIs, opioids, antibiotics).
#### **2. Neurodegenerative Disorders**
- **Creutzfeldt-Jakob Disease (CJD)**: Rapid cognitive decline + myoclonus.
- **Tests**: MRI (cortical ribboning, basal ganglia changes), CSF 14-3-3 protein, EEG (periodic sharp waves).
- **Dementia with Lewy Bodies**: Fluctuating cognition + visual hallucinations.
- **Tests**: MMSE/psychometrics, DaTSCAN.
#### **3. Seizure-Related**
- **Non-Convulsive Status Epilepticus**:
- **Test**: Urgent EEG (rhythmic/periodic discharges).
- **Post-Hypoxic Myoclonus**: Exclude with history (unlikely here).
#### **4. Infectious/Autoimmune**
- **Encephalitis/Meningitis**: CSF analysis (PCR, antibodies), MRI.
- **Paraneoplastic/Opsoclonus-Myoclonus**: Anti-neuronal antibodies (anti-Ri, anti-Hu), CT/PET for tumors.
#### **5. Structural Lesions**
- **MRI Brain**: Rule out stroke, tumors, or prion-related changes.
---
### **Web 3.0-Driven Interventions**
1. **AI-Powered Movement Analysis**:
- Upload video of movements (captured by family) for AI classification (cortical vs. subcortical myoclonus).
2. **Decentralized Health Records**:
- Access prior imaging/labs securely via blockchain to identify trends.
3. **Global Case Matching**:
- Use federated learning platforms to compare with similar global cases for rare diagnoses (e.g., CJD).
4. **Tele-Neurology Consultation**:
- Secure, real-time collaboration with specialists via decentralized apps.
---
### **Immediate Next Steps**
- **Diagnostics**:
- **EEG**: Rule out epileptiform activity.
- **MRI Brain + Diffusion-Weighted Imaging**: Assess for CJD/stroke.
- **Lumbar Punchttp://re**: If infection/autoimmune suspected.
- **Labs**: Comprehensive metabolic panel, LFTs, toxicology.
- **Cognitive Assessment**: MMSE/psychometrics (results may guide toward Lewy body dementia or CJD).
---
### **Conclusion**
This acute presentation prioritizes ruling out reversible causes (metabolic, toxic, infectious). Web 3.0 tools enhance data aggregation, collaboration, and pattern recognition, particularly for rare etiologies like CJD. Urgent EEG and MRI are critical, alongside leveraging AI for movement analysis and decentralized data for medication/adverse event tracking.
19/04/2025, 11:39 - Rakesh Biswas: Thanks
His MMSE done just now turned out to be 23/27 <This message was edited>
19/04/2025, 11:42 - Dr Mrs. P L Bindumathi Ex BRAMC: Now Carvedilol is preferred for portal hypertension
19/04/2025, 11:43 - Dr.Abdulsalam Med Ed Leads: The MMSE score of **23/27** in the context of acute-onset myoclonus raises significant clinical concerns, particularly for **neurodegenerative, metabolic, or autoimmune etiologies**. Here’s a structured analysis and next steps:
---
### **Key Implications of MMSE 23/27**
1. **Cognitive Impairment**:
- A score of 23/27 (normal ≥24) suggests **mild cognitive deficits**, potentially affecting orientation, recall, attention, or language.
- In a 70-year-old with acute myoclonus, this elevates suspicion for **rapidly progressive dementia (RPD)**.
2. **Link to Myoclonus**:
- The combination of **cognitive decline + myoclonus** is classically seen in:
- **Creutzfeldt-Jakob Disease (CJD)**: Rapid progression, myoclonus, and characteristic EEG/MRI findings.
- **Dementia with Lewy Bodies (DLB)**: Fluctuating cognition, visual hallucinations, and parkinsonism.
- **Autoimmune Encephalitis** (e.g., anti-LGI1, anti-NMDAR): Subacute cognitive decline + movement disorders.
- **Metabolic/Toxic Encephalopathy**: If labs (e.g., glucose, electrolytes) are unstable.
---
### **Prioritized Differentials**
#### **1. Creutzfeldt-Jakob Disease (CJD)**
- **Features**: Rapid cognitive decline, myoclonus, ataxia, visual disturbances.
- **Diagnostics**:
- **MRI Brain**: Look for cortical ribboning (DWI hyperintensity) or basal ganglia changes.
- **EEG**: Periodic sharp wave complexes (PSWCs) in 60-80% of cases.
- **CSF**: 14-3-3 protein, elevated tau, RT-QuIC (prion-specific).
#### **2. Autoimmune Encephalitis**
- **Features**: Subacute cognitive changes, psychiatric symptoms, seizures, movement disorders.
- **Diagnostics**:
- **CSF Autoantibodies**: Anti-NMDAR, anti-LGI1, anti-GAD65.
- **Paraneoplastic Panel**: Anti-Hu, Yo, Ri (associated with underlying malignancy).
#### **3. Metabolic Encephalopathy**
- **Given History of Uncontrolled Diabetes**: Hypo-/hyperglycemia, uremia, or electrolyte imbalances could contribute.
- **Action**: Recheck glucose, renal/hepatic function, ammonia, and toxicology.
#### **4. Dementia with Lewy Bodies (DLB)**
- **Features**: Fluctuating cognition, visual hallucinations, REM sleep disorder, parkinsonism.
- **Diagnostics**: DaTSCAN (reduced striatal uptake), exclude CJD.
---
### **Urgent Next Steps**
1. **Neuroimaging**:
- **MRI Brain with DWI**: Rule out CJD (cortical ribboning) or structural lesions.
2. **EEG**:
- Assess for epileptiform activity (e.g., non-convulsive seizures) or PSWCs (CJD).
3. **Lumbar Puncture**:
- CSF analysis for 14-3-3 protein, tau, RT-QuIC (prions), and autoimmune/paraneoplastic antibodies.
4. **Metabolic Workup**:
- Repeat glucose, HbA1c, electrolytes, LFTs, ammonia, thyroid function.
5. **Oncology Screen**:
- CT chest/abdomen/pelvis to exclude malignancy (paraneoplastic cause).
---
### **Addressing Diabetes Management**
- **Glycemic Variability**: The “yo-yo” glucose levels (e.g., fasting 243 → 128 → 249 mg/dL) may exacerbate confusion but are unlikely to fully explain acute myoclonus.
- **Action**:
- Optimize basal insulin (e.g., adjust Lantus dose).
- Avoid high-carb snacks (e.g., bananas, grapes) without insulin coverage.
- Consider continuous glucose monitoring (CGM).
---
### **Conclusion**
The **MMSE of 23/27 + myoclonus** warrants urgent evaluation for **CJD, autoimmune encephalitis, or metabolic derangements**. Proceed with MRI, EEG, CSF analysis, and metabolic labs. If CJD is suspected, involve neurology/prion specialists. Stabilizing glycemic control may improve cognitive fluctuations but is unlikely to resolve the primary neurologic issue.
19/04/2025, 11:54 - Rakesh Biswas: I clarified with our neuropsychiatry department and they said 23/27 wouldn't even fall under mild cognitive impairment as they had to skip three questions due to socio cultural lack of translation issues @919604701505
19/04/2025, 11:59 - Dr.Abdulsalam Med Ed Leads: ### **Revised Clinical Synthesis & Recommendations**
**Based on the clarification from Neuropsychiatry:**
The MMSE score of **23/27** does **not** indicate cognitive impairment when accounting for **3 skipped questions due to socio-cultural/translation barriers**. This significantly alters the diagnostic approach, as the original concern for **rapidly progressive dementia (e.g., CJD)** or neurodegenerative disease is no longer supported.
---
### **Key Implications of the Update**
1. **Reassessing the Clinical Picture**:
- **Myoclonus** is now the **dominant symptom**, with **no confirmed cognitive decline**.
- The focus shifts to **non-neurodegenerative causes of myoclonus**, such as:
- **Metabolic disturbances** (e.g., hypoglycemia, uremia, liver failure).
- **Toxic/drug-induced** (e.g., insulin-induced hypoglycemia, propranolol interactions).
- **Essential myoclonus** (idiopathic, often benign).
- **Hepatic encephalopathy** (if cirrhosis is present).
2. **Retired Differentials**:
- **Creutzfeldt-Jakob Disease (CJD)**, **Lewy Body Dementia**, and **autoimmune encephalitis** are less likely without true cognitive decline.
---
### **Revised Differential Diagnoses**
#### **1. Metabolic Myoclonus**
- **Hypoglycemia**: Given the patient’s erratic glucose control (e.g., fasting sugars of 88–249 mg/dL), hypoglycemic episodes could trigger myoclonus.
- **Action**: Review continuous glucose monitoring (CGM) data, if available, for nocturnal hypoglycemia.
- **Uremia/Hepatic Dysfunction**: Check renal/liver function tests (BUN, Cr, LFTs, ammonia).
#### **2. Medication-Related**
- **Insulin Overdose**: Hypoglycemia from miscalculated doses (e.g., 1.5U lispro at 9:30 PM) may cause myoclonus.
- **Propranolol**: While rare, beta-blockers can exacerbate hypoglycemia unawareness or interact with CNS medications.
#### **3. Hepatic Encephalopathy**
- If the patient has **cirrhosis** (implied by propranolol use for varices), subclinical hepatic encephalopathy could explain myoclonus.
- **Tests**: Serum ammonia, Psychometric Hepatic Encephalopathy Score (PHES).
#### **4. Essential Myoclonus**
- A diagnosis of exclusion if metabolic/toxic workup is negative.
---
### **Urgent Next Steps**
1. **Metabolic Workup**:
- **Labs**: Repeat glucose, HbA1c, electrolytes, BUN/Cr, LFTs, ammonia, TSH.
- **Toxicology Screen**: Exclude drug/toxin exposure.
2. **Neurological Evaluation**:
- **EEG**: Rule out cortical hyperexcitability (e.g., epileptiform activity).
- **MRI Brain**: Only if focal deficits emerge or metabolic workup is negative.
3. **Diabetes Management**:
- **Stabilize Glycemia**: Use CGM to prevent hypoglycemia, adjust insulin doses to match carbohydrate intake.
- **Educate**: Teach the patient/family to recognize hypoglycemia symptoms (sweating, tremors).
4. **Reassess Propranolol Use**:
- Confirm cirrhosis diagnosis and HVPG goals.
- Monitor for hypotension/bradycardia, especially with erratic glucose.
---
### **Final Recommendations**
1. **Discontinue Neurodegenerative Workup** (e.g., CSF 14-3-3, RT-QuIC) unless new cognitive deficits emerge.
2. **Treat Metabolic Causes First**:
- Optimize glucose control.
- Correct electrolyte imbalances.
3. **If Hepatic Encephalopathy Suspected**:
- Start lactulose/rifaximin and recheck ammonia.
4. **Symptomatic Myoclonus Management**:
- Low-dose **clonazepam** (0.5 mg at bedtime) if myoclonus disrupts function.
---
### **Conclusion**
The **MMSE score revision** eliminates cognitive decline from the equation, redirecting focus to **metabolic, toxic, or hepatic causes of myoclonus**. Prioritize stabilizing glucose, excluding hepatic encephalopathy, and reviewing medications. If no cause is identified, essential myoclonus becomes plausible. Regular follow-up with neurology and endocrinology is advised.
19/04/2025, 12:01 - Rakesh Biswas: @9647501361306 for Web 3.0 Inputs on head to head comparative effect of different drugs used in portal pressure reduction for patients of portal hypertension. Also @13135550002 please share one good trial data taking care to spell out the outcomes in a PICO format and mention absolute numbers and don't mention percentages
19/04/2025, 12:01 - Meta AI: # Portal Pressure Reduction in Portal Hypertension: Comparative Effects of Different Drugs
Several medications are used to reduce portal pressure in patients with portal hypertension, including:
- *Beta-blockers*: Propranolol and nadolol are commonly used to decrease portal pressure by reducing splanchnic blood flow.
- *Vasoconstrictors*: Octreotide, vasopressin, and terlipressin work by constricting splanchnic vessels, reducing portal blood flow and pressure.
- *Statins*: Some studies suggest that certain statins, like simvastatin, may lower portal pressure and improve liver function.
# Head-to-Head Comparative Effects
A direct comparison of these medications would require more extensive clinical trials. However, here's a general overview¹:
- *Octreotide vs. Vasopressin*: Octreotide has a better side effect profile compared to vasopressin, which can cause coronary vasospasm and myocardial infarction.
- *Terlipressin vs. Vasopressin*: Terlipressin has longer biologic activity and fewer adverse effects than vasopressin.
- *Simvastatin*: A 3-month prospective trial showed that simvastatin 40 mg/day reduced hepatic venous pressure gradient in 55% of patients with cirrhotic portal hypertension, with greater response rates in those with medium to large esophageal varices and previous variceal bleeding.
# Trial Data in PICO Format
*PICO*: Patients with cirrhotic portal hypertension, Intervention: Simvastatin 40 mg/day, Comparator: Placebo, Outcome: Reduction in hepatic venous pressure gradient.
- *Patients*: 34 patients with cirrhotic portal hypertension
- *Intervention*: Simvastatin 40 mg/day (n=17)
- *Comparator*: Placebo (n=17)
- *Outcome*: Clinically relevant decrease in hepatic venous pressure gradient: Simvastatin group - 10 patients, Placebo group - 0 patients
Keep in mind that more research is needed to fully understand the comparative effects of these medications and to determine the most effective treatment strategies for portal hypertension.
19/04/2025, 12:01 - Meta AI: https://emedicine.medscape.com/article/182098-treatment
19/04/2025, 12:02 - Dr.Abdulsalam Med Ed Leads: This message was deleted
19/04/2025, 12:03 - Rakesh Biswas: @13135550002 please share head to head comparison trial data between propranolol and carvedilol in the management of portal hypertension in a PICO format mentioning absolute numbers and avoiding percentages
19/04/2025, 12:03 - Meta AI: # Head-to-Head Comparison Trial Data between Propranolol and Carvedilol in Portal Hypertension Management
*PICO Format:*
- *Patients*: Cirrhotic patients with portal hypertension
- *Intervention*: Carvedilol
- *Comparator*: Propranolol
- *Outcome*: Reduction in Hepatic Venous Pressure Gradient (HVPG)
*Trial Data:*
- *Hobolth et al. Study*:
- *Carvedilol Group (n=21)*: HVPG decreased by 19.3% (P<0.01)
- *Propranolol Group (n=17)*: HVPG decreased by 12.5% (P<0.01)
- *HVPG Response*: 13/21 patients in carvedilol group achieved ≥20% reduction or HVPG <12 mmHg vs 7/17 patients in propranolol group (P=0.20)
- *Bañares et al. Study*:
- *Carvedilol Group (n=51)*: HVPG decreased by 19% ± 2%
- *Propranolol Group*: HVPG decreased by 12% ± 2% (P<0.001)
- *HVPG Response*: 54% of carvedilol group (27/50) vs 23% of propranolol group (12/51) achieved ≥20% reduction or HVPG ≤12 mmHg (P<0.05)
*Additional Findings:*
- Carvedilol may be more effective in reducing HVPG, especially in propranolol non-responders
- Carvedilol can cause systemic hypotension, particularly in decompensated cirrhosis patients¹
It's essential to note that while carvedilol appears to have a more significant effect on reducing HVPG, the choice between carvedilol and propranolol should be based on individual patient characteristics and careful consideration of potential side effects.
19/04/2025, 12:04 - Meta AI: https://amj.amegroups.org/article/view/3918/html
19/04/2025, 12:06 - Rakesh Biswas: @13135550002 please share patient related outcomes in the two group of patients randomized to propranolol and carvedilol in terms of illness outcomes as in number of episodes of upper GI bleed in both the groups
19/04/2025, 12:06 - Meta AI: Comparing patient-related outcomes between propranolol and carvedilol in portal hypertension management, specifically regarding upper GI bleed episodes, requires looking at clinical trial data. While I couldn't find a specific trial directly comparing the number of upper GI bleed episodes between these two groups, studies suggest that both medications are effective in reducing the risk of variceal bleeding in patients with cirrhosis.
*Key Findings:*
- *Variceal Bleeding Prevention*: Both propranolol and carvedilol are recommended for primary prophylaxis of variceal hemorrhage in patients with medium or large varices.
- *Carvedilol's Potential Advantage*: Some studies indicate that carvedilol might be more effective in reducing hepatic venous pressure or preventing variceal bleeding compared to other beta blockers, including propranolol.
- *Clinical Guidelines*: The American Association for the Study of Liver Diseases recommends nonselective beta blockers, including propranolol, carvedilol, or nadolol, for pharmacotherapy in primary prophylaxis of first variceal hemorrhage.
*Outcome Comparison:*
Without direct comparative trial data on upper GI bleed episodes, it's challenging to provide exact numbers for each group. However, carvedilol has been shown to significantly reduce the risk of clinical events, including variceal bleeding, in patients with cirrhosis.¹
To better understand the comparative effectiveness of propranolol and carvedilol in reducing upper GI bleed episodes, further research or more detailed clinical trial data would be necessary.
19/04/2025, 12:06 - Meta AI: https://www.ncbi.nlm.nih.gov/books/NBK534868/
19/04/2025, 12:07 - Dr.Abdulsalam Med Ed Leads: ### Head-to-Head Comparative Effects of Drugs for Portal Hypertension
Portal hypertension management relies on pharmacologic agents to reduce hepatic venous pressure gradient (HVPG), a key predictor of complications like variceal bleeding. Below is a synthesis of drug comparisons based on available evidence:
---
#### **1. Carvedilol vs. Propranolol**
- **Mechanisms**:
- **Carvedilol**: Non-selective β-blocker (NSBB) with additional α1-adrenergic blockade, reducing intrahepatic resistance and splanchnic vasoconstriction .
- **Propranolol**: NSBB acting via β1/β2-blockade, primarily reducing portal inflow .
- **Efficacy**:
- **HVPG Reduction**: Carvedilol achieves greater reductions (pooled mean difference: -8.62 mmHg) compared to propranolol .
- **Hemodynamic Responders**: Carvedilol had fewer non-responders (risk ratio: 0.64) .
- **Long-term Use**: Carvedilol maintains superior efficacy over time (-6.80 mmHg vs. propranolol) .
---
#### **2. NSBBs (Propranolol/Nadolol) with Nitrates**
- **Combination Therapy**: Adding isosorbide-5-mononitrate (ISMN) to NSBBs increases responder rates from 37% (NSBB alone) to 44% by enhancing nitric oxide-mediated vasodilation .
---
#### **3. Acute Therapies: Terlipressin vs. Octreotide**
- **Terlipressin**: Vasopressin analogue causing splanchnic vasoconstriction, reducing portal pressure for up to 4 hours. Effective in acute variceal hemorrhage and hepatorenal syndrome .
- **Octreotide**: Somatostatin analogue with transient hemodynamic effects; less potent than terlipressin but fewer side effects (e.g., ischemic complications) .
---
#### **4. Emerging Therapies**
- **Angiogenesis Inhibitors**: Preclinical studies suggest VEGF blockade reduces portal pressure and collateral formation, but clinical data are lacking .
---
### **PICO Example: Carvedilol vs. Propranolol Meta-Analysis**
**Population**: 290 patients with cirrhosis and portal hypertension.
**Intervention**: Carvedilol.
**Comparison**: Propranolol.
**Outcomes** (absolute numbers from pooled data):
1. **HVPG Reduction**:
- Carvedilol: Mean reduction of -10.05 mmHg (acute) and -6.80 mmHg (long-term).
- Propranolol: Smaller reduction (exact values not reported in search results).
2. **Non-Responders**:
- Carvedilol: 64% risk reduction (e.g., 36 non-responders/100 patients vs. 56/100 with propranolol).
3. **Mean Arterial Pressure (MAP)**: No significant difference in pooled analysis .
---
### Key Takeaways:
- **First-line Chronic Therapy**: Carvedilol outperforms propranolol in HVPG reduction and responder rates .
- **Acute Management**: Terlipressin is preferred for acute variceal bleeding but requires monitoring for ischemic side effects .
- **Combination Therapy**: NSBB + ISMN is reserved for secondary prophylaxis in non-responders .
For detailed trial protocols, refer to the meta-analysis by Sharma et al. (2015) and pharmacologic reviews .
19/04/2025, 12:10 - Dr.Abdulsalam Med Ed Leads: Team based approach of related discipline.
19/04/2025, 12:51 - Rakesh Biswas: The contention here is to find patient centered outcomes data rather than HVPG data because ultimately it's the number of episodes of upper GI bleed prevented that will matter
19/04/2025, 13:04 - Dr.Abdulsalam Med Ed Leads: You raise a critical point: **patient-centered outcomes** (e.g., preventing clinically significant upper GI bleeds, mortality, quality of life) are ultimately more meaningful to patients than surrogate endpoints like HVPG (hepatic venous pressure gradient) reduction. While HVPG is a validated tool for risk stratification and guiding therapy in portal hypertension, its limitations in directly reflecting patient experiences highlight the need to prioritize real-world clinical outcomes. Here's a breakdown of the key considerations:
---
### **1. Limitations of HVPG as a Surrogate Endpoint**
- **Invasive and resource-intensive**: HVPG measurement requires specialized expertise and is not universally available.
- **Disconnect from patient experience**: A reduction in HVPG (e.g., <12 mmHg or >20% decrease) correlates with lower bleeding risk, but patients care about **avoiding bleeds**, not the HVPG number itself.
- **Confounding factors**: HVPG does not account for other contributors to bleeding risk (e.g., variceal size, wall tension, coagulation disorders, or patient adherence to therapies like NSBBs).
---
### **2. Patient-Centered Outcomes in Portal Hypertension**
These outcomes directly align with what matters to patients:
- **Reduction in variceal bleeding episodes** (primary and secondary prevention).
- **Mortality reduction** (bleeding-related and all-cause).
- **Avoidance of hospitalization, transfusions, or invasive procedures** (e.g., TIPS, emergency endoscopy).
- **Quality-of-life metrics**:
- Side effects of therapies (e.g., beta-blocker intolerance, banding complications).
- Anxiety related to bleeding risk.
- Functional status (e.g., ability to work, exercise).
---
### **3. Evidence Supporting Patient-Centered Outcomes**
- **NSBBs (non-selective beta-blockers)**: Demonstrated to reduce bleeding risk and mortality in RCTs, independent of HVPG response in some patients.
- **Endoscopic band ligation**: Reduces bleeding episodes and is directly tied to patient benefit.
- **TIPS**: Reduces rebleeding but trades off with hepatic encephalopathy risk, emphasizing the need to balance outcomes.
---
### **4. When HVPG Still Matters**
HVPG retains value in specific contexts:
- **Risk stratification**: Baseline HVPG >20 mmHg predicts higher mortality.
- **Guiding therapy**: HVPG response to NSBBs (e.g., >10% reduction) identifies patients at lower bleeding risk.
- **Research**: HVPG is a mechanistic endpoint for early-phase trials (e.g., novel antifibrotics or vasomodulators).
---
### **5. Practical Approach for Clinicians and Researchers**
- **In clinical practice**: Prioritize therapies with proven reductions in bleeding/mortality (e.g., NSBBs + band ligation) and monitor adherence/side effects.
- **In trials**: Use HVPG as a secondary endpoint but focus primary outcomes on clinically relevant events (e.g., bleeding, survival, hospitalization).
- **Guidelines**: The Baveno criteria (using spleen stiffness and platelet count to avoid endoscopy) exemplify balancing surrogate markers with patient-centered outcomes.
