Saturday, January 31, 2026

50F Parotitis mths CKD filariasis years Telangana PaJR

 
31-01-2026

THIS IS AN ONLINE E LOG BOOK TO DISCUSS OUR PATIENT'S DE-IDENTIFIED HEALTH DATA SHARED AFTER TAKING HER GUARDIAN'S VIDEO CONSENT. HERE WE DISCUSS OUR PATIENT'S PROBLEMS THROUGH SERIES OF INPUTS FROM AVAILABLE GLOBAL ONLINE COMMUNITY EXPERTS WITH AN AIM TO SOLVE THOSE PATIENT'S CLINICAL PROBLEMS 
WITH COLLECTIVE CURRENT BEST EVIDENCE BASD INPUTS.

[8.27 pm, 31/01/2026] PPM 1: Handwritten history by @PPM3
                      
General examination and metabolic syn phenotype
             
                                    
                                  

                                  
                                  

[8.33 pm, 31/01/2026] PPM 1: Residual findings of palpable post inflammatory changes in left parotid following her left sided parotitis for which she was admitted 4 months back and the EMR summaries of which may be available on Monday 
[8:35 pm, 31/01/2026] PPM 1: @PPM4 there were two students from your batch currently posted in medicine today in the OPD who helped us a lot today to inquire more about this patient.
Please share the above findings and insights and discuss the case with them if possible.
[9:09 pm, 31/01/2026] PPM 4: Okay sir, will do
[10.39 am, 01/02/2026] PPM 1: Thanks.
Can check out the case report in the description box
[10:51 am, 01/02/2026] PPM 1:  Here's her first EMR summary post admission. Please note that the treating team thought it was CSOM and sjorgrens parotitis while now retrospectively it appears to be just a left sided infective parotitis that recovered. The doubt expressed about RA due to unnecessary RA testing is also not clinically compatible.
Age/Gender: 50 Years/Female
Address:
Discharge Type: Relieved
Admission Date: 18/10/2025 01:31 PM
Discharge Date: 23/10/2025 09:03 PM
Name of Treating Faculty
DR SANDEEP REDDY(AP)
DR SREETEJA (PG2)
DR HARSHINI(PG1)
Diagnosis
SEPSIS SECONDARY TO B/L CSOM AND LEFT PAROTITIS
LEFT NON HEALING ULCER OVER LEFT LOWER LIMB
ACUTE ON CHRONIC KIDNEY DISEASE WITH UREMIC ENCEPHALOPATHY(RESOLVED)
LEFT LOWER LIMB FILARIASIS SINCE 20 YRS
?RHEUMATOID ARTHRITIS
S/P 4 SESSIONS OF HEMODIALYSIS DONE ,3 PRBC TRANSFUSIONS DONE
Case History and Clinical Findings
C/O BREATHLESSNESS SINCE 4 DAYS
HOPI
PT WAS APPARENTLY ASYMPTOMATIC 10 DAYS AGO.THEN DEVELOPED FEVER -HIGH