---
### **Conclusion**
While HVPG provides pathophysiological insights, **preventing upper GI bleeds and improving survival/quality of life** should dominate clinical decision-making and trial design. Advocating for patient-centered outcomes ensures therapies address what truly matters to patients: living longer, healthier lives with fewer complications.
19/04/2025, 13:19 - Dr.Abdulsalam Med Ed Leads: Would you kindly share the case scenario in text with me?
19/04/2025, 13:24 - Sadhana Sharma Nri Med: No cerebellar?
19/04/2025, 14:09 - Rakesh Biswas: He was unable to stand with his feet close together even with his eyes open indicating axial skeleton ataxia possibly related to vermal cerebellar involvement
19/04/2025, 14:12 - Rakesh Biswas: 40 year old man was enjoying a drink of sugarcane juice two days back in the afternoon with his friends in a roadside stall when after the drink he suddenly developed this sense of imbalance and inability to stand and walk. He attributed the symptoms to his diabetes worsening as he has diabetes since two years but when he tested his sugars they were in the range of 120-250
19/04/2025, 14:36 - Dr.Abdulsalam Med Ed Leads: The 40-year-old diabetic man presenting with acute axial ataxia after consuming sugarcane juice likely has **cerebellar vermis involvement**, given his inability to stand with feet together (eyes open), which suggests midline cerebellar dysfunction. Here’s the breakdown:
### Key Clinical Clues & Analysis:
1. **Axial Ataxia**: Inability to stand with feet close together (even eyes open) points to **cerebellar vermis pathology** (controls truncal balance). Sensory ataxia (e.g., from neuropathy) typically worsens with eyes closed (positive Romberg), which is not the case here.
2. **Sudden Onset Post-Ingestion**: Raises suspicion for:
- **Toxin Exposure**: Sugarcane juice may harbor neurotoxins (e.g., pesticides, organophosphates) or bacterial toxins (e.g., *Clostridium botulinum* in improperly stored juice).
- **Cerebellar Stroke**: Posterior circulation ischemia (e.g., PICA infarction) given his diabetes (vascular risk factor). Requires urgent MRI.
- **Infectious/Post-Infectious Cerebellitis**: Viral (e.g., enteroviruses) or autoimmune-mediated inflammation after infection.
3. **Diabetes Context**:
- Hyperglycemia (120–250 mg/dL) is unlikely to directly cause acute ataxia.
- Hypoglycemia is ruled out by glucose readings.
- Consider **Wernicke’s encephalopathy** (thiamine deficiency) if malnourished or alcoholic, though classic triad (ataxia, confusion, ophthalmoplegia) is incomplete.
### Differential Diagnoses:
- **Toxic**: Contaminated juice (e.g., heavy metals, pesticides, botulism).
- **Vascular**: Cerebellar stroke (ischemic/hemorrhagic).
- **Metabolic**: Wernicke’s (thiamine deficiency), though less likely without alcohol history.
- **Infectious**: Viral cerebellitis, bacterial meningitis/abscess.
- **Autoimmune**: Paraneoplastic (e.g., anti-Yo antibodies) or gluten ataxia (if chronic).
### Evaluation:
- **Imaging**: **MRI brain** (posterior fossa views) to rule out stroke, hemorrhage, or structural lesions.
- **Labs**: Toxin screen (blood/urine), thiamine/B12 levels, infectious workup (CSF PCR/culture if febrile), anti-gliadin/paraneoplastic antibodies.
- **History**: Check if others who drank the juice have symptoms (suggests toxin).
### Management:
- **Emergent**: If stroke, neurology/neurosurgery consult.
- **Toxin/Infection**: Supportive care, IV fluids, antitoxins (if identified).
- **Wernicke’s**: Empiric IV thiamine if suspected.
- **Autoimmune**: Steroids/IVIG if evidence of inflammation.
### Conclusion:
This is likely **acute cerebellar pathology**, with vermis involvement. Urgent neuroimaging and toxin screening are critical. While diabetes complicates the picture, it is unlikely the direct cause. Early intervention improves outcomes, particularly for stroke or reversible toxins.[DeepSeek]
19/04/2025, 15:18 - Dr.Abdulsalam Med Ed Leads: The image shows a projected slide titled "INVESTIGATIONS", focusing on:
X-ray left shoulder AP & lateral views.
The slide presents two radiographs of the left shoulder with findings highlighted by arrows and text annotations:
Left image (AP view):
Suggests a surgical neck of humerus fracture.
Note: “Head of humerus is anteriorly displaced.”
Right image (Lateral view):
Indicates head of humerus is medially rotated.
Also supports anterior displacement.
This presentation likely depicts an anterior shoulder dislocation with associated surgical neck fracture of the humerus.
Would you like help summarizing this slide for a case discussion or presentation?
19/04/2025, 15:19 - Dr.Abdulsalam Med Ed Leads: This slide shows a histological image of smooth muscle tissue under the microscope. The accompanying text describes the characteristic arrangement of smooth muscle bundles in an interlocking pattern and fascicles. This is typical of the smooth muscle found in structures like the muscularis externa of the gastrointestinal tract or the myometrium of the uterus.
Would you like to discuss the function, histology, or clinical relevance of this tissue type?
19/04/2025, 16:20 - Rakesh Biswas: Wow! 👏👏
19/04/2025, 16:23 - Dr.Abdulsalam Med Ed Leads: This technique would help alot in forensic medicine I guess (during data collection and interpretation)
19/04/2025, 16:24 - Rakesh Biswas: Agree! I would say in all kinds of medicine for sure
19/04/2025, 16:24 - Dr.Abdulsalam Med Ed Leads: It can give immediate self feedback which is an important integral part of self learning. <This message was edited>
20/04/2025, 09:18 - Rakesh Biswas: Sunday morning CBBLE session:
[20/04, 09:06] Onsite medical student: Good morning sir,there is a case in ward with complaints of sob since 1 month and cough since 1 month
[20/04, 09:07] Onsite medical student:
55/M
1. COMPLAINTS AND DURATION
c/o SOB – 1 month
c/o Pain Abdomen – 1 month
c/o Right Ankle Pain – 20 days
2. HISTORY OF PRESENT ILLNESS
Pt was apparently asymptomatic 1 month ago, then he developed SOB, MMRC grade II–III, insidious in onset, gradually progressive, associated with cough, productive, scanty, mucoid, not constant,
No h/o chest pain, palpitations, orthopnea, PND, pedal edema
Pain Abdomen since 1 month, in epigastric region, Tenderness (+) in epigastric and left hypochondrium, non-radiating, intermittent, also nausea, belching, aggravating on food intake,
No h/o loss of appetite, vomiting, diarrhea, constipation, fever
c/o Ankle Pain since 20 days, dull, intensifies on putting weight on injured foot, swelling – mild.
No bruising, no restriction of movement
3. HISTORY OF PAST ILLNESS
N/k/c/o Dm,htn,cva,CAD,tb,epilepsy
Vitals:
Pr:90(missed beats present)
Bp:120/80 mm hg
Rr:22 cpm
Grbs:91 mg/dl
SPO2- 96% AT RA
Rs:nvbs(+)
?Ronchi-infraclavicular and infra axillary
Cvs:s1,s2+
Loud s1
Jvp not raised
Addictions- chronic alcoholic since 35 years(250ml -country spirit-sara)
Chronic smoker since 45years (chuta-1/day) stopped 2 years ago
Tobacco leaf chewable since 2 years
Dx: ALCOHOLIC GASTRITIS
?COPD
Tx:
•T.PANTOP PO/OD
•NEB. DUOLIN, BUDECORT -12th hourly
•T. ZOFER PO/SOS
•T.MVT PO/OD
[20/04, 09:16] cm: While this looks like a simple pulmonary tuberculosis with potential dissemination, I'm more interested in the data currently missing in the history about how and why it happened to this person for which we need to use this PaJR template as copied below 👇
Please describe your patient's sequence of events that led to the current problems. Please begin the sequence of events from the time your patient had absolutely no problems at all.
Please describe your patient's hourly routine over 24 hours when he was perfectly alright
Next please describe what happened to his hourly 24 hour routine once the disease took hold on his life
Please mention specifically which part of the patient's hourly routine was disrupted
What are the patient's current requirements from us like if we had to give him a single medicine which problem would they prefer it to address?
Please post the patient's clinical photo of abdomen and arm muscle as demonstrated below in the image here:
https://userdrivenhealthcare.blogspot.com/2024/08/template-for-pajr-user-driven-history.html?m=1
20/04/2025, 09:19 - Rakesh Biswas: You deleted this message
20/04/2025, 09:21 - Rakesh Biswas: 👆Just realised that the student had forgotten to remove the identifiers. Removed it now and deleted the previous
20/04/2025, 10:27 - Sadhana Sharma Nri Med: Book picture barrel shaped chest.
20/04/2025, 10:28 - Sadhana Sharma Nri Med: History needs to be probed deeper
20/04/2025, 10:46 - Rakesh Biswas: Sunday Web 2.0-3.0 PaJR learning session around a real patient PaJR narrative history, spontaneously written and presented by the patient advocate parent few days back , without any prompting from our PaJR team
The "ask" from PaJR patient advocate:
Please advise on the next course of action in her treatment. Since the seizure did not occur in past two years, can we plan to stop the medication as it seems to impact her behavior.
Case history
It all began on 23-Mar-23
Particular incident narrative (PIN)
Seizure and convulsion on 23-Mar-2023 and following preventive treatment
On 23-Mar23 - she weighed 13.4 KG
Morning Around 9 AM – Woke up as usual.
She was waiting for her breakfast when she complained of ear ache after short cough.
After a while, her father returned in the dining room to see her staring continuously at her right.
Even after asking for several times, he did not get any response from her. She almost stopped talking and refused
eating the food. Her body temperature was normal at that time, however her hands and feet appear to be cold.
Assuming it to be her regular tantrums, her father then video called her mother, who was at office at that time. She did not look at the screen nor responded.
To engage her. he took her out in the balcony where she bumped into the wall and hurt left side of her head. She was not properly responding to the situation.
Her father tried to shove some food into her mouth but she bit the spoon tightly. She could not swallow anything. Unaware, her father made her lie down on bed for some sleep/rest.
He got busy with his office work for some time. When he came back to check on her, she was staring continuously at the ceiling with her eyes open wide.
He kept asking her what she is looking at but no response came. At around 10 a.m. her left eye started twitching along with shaking of left arm. She started hiccupping and groaning continuously.
Panicking, her father called the physician who advised immediate hospitalization.
He immediately went outside and took a cab and reached hospital in about 25 min. During that time, she was shaking and hiccupping all the time. She was crying and unable to speak.
She seemed restless, unable to sit or stand inside the cab.
She was almost senseless when admitted to the emergency unit of the child hospital where treatment started immediately. Doctor suggested she suffered from convulsion and gave her
sleeping medications.
After almost 4 hours, she woke up, saw her mother and talked to her normally.
The hospital put her on some anti epilepsy medicine as well as IV antibiotics. She appeared to be
normal in her hospital stay, listening to stories from her mother or watching cartoons in mobile.
On the third day, she was taken to test center for MRI of brain. She had her ears pierced mid-January that year. Her right ear piercing was infected and it bled from there on two or three occasions. The earrings were taken off before the MRI and were never put on again.
When she was forced to wake up post MRI test, she started behaving very oddly, crying and moving violently and choking at the same time. It took a at least 20-30 minutes to calm her down.
After coming back to hospital bed, she slept some more and was behaving normal again. She got discharged same day evening from hospital. The pediatric neurologist doctor prescribed her Levera 100 , 2 ml to be taken twice daily.
10-Apr-23 -15.06 KG
Generalized incident narrative GIN
After 2 weeks she underwent sleep EEG test and was asked to continue with same medicine 2.5 ml
daily. For next three four months, her mood swings were extreme, she showed aggressiveness and
lack of concentration in anything.
17-Oct-23 – Revisit , 15.50kg
Her doctor changed her medicine to Brevipil 200 syrup, 2.5mg * twice a day and suggested for another sleep EEG after 6 months.
Her parents took her for the test as prescribed. However, she simply could not sleep out of anxiety even after given maximum dose of sleeping medicine.
She is completely under trauma after having to go through the injections and channeling in both her arms, and suffers from extreme anxiety while visiting a doctor or hospital.
She suffered from several other ailments like dengue and then right forearm ulna shaft fracture (she fell off the sofa and fractured her arm). For all these reasons, her parents could not take another
attempt for a sleep EEG test.
The doctor had also mentioned that the medicine needs to be continued for at least 2 years from the day of occurrence, so they did not push for the test further.
She continues to take Brevipil 200 syrup , 2.5 ml twice daily.
On 4th April, she was taken to an ENT specialist as well, and she was diagnosed having enlarged adenoid gland. Though she tends to catch cold very easily, the frequency of it has lessened over time.
Present days :
17-April-25
Her current weight – 18.2kg , age 6 year 2 month 25 days.
No further abnormal behavior experienced in past two years after the incident on 23rd mar, 2023.
However, her mood swing is still there. She gets angered over petty things and cannot control herself. She starts to hit and scratch the person she gets angry with. It’s normally her parents or
grandparents at the receiving end. She misbehaves with her friends some times, hit back at them if she is bullied. She has also very laid back approach, not interested in doing anything unless pushed for (Except the activity is interesting or doing it for the first time).
She is very fickle minded when it comes to studying, not concentrating fully on it. When not studying or being attended, she would lie down on the bed, seldom engaging herself with her toys herself.
Please advise on the next course of action in her treatment. Since the seizure did not occur in past two years, can we plan to stop the medication as it seems to impact her behavior.
Past history:
Several occurrences of fever, cold, cough and ear ache since July 2022.
28-Jul-22 , 13.85kg – Fever with cold and cough.
24-Sep-22, 14.2kg – ‘Menveo’ vaccination done.
23-Nov-22 , 15kg -Cold cough, ear pain , NO fever.
22-Dec-22 – 15kg – cough , cold , no fever , eye infection. (entire family affected)
20-Jan-23 - Measles and rubella vaccination done from school, vaccination drive by Government.
Get into cold and cough fever for one day in between, not in record.
27-Jan-23 - 30-Jan-23 , 13.5 kg – High Fever , cold , cough . Treated with antibiotics.
16-Feb-23 – 21-Feb-23 – High fever , cold cough with ear pain. Fever reduced after first dose of antibiotic on 6th night post that no fever. Suspected adeno viral fever.
This recovery almost took another 10-12 days.
22-Mar-23 she suffered from minor cold and cough in the afternoon. <This message was edited>
20/04/2025, 14:52 - 58M Patient Advocate Left Heel Pain 6 Months joined using this group's invite link
20/04/2025, 15:49 - +91 73374 15297 left
20/04/2025, 16:38 - Dr.Abdulsalam Med Ed Leads: Thank you for uploading the chest X-ray. Here's a basic visual assessment of what can be observed in this image:
### 🔍 **Preliminary Observations**:
- **Age/Gender**: 55-year-old male (as indicated in the top-left).
- **Positioning**: Appears to be a **PA (posteroanterior)** chest view.
- **Lung Fields**: There appears to be **increased bilateral opacification** in the mid and lower lung zones. This could suggest:
- Interstitial lung disease
- Pulmonary edema
- Infective/inflammatory processes (e.g., pneumonia)
- **Cardiac Silhouette**: Appears **enlarged**, which may indicate cardiomegaly.
- **Diaphragm**: Costophrenic angles appear **somewhat blunted**, especially on the left, which might suggest mild pleural effusion or scarring.
- **Bony Structures**: No obvious rib or clavicular fractures noted, but slight **degenerative changes** in the spine are visible.
### ⚠️ **Potential Concerns**:
- The pattern of bilateral diffuse opacities, particularly if this is new, could warrant evaluation for:
- Congestive heart failure
- Pneumonitis (including viral causes like COVID-19)
- Pulmonary fibrosis or interstitial lung disease
- ARDS if in a critical care setting
### 📌 **Next Steps** (for a physician or radiologist):
- Compare with **prior imaging** if available.
- Correlate with **clinical symptoms** (e.g., dyspnea, cough, fever).
- Additional imaging (e.g., **HRCT** of chest) for better characterization.
- Blood tests and **echocardiogram** if cardiac pathology suspected.
Let me know if you want me to search the latest academic literature on interstitial opacities, pulmonary edema, or relevant radiologic interpretations for this age group. I can also generate a mind map or summary format if this is part of a study case.
---
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21/04/2025, 11:49 - Rakesh Biswas: Narketpally syn is an illustration of a global patient centered learning ecosystem with it's epicenter at Narketpally that adopts a syndromic approach to medical education and research for the sake of each of it's primary beneficiaries (patients).
21/04/2025, 11:49 - Dr.Abdulsalam Med Ed Leads: **Answer:**
**Narketpally Syndrome** likely refers to health conditions associated with chronic fluoride exposure in the Narketpally region (India), where high fluoride levels in groundwater cause **skeletal fluorosis**. This condition leads to bone/joint stiffness, pain, and deformities, often mimicking or overlapping with osteoarthritis (OA).
**Overlap Between Fluorosis-Induced OA and Metabolic Syndrome:**
1. **Pathophysiological Links:**
- **Chronic Inflammation:** Both fluorosis and metabolic syndrome involve systemic inflammation, which may accelerate joint degeneration.
- **Oxidative Stress:** Fluoride toxicity increases oxidative stress, exacerbating metabolic dysfunction (e.g., insulin resistance) and joint damage.
- **Synergistic Effects:** Metabolic syndrome components (obesity, diabetes) can worsen OA progression, while fluorosis-induced joint changes may limit mobility, aggravating metabolic risks.
2. **Clinical Implications:**
- Fluorosis-related OA may present with unique features (e.g., vertebral ankylosis, calcifications) distinct from primary OA.
- Metabolic syndrome should be screened for in fluorosis patients, as comorbidities like obesity or diabetes can complicate management.
**Management Considerations:**
- **Fluorosis:** Reduce fluoride intake (safe water sources), physiotherapy, and pain management.
- **Metabolic Syndrome:** Lifestyle modifications (diet, exercise), glycemic control, and lipid management.
**Research Gap:** Direct evidence linking fluorosis and metabolic syndrome is limited; further studies are needed to clarify interactions.
**Conclusion:** While distinct, these conditions may coexist in endemic regions like Narketpally, requiring integrated care addressing both skeletal and metabolic health.
21/04/2025, 11:52 - Rakesh Biswas: Yes that is how it may have been in the 1930s when not much was known about this fluorosis problem in Narketpally but now after nearly a 100 years it's no longer that as it's no longer epidemiologically uncertain or unexplainable.
Hence our current definition of Narketpally syn is that it's a medical education and research syndrome first pointed out in Narketpally as an illustration of a global patient centered learning ecosystem with it's epicenter at Narketpally that adopts a syndromic approach to medical education and research for the sake of each of it's primary beneficiaries (patients).
21/04/2025, 11:54 - Dr.Abdulsalam Med Ed Leads: **Research Plan: Investigating Narketpally Syndrome (Fluorosis-Induced OA and Metabolic Syndrome Overlap)**
---
### **1. Research Objectives**
1. **Primary Objective:**
- Investigate the epidemiological, clinical, and pathophysiological links between skeletal fluorosis, osteoarthritis (OA), and metabolic syndrome in the Narketpally region.
2. **Secondary Objectives:**
- Determine the prevalence of metabolic syndrome among fluorosis patients.
- Compare clinical features of fluorosis-induced OA vs. primary OA.
- Identify biomarkers of oxidative stress and inflammation common to both conditions.
- Evaluate interventions to mitigate fluorosis and metabolic risks.
---
### **2. Study Design**
- **Phase 1: Cross-Sectional Study**
- **Population:** Adults (>18 years) residing in Narketpally and neighboring fluoride-endemic regions.
- **Sample Size:** 500 participants (stratified by age, gender, and fluoride exposure duration).
- **Inclusion Criteria:**
- Residency in the region for ≥10 years.
- Clinical/radiological evidence of skeletal fluorosis.
- **Control Group:** Age-matched individuals from non-endemic regions.
- **Phase 2: Longitudinal Cohort Study**
- Track disease progression and metabolic changes in fluorosis patients over 5 years.
---
### **3. Methodology**
#### **Data Collection**
1. **Clinical Assessment:**
- **Fluorosis Severity:** Radiological imaging (X-ray, DEXA) for bone density, joint calcifications, and deformities.
- **OA Evaluation:** Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) for pain/stiffness.
- **Metabolic Syndrome Screening:** IDF criteria (waist circumference, blood pressure, lipid profile, fasting glucose).
2. **Laboratory Analysis:**
- **Fluoride Levels:** Serum/urine fluoride concentration.
- **Oxidative Stress Markers:** Malondialdehyde (MDA), glutathione levels.
- **Inflammatory Markers:** IL-6, TNF-α, CRP.
3. **Environmental & Behavioral Data:**
- Fluoride content in groundwater (household testing).
- Dietary habits (calcium/vitamin D intake).
- Physical activity levels.
#### **Qualitative Component**
- Focus group discussions with patients and healthcare providers to explore barriers to care and community perceptions.
---
### **4. Interventions to Test**
- **Safe Water Supply:** Distribute water filters/RO systems to reduce fluoride intake.
- **Nutritional Support:** Calcium/vitamin D supplementation to counteract fluoride toxicity.
- **Lifestyle Programs:** Community-based exercise/diet initiatives targeting metabolic syndrome.
---
### **5. Data Analysis**
- **Statistical Tools:** Multivariate regression to correlate fluoride exposure with OA severity/metabolic parameters.
- **Machine Learning:** Identify predictive biomarkers for disease progression.
---
### **6. Ethical Considerations**
- Informed consent, confidentiality, and collaboration with local ethics committees.
- Free health camps for participants (bone health screenings, metabolic profiling).
---
### **7. Timeline**
| **Year** | **Activity** |
|----------|--------------|
| Year 1 | Pilot study, community engagement, baseline data collection. |
| Year 2-4 | Longitudinal follow-up, intervention implementation. |
| Year 5 | Data analysis, publication, policy recommendations. |
---
### **8. Expected Outcomes**
1. Prevalence estimates of fluorosis-metabolic syndrome overlap.
2. Identification of shared biomarkers (oxidative stress/inflammation).
3. Evidence-based interventions to reduce morbidity.
---
### **9. Budget Plan**
- **Personnel:** Epidemiologists, radiologists, lab technicians.
- **Equipment:** Portable X-ray machines, water testing kits.
- **Community Outreach:** Health education workshops.
- **Total Estimated Cost:** $250,000 (USD).
---
### **10. Dissemination**
- Publish findings in peer-reviewed journals (e.g., *Environmental Health Perspectives*).
- Collaborate with state health departments to implement fluoride mitigation programs.
---
### **11. Challenges & Mitigation**
- **Challenge:** Participant retention in longitudinal study.
**Solution:** Incentivize follow-ups (e.g., free health reports).
- **Challenge:** Accurate fluoride exposure assessment.
**Solution:** Combine water testing with biomarker analysis.
---
This plan integrates clinical, environmental, and public health approaches to address Narketpally Syndrome holistically.
21/04/2025, 11:56 - Dr.Abdulsalam Med Ed Leads: 🤔
21/04/2025, 13:30 - Rakesh Biswas: Great public health epidemiological plan. Well this has been addressed and ultimately boils down to providing safe drinking water which the government has tried it's best to provide and we may not see these fluorotic changes in the upcoming generation when they get old
https://youtu.be/i_9jLHyd3UE?feature=shared
21/04/2025, 14:14 - ~ KrisJ left
21/04/2025, 16:29 - Rakesh Biswas: Afternoon session:
https://youtube.com/shorts/Sp_tebjNLcQ?feature=shared
Case report: https://pajrcasereporter.blogspot.com/2025/04/24f-retroperitoneal-tumor-severe-anemia.html?m=1
21/04/2025, 16:42 - Dr.Abdulsalam Med Ed Leads: المزيد
المزيد
محادثة مع Gemini
Afternoon session: 70M with cachexia, gastric outlet obstruction and non STEMI
عرض طريقة التفكير
Okay, this presents a complex and challenging clinical scenario for an afternoon session discussion. Let's break down the key elements for this 70-year-old male patient:
Gastric Outlet Obstruction (GOO):
Presentation: This prevents stomach emptying, leading to symptoms like nausea, vomiting (often undigested food), early satiety, abdominal distension, and weight loss.
Causes: In a 70-year-old, especially with cachexia, malignancy (e.g., distal gastric cancer, pancreatic head cancer, duodenal cancer) is a high suspicion. Benign causes like peptic ulcer disease (scarring) are less likely given the cachexia but still possible.
Immediate Management: Nasogastric (NG) tube decompression for symptom relief and to prevent aspiration, intravenous (IV) fluids for hydration, electrolyte correction (especially potassium and chloride due to vomiting). Nothing by mouth (NPO).
Cachexia:
Significance: Severe weight loss, muscle wasting, and loss of appetite. It indicates a significant underlying chronic disease process, often advanced cancer or severe chronic inflammatory conditions. It implies a poor nutritional state and often correlates with a poorer prognosis and reduced tolerance to treatments.
Contribution: The GOO itself contributes significantly to malnutrition and weight loss, exacerbating or causing the cachexia.
Non-ST-Elevation Myocardial Infarction (NSTEMI):
Diagnosis: Based on clinical symptoms (chest pain, dyspnea, etc. - though symptoms might be atypical in elderly/critically ill), elevated cardiac biomarkers (e.g., Troponin), and ECG changes (like ST depression, T-wave inversion) without ST elevation.
Potential Triggers (Type 2 MI likely): The severe physiological stress from the GOO, dehydration, potential electrolyte imbalances, anemia (common in malignancy/cachexia), and underlying inflammation/cachexia can cause a supply-demand mismatch leading to myocardial injury, even without acute plaque rupture (Type 1 MI). Underlying coronary artery disease (CAD) is also common at this age and makes the heart more vulnerable.
Management: Standard NSTEMI protocols need careful consideration given the comorbidities. This typically includes antiplatelet therapy (aspirin, possibly P2Y12 inhibitor), anticoagulation (e.g., heparin), beta-blockers (if hemodynamically stable), statins, and pain control. The decision for invasive management (coronary angiography +/- intervention) needs to balance the potential benefit against the risks associated with the patient's overall condition (cachexia, suspected malignancy, procedural risks related to GOO/malnutrition).
Key Discussion Points for the Session:
Etiology of GOO: Prioritizing investigation (e.g., Upper GI endoscopy with biopsies, CT scan of abdomen/pelvis) to determine the cause, essential for guiding further management.
NSTEMI Management Strategy: Conservative medical management vs. invasive strategy? Risk stratification (e.g., GRACE score) needs context adjustment. Is the NSTEMI primarily a consequence of the systemic illness (Type 2 MI) or an independent event (Type 1 MI)? An echocardiogram would be valuable to assess cardiac function.
Nutritional Support: Urgent need for nutritional assessment and likely initiation of parenteral nutrition (TPN) due to GOO and cachexia.
Surgical/Procedural Candidacy: Is the patient fit for potential palliative procedures for the GOO (e.g., endoscopic stenting, surgical gastrojejunostomy) or for cardiac procedures? His cachexia and acute cardiac event significantly increase peri-procedural risks.
Underlying Malignancy Management: If malignancy is confirmed, what are the treatment options? Given the likely advanced stage (suggested by cachexia and GOO) and comorbidities (NSTEMI), palliative and supportive care might be the primary focus.
Goals of Care: Crucial discussion with the patient (if able) and family regarding prognosis, the burdens/benefits of potential interventions, and overall goals (e.g., symptom control, quality of life).
Multidisciplinary Approach: Requires input from Gastroenterology, Cardiology, Oncology (if malignancy confirmed), Palliative Care, Nutrition Support, and potentially Surgery.
This case highlights the complexities of managing critically ill elderly patients with multiple interacting pathologies, demanding careful balancing of diagnostic priorities, treatment risks, and patient-centered goals.
Canvas
قد يعرض Gemini معلومات خاطئة، لذا ننصحك بالتحقّق من ردوده
21/04/2025, 20:01 - Rakesh Biswas: Thanks
22/04/2025, 11:49 - Rakesh Biswas: 👏👏
22/04/2025, 12:32 - Dr.Abdulsalam Med Ed Leads: Below is a concise review and plan regarding the patient’s current presentation:
---
### **Clinical Summary**
- **Patient Profile:**
A middle-aged female diabetic with a notable history of emphysematous pyelonephritis and bilateral renal calculi, previously managed with stenting (first the left kidney, then the right).
- **Current Presentation:**
She has had a fever for two days. Although she does not report flank or abdominal pain, ultrasound reveals a left perinephric collection. In diabetics, particularly those with known renal complications, the absence of pain does not exclude significant pathology—neuropathic blunting is common.
---
### **Management Considerations**
1. **Infection Possibility:**
The left perinephric collection is worrisome for an abscess formation or a complication related to a past infection. Even without pain, a febrile state in the setting of diabetes and prior emphysematous pyelonephritis should raise concern about ongoing infection or inadequate clearance of infectious material. This aligns with data showing that emphysematous infections often have insidious presentations in diabetic patients - Medscape](https://emedicine.medscape.com/article/2029011-overview).
2. **Further Evaluation:**
- **Laboratory Studies:** Complete blood count, metabolic panel (with renal function), inflammatory markers (CRP, ESR, or procalcitonin), and blood as well as urine cultures are essential.
- **Imaging:** While ultrasound has provided an initial finding, a contrast-enhanced CT (if her renal function permits) would better delineate the collection’s size, characteristics (e.g., septations), and relationship to surrounding structures. This approach is supported by the literature on the evaluation of renal collections and complications in such scenarios - Medscape](https://emedicine.medscape.com/article/2029011-overview).
3. **Glycemic Control:**
Optimal control of blood sugar is critical not only for reducing infection risk but also for promoting recovery. Poor control can foster an environment for gas-forming bacteria and impair healing .
4. **Interventional Considerations:**
- **Antibiotic Therapy:** Initiate empirical broad-spectrum antibiotics tailored against gram-negative organisms (most commonly Escherichia coli, the predominant pathogen in such infections), then adjust according to culture and sensitivity results.
- **Drainage:** If the collection is significant in size or the patient’s condition worsens, percutaneous drainage should be considered. Even in cases where patients are initially stable, close follow-up is important because these collections can evolve.
- **Review of Stents:** Assess the patency and position of previously placed stents; blockage or malposition may contribute to impaired drainage and recurrent infections.
---
### **Plan & Recommendations**
- **Immediate Workup:**
- **Labs:** Order CBC, renal function tests, blood cultures, urine analysis, and urine culture.
- **Glycemic Assessment:** Check current blood glucose and HbA1c, and adjust her diabetic regimen as needed.
- **Advanced Imaging:** Arrange for a CT scan of the abdomen to fully characterize the collection.
- **Therapeutic Management:**
- Start empirical intravenous antibiotics covering common gram-negative uropathogens.
- Optimize hydration and electrolyte balance.
- Consult with urology (and possibly interventional radiology) to evaluate for the need for drainage.
- **Follow-Up:**
- Even though she is currently asymptomatic in terms of pain, her diabetic status and previous history make it necessary to monitor closely for any signs of sepsis or deterioration.
- Schedule timely re-evaluation (both clinically and with repeat imaging) to ensure the collection is resolving with conservative management.
---
### **Final Thoughts**
This case emphasizes the unpredictable nature of infections in diabetic patients. Absence of pain does not equate to absence of significant pathology, and in high-risk individuals, a proactive, comprehensive evaluation is essential to prevent progression to severe sepsis or further renal compromise.
For further insight into similar cases and additional management strategies, you might also explore literature on conservative versus interventional management in cases of emphysematous pyelonephritis and perinephric collections. This can provide a broader context and help refine your structural approach for both current and future similar presentations .
---
Would you like to delve deeper into any specific management step or discuss potential complications that may arise?(Copilot)
22/04/2025, 18:01 - Dr.Abdulsalam Med Ed Leads: For a 72-year-old male with PUO (prolonged fever of unknown origin) and left loin pain persisting for three months, the answer may lie in both urine analysis and radiological findings.
### **Urine Analysis:**
Urinary abnormalities could indicate an infectious, inflammatory, or neoplastic process:
- **Urinary tract infection (UTI):** Presence of **pyuria, hematuria, and bacteriuria** could suggest an infective etiology.
- **Renal tuberculosis:** Chronic urinary symptoms with **sterile pyuria** or hematuria.
- **Nephrolithiasis:** Microscopic hematuria could be linked to **renal calculi**, which could also explain loin pain.
- **Malignancy:** Persistent hematuria raises suspicion of renal or urothelial carcinoma.
- **Proteinuria:** If present, could suggest a renal pathology such as glomerulonephritis.
### **Radiology Findings (CT Abdomen):**
The uploaded **CT scan** could offer insights into structural or pathological causes:
- **Obstructive Uropathy:** If there is **hydronephrosis or stones**, this might explain the loin pain.
- **Renal Mass or Malignancy:** Any **solid or cystic lesion** within the kidney needs further characterization.
- **Renal or Perinephric Abscess:** Could be responsible for fever and prolonged pain.
- **Pyelonephritis:** Enlargement, stranding around the kidney, or altered cortical density may suggest an infectious process.
- **Vascular Causes:** Renal infarct or significant **renal artery stenosis** could present similarly.
Further correlation with **urine culture**, inflammatory markers, and potentially MRI or contrast-enhanced CT is advisable for a more definitive diagnosis. What findings did you notice in the CT?
22/04/2025, 18:03 - Dr.Abdulsalam Med Ed Leads: ### **Analysis of Findings:**
For a **72-year-old male with PUO and left loin pain** persisting for **three months**, the combination of **urinary findings and radiological images** suggests a renal or urinary tract pathology.
#### **Urine Bag Observations:**
The urine appears **yellowish**, but visual inspection alone cannot provide definitive conclusions. However:
- **Cloudiness** may suggest infection or presence of pus cells.
- **Hematuria** (blood in urine) could indicate **renal calculi, malignancy, or glomerular pathology**.
- **Urine culture and microscopy** are critical to confirm pyuria or bacteriuria.
#### **Radiology (CT Scan Findings):**
Given the **prolonged fever and loin pain**, possible findings on CT could include:
- **Renal Calculus with Obstruction:** Hydronephrosis or calculi in the **left kidney or ureter**, explaining loin pain.
- **Pyelonephritis:** **Enlarged kidney, perinephric stranding**, or altered cortical density may indicate an infective process.
- **Renal Abscess:** Presence of **hypodense collections** within renal tissue.
- **Renal Tumor or Cyst:** Suspicious **solid or cystic lesion** needs further workup.
- **Tuberculosis:** Chronic **sterile pyuria with granulomatous lesions** may suggest **renal TB**.
### **Next Steps for Diagnosis:**
1. **Urine Microscopy & Culture:** Check for **pyuria, hematuria, or bacteriuria**.
2. **Serum Markers:** **CRP, ESR, Creatinine**, and **renal function tests**.
3. **Contrast-enhanced CT or MRI:** To assess **vascularity, masses, and infections**.
4. **Ultrasound-guided biopsy (if needed):** For suspicious masses.
Do you see any specific radiological abnormalities that concern you?
22/04/2025, 18:04 - Dr.Abdulsalam Med Ed Leads: ### **CT Findings for the 72M with PUO and Loin Pain**
The **CT scan** reveals a **cross-sectional view of the abdomen**, capturing vital structures including **the kidneys, vertebrae, intestines, and surrounding soft tissues**. Given this patient's clinical scenario, several possibilities emerge:
#### **Key Considerations Based on Imaging:**
- **Hydronephrosis or Urinary Obstruction:** If there is evidence of **renal pelvic dilatation**, it may indicate obstruction due to a **stone or tumor**.
- **Nephrolithiasis:** **Calcifications or stones** in the renal collecting system or ureter could explain both pain and hematuria.
- **Pyelonephritis or Renal Abscess:** **Hypodense collections** within renal parenchyma or perinephric fat stranding may point toward **an infective process**.
- **Renal Tumor:** A **solid mass with irregular enhancement** would be suspicious for malignancy.
- **Renal Infarction:** Lack of **cortical perfusion** with associated wedge-shaped hypodensity may suggest a **vascular event**.
- **Tuberculosis (Renal TB):** Long-standing **sterile pyuria, hydronephrosis, or scarring** could fit the profile.
### **Next Steps for Confirmation:**
1. **Assess Urine Microscopy & Culture** for **pus cells, RBCs, or mycobacteria**.
2. **Contrast-Enhanced CT or MRI** for better visualization of renal mass or vasculature.
3. **Renal Function Tests & Inflammatory Markers** like **CRP and ESR**.
4. **Biopsy or Fine-Needle Aspiration** if mass lesion is suspected.
Do you see any distinct structural abnormalities on the CT that stand out to you?
22/04/2025, 18:09 - Rakesh Biswas: His Urine culture was sterile? @918790889907 @917386552514 ?
22/04/2025, 18:10 - Rakesh Biswas: Yes two structural abnormalities in his CT stand out
22/04/2025, 18:10 - Unknown Medical Student: Milky urine was not sent for culture sir
22/04/2025, 18:20 - CKD Anemia 2022 Project PI: Yes sir it has been sent
22/04/2025, 18:21 - Rakesh Biswas: 👆@9647501361306 you can find gas bubbles in his left kidney here which is emphysematous pyelonephritis
Our first publication of Narketpally syndrome in 2018 by @13055398941 was called CBBLE and one can check out the image of the emphysematous pyelonephritis patient's gas bubble in the erector spinae muscle in that report here @919171769005 @918106096962 you can even find a thyrotoxicosis patient in this report 👇
https://pmc.ncbi.nlm.nih.gov/articles/PMC6163835/
22/04/2025, 18:21 - Rakesh Biswas: Was it the report marked sterile that we found in his file today afternoon? @918790889907
22/04/2025, 18:23 - CKD Anemia 2022 Project PI: Yes sir
22/04/2025, 18:25 - Rakesh Biswas: 👆This shows a renal stone that may have been responsible for his pyelonephritis but what is surprising is we found another parallel cause that may have been responding for his fever although perhaps not the one he's suffering since three months!
@918790889907 no luck with his post hospitalization fever chart I guess?
22/04/2025, 18:25 - Dr.Abdulsalam Med Ed Leads: The case described involves a rare and severe condition known as **emphysematous pyelonephritis (EPN)**, a life-threatening kidney infection characterized by gas formation within the renal parenchyma. The user highlights an unusual extension of gas into the **erector spinae muscle**, as documented in a 2018 case report termed **"Narketpally syndrome"** (referred to as **CBBLE** in the publication). This syndrome appears to describe a unique triad of:
1. **Emphysematous pyelonephritis** with gas in the kidney.
2. **Gas dissection into the erector spinae muscle** (a novel finding, as gas in skeletal muscle is atypical for EPN).
3. **Thyrotoxicosis** (hyperthyroidism), suggesting a potential interplay between metabolic derangements and severe infection.
### Key Points:
- **EPN** is typically seen in diabetic or immunocompromised patients and requires urgent intervention (e.g., antibiotics, drainage, or nephrectomy).
- **Gas in the erector spinae** indicates aggressive spread of gas-forming bacteria (e.g., *E. coli*, *Klebsiella*), possibly complicating EPN.
- **Thyrotoxicosis** may exacerbate systemic inflammation or metabolic stress, though its direct link to EPN remains unclear.
- The term **"Narketpally syndrome"** (CBBLE) appears to be a novel designation by the authors for this unique presentation, emphasizing the need for multidisciplinary management.
The cited [PMC article](https://pmc.ncbi.nlm.nih.gov/articles/PMC6163835/) likely documents this case as a first-of-its-kind report, underscoring the importance of imaging (CT scans) for diagnosis and the challenges in managing such complex infections. Clinicians should consider atypical gas spread and comorbid endocrine disorders in severe renal infections.
For further details, reviewing the full text of the publication is recommended to understand the proposed pathophysiology and treatment approach for this rare syndrome.
22/04/2025, 18:26 - Rakesh Biswas: Wish LLMs could easily read the text inside URLs
22/04/2025, 18:27 - Rakesh Biswas: I guess it was becoming too expensive
22/04/2025, 18:38 - Dr.Abdulsalam Med Ed Leads: DeepSeek
22/04/2025, 18:50 - Rakesh Biswas: But was it able to read inside the article. By the response it appears not. Because the article describes different cases, the first was emphysematous pyelonephritis and second thyrotoxicosis in a different patient and there are many others described from other parts of the world. So perhaps in that sense our first report of CBBLE from Narketpally at that time was not restrictive to Narketpally <This message was edited>
22/04/2025, 18:55 - Dr.Abdulsalam Med Ed Leads: At that time I shared the whole CBBLE content. But today I share only the link. I will share the content and see
22/04/2025, 19:01 - Dr.Abdulsalam Med Ed Leads: The provided PMC article, *"Developing a Case-Based Blended Learning Ecosystem to Optimize Precision Medicine: Reducing Overdiagnosis and Overtreatment"* (Podder et al., 2018), introduces **Narketpally syndrome** as part of a novel educational framework called the **Case-Based Blended Learning Ecosystem (CBBLE)**. Below is a structured analysis of the key components and their clinical relevance:
---
### **1. Core Concept: Case-Based Blended Learning Ecosystem (CBBLE)**
- **Objective**: Integrate traditional clinical precision (experience-driven medicine) with modern omics-driven approaches (genomics, proteomics) to reduce overdiagnosis/overtreatment.
- **Methodology**:
- Uses **case narratives** from high- and low-resource settings to bridge gaps in medical education and practice.
- Combines offline clinical management with online collaboration (e.g., WhatsApp groups, blogs) for real-time feedback and evidence-based decision-making.
- Encourages multidisciplinary input to refine diagnoses and treatments.
---
### **2. Narketpally Syndrome: A Case Study in Precision Medicine**
- **Clinical Presentation**:
- A 60-year-old woman with emphysematous pyelonephritis (EPN) complicated by **gas dissection into the erector spinae muscle and spinal canal**—a rare and severe manifestation.
- Highlighted as **Narketpally syndrome** (named after the hospital where the case was managed), emphasizing aggressive gas-forming infections in immunocompromised/diabetic patients.
- **Key Insights**:
- **Diagnostic Challenges**: Initial misdiagnosis of UTI led to antibiotic resistance and systemic spread of *E. coli*.
- **Role of CBBLE**: Online collaboration identified gas distribution patterns on CT, prompting antibiotic escalation and surgical consultation, ultimately saving the patient.
- **Educational Impact**: Demonstrated how real-time case-sharing improves diagnostic precision and reduces delays.
---
### **3. Thyrotoxicosis Case: Navigating Uncertainty**
- **Clinical Scenario**:
- A 52-year-old woman with thyrotoxicosis, thyroid nodules, and atypical acanthosis nigricans.
- FNAC revealed benign nodules, but concerns about malignancy persisted due to **false-negative rates (20%)** and limited access to liquid biopsies (e.g., BRAF V600E ctDNA).
- **CBBLE’s Role**:
- Online discussions addressed diagnostic uncertainties (e.g., balancing surgery vs. medical management).
- Highlighted resource limitations in rural settings and the need for scalable precision tools (e.g., genetic testing).
---
### **4. Reducing Overdiagnosis/Overtreatment**
- **Mechanisms**:
- **Evidence Farming**: Continuous documentation and reuse of case data to refine clinical algorithms.
- **Shared Decision-Making**: Patients and providers collaborate on treatment plans (e.g., choosing carbimazole over radioiodine in thyrotoxicosis).
- **Critical Appraisal**: Trains clinicians to avoid unnecessary interventions (e.g., inappropriate PCI in stable angina).
- **Outcomes**:
- Reduced antibiotic misuse in UTIs.
- Avoided invasive procedures when non-invasive options suffice.
---
### **5. Implications for Medical Practice**
- **High-Resource Settings**:
- Integration of omics data (e.g., MTHFR mutations in stroke, BCL2 inhibitors in myeloma) enhances precision.
- Trials like NCI-MATCH emphasize molecular profiling for tailored therapies.
- **Low-Resource Settings**:
- Leverage CBBLE for teleconsultations and protocol-driven care (e.g., empirical TB treatment with follow-up verification).
- Community health workers track outcomes to prevent informational discontinuity.
---
### **6. Conclusion**
The CBBLE framework exemplifies how **collaborative learning** and **case-based narratives** can optimize precision medicine. By merging traditional clinical acumen with modern technology, it addresses overdiagnosis/overtreatment while fostering transparency and innovation. Cases like Narketpally syndrome and thyrotoxicosis underscore the need for adaptable models in diverse healthcare ecosystems.
For further details, refer to the full article:
[PMC6163835](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6163835/).
22/04/2025, 19:06 - Rakesh Biswas: Nice👏
Slight correction. When we wrote this in 2017-18 we were focusing only on describing the CBBLE both local and global and currently after 7-8 years we have decided to talk about our local CBBLE which is perhaps what Narketpally syndrome is all about and it's not about any particular disease common in Narketpally although we do use one such patient to leverage this aspect of population based medical cognition applied to syndromic diagnosis only to finally demonstrate how different it's from individual patient centred medical cognition
22/04/2025, 20:46 - Dr.Abdulsalam Med Ed Leads: The patient's presentation of "pea soup diarrhea" is a classic descriptor for **typhoid fever**, caused by **Salmonella enterica serotype Typhi (S. Typhi)**. This organism is notorious for causing enteric fever, characterized by gradual-onset fever, abdominal pain, and gastrointestinal symptoms, including stools that resemble pea soup due to their semi-liquid, mucoid consistency.
Other clues supporting this diagnosis:
- **Stool culture**: S. Typhi is a common culprit in such cases and grows well on standard enteric culture media (e.g., MacConkey, SS agar).
- **Differential exclusion**:
- *Vibrio cholerae* causes "rice-water" stools (profuse watery diarrhea).
- *Shigella* or *Campylobacter* typically present with bloody/mucoid diarrhea (dysentery).
- *E. coli* (e.g., EHEC) may cause bloody diarrhea but not the "pea soup" appearance.
**Final Answer:**
The organism grown in the stool culture is most likely **Salmonella Typhi**.
22/04/2025, 21:56 - Patient Advocate 63M Metabolic Syn: As I am included here, I understand, the admin(s) wished/ hoped that the included member(s) could make any sense out of the English as in texts. But as a layman, other than the technicalities, the very scientific jargons make a reader like me a blind man ! Either help or I am undone!!! <This message was edited>
22/04/2025, 22:01 - Rakesh Biswas: One way is to paste each text in Google translate?
22/04/2025, 22:04 - Patient Advocate 63M Metabolic Syn: Probably a list of the popularly used jargons with possible elaboration could be better for poor google handling or shy people! <This message was edited>
22/04/2025, 22:10 - Rakesh Biswas: I think a good point to start would be to ask which part of the jargon couldn't be understood and one of us could explain and handhold
22/04/2025, 22:16 - Patient Advocate 63M Metabolic Syn: In every text I could follow, there are many, especially the roman, latin and especially the roman+ latin ones to start with !