GRADE ON AND OFF .H/O WELLING IN LEFT EAR AURICULAR SINCE 5 DAYS .H/O LOCAL
TRAUMA IN LEFT EAR .H/O OF NAUSEA AND VOMITING PRESENT. H/O OF ULCER OVER LEFT LEG AND THIGH SINCE 2 MONTHS WHICH Gradually PROGRESSED TO PRESENT SIZE PAST HISTORY
K/C/O CKD SINCE 2 YEARS WITH ANEMIA OF CHRONIC KIDNEY
H/O 1 SESSION OF HEMODIALYSIS SUE ON 7/24
PERSONAL HISTORY: MARRIED, NORMAL APPETITE, MIXED DIET, REGULAR BOWEL AND BLADDER HABITS, NO KNOWN ALLERGIES, NO KNOWN ADDICTIONS.
NO SIGNIFICANT FAMILY HISTORY.
GENERAL EXAMINATION: NO PALLOR, NO ICTERUS, NO CYANOSIS, NO CLUBBING, NO LYMPHADENOPATHY, NO
EDEMA.
VITALS: TEMP- 99, BP-100/60 MMHG, PR- 80 BPM, RR-20CPM, SPO2-100%AT RA, GRBS-
90MG/DL
SYSTEMIC EXAMINATION:
RS- BLAE+, B/L CREPTS+
CVS- S1S2+, NO MURMURS
CNS- NFND
PER ABDOMEN- SOFT, NON TENDER
DIALYSIS DONE ON 18/10/25,19/10/15,20/10/25,21/10/25
TRANSFUSIONS DONE ON 18/10/25,20/10/25,21/10/25
GENERAL SURGERY REFFERAL I/V/O ULCER ON LEFT LEG AND LEFT THIGH ON 23/10/25:
INSPECTION: A SWELLING OF SIZE 15X10CMS IN LEFT CHEEK EXTENDING INFRONT BELOW
AND BEHIND THE EAR LOBULE, SKIN OVER THE SWELLING IS NODULAR AND SHINY,
MARGINS APPEAR TO BE IRREGULAR, SEROPURULENT DISCHARGE PRESENT IN THE LEFT EXTERNAL AUDITORY MEATUS, LEFT EAR LOBE IS RAISED
PALPITATION: LOCAL RISE OF TEMP PRESENT, SEVERE TENDERNESS PRESENT,
SURFACE IS NODULAR AND FIRM-HARD IN CONSISTENCY, ON BIMANUAL PALPATION DEEP LOBE IS PALPABLE WITH ANTERIOR AND POSTERIOR LOBES, POSTERIOR CERVICAL Lymph Nodes AND PALPABLE.
ENT REFFERAL ON 18/10/25 I/V/O EAR PAIN AND SWELLING: LEFT EAR PREAURICULAR
SWELLING OF 5X5 PRESENT T, TENDERNESS WITH NO LOCAL RISE OF TEMPERATURE
PRESENT, MUCOID DISCHARGE PRESENT IN BOTH EARS, A SINGLE PINHOLE
PERFORATION IN RIGHT EAR AND A SINGLE MEDIUM CENTRAL PERFORATION IN LEFT EAR IS PRESENT.
Investigation
HEMOGRAM 1: HB-6.1, TLC-28000, RBC-2.2, PCV-17.9, PLT- 2.5.......ON 19/10/25: HB-6.1, TLC-
27.95, RBC-2.17, PCV-17.9, PLT- 224....ON 21/10/25: HB-6.7, TLC-25.90, RBC-2.3, PCV-19.8, PLT-
1.9 ...23/10/25: HB-8.3, TLC-17300, RBC-2.8, PCV-24.8, PLT- 1.5
CUE: ALB- +30MG/DL, SUG- NI, PUS-3-4, EPI- 2-3, RBC-NIL...ON 19/10/25 ALB- +, SUG- NI, PUS-3-4, EPI- 2-3, RBC-NIL
RFT: UR-294, CR-7.70, UA-10.80, CA+8.7, P-9, NA+-135, K+-4.3, CL-98...ON 20/10/25 UR-94, CR-
2.70, UA-2.90, CA+10.1, P-4.5, NA+-140, K+-3.3, CL-101
RFT ON 23/10/25 UREA-50, CREAT 2.4 NA-138, K+-2.9, CL-101