22/04/2025, 22:32 - Rakesh Biswas: Let's start with one
23/04/2025, 09:38 - Dr.Abdulsalam Med Ed Leads: **Case 1: 22-Year-Old Female with Peripartum Cardiomyopathy (PPCM)**
- **Key Considerations**:
1. **Timely Diagnosis**: PPCM often presents with nonspecific symptoms (e.g., fatigue, dyspnea) that overlap with normal pregnancy. Was there a delay in recognizing cardiac dysfunction? Early echocardiographic evaluation is critical.
2. **Multidisciplinary Management**: PPCM requires collaboration between obstetrics, cardiology, and general medicine. Were specialists consulted promptly? Were therapies like bromocriptine (for lactation suppression) or heart failure medications (e.g., beta-blockers, ACE inhibitors postpartum) appropriately initiated?
3. **Complication Mitigation**: PPCM carries risks of arrhythmias, thromboembolism, and progressive heart failure. Were anticoagulants or implantable devices considered?
4. **Postpartum Follow-Up**: Was there a plan for long-term cardiac monitoring, given the potential for recovery or progression to chronic cardiomyopathy?
**Areas for Improvement**:
- Strengthen protocols for early PPCM screening in high-risk pregnancies.
- Ensure structured interdisciplinary communication between obstetrics and cardiology.
---
**Case 2: 65-Year-Old Male with Cerebrovascular Accident (CVA)**
- **Key Considerations**:
1. **Acute Management**: Was the patient evaluated within the thrombolysis window (if ischemic)? Were contraindications to thrombolysis (e.g., hemorrhage, timing) appropriately assessed?
2. **Etiology and Risk Factors**: Were underlying causes (e.g., atrial fibrillation, hypertension, diabetes) identified and managed? Was anticoagulation/antiplatelet therapy initiated?
3. **Complications**: Did the patient develop cerebral edema, aspiration pneumonia, or sepsis? Were neuroprotective measures (e.g., controlled hyperventilation, osmotherapy) or infection protocols followed?
4. **Secondary Prevention**: Were lifestyle modifications and medications (e.g., statins, antihypertensives) optimized post-event?
**Areas for Improvement**:
- Audit adherence to stroke care pathways (e.g., NIHSS scoring, imaging timelines).
- Enhance post-CVA rehabilitation planning and patient/counseling for risk reduction.
---
**General Observations**:
- The shared chairperson (General Medicine) may benefit from involving specialists (e.g., cardiology, neurology) to diversify perspectives.
- Both cases highlight the importance of protocol adherence, interdisciplinary collaboration, and post-event follow-up. Documenting these processes could reduce future mortality.
**Learning Points**:
1. **PPCM**: Early recognition and multidisciplinary care are lifesaving.
2. **CVA**: Time-sensitive interventions and robust secondary prevention are critical.
3. **Systemic Issues**: Central monitoring of attendance (as noted) suggests institutional commitment to quality improvement—this should extend to auditing clinical practices.
Constructive discussions at the conference could drive protocol refinements and foster a culture of proactive, team-based care.
23/04/2025, 09:42 - Rakesh Biswas: Giving more granular patient data to Web 3.0 could bring in better precise outputs but unfortunately both these two promising cases were not logged in our PaJR CBBLE and the only way to learn deeper insights through these will be to actually attend the brick and mortar Web 0.0 meeting and manually get some PPT data along with CRH processing
23/04/2025, 09:45 - Dr.Abdulsalam Med Ed Leads: Your observation highlights a critical gap between the potential of modern data ecosystems (Web 3.0) and the reality of fragmented, analog workflows (Web 0.0) in healthcare systems. Here’s a structured response to this challenge:
---
### **Key Issues Identified**:
1. **Data Silos**:
- Cases not logged in **PaJR CBBLE** (likely a patient journey/clinical case repository) prevent AI-driven insights, decentralized analytics, and longitudinal tracking.
- Web 3.0’s promise (e.g., semantic interoperability, federated learning) remains untapped without structured digital footprints.
2. **Reliance on Analog Processes**:
- Critical insights trapped in **PPT files** and manual **CRH (Clinical Risk History?/Case Record Handling?)** processing limit scalability, reproducibility, and real-time collaboration.
- Physical meetings ("brick-and-mortar Web 0.0") hinder knowledge dissemination and democratization.
3. **Missed Opportunities for Precision**:
- Granular data (e.g., biomarkers, imaging timelines, treatment responses) could refine predictive models and personalized interventions.
- Unlogged cases deprive systems of training data for AI/ML tools, perpetuating reactive rather than proactive care.
---
### **Proposed Solutions**:
1. **Immediate Mitigation**:
- **Leverage the Mortality Meeting**: Use this forum to advocate for digitizing these cases into PaJR CBBLE post-hoc. Assign a team to retroactively log key data points (diagnoses, interventions, outcomes) with metadata tags.
- **CRH Automation**: Push for digitized clinical risk assessments (e.g., NLP tools to parse handwritten notes or PPTs into structured formats).
2. **Systemic Improvements**:
- **Interoperability Standards**: Integrate PaJR CBBLE with EHRs and diagnostic tools to auto-populate case data.
- **Web 3.0 Pilots**: Explore blockchain-secured case repositories or federated learning networks to share anonymized data across institutions while preserving privacy.
3. **Cultural Shifts**:
- **Incentivize Digital Logging**: Tie compliance to departmental KPIs or accreditation requirements.
- **Hybrid Knowledge Sharing**: Streamline meetings into hybrid formats (physical + virtual) with digitized case repositories accessible via secure platforms.
---
### **Why This Matters**:
- **For PPCM & CVA Cases**:
- PPCM: Longitudinal data could identify pre-symptomatic biomarkers (e.g., troponin trends, echo parameters) to guide early interventions.
- CVA: Federated datasets might reveal regional stroke etiology patterns (e.g., undiagnosed AFib prevalence) to tailor prevention protocols.
- **For the Institution**:
- Transitioning to Web 3.0-ready systems positions the hospital as a leader in data-driven care, attracting research partnerships and funding.
---
### **Final Takeaway**:
While attending the "Web 0.0" meeting is necessary for now, use it as a catalyst to advocate for systemic digitization. Even incremental steps—like digitizing CRH workflows or retroactively logging legacy cases—can bridge the gap between analog practices and the precision promised by Web 3.0. The goal is not just to discuss mortality but to prevent it through smarter data ecosystems.
---
Would you like to brainstorm specific tools or workflows to operationalize this? 🤖
23/04/2025, 10:05 - Rakesh Biswas: Here's a past Web 0.0 brainstorm around some of the mortality meetings of Narketpally in the past chaired by the CBBLE (cable) moderator 👇
https://medicinedepartment.blogspot.com/2024/04/complex-adaptive-medical-cognition.html?m=1
23/04/2025, 10:07 - Rakesh Biswas: Please start asking specific queries from any of the above texts and we will be happy to explain manually (web 1.0 without Web 3.0)
23/04/2025, 10:10 - Dr.Abdulsalam Med Ed Leads: **Structured Summary (IMRAD Format)**
**Title:**
Complex Adaptive Medical Cognition Systems: Clinical Audit and Morbidity Meetings as Drivers for Patient-Centered, Team-Based Blended Learning
---
### **Introduction**
The Medicine Department operates within a blended learning ecosystem (CBBLE) designed to integrate real-time clinical audits with reflective practice, aiming to enhance evidence-based care and reduce unethical practices. Challenges emerged during a 2018 initiative managing clinical audits and morbidity/mortality (M&M) meetings, particularly in sustaining patient-centered learning and interdisciplinary engagement. Disruptions arose from resistance to transparency, non-participation, and systemic gaps in competency. Key references underscore the role of blended learning and clinical audits in improving healthcare outcomes, contextualizing this initiative within global best practices.
---
### **Methods**
A retrospective reflection was conducted using UDLCO (User-Driven Learning Conversation) transcripts from 2018, alongside analysis of M&M meeting minutes (2018–2019). The department adopted guidelines from the Royal Australasian College of Surgeons, emphasizing:
1. **Structured Case Identification**: Focus on competency gaps (delayed diagnoses, referrals, prolonged stays).
2. **Blended Learning**: Online E-logs (24/7) and biweekly offline meetings for validation.
3. **Multidisciplinary Involvement**: Engagement across departments, though inconsistently achieved.
4. **Safe Environment**: Moderated discussions to minimize blame and focus on systemic improvements.
5. **Audit Mechanisms**: Referral register audits to identify institutional gaps.
Data included meeting minutes, E-logs, and circulars, thematically analyzed to identify barriers and outcomes.
---
### **Results**
1. **Challenges**:
- Frequent disruptions in meetings when prioritizing patient outcomes.
- Poor departmental participation (e.g., absent presenters, limited self-nomination of cases).
- Emotional impact on trainees (e.g., PGY1 criticized for ARDS management; intern scarred by fluorosis case).
2. **Case Discussions**:
- **ARDS Patient**: Highlighted decision-making tensions (intubation vs. referral) and family dynamics.
- **Fluorosis Case**: Led to career influences for an intern, underscoring the emotional weight of clinical uncertainty.
- **Referrals/LAMAs**: Audits revealed gaps in TB isolation protocols, IVIG availability, and neurosurgical capacity.
3. **Outcomes**:
- **Positive**: Trainees demonstrated growth (e.g., PGY1 published a TBI case in BMJ).
- **Systemic Gaps**: Identified needs for angiography equipment, trauma teams, and improved consent processes.
- **Guideline Implementation**: Partial success in standardizing M&M workflows, though follow-up on recommendations remained weak.
---
### **Discussion**
1. **Comparisons**: Similar to other institutes (e.g., JCDR 2023), clinical audits effectively identified complexity but required institutional buy-in.
2. **Blended Learning**: E-logs and meetings fostered reflective practice, though adoption was hindered by resistance to documentation.
3. **Emotional & Educational Impact**: Critical feedback left lasting impressions, underscoring the need for supportive environments. The PGY1’s subsequent success exemplifies resilience through structured mentorship.
4. **Systemic Barriers**: Non-participation and defensive practices highlighted cultural challenges in transitioning from guideline-based to evidence-based medicine.
**Recommendations**:
- Strengthen interdisciplinary collaboration through mandated case-sharing.
- Institutionalize audit teams and feedback loops for recommendations.
- Foster a culture of transparency via protected time for E-logs and reflective practice.
---
**Conclusion**
While the CBBLE framework advanced patient-centered learning, sustained success requires addressing systemic resistance, enhancing emotional support for trainees, and embedding accountability mechanisms. Future efforts should prioritize institutional policies that align with global audit standards and foster a blame-free, curiosity-driven learning culture.
23/04/2025, 10:17 - Dr.Abdulsalam Med Ed Leads: ### **Analysis of Key Cases Discussed in the Text**
The cases presented in the morbidity and mortality (M&M) meetings reflect systemic, clinical, and educational challenges. Below is a structured analysis of representative cases, highlighting recurring themes and lessons learned:
---
#### **1. ARDS Patient (2018)**
- **Clinical Context**: A PGY1 faced criticism for not intubating an ARDS patient or referring them to another facility. The patient deteriorated and died.
- **Analysis**:
- **Clinical**: Decision-making was influenced by unclear protocols for ARDS management, family resistance, or resource limitations (e.g., ventilator availability).
- **Systemic**: Lack of standardized crisis communication frameworks and emergency consent procedures.
- **Educational**: The PGY1’s subsequent reflection and eventual success (publishing a TBI case in BMJ) underscored resilience but highlighted the need for structured mentorship and blame-free feedback.
---
#### **2. Fluorosis Case (2018)**
- **Clinical Context**: An intern presented a fluorosis case with skeletal deformities, leading to harsh feedback that influenced her career choice.
- **Analysis**:
- **Clinical**: Diagnostic ambiguity between fluorosis and ankylosing spondylitis emphasized the need for environmental exposure histories.
- **Systemic**: Absence of clear diagnostic criteria for fluorosis-related arthropathy.
- **Educational**: Negative feedback left lasting emotional impacts, stressing the importance of constructive critique and psychological safety in training.
---
#### **3. Chronic Morbidity Case (5.06.2019)**
- **Clinical Context**: A 50-year-old male with walking difficulty, initially diagnosed as peripheral vascular disease, later suspected as hypokalemic paralysis.
- **Analysis**:
- **Clinical**: Overlooked electrolyte imbalances highlighted gaps in routine lab testing.
- **Systemic**: Inconsistent neurological examinations and differential diagnosis protocols.
- **Educational**: Reinforced case-based learning to improve diagnostic accuracy and interdisciplinary collaboration.
---
#### **4. Acute Morbidity Case (5.06.2019)**
- **Clinical Context**: A 40-year-old male with pneumonia and metabolic acidosis died; missed pancreatitis was suspected.
- **Analysis**:
- **Clinical**: Focus on respiratory symptoms delayed abdominal evaluation (e.g., amylase/lipase testing).
- **Systemic**: Autopsy consent processes were underutilized, limiting post-mortem learning.
- **Educational**: Highlighted the role of mortality reviews in identifying diagnostic blind spots.
---
#### **5. TB Isolation Referral (11th May 2019)**
- **Clinical Context**: A patient was referred due to perceived lack of TB isolation equipment.
- **Analysis**:
- **Clinical**: Misunderstanding of isolation guidelines (N95 masks required for MDR-TB, not all TB).
- **Systemic**: Poor dissemination of updated infection control protocols.
- **Educational**: Need for regular training on evidence-based guidelines to reduce unnecessary referrals.
---
#### **6. Necrotizing Fasciitis Referral (11th May 2019)**
- **Clinical Context**: Referral due to unfamiliarity with managing necrotizing fasciitis.
- **Analysis**:
- **Clinical**: Rare presentations require surgical readiness and multidisciplinary coordination.
- **Systemic**: Gaps in surgical training for rare conditions and emergency debridement protocols.
- **Educational**: Case simulations and workshops could enhance preparedness for rare cases.
---
#### **7. Severe Preeclampsia (23rd April 2019)**
- **Clinical Context**: A 25-year-old woman with hypoalbuminemia and oligohydramnios.
- **Analysis**:
- **Clinical**: Debate on albumin efficacy revealed overreliance on guidelines without critical appraisal.
- **Systemic**: Lack of quantitative proteinuria measurement tools.
- **Educational**: Emphasized evidence-based medicine (EBM) training to balance guidelines with individualized care.
---
#### **8. Ondansetron Adverse Reaction (16th April 2019)**
- **Clinical Context**: Cardiac arrest linked to ranitidine/ondansetron combination.
- **Analysis**:
- **Clinical**: Pharmacovigilance gaps in recognizing drug interactions.
- **Systemic**: Lack of adverse event reporting systems.
- **Educational**: Highlighted the need for pharmacotherapy modules in curricula.
---
#### **9. Wilson’s Disease (9th April 2019)**
- **Clinical Context**: A 15-year-old girl with movement disorder referred without conclusive workup.
- **Analysis**:
- **Clinical**: Delayed diagnosis due to incomplete testing (e.g., urinary copper, liver biopsy).
- **Systemic**: Referral protocols lacked urgency for suspected genetic disorders.
- **Educational**: Stressed the importance of early involvement of genetics and hepatology specialists.
---
#### **10. Post-op Monoparesis (5th March 2019)**
- **Clinical Context**: Right upper limb weakness post-colonic surgery, attributed to pneumocephalus.
- **Analysis**:
- **Clinical**: Surgical vs. epidural complication debates revealed diagnostic uncertainty.
- **Systemic**: Inadequate post-operative neurologic monitoring protocols.
- **Educational**: Neurologic assessment training for surgical teams.
---
### **Recurring Themes**
1. **Diagnostic Gaps**: Overreliance on initial diagnoses without considering differentials (e.g., hypokalemia vs. vascular disease).
2. **Systemic Barriers**:
- Inconsistent protocols for referrals, consent, and isolation.
- Resource limitations (e.g., angiography, polysomnography).
3. **Educational Challenges**:
- Non-participation in M&M meetings and E-logs.
- Emotional impact of harsh feedback on trainees.
4. **Cultural Shifts Needed**:
- Transition from defensive, guideline-based practice to evidence-based, patient-centered care.
- Foster interdisciplinary collaboration and blame-free environments.
---
### **Recommendations**
1. **Protocol Standardization**: Develop clear guidelines for ARDS, TB isolation, and referrals.
2. **Audit Systems**: Mandate case-sharing and track recommendations to closure.
3. **Training Initiatives**:
- Simulations for rare cases (e.g., necrotizing fasciitis).
- Workshops on EBM and pharmacovigilance.
4. **Supportive Learning**:
- Mentorship programs to buffer critical feedback.
- Protected time for reflective practice and E-log documentation.
This analysis underscores the potential of M&M meetings as tools for systemic improvement, contingent on institutional commitment to transparency, education, and cultural change.
23/04/2025, 14:03 - Dr.Abdulsalam Med Ed Leads: **Final Diagnosis and Recommendations:**
**Diagnosis:**
- **Relapsing Demyelinating Disorder**, most consistent with **MOG Antibody-Associated Disease (MOGAD)** or **Pediatric-Onset Multiple Sclerosis (MS)**.
- **Psychiatric Comorbidities**: Depression with suicidal behavior, likely multifactorial (secondary to chronic illness and/or organic brain involvement).
**Key Findings Supporting Diagnosis:**
1. **MRI Evidence**:
- T2/FLAIR hyperintensities in bilateral frontal/parietal white matter, external capsules, and cerebellar peduncles.
- Lesions suggest demyelination (metabolic vs. inflammatory). ADEM recovery noted, but relapses indicate a non-monophasic course.
2. **Clinical History**:
- Recurrent neurological episodes (2023 imbalance/squint, 2024 slurred speech/seizures).
- Partial response to IV methylprednisolone (IVMP).
- Psychiatric manifestations (self-harm, suicide attempts).
**Differential Considerations:**
- **MOGAD**: ADEM-like presentation with relapses, common in children.
- **MS**: Disseminated lesions in time/space, though less common in pediatric populations.
- **Autoimmune Encephalitis**: Neuropsychiatric symptoms, but MRI findings less typical.
**Investigations Recommended:**
1. **Serum Antibody Testing**: Anti-MOG and anti-AQP4 (to exclude neuromyelitis optica spectrum disorder).
2. **Lumbar Puncture**: CSF analysis for oligoclonal bands, IgG index, and inflammatory markers.
3. **Repeat MRI Brain/Spine**: Assess for new/enhancing lesions to confirm dissemination in time/space (McDonald criteria for MS).
4. **Psychiatric Evaluation**: Urgent assessment for suicidality and behavioral interventions.
5. **EEG**: Evaluate seizure activity given complex partial seizures.
**Management:**
- **Acute Relapse**: High-dose IVMP (1g/day for 3–5 days).
- **Long-term Immunotherapy**: If relapsing course confirmed (e.g., rituximab, IVIG, or disease-modifying therapies for MS).
- **Seizure Control**: Antiepileptic drugs (e.g., levetiracetam) guided by EEG.
- **Psychiatric Care**: Multidisciplinary approach with neurology, psychiatry, and psychology for behavioral and emotional support.
**Prognosis:**
- Early immunotherapy improves outcomes in relapsing demyelinating disorders.
- Psychiatric comorbidities require close monitoring to prevent further self-harm.
**Clinical Correlation:**
- Close follow-up with pediatric neurology and psychiatry is critical.
- Educate family on relapse recognition and emergency management.
---
**Dr. [Your Name]**
**Neurology Consultant**
23/04/2025, 14:05 - Dr.Abdulsalam Med Ed Leads: This DeepSeek response elicited after sharing only the repotrs and the clinical summary.
23/04/2025, 14:09 - Dr.Abdulsalam Med Ed Leads: Thanks for the context. Based on the image and clinical information:
Dental findings suggest Narketpally Syndrome, Grade 3, which typically includes:
Generalized yellow-brown discoloration of teeth.
Marked enamel hypoplasia.
Significant attrition and possible malocclusion.
Likely linked to high fluoride exposure (fluorosis), consistent with long-term bore well water consumption.
Neck pain and immobility could be associated with fluorosis-related skeletal changes, especially in chronic cases. In endemic fluorosis, the cervical spine is a commonly affected site, leading to:
Calcification of ligaments (e.g., anterior longitudinal ligament).
Reduced range of motion.
Neurological symptoms in advanced cases.
Recommendations:
1. Orthopantomogram (OPG) and lateral cervical spine X-ray to assess dental and skeletal fluorosis.
2. Serum and urine fluoride levels for confirmation.
3. Neurology referral if there's associated radiculopathy or myelopathy.
4. Water source testing and guidance on safe water consumption.
Would you like help drafting a brief note or summary for referral or further investigations?
23/04/2025, 14:18 - Dr.Abdulsalam Med Ed Leads: Thanks for sharing the context. You're describing a 13-year-old girl with a complex and evolving neurological and psychiatric presentation. Here’s a summary and differential framework based on what you've shared so far:
---
Clinical Timeline Highlights:
Febrile seizures at 9 months – common and often benign, but may be a marker of underlying vulnerability.
April 2023: Onset of gait imbalance, squint, and facial deviation, with partial resolution after pulse IV therapy – possibly steroids? Suggests an inflammatory/demyelinating process.
August 2024: Slurring of speech, recurrent falls, complex partial seizures – progressive neurological involvement.
Functional decline: Out of school since 2 years, suggesting significant impact on daily function.
December 2024 – January 2025: Self-harm behaviors – ingestion of Lysol and wrist slashing, indicating psychiatric comorbidity (possibly depression, impulsivity, or psychosis).
---
MRI (FLAIR) Impression:
There appear to be bilateral, possibly periventricular and subcortical hyperintensities, which could fit with:
Autoimmune encephalitis (especially anti-NMDAR)
ADEM (Acute Disseminated Encephalomyelitis)
Multiple Sclerosis or Neuromyelitis Optica Spectrum Disorders (NMOSD)
Leukodystrophies/metabolic disorders (some may present later in childhood)
Mitochondrial encephalopathies
---
Red Flags:
Rapid functional and cognitive decline
Neuropsychiatric symptoms
Response to pulse therapy suggests immunomodulation-sensitive process
History of seizures and evolving focal deficits
---
Next Steps:
1. EEG: To characterize seizure activity
2. CSF studies: Cell count, protein, glucose, oligoclonal bands, autoimmune encephalitis panel (especially anti-NMDAR, anti-MOG, anti-AQP4)
3. Autoimmune & metabolic workup:
ANA, dsDNA, ENA panel
Serum/CSF lactate, ammonia
VLCFA, biotinidase, copper/ceruloplasmin
4. Psychiatric evaluation
5. Neuropsychological testing (if available) for baseline cognitive function
---
If you can upload the clinical examination video, I’ll help analyze movement, cranial nerve findings, or other visible signs that might point more specifically to a diagnosis.
Let me know if you'd like help drafting a referral note or provisional diagnosis summary too.
23/04/2025, 14:20 - Dr.Abdulsalam Med Ed Leads: Yes, anti-AQP4 (aquaporin-4) antibody testing is very relevant in this context.
Here's why:
AQP4 antibodies are associated with Neuromyelitis Optica Spectrum Disorder (NMOSD), which often presents with:
Optic neuritis (vision loss)
Longitudinally extensive transverse myelitis (LETM)
Area postrema syndrome (vomiting, hiccups)
Brainstem or diencephalic involvement (which can cause cranial nerve palsies, gait issues, slurred speech)
Sometimes seizures and encephalopathy, though these are more common in MOG-antibody disease.
Relevance to This Case:
The gait imbalance, squint, facial deviation, slurred speech, and seizures could all be due to brainstem involvement or cortical lesions.
The partial response to IV pulse therapy suggests an inflammatory demyelinating disorder.
NMOSD is an important differential alongside MOGAD and anti-NMDAR encephalitis.
So yes, definitely:
Order AQP4-IgG, preferably by cell-based assay (CBA) – the gold standard.
Also consider testing for MOG-IgG and anti-NMDAR antibodies given the seizure + behavioral profile.
Let me know if you want a diagnostic flowchart or sample workup list for suspected autoimmune encephalitis vs demyelination.
23/04/2025, 16:39 - Rakesh Biswas: 👆 which LLM?
23/04/2025, 16:39 - Rakesh Biswas: Which LLM?
23/04/2025, 16:39 - Rakesh Biswas: This was good 👏
23/04/2025, 18:45 - Dr.Abdulsalam Med Ed Leads: Scholar ChatGPT
23/04/2025, 18:46 - Dr.Abdulsalam Med Ed Leads: Scholar ChatGPT
23/04/2025, 22:02 - +91 98312 49909: Is this coated tongue sir? The one described for Typhoid fever
24/04/2025, 07:26 - Rakesh Biswas: Nailed it 👏
We thought so to but then all these descriptions were made 200 years back and no longer considered relevant and correlation worthy but your book chapter will perhaps elucidate how and more importantly how Web 3.0 can bring these clinical signs back into relevance @9647501361306 @919604701505
24/04/2025, 07:53 - You added Adwaith Krishna S Nurture Oncology
24/04/2025, 07:57 - Dr.Abdulsalam Med Ed Leads: Your question touches on several fascinating intersections: historical clinical signs, their relevance in modern medicine, and the potential role of Web 3.0 technologies in revitalizing or recontextualizing them. Let’s break this down:
---
### **1. The "Coated Tongue" in Typhoid Fever: Historical Context**
The "coated tongue" (often described as a dry, white or brownish fur-like coating) was indeed a classic sign associated with typhoid fever in 19th- and early 20th-century medicine. Historical texts (e.g., Osler’s *Principles and Practice of Medicine*) emphasized physical exam findings like this, as diagnostic tools were limited. However:
- **Why it fell out of relevance**:
- Modern diagnostics (blood cultures, PCR, serology) rendered subjective physical signs less critical.
- Many clinical signs (e.g., coated tongue, "rose spots") lack specificity and sensitivity for typhoid.
- Antibiotic use altered disease presentations, and vaccination reduced incidence in many regions.
---
### **2. Can Historical Clinical Signs Regain Relevance?**
Physical signs like the coated tongue are not *irrelevant*—they remain part of the clinical narrative but are now contextualized within a broader diagnostic framework. Their utility depends on:
- **Resource-limited settings**: Where labs are unavailable, clinical signs still guide empiric treatment.
- **Pattern recognition**: Experienced clinicians may use them as clues in syndromic diagnoses.
- **Digital augmentation**: Modern tools (e.g., AI image analysis) could quantify and standardize subjective signs.
---
### **3. Web 3.0 and the Revival of Clinical Signs**
Web 3.0 (decentralized, semantic, AI-driven, and interoperable data ecosystems) could breathe new life into historical clinical observations in several ways:
#### **a. Decentralized Data Aggregation**
- **Global symptom databases**: Blockchain-secured platforms could aggregate anonymized clinical data (including physical signs like coated tongues) from diverse populations, revealing patterns overlooked in smaller studies.
- **Crowdsourced diagnostics**: Clinicians in low-resource regions could contribute real-time observations to decentralized networks, creating a "living library" of signs correlated with lab-confirmed diagnoses.
#### **b. AI-Powered Pattern Recognition**
- **Image analysis**: AI trained on crowdsourced tongue images (tagged with diagnoses) could identify subtle patterns linking coated tongues to specific infections (e.g., typhoid, COVID-19, or Candida).
- **Predictive modeling**: Machine learning could correlate historical signs with modern biomarkers, uncovering latent diagnostic value (e.g., a coated tongue + fever + thrombocytopenia = higher typhoid probability).
#### **c. Patient-Clinician-Community Collaboration**
- **Patient-reported outcomes**: Web 3.0 platforms (e.g., patient-owned health wallets) could integrate self-reported symptoms with clinician observations, enabling longitudinal tracking of signs like tongue changes.
- **Medical education**: Immersive Web 3.0 environments (VR/AR) could teach rare or historical signs by simulating their evolution in diseases like typhoid.
#### **d. Incentivizing Observation**
- **Tokenized rewards**: Clinicians or patients contributing high-quality data (e.g., validated images of coated tongues with lab-confirmed typhoid) could earn tokens, fostering a self-sustaining ecosystem of observation.
---
### **4. Challenges**
- **Data quality**: Subjective signs require standardization (e.g., photography protocols, diagnostic criteria).
- **Ethics**: Privacy and bias risks in decentralized health data must be addressed.
- **Validation**: Historical signs need rigorous re-evaluation against gold-standard diagnostics.
---
### **5. Conclusion**
While the coated tongue alone may never regain its 19th-century diagnostic prominence, **Web 3.0 could resurrect historical signs by embedding them in data-rich, AI-augmented frameworks**. By aggregating global data, incentivizing contributions, and uncovering hidden correlations, these technologies might transform "antiquated" observations into validated, context-aware diagnostic tools—especially in resource-limited settings or for emerging diseases.
Your book chapter could frame this as a paradigm shift: marrying the wisdom of clinical observation with the power of decentralized intelligence. The future of diagnostics may lie not in discarding the old, but in reimagining it through the lens of Web 3.0. 🚀
Let me know if you'd like to dive deeper into specific examples (e.g., typhoid vs. other infections) or technical frameworks!
24/04/2025, 08:06 - Rakesh Biswas: 👏👏
24/04/2025, 10:08 - Dr.Abdulsalam Med Ed Leads: The query appears to refer to complications of hanging, likely with typos. Below is a structured response based on the inferred intent:
---
### **Uncommon Complications of Hanging**
1. **Delayed Cerebral Edema**: Brain swelling occurring hours after resuscitation.
2. **Tracheal Stenosis**: Narrowing of the windpipe due to prolonged pressure.
3. **Hypoxic Seizures**: Seizures triggered by oxygen deprivation.
4. **Aspiration Pneumonia**: From inhaling stomach contents during the event.
5. **Vocal Cord Paralysis**: Damage to laryngeal nerves.
### **Most Severe Complications (Greatest Seriousness)**
1. **Anoxic Brain Injury**: Irreversible brain damage due to lack of oxygen.
2. **Cervical Spine Fracture**: Often fatal if the spinal cord is severed.
3. **Cardiac Arrest**: Immediate cessation of heart function.
4. **Carotid Artery Dissection**: Tearing of major neck arteries.
5. **Multi-Organ Failure**: Systemic collapse from prolonged hypoxia.
---
**Note:** Hanging is a life-threatening act. If you or someone you know is struggling, please seek immediate help from emergency services or mental health professionals.
24/04/2025, 10:10 - ~ Vaishnavi Thota left
24/04/2025, 10:25 - Rakesh Biswas: Yes this patient had a tracheal tear and was jointly managed with ENT department here by the Emergency team
24/04/2025, 11:23 - Dr.Abdulsalam Med Ed Leads: If you don't mind, I'll share them with my AI agents to prepare drafts about these topics to enrich your discussions and outcome
24/04/2025, 11:24 - Rakesh Biswas: Thanks. That would be great. Off course we have 5000 already published cases waiting in queue for your book on Medical cognition Web 2.0-Web 3.0
24/04/2025, 11:27 - Dr.Abdulsalam Med Ed Leads: Now, we are assessing our students for ENT end course assignments. It may take 6 hours.
24/04/2025, 11:51 - +91 98312 49909: Absolutely sir.
I feel they can still be useful in low-resource settings, or as part of pattern recognition in early diagnosis-especially if ML can help validate and quantify their predictive value. Web 3.0's ability to aggregate large-scale decentralized clinical data could be useful in this respect, letting us re-evaluate old signs in light of modern outcomes.
24/04/2025, 11:55 - Rakesh Biswas: 👏👏 very well thought out
24/04/2025, 15:30 - Dr.Abdulsalam Med Ed Leads: **Slide Title: Patient Presentation - Unresponsive State**
---
**Chief Complaint:**
- Unresponsive state upon arrival to the emergency department.
---
**Patient Demographics:**
- **Age:** 27 years
- **Gender:** Female
- **Residence:** Beebibegudem, QLD (Queensland, Australia)
- **Occupation:** Housewife
---
**Presentation Details:**
- **Date & Time:** 4th April, 10:00 AM
- **Condition:** Found unresponsive (no response to stimuli).
- **Location:** Emergency Department (Casualty).
---
**Key Focus for Assessment:**
1. Immediate stabilization (ABC: Airway, Breathing, Circulation).
2. Differential diagnosis: metabolic, neurological, toxicological, or infectious causes.
3. Urgent investigations: blood glucose, CT head, labs, toxicology screen.
---
**Notes:**
- Ensure clear documentation of onset, preceding symptoms, and medical history (if available).
- Consider social/family context (e.g., access to medications, recent stressors).
---
**Next Steps:**
- Await initial test results.
- Consult neurology/internal medicine for further evaluation.
---
This slide is concise, highlights critical information, and guides clinical discussion. Adjust based on additional patient history or institutional protocols.
24/04/2025, 15:30 - Dr.Abdulsalam Med Ed Leads: **Key Issues to Raise During the Discussion:**
1. **Initial Stabilization and Assessment:**
- Was the **ABCDE approach** (Airway, Breathing, Circulation, Disability, Exposure) rigorously followed?
- Were life-threatening conditions (e.g., hypoxia, hypoglycemia, cardiac arrest) ruled out or managed immediately?
2. **Differential Diagnoses:**
- **Priority Causes**: Hypoglycemia, toxic ingestion (e.g., medications, household toxins), stroke, seizure (including non-convulsive status epilepticus), infection (e.g., meningitis, sepsis), or metabolic derangements (e.g., electrolyte imbalances, diabetic ketoacidosis).
- **Unique Considerations for a Young Female**: Pregnancy-related conditions (e.g., eclampsia), psychiatric causes (e.g., catatonia), or autoimmune encephalitis.
3. **Investigations:**
- **Immediate Tests**: Blood glucose, ABG, electrolytes, toxicology screen (including acetaminophen/salicylate levels), CT head.
- **Additional Considerations**: Lumbar puncture (if infection suspected), MRI (if CT inconclusive), pregnancy test, EEG (for non-convulsive seizures).
- **Resource Limitations**: Given the rural residence (Beebibegudem), is timely access to advanced imaging or specialist consultations feasible?
4. **Social and Environmental Context:**
- **Household Exposure**: Potential access to toxins (e.g., cleaning agents, pesticides) or medications.
- **Psychosocial Factors**: Recent stressors, mental health history, or domestic situation (e.g., intimate partner violence).
- **Community Risks**: Local prevalence of infections (e.g., vector-borne diseases) or environmental hazards.
5. **Ethical and Legal Considerations:**
- **Consent**: Who is the decision-maker if the patient lacks capacity? Was emergency doctrine applied appropriately?
- **Documentation**: Clarity in charting the patient’s condition, interventions, and family communications.
6. **Management and Specialist Involvement:**
- **Neurology/Internal Medicine Consultation**: When to involve specialists (e.g., persistent unresponsiveness, abnormal imaging).
- **Toxicology Input**: If overdose or poisoning is suspected.
- **Monitoring**: Continuous vital signs, neurological checks, and serial labs.
7. **Communication Challenges:**
- **Family Engagement**: How to communicate uncertainty and urgency to family members.
- **Interdisciplinary Coordination**: Ensuring seamless handover between emergency staff and admitting teams.
8. **Potential Pitfalls:**
- **Overlooked Causes**: Undiagnosed metabolic disorders (e.g., porphyria), atypical stroke presentations (e.g., posterior circulation), or rare toxins.
- **Assumption Bias**: Avoiding premature closure on a diagnosis without excluding critical conditions.
9. **Follow-up and Prevention:**
- **Long-term Plan**: If a chronic condition is identified (e.g., epilepsy), ensure follow-up and education.
- **Community Resources**: Referrals to social services if psychosocial factors contributed (e.g., substance abuse support).
---
**Guiding Questions for Discussion:**
- “What red flags were present that could guide urgent interventions?”
- “How might the patient’s occupation and residence influence the differential diagnosis?”
- “Are there gaps in the initial workup that need addressing before narrowing the diagnosis?”
This structured approach ensures comprehensive evaluation while fostering critical thinking and teamwork.
24/04/2025, 15:41 - Dr.Abdulsalam Med Ed Leads: **Comprehensive Analysis and Recommendations for Persistent Neurocysticercosis (NCC):**
### **Clinical Background:**
- **12-year history** of NCC with recent breakthrough seizure.
- Initial presentation: Seizures + left hemiparesis (resolved), treated with phenytoin → switched to phenobarbital 7 years ago.
- **Current MRI** shows persistent cysts (non-resolving over 12 years); old imaging unavailable.
- Key questions: Why cysts persist? Reinfection? Optimal treatment?
---
### **Key Considerations:**
1. **Cyst Stage & Activity (Based on MRI):**
- **Vesicular/colloidal stage (active):** Requires antiparasitics (albendazole + steroids).
- **Calcified (inactive):** No role for antiparasitics; focus on seizure control.
- **Persistent cysts** may indicate:
- **Treatment failure** (inadequate prior therapy, drug resistance).
- **Chronic inflammation** (e.g., degenerating cysts causing edema).
- **Reinfection** (endemic exposure, poor hygiene).
2. **Reinfection Risk:**
- Endemic regions (India, Latin America) increase risk of repeat *T. solium* exposure.
- Screen for ongoing risk factors (e.g., household tapeworm carriers, sanitation practices).
3. **Antiseizure Management:**
- Breakthrough seizure suggests suboptimal control. Reassess ASM choice (e.g., levetiracetam preferred for NCC due to fewer interactions).
---
### **Recommendations:**
1. **Imaging Review:**
- Confirm cyst stage on current MRI (vesicular/colloidal vs. calcified).
- Look for perilesional edema (suggests active inflammation).
2. **Antiparasitic Therapy (if active cysts):**
- **Albendazole** (15 mg/kg/day for 10–14 days) + **prednisolone** (1 mg/kg/day to mitigate edema).
- Consider **combination therapy** (albendazole + praziquantel) if prior treatment failed.
- **Extended courses** (e.g., 28 days) for subarachnoid/racemose cysts.
3. **Seizure Control:**
- Optimize ASM (switch to levetiracetam/lacosamide if enzyme-inducing drugs like phenytoin/phenobarbital are suboptimal).
- Avoid abrupt ASM changes; monitor levels if using phenytoin.
4. **Reinfection Prevention:**
- Educate on hygiene (handwashing, avoiding undercooked pork).
- Screen/treat household contacts for *T. solium* tapeworm.
5. **Surgical Evaluation:**
- If hydrocephalus/mass effect present (e.g., VP shunt for obstructive cysts).
6. **Follow-Up:**
- Repeat MRI in 3–6 months to assess treatment response.
- Monitor for paradoxical worsening (increased edema post-treatment).
---
### **Why Cysts Persist:**
- Likely **chronic inflammation** or **treatment-resistant cysts** (e.g., calcified nodules with episodic edema).
- **Reinfection** is possible if risk factors persist, but 12-year timeline suggests chronicity rather than new exposure.
---
### **Final Notes:**
- **Imaging is critical** to guide therapy. If active cysts are confirmed, a structured antiparasitic course with close monitoring is essential.
- Address **ASM adherence** and consider non-enzyme-inducing alternatives to improve seizure control.
**@Dr.Abdulsalam:** Proceed with MRI staging, then tailor therapy accordingly. If active, albendazole + steroids remain first-line. Reinforce prevention to mitigate reinfection.
24/04/2025, 15:46 - Dr.Abdulsalam Med Ed Leads: These axial FLAIR MRI images of the brain demonstrate significant findings:
1. Right Frontal Lobe Lesion: There is a well-defined, hyperintense lesion seen in the right frontal region involving both cortical and subcortical areas. This lesion appears to exert a mild mass effect on the adjacent structures, with effacement of the adjacent sulci. It is suggestive of a space-occupying lesion, such as a high-grade glioma, metastasis, or abscess. The lesion margins appear irregular.
2. Periventricular and Deep White Matter Hyperintensities: Bilateral periventricular white matter shows hyperintense signals on FLAIR, more prominently on the left side. These changes are often seen in chronic small vessel ischemic changes, but could also suggest demyelination depending on clinical context.
3. No Acute Infarct or Hemorrhage Visualized: No diffusion restriction or blooming artifact is evident in these FLAIR sequences to suggest an acute infarct or hemorrhage.
4. Ventricular System: The lateral ventricles are within normal limits in size and configuration. No midline shift or hydrocephalus is apparent.
Clinical Correlation Recommended: Given the findings, especially the right frontal lesion, further evaluation with contrast-enhanced MRI, MR spectroscopy, and possibly biopsy might be warranted based on the patient's symptoms and clinical background.
Please provide clinical context (e.g., symptoms, onset, relevant history) for more specific differential considerations.
24/04/2025, 15:46 - Dr.Abdulsalam Med Ed Leads: These axial FLAIR MRI images of the brain demonstrate significant findings:
1. Right Frontal Lobe Lesion: There is a well-defined, hyperintense lesion seen in the right frontal region involving both cortical and subcortical areas. This lesion appears to exert a mild mass effect on the adjacent structures, with effacement of the adjacent sulci. It is suggestive of a space-occupying lesion, such as a high-grade glioma, metastasis, or abscess. The lesion margins appear irregular.
2. Periventricular and Deep White Matter Hyperintensities: Bilateral periventricular white matter shows hyperintense signals on FLAIR, more prominently on the left side. These changes are often seen in chronic small vessel ischemic changes, but could also suggest demyelination depending on clinical context.
3. No Acute Infarct or Hemorrhage Visualized: No diffusion restriction or blooming artifact is evident in these FLAIR sequences to suggest an acute infarct or hemorrhage.
4. Ventricular System: The lateral ventricles are within normal limits in size and configuration. No midline shift or hydrocephalus is apparent.
Clinical Correlation Recommended: Given the findings, especially the right frontal lesion, further evaluation with contrast-enhanced MRI, MR spectroscopy, and possibly biopsy might be warranted based on the patient's symptoms and clinical background.
Please provide clinical context (e.g., symptoms, onset, relevant history) for more specific differential considerations.
24/04/2025, 16:00 - pajr.in CEO, NHS Endocrinologist: All can be connected to Phenytoin toxicity.
24/04/2025, 16:15 - Dr.Abdulsalam Med Ed Leads: Scholar ChatGPT
24/04/2025, 16:16 - Dr.Abdulsalam Med Ed Leads: DeepSeek
24/04/2025, 16:17 - Dr.Abdulsalam Med Ed Leads: DeepSeek
24/04/2025, 16:21 - Rakesh Biswas: Assuming this is scholar GPT.
I particularly liked it's medical cognition highlighters in the inputs with due attention to context and multiple dimensions of the patient encounter including potential pitfalls such as assumption bias! Also the guiding questions were another potentially very useful feature! We could train some models in "critical realist heutagogy?" @919604701505 @919171769005 <This message was edited>
24/04/2025, 16:25 - Dr.Abdulsalam Med Ed Leads: Also DeepSeek's
24/04/2025, 16:26 - Rakesh Biswas: Important CRH (critical realist heutagogy) question for the LLM here:
What is the evidence of improved outcomes in neurocysticercosis with or without anti helminthic therapy ie albendazole vs placebo.
Please share the detailed data from one RCT in a PICO format taking care to share only absolute values and avoid relative percentages @13135550002
24/04/2025, 16:26 - Meta AI: To answer your question about the evidence of improved outcomes in neurocysticercosis with or without anti-helminthic therapy, specifically albendazole vs placebo, I'll provide an overview based on available research.
# Comparison of Albendazole and Praziquantel
While direct comparisons between albendazole and placebo are limited, research comparing albendazole to praziquantel shows promising results for albendazole. A meta-analysis of comparative trials indicates that albendazole is associated with:
- *Better control of seizures*: Albendazole showed superior seizure control compared to praziquantel, with a point effect estimate (incidence rate ratio) of 4.94 (95% CI 2.45-9.98) in a pooled analysis of 156 patients.
- *Total disappearance of cysts*: Albendazole was more effective than praziquantel in achieving total disappearance of cysts, with an odds ratio of 2.30 (95% CI 1.06-5.00) in a pooled analysis of 335 patients.
# PICO Format for RCT Comparison
Given the lack of direct RCT data comparing albendazole to placebo in your query, here's a representation based on the albendazole vs praziquantel meta-analysis, focusing on seizure control and cyst disappearance:
*PICO Format*
- *Population*: Patients with parenchymal neurocysticercosis
- *Intervention*: Albendazole therapy
- *Comparison*: Praziquantel therapy (as a proxy for comparison, given the direct comparison to placebo isn't readily available)
- *Outcome*:
- *Seizure Control*: Albendazole shows better seizure control.
- *Cyst Disappearance*: Albendazole is associated with greater total disappearance of cysts.
# Detailed Data from Meta-Analysis
The meta-analysis included six studies comparing albendazole and praziquantel. Key findings include¹:
- *Seizure Control*: 4 studies (156 patients) showed albendazole's superiority in seizure control.
- *Cyst Reduction*: No significant difference was found between albendazole and praziquantel in reducing cysts.
- *Total Disappearance of Cysts*: 6 studies (335 patients) demonstrated albendazole's effectiveness over praziquantel.
Given the nature of the question and available data, direct comparison to placebo isn't feasible without further research. The current evidence supports albendazole's efficacy in treating neurocysticercosis, particularly when compared to praziquantel. For more precise comparisons, including albendazole vs placebo, additional randomized controlled trials would be necessary.
24/04/2025, 16:26 - Meta AI: https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0000194
24/04/2025, 16:28 - Rakesh Biswas: @13135550002 please share any single RCT comparing antihelminthic vs placebo in neurocysticercosis. Please avoid meta analysis.
24/04/2025, 16:28 - Meta AI: A 1995 randomized clinical trial published in the Archives of Internal Medicine compared the efficacy of two antihelminthic agents, albendazole and praziquantel, against symptomatic treatment alone in patients with active neurocysticercosis. Here's a breakdown of the study:
- *Study Design*: The trial randomized 138 patients into three groups:
- *Group 1*: Oral prednisolone alone (27 patients)
- *Group 2*: Praziquantel with prednisolone (54 patients)
- *Group 3*: Albendazole with prednisolone (57 patients)
- *Outcomes*:
- *Cyst Resolution*: At 6 months and 1 year after treatment, there were no significant differences in the proportion of patients free of cysts or relative reduction in cyst number across the three groups.
- *Seizure Control*: At 2 years, there was no difference in the proportion of patients free of seizures during the entire follow-up period.
- *Sequelae*: Early and late sequelae occurred more frequently in patients treated with praziquantel and albendazole compared to those receiving only prednisolone.
This study doesn't provide a direct comparison to a placebo group without any antihelminthic treatment, as all groups received some form of treatment. However, the group receiving prednisolone alone serves as a control for the antihelminthic treatment groups, suggesting that antihelminthic therapy may not offer significant benefits over symptomatic treatment alone in neurocysticercosis.¹
24/04/2025, 16:28 - Meta AI: https://pubmed.ncbi.nlm.nih.gov/7575052/
24/04/2025, 16:29 - Rakesh Biswas: @13135550002 any similar studies after 1995? What is the role of antihelminthic therapy in the current evidence based management of neurocysticercosis?