LFT 18/10/25: TB-1.18, DB-0.33, SGOT-15 SGPT-10, ALP-348, TP-6.5, ALB-2.05, G-4.45, AG
RATIO-0.46.....23/10/25: TB-1.16, DB-0.19, SGOT-18 SGPT-14, ALP-376, TP-5.5, ALB-2.0, G-3.50,
AG RATIO-0.57
RBS: 82MG/DL; HBA1C: 6.7
SERUM IRON:32, PT-17,INR-1.25,APTT-34
RA FACTOR ON 23/10/5:POSITIVE (192)
PERIPHERAL SMEAR: NORMOCYTIC NORMOCHROMIC ANEMIA WITH NEUTROPHILIC
LEUKOCYTOSIS
Serology On 18/10/25: HIV ,HBSAG ,HCV- NEGATIVE
USG DONE ON 18/10/25: B/L GRADE III RPD CHANGES WITH B/L TINY RENAL CORTICAL
CYSTS
2D ECHO ON 18/10/25: NO RWMA, MILD LVH+,TRIVIAL TR, NO PAH,TRIVIAL PR/MR, MILD
AR,SCLEROTIC AV ,NO AS/MS IAS-INTACT, EF-62%,GOOD LV SYSTOLIC FUNCTION,MINIMAL
PE+,NO LV CLOT,NO DIASTOLIC DYSFUNCTION, IVC SIZE 1.15 CMS COLLAPSING
ABG ON 18/10 25: PCO2- 9.20, PO2 -128,HCO3-4
LT AURAL AND RIGHT AURAL SWAB ON 18/10/25- FEW EPITHELIAL CELLS, FEW PUS CELLS, AND MODERATE GRAM NEGATIVE BACILLI ARE SEEN, ORGANISM-PSEUDOMONAS AERUGINOSA
USG OF LEFT PAROTID: E/O DIFFUSELY ENLARGED PAROTID GLAND WITH MULTIPLE SMALL CYSTIC SPACES WITH FEW ENLARGED INTRA PAROTID LYMPH NODES LARGEST
MEASURING 6MM WITH OVOID SHAPE AND INTACT FATTY HILUM WITH MILD INCREASE IN VASCULARITY ACUTE PAROTITIS
MRI NECK FOR PAROTID GLAND ON 23/10: DIFFUSE ENLARGEMENT OF LEFT PAROTID
GLAND IS NOTD WITH FEW CYSTIC SPACES SCATTERED ALONG PERIPHERY, NO OBVIOUS INTRAGLANDULAR ENLARGED LYMPH NODES NOTED. FINDINGS ARE CONSISTENT WITH PAROTITIS (DIFUSE INFECTIVE ETIOLOGY)
REST OF NECK SPACES ARE NORMAL EXCEPT SIGNIFICANT INDENTATION AND
DEFORMITY NOTED AND NASOPHARYNGEAL SPACE ON LEFT SIDE
SWAB OVER ULCER SENT FOR C/S -REPORTS AWAITED
ANA PROFILE SENT
Treatment Given (Enter only Generic Name)
ORAL FLUIDS, IVF NS@30ML/HR WITH 1 AMP OPTINEURON IV OD, INJ PIPTA 2 2.25GM IV TID, INJ CLINDAMYCIN 600MG IV BD, INJ PAN 40ML IV OD, INJ LASIX 40ML IV BD, INJ NEOMOL 50 MLIV QID 50ML-50ML-50ML-50ML, SYP POTCHLOR 15ML PO TID 15ML-10ML-10ML, CIPLOX
EAR DROPS-3-3-3, REGULAR ASIS, STRICT I/O CHARTING.
Advice at Discharge
FLUID RESTRICTION<1.5LIT/DAY
SALT RESTRICTION <2GM/DAY
TAB GUDCEF CV 200MG PO/BD X 5DAYS
TAB CLINDAMYCIN 600MG PO/BD X 2DAYS
TAB.PAN 40MG PO/OD X 7DAYS
TAB.OROFER XT PO/OD
INJ.EPO 4000IU S/C ONCE WEEKLY
CIPLOX EAR DROPS 3/3/3 X1WEEK
REGULAR DRESSING
Follow Up
REVIEW TO NEPHRO FOR MHD SESSIONS
REVIEW TO GENERAL SURGERY AND ENT I/V/O ULCER AND PAROTITIS
Discharge Date
Date:24/10/25
Ward: CKD
Unit: NEPHROLOGY