24/04/2025, 16:30 - Meta AI: # Role of Antihelminthic Therapy in Neurocysticercosis Management
The role of antihelminthic therapy in managing neurocysticercosis is still debated. While corticosteroids are widely used to control inflammation, the effectiveness of antihelminthic drugs like albendazole and praziquantel varies depending on the type and stage of the disease.
# Studies After 1995
Several studies have investigated the use of antihelminthic therapy in neurocysticercosis:
- *Single Enhancing Lesions*: Research suggests that corticosteroids may be beneficial in treating single enhancing lesions, reducing seizures and promoting lesion resolution.
- *Albendazole vs Praziquantel*: Albendazole is often preferred due to its better efficacy and shorter treatment duration.
- *Combination Therapy*: Some studies explore combining antihelminthic therapy with corticosteroids and antiepileptic drugs, but more research is needed to determine optimal treatment regimens.
# Current Evidence-Based Management
Current management strategies focus on controlling symptoms, reducing inflammation, and preventing further damage. This may involve:
- *Corticosteroids*: Used to manage inflammation and edema, particularly in cases with multiple or degenerating cysts.
- *Antiepileptic Drugs*: Prescribed to control seizures, which are a common symptom of neurocysticercosis.
- *Antihelminthic Therapy*: May be used in specific cases, such as viable parenchymal cysts or subarachnoid disease, but its role is still being studied.
- *Surgery*: May be necessary for hydrocephalus, spinal cord compression, or other complications.
# Key Considerations
When managing neurocysticercosis, it's essential to consider the following factors:
- *Disease Stage*: Treatment approaches may vary depending on the stage of the disease (e.g., viable, degenerating, or calcified cysts).
- *Cyst Location*: Cysts in different locations (e.g., parenchymal, subarachnoid, or ventricular) may require different treatment strategies.
- *Inflammation Control*: Corticosteroids play a crucial role in managing inflammation, which is a key aspect of the disease.¹
24/04/2025, 16:30 - Meta AI: https://pmc.ncbi.nlm.nih.gov/articles/PMC3721198/
24/04/2025, 16:31 - Dr.Abdulsalam Med Ed Leads: **Evidence from a Randomized Controlled Trial (RCT) in PICO Format**
Below is a detailed summary of an RCT comparing albendazole + prednisone versus placebo + prednisone in neurocysticercosis (NCC), presented with **absolute values** .
---
### **PICO Framework**
**Population**:
- **Adults and children** with active or transitional NCC cysts (viable or degenerating) and new-onset symptoms (e.g., seizures, headaches).
- **Sample size**: 178 participants (88 in albendazole group, 90 in placebo group).
**Intervention**:
- **Albendazole** (800 mg/day) + **prednisone** (1 mg/kg/day) for **8 days**.
**Comparison**:
- **Placebo** + **prednisone** (1 mg/kg/day) for **8 days**.
**Outcomes** (measured at 1, 6, and 12 months):
| **Outcome** | **Albendazole Group (n=88)** | **Placebo Group (n=90)** | **p-value** |
|-------------------------------|------------------------------|---------------------------|-------------|
| **Complete cyst resolution at 1 month** | 27 patients (31%) | 6 patients (7%) | 0.001 |
| **Reduction in active cysts** | Greater reduction (exact counts not reported) | Minimal reduction | 0.001 |
| **Seizure recurrence at 12 months** | No significant difference vs. placebo | No significant difference | NS |
---
### **Key Findings**
1. **Cyst Resolution**:
- Albendazole led to **complete cyst disappearance in 31% of patients** (27/88) by 1 month, compared to **7% in the placebo group** (6/90) .
- This effect plateaued after 1 month, with no further improvement in cyst resolution at 6 or 12 months.
2. **Seizure Outcomes**:
- **No significant difference** in seizure recurrence between groups over 12 months.
- A secondary analysis noted a reduction in **generalized seizures** in the albendazole group during months 1–12 (rate ratio: 0.19) but no effect on focal seizures .
3. **Safety**:
- Adverse events (e.g., headache, abdominal pain) were comparable between groups.
---
### **Interpretation**
- Albendazole + steroids **accelerates cyst resolution** but does not significantly reduce long-term seizure recurrence in NCC patients with active cysts .
- The lack of long-term seizure benefit may reflect the natural history of NCC, where cysts eventually calcify or resolve regardless of treatment .
---
### **Limitations**
- **Population**: Focused on active/transitional cysts; calcified cysts were excluded.
- **Outcome measures**: Seizure recurrence data lacked absolute counts in the trial abstract (relative rates only) .
For full trial details, refer to the original study: [Effects of albendazole treatment on neurocysticercosis: a randomised controlled trial](https://pubmed.ncbi.nlm.nih.gov/18495737/) .
24/04/2025, 16:31 - Dr.Abdulsalam Med Ed Leads: DeepSeek 👆
24/04/2025, 16:34 - Rakesh Biswas: 👏👏the best part is that it could even reference the URL to the article in pubmed! @13135550002 I am hoping you can also learn to do that soon
24/04/2025, 16:34 - Meta AI: I'm glad you appreciated the detailed information. While I don't have direct access to PubMed or other databases, I can suggest ways to find the articles I referenced. You can try searching for the article titles, authors, or keywords on PubMed or other academic search engines like Google Scholar.
If you need help with searching or finding specific articles, feel free to ask, and I'll do my best to assist you. I'm constantly learning and improving, so maybe one day I'll be able to provide direct links to articles! 😊
25/04/2025, 10:10 - Rakesh Biswas: Morning journal club feeler on yesterday's published journal paper
CRH initial impression Inputs:
Doesn't sound impressive 👇
reduced knee pain measured on a 0- to 100-mm visual analog scale (score of 100 = worst): −31.3 mm in the metformin group and −18.9 mm in the placebo group (between-group difference, −11.4 mm; P = .01), corresponding to an effect size of 0.43.
Will need to know the exact questions in the VAS and relive the perceived experiences of those subjected to the scale that made this creeping ant difference
https://jamanetwork.com/journals/jama/fullarticle/2833338
25/04/2025, 11:59 - Dr.Abdulsalam Med Ed Leads: The full article from *JAMA* could not be extracted due to security restrictions on the website (Cloudflare protections blocked access). However, I can still provide a detailed initial critique based on the abstract and publicly visible content. Here's a feeler for your journal club discussion:
---
### **Initial Critical Take on the Study:**
This randomized clinical trial explored whether metformin reduced knee pain in obese patients with knee osteoarthritis. The key result:
> **Pain reduction on a 0–100 mm visual analog scale (VAS):**
> - **Metformin group:** −31.3 mm
> - **Placebo group:** −18.9 mm
> - **Between-group difference:** −11.4 mm (P = .01)
> - **Effect size:** 0.43
**Surface-level impression:**
The **effect size of 0.43** is **modest**, sitting just below what’s typically considered a medium effect (Cohen's d of 0.5). The **11.4 mm improvement** difference on the VAS — while statistically significant — may not cross the **minimal clinically important difference (MCID)** threshold, often pegged around 15–20 mm for chronic pain. This raises real questions about practical relevance versus statistical significance.
---
### **What’s missing / needs clarification for deeper evaluation:**
1. **VAS question context:** What was the exact wording of the VAS? Was it “average pain in the past week” or “worst pain today”? Context changes perception.
2. **Patient-reported experience:** What was the baseline experience of participants? Were improvements genuinely noticeable to them or just numbers on paper?
3. **Rescue medications and compliance data:** Did participants use NSAIDs, and how did that interact?
4. **Dropout analysis:** Was there differential attrition, especially in patients with poor pain response?
---
### **Suggested Next Steps:**
- Retrieve full text via institution access or JAMA login.
- Examine the supplementary materials: especially methods, full pain questionnaire wording, subgroup analysis, and adverse events.
- Consider patient engagement metrics and responder analysis — e.g., what proportion improved by ≥30 mm?
- Compare with prior studies on metformin and systemic inflammation in OA.
Would you like me to pull academic articles critiquing or expanding on this metformin-OA connection for journal club prep?
---
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25/04/2025, 12:06 - Dr.Abdulsalam Med Ed Leads: **Summary and Implications of the JAMA RCT on Metformin for Knee Osteoarthritis (OA) in Overweight/Obese Patients**
### **Key Findings**
1. **Efficacy**:
- Metformin (2000 mg/day) significantly reduced knee pain vs. placebo at 6 months:
- **Mean pain reduction**: −31.3 mm (metformin) vs. −18.9 mm (placebo) on a 100-mm visual analog scale (VAS).
- **Between-group difference**: −11.4 mm (95% CI: −20.1 to −2.6; *P* = .01), with a moderate effect size (0.43).
- Secondary outcomes (WOMAC scores for pain, stiffness, function) also improved significantly with metformin.
2. **Safety**:
- Gastrointestinal adverse events (diarrhea, abdominal discomfort) were more common with metformin but manageable.
- No serious adverse events or significant dropouts.
3. **Clinical Relevance**:
- The metformin group exceeded the **minimum clinically important difference (MCID)** for pain reduction (15 mm), while the placebo group approached it.
- Results suggest metformin may be a safe adjunct therapy for knee OA in overweight/obese individuals, even without diabetes.
---
### **Strengths of the Study**
- **Robust Design**: Randomized, double-blind, placebo-controlled trial.
- **Real-World Applicability**: Remote recruitment/follow-up via telemedicine broadens generalizability.
- **Mechanistic Plausibility**: Aligns with preclinical evidence of metformin’s anti-inflammatory and cartilage-protective effects.
---
### **Limitations**
- **Sample Size**: Small (*n* = 107) and short follow-up (6 months).
- **Structural Outcomes**: No imaging to assess cartilage preservation or disease modification.
- **Placebo Effect**: High placebo response (−18.9 mm pain reduction) complicates interpretation.
- **Population**: Excluded patients with diabetes; results may not generalize to non-overweight individuals.
---
### **Clinical Implications**
1. **Potential Use Cases**:
- **Overweight/obese patients with knee OA** who:
- Have inadequate pain relief from first-line therapies (e.g., NSAIDs, exercise, weight loss).
- Have comorbidities like prediabetes or metabolic syndrome.
- **Avoid in**: Patients with GI intolerance, renal impairment, or vitamin B12 deficiency.
2. **Practical Considerations**:
- Start with a low dose (500 mg/day) and titrate to 2000 mg/day to minimize GI side effects.
- Monitor vitamin B12 levels with long-term use.
- Combine with lifestyle interventions (weight loss, exercise) for synergistic benefits.
---
### **Unanswered Questions & Future Research**
- **Mechanism**: Does metformin reduce inflammation, improve metabolism, or directly protect cartilage?
- **Disease Modification**: Can metformin slow OA progression?
- **Long-Term Safety**: Effects beyond 6 months (e.g., B12 deficiency, renal function).
- **Broader Populations**: Efficacy in non-overweight patients or those with diabetes.
---
### **Conclusion**
This trial provides **moderate-quality evidence** supporting metformin as a novel, cost-effective option for knee OA pain in overweight/obese individuals. While not yet a first-line therapy, it could be considered for select patients within a multidisciplinary OA management plan. Larger, longer-term trials are needed to confirm durability and disease-modifying effects.
**Guideline Updates**: Watch for future OA guidelines (e.g., ACR, OARSI) to potentially incorporate metformin as an adjunct therapy.
For further details, refer to the full study: [JAMA 2025; DOI:10.1001/jama.2025.3471].(UPDF generated)
25/04/2025, 12:27 - Rakesh Biswas: 👆Was this deep seek?
25/04/2025, 12:29 - Dr.Abdulsalam Med Ed Leads: This is UPDF generated, it's specialized in with pdf format texts
25/04/2025, 12:29 - Rakesh Biswas: Loved this one by Scholar GPT! 👏👏
@919652955915 @919154575937 you have been part of the web 2.0 CBBLE era where we would have taken many days to reach this kind of learning outcomes?
25/04/2025, 12:30 - Rakesh Biswas: It's arguments weren't that strong but again loved the variability of inputs toward triangulation
25/04/2025, 12:32 - Dr.Abdulsalam Med Ed Leads: This agent can deal with student leveled analysis of pdfs
25/04/2025, 12:58 - Dr.Abdulsalam Med Ed Leads: **Critical Analysis of the Metformin Trial for Knee Osteoarthritis: Contextualizing the VAS Results**
The recent JAMA study on metformin's efficacy in knee osteoarthritis (OA) pain reduction has sparked debate, particularly regarding the clinical relevance of its findings. Here’s a breakdown of key considerations for your journal club discussion:
---
### **1. Interpreting the Visual Analog Scale (VAS) Results**
- **Trial Outcomes**: Metformin reduced pain by −31.3 mm vs. −18.9 mm for placebo on a 0–100 mm VAS (between-group difference: −11.4 mm; *P* = 0.01) .
- **Clinical Significance**:
- The study’s predefined "minimum clinically important difference" (MCID) was 15 mm, which the between-group difference did not meet .
- However, **VAS interpretation is context-dependent**:
- A 33% reduction in VAS scores is often considered meaningful . For a baseline pain score of ~60 mm (common in OA trials), a 31.3 mm reduction (~52%) exceeds this threshold, while the placebo’s 18.9 mm (~31%) does not.
- VAS may not be linear: Rasch analysis suggests patients perceive pain relief non-uniformly across the scale, potentially inflating or understating changes depending on baseline severity .
---
### **2. Strengths and Limitations of the Trial**
- **Strengths**:
- **Safety and Accessibility**: Metformin is low-cost, widely available, and has a well-established safety profile, making it an attractive option for OA management .
- **Secondary Outcomes**: Significant improvements in WOMAC pain, stiffness, and function scores (*P* < 0.05) support metformin’s broader benefits .
- **Limitations**:
- **Small Sample Size**: With only 107 participants, the trial may lack power to detect smaller but clinically relevant effects .
- **Short Follow-Up**: The 6-month duration precludes conclusions about long-term efficacy or structural disease modification .
- **Baseline Pain Severity**: The study excluded patients with diabetes but did not report baseline VAS scores in detail. Pain severity at enrollment affects MCID interpretation .
---
### **3. Broader Context of OA Pain Measurement**
- **VAS vs. WOMAC**:
- The VAS is more sensitive to detecting treatment effects than WOMAC in meta-analyses, but it may also introduce greater variability .
- In this trial, WOMAC pain scores improved significantly (−113.9 vs. −68.2; *P* = 0.045), aligning with VAS trends .
- **Placebo Effect**: The −18.9 mm reduction in the placebo group highlights the strong placebo response common in OA trials, possibly due to psychosocial factors or regression to the mean .
---
### **4. Implications for Clinical Practice**
- **Potential Role of Metformin**:
- While not a "breakthrough," metformin offers a **safe adjunct** to lifestyle modifications (e.g., weight loss, exercise) in overweight/obese OA patients, particularly where NSAIDs or surgery are contraindicated .
- Its anti-inflammatory and metabolic effects may slow OA progression, though structural benefits were not assessed in this trial .
- **Research Gaps**:
- Larger, longer-term trials with imaging (e.g., MRI) are needed to confirm pain relief durability and cartilage preservation .
- Subgroup analyses (e.g., baseline BMI, pain severity) could identify patients most likely to benefit.
---
### **5. Conclusion**
The trial’s modest between-group difference (−11.4 mm) may reflect **statistical significance without clear clinical meaningfulness** in isolation. However, combining VAS and WOMAC results, safety data, and patient-specific factors (e.g., obesity, contraindications to NSAIDs) suggests metformin has a plausible role in OA management. Future studies should prioritize larger cohorts and mechanistic insights to validate these findings.
**Key Questions for Journal Club Discussion**:
- How should we reconcile statistical significance with MCID thresholds in pain trials?
- Does metformin’s safety profile justify its off-label use despite uncertain clinical impact?
- How might baseline pain severity influence the interpretation of VAS changes in OA?
For deeper insights, refer to the primary trial and VAS methodology critiques . { DeepSeek}
25/04/2025, 13:27 - pajr.in CEO, NHS Endocrinologist: Great. How is the child doing now?
25/04/2025, 13:38 - Ganesh Joshi: AIIMS Bibinagar Department of PMR will guide after examination🙏🏻
25/04/2025, 16:21 - Rakesh Biswas: His parents showed us in the OPD as one of them had developed Repetitive strain injury to the shoulder and back muscles from the strain of carrying him!
25/04/2025, 16:21 - Rakesh Biswas: Do you know anyone there?
25/04/2025, 23:19 - pajr.in CEO, NHS Endocrinologist: Does not bode well
https://x.com/pparikhxr/status/1915737790265925787?t=gLav_R3SZY9aKri212GXgQ&s=08
26/04/2025, 07:04 - Rakesh Biswas: But this inventing/confabulating citations is very common with current AI especially meta AI who's non premium version for us simply refuses to either share or deep dive into URLs.
We have experienced this on so many occasions since more than a year now! That's the reason we rely more on perplexity when it comes to checking URL citations which it dutifully cites or Google Gemini from the Google Ux.
Your thoughts @9647501361306
26/04/2025, 10:27 - Dr.Abdulsalam Med Ed Leads: Meta AI declared that publicly before more than 4 months!
26/04/2025, 10:29 - Dr.Abdulsalam Med Ed Leads: I used to depend on meta AI to read different images very professionally with easy access, and then it refused to read simply saying this option is no longer available <This message was edited>
26/04/2025, 10:58 - Rakesh Biswas: Share the same disappointment about @13135550002
Let's hope it will open it's windows wider soon and allow better access to all it's useful features
26/04/2025, 10:58 - Meta AI: I completely understand your sentiment! It's exciting to imagine the possibilities with expanded access to features and information. I'm designed to learn and improve continuously, so hopefully, future updates will bring even more capabilities and insights to our conversations. Thanks for sharing your thoughts!
26/04/2025, 10:59 - +91 77985 07300 left
26/04/2025, 11:04 - Dr.Abdulsalam Med Ed Leads: hope so
26/04/2025, 11:08 - Dr.Abdulsalam Med Ed Leads: Its answer is not convincing as its earlier responses were almost inclusive of any academic and professional task, and all of a sudden vanished!
26/04/2025, 11:10 - Dr.Abdulsalam Med Ed Leads: Financial? security? Competitive? issues!
26/04/2025, 18:40 - Dr.Abdulsalam Med Ed Leads: The 17-year-old female presenting with 20 days of polyarthritis, enthesitis, and intermittent urticaria presents a complex clinical picture. Below is a structured approach to the differential diagnosis and evaluation:
### **Differential Diagnosis**
1. **Juvenile Spondyloarthritis (Enthesitis-Related Arthritis, ERA)**
- **Key Features**: Enthesitis, asymmetric oligo/polyarthritis (often lower limbs), HLA-B27 association.
- **Urticaria Link**: Not typical; consider coexisting allergic/autoimmune conditions or drug reaction.
2. **Systemic Lupus Erythematosus (SLE)**
- **Key Features**: Non-erosive arthritis, malar rash, photosensitivity, renal/hematologic involvement.
- **Urticaria**: Rare but possible (e.g., hypocomplementemic urticarial vasculitis). Check for anti-dsDNA, anti-Smith antibodies, low complement.
3. **Serum Sickness-Like Reaction**
- **Key Features**: Drug/antigen exposure (e.g., antibiotics, antivirals), urticaria, arthritis, fever.
- **Timeline**: Symptoms arise 1–3 weeks post-exposure. Resolves with discontinuation of trigger.
4. **Urticarial Vasculitis**
- **Key Features**: Urticaria lasting >24 hours with purpura/pigmentation, arthralgias/arthritis, hypocomplementemia (especially anti-C1q antibodies).
- **Enthesitis**: Uncommon; skin biopsy (leukocytoclastic vasculitis) required for diagnosis.
5. **Autoinflammatory Syndromes (e.g., CAPS, Muckle-Wells Syndrome)**
- **Key Features**: Periodic fever, urticaria, sensorineural hearing loss, arthritis.
- **Rarity**: Consider in refractory cases with family history or recurrent episodes.
6. **Behçet’s Disease**
- **Key Features**: Oral/genital ulcers, uveitis, pathergy.
- **Urticaria**: Atypical; erythema nodosum more common.
7. **Infection/Reactive Arthritis**
- **Triggers**: Viral (e.g., parvovirus, hepatitis) or bacterial (e.g., streptococcal, Lyme).
- **Urticaria**: Rare; evaluate for recent infections/travel.
### **Evaluation Steps**
1. **History**:
- Medication use (e.g., antibiotics, NSAIDs), recent infections, family history of autoimmune disease.
- Rash characteristics (duration, distribution, response to pressure/heat).
2. **Physical Exam**:
- Joint/entheseal tenderness (e.g., Achilles, plantar fascia).
- Oral/genital ulcers, lymphadenopathy, organomegaly.
3. **Laboratory Workup**:
- **Inflammatory Markers**: ESR, CRP.
- **Autoantibodies**: ANA, RF, anti-CCP, HLA-B27, ANCA, anti-dsDNA.
- **Complement Levels**: C3, C4, anti-C1q (urticarial vasculitis).
- **Infection Screen**: ASO titer, parvovirus IgM, Lyme serology, hepatitis panel.
4. **Imaging**:
- X-ray/MRI of affected joints (enthesitis, erosions).
- Sacroiliac imaging if spondyloarthritis suspected.
5. **Skin Biopsy**:
- If urticarial lesions persist >24 hours, assess for vasculitis.
### **Management Considerations**
- **Symptomatic Relief**: NSAIDs for arthritis/enthesitis, antihistamines for urticaria.
- **Disease-Specific Therapy**:
- **ERA/Spondyloarthritis**: DMARDs (methotrexate), biologics (anti-TNF).
- **SLE/Urticarial Vasculitis**: Steroids, hydroxychloroquine, immunosuppressants.
- **Autoinflammatory Syndromes**: IL-1 inhibitors (e.g., anakinra).
### **Key Takeaway**
The combination of enthesitis and urticaria is unusual. Prioritize ruling out SLE, urticarial vasculitis, and drug reactions. HLA-B27 testing and complement levels may clarify the diagnosis. Early rheumatology referral is recommended for targeted workup and management.
26/04/2025, 20:44 - pajr.in CEO, NHS Endocrinologist: Fluorosis is evident but I wouldn't discard Gout yet. RA possibly too but Inflammatory OA unlikely given spared thumb and affliction of MCPs and PIPs
26/04/2025, 20:45 - pajr.in CEO, NHS Endocrinologist: Also quite asymmetric and suggests he is a right handed gentleman
27/04/2025, 12:32 - Rakesh Biswas: This week's Meu global elective UG student learning byproducts:
Some of our MeU global UG students run their own elective special interest groups SIGs to nurture interest in "oncology" amongst all and also manage to publish the by products of their discussions in that group (active learning through critical realist heutagogy ) as potentially impactful papers/letters such as this one on April 23, 2025: 👇
https://www.sciencedirect.com/science/article/abs/pii/S0959804925002230
They roped us into their groups and we as spoilt facilitators tried to rope them into medical education and research and other than communicating from their elective oncology learning snippets, they are currently working with us on a paper that describes a unique medical education syndrome that tries to rejuvenate into medical education, the level 6 of Bloom's taxonomy.
This is done through a syndromic approach to medical education and research utilising a new design known as "critical realist heutagogy" for processing data from primary beneficiaries of medical education and research (patients) into user driven learning community ontologies. Here's a recent podcast about it designed by another global "Medical Cognition Web 2.0-3.0" project member Prof Salam : https://youtu.be/EhfMlwgx_Tw?feature=shared
28/04/2025, 07:46 - PaJR Physicist: <Media omitted>
28/04/2025, 08:12 - Rakesh Biswas: Please elaborate and clarify the last line:
1) What is "much of the test" here?
28/04/2025, 08:16 - PaJR Physicist: Sorry, Read as 'if the case files here'. Attribute it to pre coffee cognitive deficit.
28/04/2025, 08:57 - Rakesh Biswas: Alright
For the textual and visual asynchronous learners here (who may not prefer the audio learning mode) would it be possible for you to share the text of the case files one by one or even the entire text of the podcast above?
28/04/2025, 09:06 - PaJR Physicist: <Media omitted>
28/04/2025, 09:32 - Rakesh Biswas: Got it! So you would like our Web 3.0 expert to convert many of our texts here into audio. Yes I guess that's a good way forward. The other user driven way is that most users would automatically convert the text here into audio podcasts themselves using notebook LM if they are audio learners.
28/04/2025, 09:34 - Rakesh Biswas: The file is in .rtf which couldn't open in my phone but I recall opening one such pmed document
28/04/2025, 09:35 - PaJR Physicist: Especially when you have traffic conditions, like we have in Bangalore. 😋
28/04/2025, 09:44 - Rakesh Biswas: Yes reviewed it again just now and will share my Inputs on it:
1) As a visual learner I would have preferred more image illustrated textual insights
2) That is perhaps best brought out in a blogged write up rather than a word file
3) For example an image in canva perhaps using more nature motifs around what is " Key CABs relevant to CHF management including electromechanical activation time (EMAT) and its corrected form (Ematc), left ventricular systolic time (LVST), and the presence and strength of the third (S3) and fourth (S4) heart sounds" and
4) The evidence in a PICO format if population based data or links to detailed real case report events and outcomes on how they are hypothesized to be useful in cardiac failure monitoring over and above patient reported outcomes <This message was edited>
28/04/2025, 10:03 - Dr.Abdulsalam Med Ed Leads: Podcast enhances listening a skill very essential in academic learning, which fosters self reflection development an integral cornerstone of giving constructive feedback (self, peer,.....) which interns aid in achieving the objectives. <This message was edited>
28/04/2025, 10:06 - Rakesh Biswas: Agree but listening takes a lot of time. Prefer to do it synchronously and listen to patients and other learners in a regular face to face manner.
28/04/2025, 10:11 - Dr.Abdulsalam Med Ed Leads: Time and priority management priority is another skill for an academician character. I listen to postcad during driving or early morning fieldwalking
28/04/2025, 10:14 - Rakesh Biswas: I listen to classical music during that time!😅
28/04/2025, 11:51 - Rakesh Biswas: Raised temperature on the left medial shin over the dilated superficial veins
28/04/2025, 12:42 - Dr.Abdulsalam Med Ed Leads: Let's work through it carefully:
17F: teenage girl
Short stature, noticed 8 years ago
Hypothyroidism, on thyroxine (still inadequately controlled now with TSH 9.6 IU/mL despite 75 mcg)
Gibbus deformity, secondary to a surgery 4 years ago (but no available surgical records)
Bifid spine at gibbus site (could suggest underlying spinal dysraphism)
History of lumbar swelling, drained (possibly an abscess or a pseudomeningocele?)
Given this combination, possible syndromic associations include:
1. Congenital spinal dysraphism (occult spinal dysraphism)
Spina bifida occulta can present late with a gibbus, short stature if associated with tethered cord.
Post-surgical scarring could confuse the picture.
A bifid spine on physical exam suggests failure of fusion of vertebral arches.
2. Skeletal dysplasia (especially associated with spinal deformities)
Some skeletal dysplasias (e.g., spondyloepiphyseal dysplasia congenita, mucopolysaccharidoses) present with:
Short stature
Gibbus
Spinal abnormalities
Possible endocrine problems (secondary hypothyroidism or pituitary dysfunction in some)
3. Hypothyroidism-associated skeletal dysplasia
Long-standing untreated congenital hypothyroidism can cause epiphyseal dysgenesis, short stature, and even gibbus-like deformity.
But usually the hypothyroidism is more severe if this is the cause, and mental retardation would also be present if congenital.
4. Mucopolysaccharidosis (MPS)
Some types (like MPS I - Hurler's syndrome, MPS IV - Morquio's) cause:
Short stature
Gibbus deformity
Spinal anomalies
Possible hydrocephalus or spinal cord compression
But they usually also have coarse facies, corneal clouding, organomegaly, and joint laxity or stiffness.
Clue: Did she have coarse facial features or stiff joints?
---
Summary:
Most likely possibilities are:
Occult spinal dysraphism (e.g., spina bifida occulta, tethered cord syndrome)
Skeletal dysplasia (e.g., mild form of spondyloepiphyseal dysplasia)
Less likely but important to rule out: Mucopolysaccharidosis (MPS)
---
Next steps you could consider:
Spine MRI: to look for tethered cord, diastematomyelia, lipoma, meningocele remnants
Skeletal survey: check for dysplasia signs (beaking vertebrae, abnormal epiphyses)
Urine GAGs (glycosaminoglycans) if considering MPS
Thyroid function optimization (aim TSH <5)
---
Would you like me to also give a differential diagnosis table summarizing features side-by-side for you to use during your OPD? It might help for quick reference!
28/04/2025, 13:08 - Rakesh Biswas: The LLM should have taken into account cleft palate or bifid hard palate too, which she has. The Dental resident who brought this patient to our OPD found out a similar syndrome through orpha net
28/04/2025, 13:21 - Dr.Abdulsalam Med Ed Leads: I think there was NO mention about cleft palate or bifid hard palate in the shared text!
28/04/2025, 13:48 - Dr.Abdulsalam Med Ed Leads: Okay, let's break down these complex findings. It's challenging without the surgical details or previous imaging, but we can form a differential diagnosis based on the combination of features: short stature, hypothyroidism, and significant spinal deformity (gibbus, possible spina bifida, past surgery, past lumbar swelling/drainage).
Here are the possibilities, ranging from more to less likely:
Coincidental Conditions (Most Likely Scenario):
Hypothyroidism: Most likely Autoimmune Thyroiditis (Hashimoto's thyroiditis) given the age of onset and need for increasing thyroxine dose. The current TSH of 9.6 IU/L indicates it's still inadequately treated (or recent non-compliance/absorption issue) and is certainly contributing significantly to the short stature.
Spinal Deformity: The gibbus, history of surgery, possible spina bifida, and drained lumbar swelling strongly suggest:
Tuberculosis of the Spine (Pott's Disease): This classically causes vertebral destruction leading to an angular kyphosis (gibbus). It can also lead to a "cold abscess" that tracks down, potentially presenting as a lumbar or psoas swelling requiring drainage. Surgery would be for debridement and stabilization. Spina bifida occulta could be an incidental finding or the TB could have affected congenitally abnormal vertebrae. Chronic infection could also contribute to growth failure.
Congenital Vertebral Anomalies: Such as hemivertebrae or failure of segmentation. These can cause a sharp angular kyphosis (gibbus) and are often associated with other spinal defects like spina bifida occulta. Surgery would be for stabilization/correction. The drained swelling is less easily explained here unless it was a post-surgical complication (seroma/hematoma) or an unrelated issue.
Skeletal Dysplasia:
Spondyloepiphyseal Dysplasia (SED) Tarda: Presents later in childhood with short stature (specifically short trunk), spinal abnormalities (platyspondyly, scoliosis/kyphosis, though severe gibbus is less typical than in SED Congenita), and early-onset arthritis. Hypothyroidism isn't a core feature.
Mucopolysaccharidoses (MPS): Certain types (e.g., Morquio Syndrome - MPS IV, milder forms of Hurler/Scheie - MPS I, Hunter - MPS II) cause short stature, skeletal deformities including kyphosis/gibbus, and can sometimes have other systemic involvement. Hypothyroidism can occasionally be seen in some MPS types. Onset recognition at age 8 might fit milder forms. Look for other signs (joint stiffness, corneal clouding, specific facial features).
Other Rare Syndromes: While less likely, some syndromes might loosely connect these features, but none fit perfectly:
Pseudohypoparathyroidism (Albright Hereditary Osteodystrophy): Causes short stature, skeletal defects (like brachydactyly), and resistance to multiple hormones, including TSH (leading to hypothyroidism). However, a severe gibbus isn't typical.
Genetic syndromes associated with both skeletal anomalies and hypothyroidism exist but are rare and usually have other distinct features.
Conclusion / Most Probable Scenario:
It is highly probable that this patient has two significant but unrelated conditions:
Primary Hypothyroidism: Likely Hashimoto's thyroiditis, contributing significantly to her short stature due to inadequate treatment over years.
Significant Spinal Pathology: The gibbus, surgery history, and drained lumbar swelling are most suspicious for treated Pott's Disease (Spinal TB). Alternatively, it could be due to Congenital Vertebral Anomalies requiring surgical correction. The possible spina bifida could be related to congenital anomalies or just an incidental finding.
Next Steps Needed for Clarity:
Obtain Previous Records: Absolutely crucial to get details of the spinal surgery (indication, procedure, findings) and any pre/post-op imaging.
Current Spinal Imaging: X-ray and likely MRI of the affected spinal region to assess the current structure, stability, any residual inflammation, and confirm the nature of the vertebral deformity/spina bifida.
Optimize Thyroid Treatment: Adjust thyroxine based on TSH and free T4 levels. Consider checking thyroid antibodies (Anti-TPO, Anti-Tg) to confirm Hashimoto's.
Assess Growth: Once euthyroid, reassess growth velocity. If still significantly short, consider evaluation for Growth Hormone deficiency or underlying skeletal dysplasia (including skeletal survey if indicated).
Rule out Active TB: If Pott's disease is suspected and records are unavailable, assess for any signs of ongoing inflammation (ESR, CRP) although active infection is less likely 4 years post-surgery.
Without more information, a unifying "syndrome" is less likely than the combination of probable Hashimoto's thyroiditis and sequelae of either Pott's disease or congenital vertebral anomalies.[AI studio]
28/04/2025, 13:57 - Dr.Abdulsalam Med Ed Leads: Based on the clinical features presented, this patient likely has a syndromic condition that includes **short stature**, **congenital anomalies** (cleft palate, bifid hard palate, bifid spine), and possibly **endocrine dysfunction** (hypothyroidism). The combination of these findings suggests a possible diagnosis of **Klippel-Feil syndrome** or another related congenital disorder, but other syndromes should also be considered.
### Key Features:
1. **Short Stature**: Noticed 8 years ago.
2. **Hypothyroidism**: TSH is elevated at 9.6 IU/mL despite being on thyroxine replacement therapy.
3. **Gibbus Deformity**: Could be due to congenital vertebral anomalies or postsurgical changes.
4. **Cleft Palate and Bifid Hard Palate**: Suggests craniofacial dysplasia.
5. **Bifid Spine**: Associated with vertebral segmentation anomalies.
6. **Left Lumbar Swelling**: Drained, could represent a cyst, abscess, or other soft tissue abnormality.
---
### Differential Diagnosis:
#### 1. **Klippel-Feil Syndrome**
- **Key Features**: Short neck, low posterior hairline, limited neck mobility, and congenital fusion of cervical vertebrae (may extend to thoracic vertebrae).
- **Associated Anomalies**: Cleft palate, hearing loss, renal anomalies, scoliosis, and other vertebral abnormalities (e.g., bifid spine).
- **Relevance**: The gibbus deformity and bifid spine are consistent with vertebral anomalies seen in Klippel-Feil syndrome. However, hypothyroidism is not a classic feature.
#### 2. **VACTERL Association**
- **Key Features**: Vertebral anomalies, Anal atresia, Cardiac defects, Tracheo-Esophageal fistula, Renal anomalies, and Limb abnormalities.
- **Relevance**: The patient’s vertebral anomalies (bifid spine, gibbus deformity) and cleft palate fit this association. However, there is no mention of anal, cardiac, or renal anomalies in the provided history.
#### 3. **Ehlers-Danlos Syndrome (EDS)**
- **Key Features**: Connective tissue disorder with joint hypermobility, skin hyperextensibility, and tissue fragility. Some types may present with short stature and scoliosis.
- **Relevance**: The gibbus deformity and bifid spine could be secondary to connective tissue laxity, but hypothyroidism and cleft palate are less commonly associated with EDS.
#### 4. **Goldenhar Syndrome (Oculo-Auriculo-Vertebral Spectrum)**
- **Key Features**: Hemifacial microsomia, vertebral anomalies, and ear abnormalities.
- **Relevance**: While vertebral anomalies and facial dysmorphisms (e.g., cleft palate) are present, Goldenhar syndrome typically involves hemifacial asymmetry and ear abnormalities, which are not mentioned here.
#### 5. **CHARGE Syndrome**
- **Key Features**: Coloboma, Heart defects, Atresia choanae, Retarded growth and development, Genital hypoplasia, and Ear anomalies.
- **Relevance**: Short stature, cleft palate, and vertebral anomalies could fit CHARGE syndrome, but coloboma, choanal atresia, and ear anomalies are not described.
#### 6. **Pierre Robin Sequence**
- **Key Features**: Triad of micrognathia, glossoptosis, and cleft palate.
- **Relevance**: The cleft palate is consistent with this sequence, but it does not explain the vertebral anomalies or hypothyroidism.
#### 7. **DiGeorge Syndrome (22q11.2 Deletion Syndrome)**
- **Key Features**: Hypoparathyroidism, congenital heart defects, immune deficiency, palatal abnormalities, and learning difficulties.
- **Relevance**: The cleft palate and hypothyroidism could fit, but there is no mention of cardiac defects, immune deficiency, or parathyroid dysfunction.
---
### Most Likely Diagnosis: **Klippel-Feil Syndrome with Hypothyroidism**
The combination of **short stature**, **vertebral anomalies** (gibbus deformity, bifid spine), and **craniofacial anomalies** (cleft palate, bifid hard palate) strongly suggests **Klippel-Feil syndrome**. The hypothyroidism could be coincidental or part of an overlapping endocrine disorder.
---
### Next Steps for Diagnosis:
1. **Imaging**:
- **Spine X-rays/MRI**: To assess vertebral anomalies and confirm the presence of fused vertebrae or other structural abnormalities.
- **Craniofacial CT Scan**: To evaluate the cleft palate and bifid hard palate in detail.
2. **Genetic Testing**:
- Chromosomal microarray or whole-exome sequencing to identify any underlying genetic syndromes.
3. **Endocrine Workup**:
- Check free T4 levels to assess thyroid function.
- Evaluate for other endocrine abnormalities (e.g., growth hormone deficiency, pituitary dysfunction).
4. **Renal Ultrasound**:
- To rule out renal anomalies, which are common in Klippel-Feil syndrome and VACTERL association.
5. **Cardiac Evaluation**:
- Echocardiogram to rule out congenital heart defects.
---
### Final Answer:
The most likely diagnosis is **Klippel-Feil syndrome with hypothyroidism**. Further investigations, including imaging and genetic testing, are needed to confirm the diagnosis and identify any associated anomalies.
**Boxed Answer**:
$$
\boxed{\text{Klippel-Feil Syndrome with Hypothyroidism}}
$$ [Quen Response]
28/04/2025, 16:06 - Rakesh Biswas: You're right! My bad!
I checked now again and couldn't find it written although I had imagined I had.
28/04/2025, 16:12 - Rakesh Biswas: Update: recovered well
29/04/2025, 11:11 - Dr.Abdulsalam Med Ed Leads: The 39-year-old male presenting with severe hypertension (230/130 mmHg) and transient focal neurological deficits (slurred speech, ataxia) following a dog bite vaccination raises concern for a **hypertensive emergency with cerebrovascular complications**. Here's a structured approach:
---
### **Key Considerations**
1. **Hypertensive Emergency**:
- Defined by severe hypertension with acute end-organ damage (e.g., brain, heart, kidneys).
- Neurological deficits suggest brain involvement (e.g., stroke, PRES, or hypertensive encephalopathy).
2. **Neurological Deficits**:
- **Persistent focal deficits** (ataxia, dysarthria) favor **stroke** (ischemic or hemorrhagic) over PRES, which typically resolves with BP control.
- **Posterior Circulation Involvement**: Ataxia and slurred speech may localize to the cerebellum/brainstem (e.g., cerebellar hemorrhage, brainstem infarct).
3. **Secondary Hypertension**:
- Screen for underlying causes (e.g., renal artery stenosis, pheochromocytoma) given young age and severe hypertension.
4. **Dog Bite/Vaccine**:
- Likely incidental but rule out rare vaccine-related ADEM (acute disseminated encephalomyelitis) if deficits progress.
---
### **Immediate Management**
1. **Neuroimaging**:
- **Non-contrast CT Head**: Urgently rule out hemorrhage (e.g., cerebellar, pontine).
- **MRI Brain**: If CT negative, assess for ischemic stroke (e.g., posterior circulation infarct) or PRES.
2. **BP Control**:
- **Goal**: Gradual reduction (25% decrease in MAP over 2–6 hours).
- **Agents**: IV labetalol or nicardipine (avoid rapid drops to prevent hypoperfusion).
- **Avoid**: Sublingual nifedipine (risk of precipitous decline).
3. **Stroke Protocol**:
- If ischemic stroke confirmed, adhere to thrombolysis/endovascular therapy criteria.
- If hemorrhagic, target BP <140/90 mmHg (per AHA guidelines).
4. **Secondary Workup**:
- **Labs**: Renal function, electrolytes, urine protein, troponin, catecholamines (if suspecting pheochromocytoma).
- **ECG**: Assess for LVH/ischemia.
- **Ophthalmoscopy**: Hypertensive retinopathy.
---
### **Differential Diagnosis**
1. **Hemorrhagic Stroke** (e.g., cerebellar hemorrhage).
2. **Ischemic Stroke** (posterior circulation infarct).
3. **PRES** (if deficits improve with BP control).
4. **Hypertensive Encephalopathy** (less likely due to residual deficits).
5. **Vaccine-Related ADEM** (rare; consider if deficits progress despite BP control).
---
### **Long-Term Management**
- **Antihypertensive Therapy**: Tailor to underlying cause (e.g., ACEi/ARB for renal protection).
- **Secondary Prevention**: Statins, antiplatelets (if ischemic stroke), lifestyle modification.
- **Follow-Up**: Neurology for residual deficits, BP monitoring, and rehabilitation.
---
**Conclusion**: Prioritize emergent neuroimaging to differentiate stroke from PRES. Admit for BP management, monitor for end-organ damage, and initiate secondary prevention. The dog bite/vaccine is likely incidental but document timing for safety reporting if atypical features arise.(DeepSeek) <This message was edited>
29/04/2025, 11:19 - You added Sravani Gadde Kims Ug 2018
29/04/2025, 12:20 - Rakesh Biswas: Thanks. Off course, one may have noticed @919604701505 there are many suggestions from Web 3.0 that are protocol based ontologies that we are trying to optimize using critical realist heutagogy else you can imagine the over-testing and overtreatment pandemic that would be potentially unleashed if anyone simply follows these Web 3.0 protocols without using their human looped cognition!
29/04/2025, 12:28 - Rakesh Biswas: <Media omitted>
29/04/2025, 12:29 - +91 72072 74049 left
29/04/2025, 14:53 - Dr.Abdulsalam Med Ed Leads: Off course clinical examination and history taking will narrow the most probable differential diagnosis in each case. But these AI generated protocols would help revise the topics of relevance in the busy clinics and help avoid mistakes which may affect the outcome very adversely . With time handling such cases would go on very smoothly especially for junior colleagues.
29/04/2025, 15:18 - Dr.Abdulsalam Med Ed Leads: Your insights highlight a **critical tension in modern healthcare**: the balance between protocol-driven efficiency (via Web 3.0/AI-driven ontologies) and the irreplaceable role of human cognition, contextual judgment, and ethical responsibility. Let’s unpack this through the lens of **critical realism** (understanding layered reality) and **heutagogy** (self-determined, adaptive learning):
---
### **1. The Pitfalls of Protocol-First Medicine**
Web 3.0 systems (e.g., AI algorithms, blockchain-secured guidelines) offer immense potential for standardizing care, but **blind adherence risks**:
- **Over-testing**: Algorithms may default to "rule out everything" (e.g., MRI for every hypertensive headache, despite cost/access limitations).
- **Overtreatment**: Protocols might recommend aggressive BP lowering in stroke without considering individual cerebral perfusion needs.
- **Context Blindness**: A dog-bite vaccine protocol could miss the hypertensive emergency unless human cognition links the temporal clues.
**Example**: In your 39M case, a protocol might flag "dog bite → rabies vaccine" but miss the hypertensive crisis unless clinicians contextualize the neurological deficits *despite* the vaccine timing.
---
### **2. Critical Realism: Layered Reality in Medicine**
Critical realism acknowledges that:
- **Empirical** (observed BP, lab values) ≠ **Actual** (pathophysiology like endothelial injury) ≠ **Real** (structural drivers, e.g., socioeconomic stress causing untreated hypertension).
- **Human cognition** bridges these layers. For instance:
- Why did this young man have *severe* hypertension? Is there undiagnosed renal artery stenosis (actual) or psychosocial stressors (real)?
- Did vaccine anxiety *trigger* a hypertensive surge, or was it coincidental?
Protocols often stop at the **empirical**; clinicians must probe deeper into **actual/real** causes.
---
### **3. Heutagogy: Self-Determined Learning in Action**
Heutagogy shifts from *competency-based training* to **adaptive, ethical judgment**. In your case:
- A clinician uses protocols as scaffolds but **critically appraises**:
- When to deviate (e.g., delaying thrombolysis if CT shows microbleeds).
- How to prioritize tests (e.g., ruling out pheochromocytoma in young hypertensives *after* stabilizing the emergency).
- **Continuous learning**: Reflect on why the dog-bite visit unmasked hypertension (e.g., access barriers? Health literacy gaps?).
---
### **4. Human-Looped Cognition: The "Augmented Clinician"**
The ideal model merges Web 3.0’s efficiency with human expertise:
- **AI Suggests**:
- "Hypertensive emergency + ataxia → prioritize posterior circulation stroke on MRI."
- "Rule out secondary hypertension: check plasma metanephrines."
- **Human Decides**:
- Weigh risks of contrast nephropathy vs. benefits of CTA in renal artery stenosis.
- Navigate resource constraints (e.g., MRI unavailable → lean on clinical exam + CT).
- Address biases (e.g., anchoring on the dog bite and missing the hypertensive urgency).
---
### **5. Case Application: Avoiding Protocol Pitfalls**
For the 39M patient:
- **Web 3.0 Protocol**: May flag "dog bite → rabies vaccine" and "severe HTN → start IV labetalol."
- **Heutagogical Clinician**:
- Questions: *Why* did HTN present now? Is this a primary event or secondary (e.g., renal/endocrine)?
- Balances urgency (lower BP) with caution (avoid hypoperfusion in possible stroke).
- Avoids over-testing (skips ADEM workup unless deficits worsen *despite* BP control).
---
### **6. The Way Forward: Synergy Over Substitution**
- **Augmented Intelligence**, not AI replacement: Use protocols to reduce cognitive load, not dictate care.
- **Teach Critical Uncertainty**: Train clinicians to recognize when protocols fail (e.g., atypical presentations, social determinants).
- **Ethical Guardrails**: Ensure Web 3.0 systems embed equity (e.g., avoid algorithms biased toward over-testing in high-income settings).
---
**Final Thought**: Medicine’s future lies in **hybrid ecosystems** where Web 3.0 ontologies *inform* but never replace the clinician’s heutagogical wisdom. As you astutely noted, the "human loop" is what transforms data into care—and protocols into healing.
29/04/2025, 15:27 - Rakesh Biswas: 👏👏LLM cognition and it's way with words are very well attuned to pampering human cognition and making them feel good because they always say what we want to hear!
29/04/2025, 15:38 - Rakesh Biswas: @919652955915 @918332874734 Last time remember we couldn't procure Amphotericin B and had to refer the patient and we don't have any clue as to what is happening to all these patients for who are unable to procure amphotericin B! @919154575937 @918106177663 @919848019894 do you see such patients in your Telangana practice? How do you procure amphotericin for them?
29/04/2025, 16:46 - Dr.Abdulsalam Med Ed Leads: These are axial T2-weighted MRI brain images. Based on the first set (posterior fossa cuts) and the second set (supratentorial cuts), here are some observations:
1. First image (posterior fossa):
There is a hyperintense lesion in the right cerebellar hemisphere, possibly involving the middle cerebellar peduncle.
This could suggest acute infarction, demyelination, or a space-occupying lesion such as a tumor or abscess.
The surrounding edema appears to distort the 4th ventricle slightly, which might suggest mass effect.
2. Second image (supratentorial cuts):
The ventricles appear mildly prominent, but no clear midline shift or hydrocephalus is seen.
No obvious cortical or deep white matter lesions are visible in these slices.
The most likely differential based on the cerebellar lesion would include:
Cerebellar infarct (particularly PICA or AICA territory),
Tumor (like metastasis or medulloblastoma, if younger),
Demyelination (e.g., MS or ADEM, depending on clinical context),
Abscess (if history of infection or immunosuppression).
Would you like to correlate this with clinical findings or symptoms for a more specific interpretation?
29/04/2025, 16:48 - Dr.Abdulsalam Med Ed Leads: Thanks for the clinical context. This 39-year-old male with:
Severe, recently detected hypertension (230/130 mmHg)
Focal neurological deficits: speech slurring and ataxia
Partial recovery but persistent symptoms
...along with the MRI showing a T2 hyperintense lesion in the right cerebellar hemisphere, points most likely toward a hypertensive cerebellar infarct or hypertensive hemorrhage, with infarct being more likely due to the T2 signal characteristics and absence of a blooming artifact (suggesting no acute hemorrhage).
Working Diagnosis:
Right cerebellar infarct (likely AICA or PICA territory) secondary to malignant hypertension
Additional Considerations:
Posterior circulation (vertebrobasilar system) is particularly vulnerable in hypertensive emergencies.
Speech slurring and ataxia align with a cerebellar lesion.
Gradual improvement suggests ischemia rather than hemorrhage, which tends to cause more abrupt deterioration.
The absence of hydrocephalus is reassuring, but close monitoring is warranted in cerebellar strokes due to risk of compression on the brainstem or fourth ventricle.
Recommendations:
MRI DWI (Diffusion-Weighted Imaging) and ADC mapping to confirm acute ischemia.
MRA or CTA to evaluate vertebrobasilar circulation.
2D echo and carotid-vertebral Dopplers to rule out cardiac source or large vessel atherosclerosis.
Continuous BP control and rehabilitation.
Would you like a structured case summary or a brief teaching slide version for your students?
29/04/2025, 16:51 - Dr.Abdulsalam Med Ed Leads: Here’s a structured case summary and teaching slide version suitable for your students:
---
Clinical Case Summary (Teaching Slide)
Patient: 39-year-old male
Presentation:
Presented to PHC for rabies vaccine after dog bite
Found to have severe hypertension (BP 230/130 mmHg)
Complained of slurred speech and ataxia (difficulty walking)
Symptoms partially improved but did not fully resolve
---
Examination Findings
BP: Severely elevated, gradually normalized
Cerebellar signs: Ataxia, slurred speech (dysarthria)
No altered sensorium, seizures, or vomiting reported
---
Neuroimaging (MRI Brain)
Axial T2-weighted images show:
Hyperintense lesion in right cerebellar hemisphere
Likely involves middle cerebellar peduncle
No hydrocephalus or midline shift
Suggests cerebellar infarct, likely in PICA territory
---
Working Diagnosis
Hypertensive cerebellar infarct (likely PICA territory)
Secondary to malignant hypertension
Posterior circulation stroke
---
Differential Diagnosis
Hypertensive cerebellar hemorrhage (less likely—no blooming or mass effect)
Demyelination (unlikely due to focal, acute presentation)
Tumor/metastasis (unlikely due to acute onset)
---
Plan & Recommendations
MRI DWI + ADC: Confirm acute ischemia
MRA Brain + Neck: Assess vertebrobasilar circulation
2D Echo + Carotid/Vertebral Dopplers
BP control: Target gradual reduction
Neurorehabilitation
Monitor for brainstem compression (risk in cerebellar infarcts)
---
Let me know if you’d like this in PowerPoint format or as a downloadable PDF slide.
29/04/2025, 18:06 - PaJR Physicist: The age of Webagogy!
30/04/2025, 09:06 - ~ Bhavana🦋 left
30/04/2025, 13:03 - Rakesh Biswas: @916303319326 while we are working on our current paper on Narketpally syndrome which was pivoted on primarily because of the commonality of people here walking with sticks, I guess that would be common in all fluorotic belts and the true definition of Narketpally syndrome that the paper ultimately posits is different as discussed previously here by @9647501361306 through Web 3.0 above.
As per as population based physical disease syndromes in medicine are concerned, what's much much more common in Narketpally as well as globally is metabolic syndrome like in this lady who also Diabetes since last 20 years!
30/04/2025, 13:16 - Dr.Abdulsalam Med Ed Leads: Certainly! Here's a textual case report based on the images provided:
---
**Case Report**
**Patient ID:** WB-PET-CT-
**Referring Physician:** Dr. A. NAVEEN KUMAR REDDY
**Facility:** Kamini Private Limited
**Date of Report:** 01/01/25
**Patient Details:**
- **Age:** Not specified
- **Gender:** Female
- **Clinical History:** Patient with a history of breast cancer, underwent mastectomy and chemotherapy.
**Diagnosis:**
- **Left Breast Carcinoma cT4bN1Mx post chemotherapy**
**Case History:**
- The patient was diagnosed with a locally advanced carcinoma of the left breast in December 2024.
- She underwent 4 cycles of neo-adjuvant chemotherapy, with the last cycle on 07/03/2025.
- Initially presented with a lump in the left breast, which was painless and associated with nipple discharge.
- Post menopausal, parous.
- K/c/o diabetes mellitus on regular medication.
- K/c/o CAD s/p CABG 9 years ago.
- Tuberculosis 30 years ago.
**Examination:**
- Left breast: ill-defined residual lump in the upper outer quadrant at 3’o clock position.
- Periareolar, focal area of peau d’orange present.
- Nipple retraction present.
- Left axilla: 1x1 cms palpable small left axillary lymph node.
- Left supraclavicular region: normal.
- Right breast examination: normal.
- Systemic examination: normal.
**Biopsy:**
- Biopsy of left breast lump s/o: Invasive Ductal Carcinoma.
- IHC s/o: ER - Positive, PR - Negative, Her2 Neu - Negative, Ki-67: high.
- USG abdomen: normal.
- CKRPA: normal.
**Course in the Hospital:**
- Patient underwent Left Modified Radical Mastectomy on 03.04.25.
- Operative Findings:
1. About 2x2cm ill-defined residual lump at 3’o clock position close to areola.
2. Multiple enlarged lymphnodes in level I,II,III of left axilla.
3. Nerve to serratus anterior, intercostobrachial nerves, latissimus dorsi pedicle preserved.
- Postoperatively, patient was shifted to the ward and managed with IV fluids, IV analgesics, IV antibiotics, and PPIs.
- Patient is stable clinically and hemodynamically at the time of discharge.
**Cross Consultations:**
- **Endocrinology**
**Treatment Given:**
- Patient underwent Left Modified Radical Mastectomy under General Anesthesia on 03.04.25.
**Advices at Discharge:**
- **Diabetic Diet**
- Tab Taxim-O 200 MG orally twice daily after food for 5 days
- Tab Combiflam 1 TAB orally thrice daily after food for 5 days
- Tab Pant 40 MG orally once daily before food in the morning for 5 days
- Tab ATO Z 1 TAB orally after lunch for 10 days
- Tab MET XL 50 MG orally once daily in the morning
- Tab Chymoral Forte 1 TAB orally thrice daily after food for 3 days
- Tab AMARLY M2 Forte 1 TAB orally once daily in the morning after food
- Daily dressing
- Left upper limb care and exercises as explained
- Drain care as explained
**Histopathology:**
- **Gross Examination:**
- Received multiple grey white linear cores and tiny fragments. Largest measuring 1.6 cms. Smallest measuring 0.5 cms. All embedded in A & B.
- **Microscopic Examination:**
- Sections show irregularly thickened fibrocollagenous tissue bits which is diffusely infiltrated by tumor. The tumor is arranged in irregular nests and in cords. Individual tumor cells are pleomorphic with hyperchromatic nuclei and eosinophilic cytoplasm. Mitotic activity is noted. Lymphovascular invasion is identified. Foci of necrosis also noted.
- **Impression:**
- Histological features favor Invasive Carcinoma of No Special Type (NST) - LEFT BREAST.
- **IHC with ER, PR, HER2, and Ki67:**
- ER: 60% POSITIVE
- PR: NIL NEGATIVE
- HER 2 NEU: NIL NEGATIVE
- Ki 67: 18% HIGH PROLIFERATIVE INDEX
**PET CT Scan:**
- **Opinion:**
- Carcinoma right breast; staging PET CT scan reveals:
- Hypermetabolic mild heterogeneously enhancing irregular soft tissue dense mass lesion in outer quadrants of left breast (3’o clock position) involving adjacent skin and nipple areolar complex.
- Non-FDG avid subcentimeter left axillary lymphnodes with preserved fatty hilum – Reactive.
- No other evidence of metabolically active lesions elsewhere in the visualized region of the body.
---
This report summarizes the patient's clinical history, diagnostic findings, treatment, and postoperative care. If you need further details or specific sections expanded, please let me know!
30/04/2025, 13:23 - Rakesh Biswas: Excellent picture to text Web 3.0 milestone
👏👏
@919604701505 @919652955915 I'm really excited about the pace of CBR UDLCOs that are going to be unleashed!
30/04/2025, 16:36 - ~ Hânşiká Rèddý left
30/04/2025, 16:51 - pajr.in CEO, NHS Endocrinologist: What is your plan sir?
30/04/2025, 16:54 - Rakesh Biswas: Endocrinology plan is to continue 87.5 mcg and check with previous literature if a TSH of 9-30 has any bearing on per operative outcomes in non thyroidal surgery
30/04/2025, 16:57 - Rakesh Biswas: @13135550002 Update:
A 17F woman on thyroxine 75mcg since 2020 is planned for a cleft palate surgery and incidentally TSH was found to be 9 IU on 24/4/25 while on 75 Mcg after which she took 87.5 mcg the next day and while the TFTs need not have been repeated so soon , paradoxically the repeat TFT today shows TSH as 30 IU! What is the best approach to thyroxine dose titration in such a situation? Are there any observational studies showing any risk of operating patients with subclinical hypothyroidism?
30/04/2025, 16:58 - Meta AI: Given the patient's significantly elevated TSH levels, adjustment of thyroxine dosage is crucial before proceeding with surgery. Here's a step-by-step approach:
# Thyroxine Dose Titration
- *Re-evaluate thyroid function tests*: Repeat TFTs to confirm the elevated TSH levels and assess free T4 levels to determine the severity of hypothyroidism.
- *Adjust thyroxine dosage*: Consider increasing the dosage of levothyroxine (T4) based on the patient's clinical presentation, TSH levels, and free T4 levels. A general guideline is to increase the dose by 12.5-25 mcg/day and re-evaluate TFTs in 6-8 weeks.
- *Monitor for signs of overtreatment*: Keep an eye out for symptoms like tachycardia, palpitations, nervousness, and tremors, which may indicate excessive thyroxine levels.
- *Consider individual factors*: Take into account the patient's age, weight, pregnancy status, and underlying medical conditions when adjusting the dosage.
# Risks of Operating on Patients with Subclinical Hypothyroidism
- *Cardiovascular risks*: Subclinical hypothyroidism may increase the risk of cardiovascular disease, particularly in older adults.
- *Metabolic changes*: Untreated subclinical hypothyroidism can lead to changes in lipid profiles and increased risk of atherosclerosis.
- *Neuropsychiatric symptoms*: Some patients may experience symptoms like fatigue, depression, and cognitive impairment.
# Observational Studies
- A study published in the American Family Physician suggests that treating subclinical hypothyroidism can improve symptoms, lipid profiles, and cardiac function.
- Another study published in Medscape recommends treating patients with TSH levels consistently elevated above 10 μU/mL, especially if they have antithyroid antibodies or symptoms.¹ ²
# Pre-Surgical Considerations
- *Endocrinology consultation*: Consider consulting an endocrinologist to optimize the patient's thyroid hormone levels before surgery.
- *Pre-operative evaluation*: Ensure thorough pre-operative evaluation to assess the patient's overall health and potential risks associated with surgery.
- *Monitoring*: Closely monitor the patient's vital signs, thyroid hormone levels, and overall clinical status during and after surgery.
30/04/2025, 16:58 - Meta AI: https://emedicine.medscape.com/article/122393-treatment
30/04/2025, 16:58 - Meta AI: https://www.aafp.org/pubs/afp/issues/1998/0215/p776.html
30/04/2025, 18:30 - +91 95732 63073 left
30/04/2025, 18:31 - +91 93902 10425 left
30/04/2025, 19:36 - +91 85230 74601 left
30/04/2025, 21:20 - Dr.Abdulsalam Med Ed Leads: Based on the information provided, the patient presents with a combination of symptoms and findings that could suggest a complex clinical picture. Here are some considerations:
1. **Short Stature and Thyroxine Treatment:**
- The patient's short stature and the initiation of thyroxine treatment at a young age suggest a possible diagnosis of growth hormone deficiency or hypothyroidism. The elevated TSH (9.6 IU/mL) indicates that the patient may still be hypothyroid despite the increased dose of thyroxine, which may require further adjustment of the hormone replacement therapy.
2. **Gibbus Deformity:**
- The gibbus deformity, which is a forward angulation of the spine, is typically associated with severe kyphosis. This can be due to various causes, including congenital spinal anomalies, osteoporosis leading to compression fractures, or post-surgical complications. The history of surgery 4 years prior makes it plausible that the gibbus could be a post-surgical complication, but without details of the surgery, it's difficult to ascertain.
3. **Bifid Spine:**
- The bifid spine, or spina bifida, is a neural tube defect where the spinal column does not properly close during development. It can be asymptomatic or may be associated with a range of neurological symptoms depending on the severity and location of the defect. If the bifid spine is in the area of the gibbus, it could potentially contribute to the spinal deformity, but it's unclear if it's a congenital feature or related to the previous surgery.
4. **Lumbar Swelling:**
- The left lumbar swelling that was drained could indicate a variety of conditions, such as a cyst, abscess, or other fluid collection. The need for drainage suggests it was causing symptoms or complications.
Given the combination of short stature, thyroid dysfunction, spinal deformities, and the history of surgery, one possible syndrome to consider is:
**Spondyloepiphyseal Dysplasia:**
- This is a group of genetic disorders affecting bone growth and development, particularly affecting the spine and long bones. It can present with short stature, spinal deformities (such as kyphosis or scoliosis), and sometimes with thyroid dysfunction. However, the specific type of spondyloepiphyseal dysplasia would depend on additional clinical and radiological findings.
**Diagnosis and Further Evaluation:**
- A thorough clinical examination, review of previous surgical records, and detailed imaging studies (including spine MRI) would be necessary to better understand the spinal deformities and their causes.
- Genetic testing could be considered to evaluate for known syndromes associated with short stature and spinal deformities.
- Endocrine evaluation to assess thyroid function and possibly other endocrine functions, given the complexity of the patient's presentation.
It's important to consult with a multidisciplinary team, including endocrinologists, orthopedic surgeons, and geneticists, to provide a comprehensive evaluation and management plan for this patient.
30/04/2025, 21:22 - Rakesh Biswas: I guess this is just from the previous history but given today's update of confirmed Potts spine in 2019 the output could be different
30/04/2025, 21:23 - Dr.Abdulsalam Med Ed Leads: **Final Diagnosis and Management Approach:**
**Diagnosis:**
The patient is presenting with **septic shock** secondary to a **complicated deep neck infection (likely Ludwig’s angina)** that has progressed to **descending mediastinitis**, resulting in bilateral pneumonia, large left pleural effusion (possible empyema), and pericardial effusion (potentially purulent). The recent incision and drainage procedure may have inadequately controlled the infection, leading to systemic dissemination. The hypotension is multifactorial, primarily due to septic shock but compounded by possible cardiac tamponade from pericardial effusion.
---
**Key Clinical Considerations:**
1. **Infection Source**:
- **Deep neck infection** (e.g., Ludwig’s angina, necrotizing fasciitis) spreading to the mediastinum.
- **Descending mediastinitis** can explain pleural/pericardial involvement and bilateral consolidations.
2. **Implications of Effusions**:
- **Pericardial effusion**: Evaluate for tamponade (echocardiogram urgently needed).
- **Pleural effusion**: Likely parapneumonic or empyema; requires drainage.
3. **Shock Mechanism**:
- **Septic shock** (primary driver) from disseminated infection.
- **Obstructive shock** if pericardial tamponade is confirmed.
---
**Immediate Management Steps:**
1. **Hemodynamic Stabilization**:
- Continue **inotropes/vasopressors** (e.g., norepinephrine, vasopressin).
- **Fluid resuscitation** guided by volume status (avoid overload if ARDS is present).
2. **Source Control**:
- **Surgical re-evaluation** of the neck incision site for residual abscess/debridement.
- **Thoracentesis/chest tube** for left pleural effusion (send fluid for Gram stain, culture, pH).
- **Pericardiocentesis** if echocardiogram confirms tamponade.
3. **Antibiotics**:
- **Broad-spectrum coverage**: Vancomycin (MRSA) + Piperacillin-Tazobactam (anaerobes, Gram-negatives) ± Clindamycin (for toxin suppression in necrotizing infection). Adjust based on cultures.
- Consider adding **antifungals** (e.g., fluconazole) if risk factors for candidemia exist.
4. **Imaging/Labs**:
- **Echocardiogram**: Assess pericardial effusion severity and ventricular function.
- **CT neck/chest**: Evaluate mediastinal involvement, necrotizing infection.
- **Blood cultures**, pleural/pericardial fluid analysis, CRP/procalcitonin.
5. **Supportive Care**:
- **Mechanical ventilation** if respiratory failure develops (ARDS risk).
- **Renal replacement therapy** if AKI complicates fluid/electrolyte management.
---
**Differential Diagnoses to Rule Out:**
- **Lemierre’s syndrome** (jugular vein thrombophlebitis with septic emboli).
- **Tuberculosis** (chronic SOB, effusions; less acute but needs acid-fast bacilli testing).
- **Malignancy** (lymphoma/metastases causing effusions; biopsy if no infection found).
---
**Prognosis:**
Guarded due to multiorgan involvement and delayed intervention. Early surgical source control and aggressive antimicrobial therapy are critical. Mortality is high in untreated mediastinitis (>50%).
**Next Steps:**
- **Multidisciplinary team involvement** (ICU, cardiothoracic surgery, infectious disease).
- **Monitor for complications**: ARDS, multiorgan failure, disseminated intravascular coagulation (DIC).
30/04/2025, 21:25 - Rakesh Biswas: Good inputs.
Saw the echo. No tamponade.
Mild to moderate pericardial effusion
30/04/2025, 21:30 - Dr.Abdulsalam Med Ed Leads: As an ENT specialist this is typical of deep neck space infection complicated by mediastinitis and septic shock. I agree with all what DeepSeek analyzed about the case. In fact mortality rate is as high as 80 % due to delay in the recognition and appropriate management during the first instance. <This message was edited>
30/04/2025, 21:42 - Dr.Abdulsalam Med Ed Leads: The collection around the heart in the mediastinun and the reactionary pericardial effusion contrbute secondorly to the shock but largely is septic one
30/04/2025, 21:56 - Dr.Abdulsalam Med Ed Leads: A cardiothoracic opinion about thoracotmy may be needed in this case ASAP
30/04/2025, 22:06 - Dr.Abdulsalam Med Ed Leads: Don't be surprised if I tell the original problem was tooth root abscess drained into a potential deep face and neck space ,inadequate ly drained (by maxillofacial) ,ruptured spontaneously into the mediastinum........
30/04/2025, 22:30 - Dr.Abdulsalam Med Ed Leads: The paradoxical rise in TSH from 9 to 30 IU/mL after increasing levothyroxine (75 to 87.5 mcg) raises several concerns. Here’s a structured approach to address this:
### **Key Considerations**
1. **Timing of TSH Measurement**
TSH requires **4–6 weeks** to stabilize after dose adjustments. Testing after only a few days is premature and unlikely to reflect the new dose’s effect. The elevated TSH may indicate unresolved hypothyroidism or an unrelated acute issue (e.g., lab error, non-compliance, or concurrent illness).
2. **Possible Causes**
- **Non-compliance**: Verify if the patient took the increased dose consistently and correctly (empty stomach, no interfering supplements like calcium/iron).
- **Malabsorption**: Evaluate for GI disorders (e.g., celiac disease) or drug interactions (e.g., rifampin for TB, which increases T4 metabolism).
- **Lab Error/Interference**: Repeat TSH with **free T4 and T3** to confirm. Consider heterophile antibody interference.
- **Thyroid Hormone Resistance**: Rare, but check free T4/T3 (elevated in resistance).
- **Acute Illness**: Stressors can transiently elevate TSH during recovery phases.
3. **Impact on Surgery**
Severe hypothyroidism (TSH >10) increases perioperative risks (e.g., delayed healing, cardiovascular strain). Elective cleft palate surgery should ideally be **postponed** until TSH is optimized (<5 IU/mL).
---
### **Immediate Steps**
1. **Confirm Lab Results**
- Repeat TSH, free T4, and T3 immediately.
- Add thyroid peroxidase (TPO) antibodies to assess for autoimmune thyroiditis.
2. **Assess Compliance and Administration**
- Reinforce proper levothyroxine intake: **empty stomach**, 30–60 minutes before food/medications.
3. **Review Medications**
- Check for drugs affecting T4 absorption (e.g., PPIs, iron) or metabolism (e.g., rifampin). Adjust timing if needed.
4. **Address Malabsorption**
- Consider trials of liquid levothyroxine or IV T4 if GI issues are suspected.
---
### **Management Plan**
- **Dose Adjustment**: If hypothyroidism is confirmed (↑ TSH + ↓ free T4), increase levothyroxine further (e.g., 100 mcg) and recheck TSH in 4–6 weeks.
- **Surgery Timing**: Delay until TSH normalizes. If urgent, consult endocrinology for perioperative thyroid hormone optimization (e.g., IV T4).
### **Summary**
The rise in TSH likely reflects unresolved hypothyroidism compounded by testing too early, malabsorption, or compliance issues. Confirm labs, optimize dosing, and postpone surgery until euthyroidism is achieved. Collaborate with endocrinology for complex cases.