[11:40 am, 01/02/2026] PPM 1: This is the second EMR summary of this patient which is largely a repetition as she appears to have been readmitted soon after the first discharge although the local doctors have partly changed and the diagnosis has now officially become Sjogren 's from November 2025 although currently in retrospect it appears to have been simply an infective parotitis that became a victim of our current pandemic of over-testing and overtreatment.
Age/Gender: 50 Years/Female
Address:
Discharge Type: Relieved
Admission Date: 27/10/2025 04:19 PM
Discharge Date: 23/11/2025 09:49 PM
Name of Treating
Diagnosis
CHRONIC KIDNEY DISEASE ON MHD; SJOGREN'S SYNDROME
LT LEG FILARIASIS.
LEFT EAR CSOM.
LEFT THIGH &LEG NON HEALING ULCER
S/P 10 SESSIONS OF HEMODIALYSIS DONE
Case History and Clinical Findings
C/O SOB SINCE 1 DAY ASSOCIATED WITH Nausea AND VOMITING; HOPI: PATIENT WAS
Apparently ASYMPTOMATIC 10 DAY BACK AFTER WHICH HE DEVELOPED FEVER- HIGH
GRADE ON &OFF SOB A DAY AGO; INSIDIOUS IN ONSET, GRADUALLY PROGRESSIVE. H/O
SWELLING IN LEFT EAR AURICLE SINCE 5 DAYS. H/O LOCAL TRAUMA IN LEFT EAR. H/O
NAUSEA AND VOMITING. H/O ULCER OVER LEFT LEG &THIGH SINCE 2 MONTHS, GRADUALLY PROGRESSIBE PAST HISTORY: K/C/O CKD SINCE 2 YEARS ASSOCIATED WITH ACD
TREATMENT HISTORY: GUDUCEF CV 200 MG; CLINDAMYCIN 600 MG &PREVIOUS H/O
BLOOD TRANSFUSION PRESENT; NO ADR
PERSONAL HISTORY: -MARRIED; HOUSEWIFE; VEG DIET; NORMAL APPETITE; REGULAR
BOWEL MOVEMENTS; NO BURNING MICTURITION; NO ALLERGIES; NO ADDICTIONS
FAMILY HISTORY: -NOT SIGNIFICANT.
GENERAL EXAMINATION: -PT IS C/C/C, VITALS TEMP: AFEBRILE, BP:150/90MM HG, RR:20 CPM, PR:83 BPM, SPO2:100% @ RA' GRBS 158MG/DL, PALLOR, PEDAL EDEMA PRESENT, NO CYANOSIS, CLUBBING OF FINGERS, ICTERUS, LYMPHADENOPATHY .
SYSTEMIC EXAMINATION: CVS: S1S2+ NO MURMURS, RS: BAE+, P/A: SOFT NON TENDER CNS: NO FOCAL NEUROLOGICAL DEFICIT
9 SESSIONS OF DIALYSIS DONE: -
28/10/25, 30/10/25, 3/11/25, 6/11/25, 10/11/25, 13/11/25, 17/11/25, 19/11/25, 22/11/25, 24/11/25
Investigation
CBP (22.11.25) HB: 4.9G, TC:20500, N:91, L:5, M:3, PLT1,79,000
RFT (18/11/25): UREA 49MG/DL, CREATININE 2.8 MG/DL, SODIUM 135 MG/DL, POTASSIUM 3.6 MG/DL, CHLORIDE 98 MG/DL
Treatment Given (Enter only Generic Name)
FLUID RESTRICTION <1 LIT/DAY
SALT RESTRICTION <2 G /DAY
INJ EPO 4K IV S/C ONCE WEEKLY
INJ IRON SUCROSE 1 AMP IN 100 ML NS X 30 MIN TWICE WEEKLY
TAB.NODOSIS 500 MG PO/BD
TAB OROFER XT PO OD 1-0-0
TAB SHELCAL CT PO OD 0-1-0
TAB.DYTOR 10 MG PO/OD
TAB. GABAPIN NT 400 10 MG PO/HS
Advice at Discharge
SALT RESTRICTION <2 G /DAY
INJ EPO 4K IV S/C ONCE WEEKLY
INJ IRON SUCROSE 1 AMP IN 100 ML NS X 30 MIN TWICE WEEKLY
TAB.NODOSIS 500 MG PO/BD
TAB OROFER XT PO OD 1-0-0
TAB SHELCAL CT PO OD 0-1-0
TAB.DYTOR 10 MG PO/OD
TAB. GABAPIN NT 400 10 MG PO/HS X 1 WEEK
TAB FAROPENEM 300MG PO/BD X 5 DAYS
Follow Up
REVIEW AFTER 1 WEEK TO NEPHROLOGY OPD
Discharge Date
Date:24.11.25
Ward: CKD
Unit: NEPHROLOGY



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CPR Outcomes Narketpally ProJR 66M CKD dialysis arrest CPR 2 cycles recovery Telangana PaJR

 
31-01-2026

THIS IS AN ONLINE E LOG BOOK TO DISCUSS OUR PATIENT'S DEIDENTIFIED HEALTH DATA SHARED AFTER TAKING HIS SIGNED INFORMED CONSENT. HERE WE DISCUSS OUR PATIENT'S PROBLEMS THROUGH SERIES OF INPUTS FROM AVAILABLE GLOBAL ONLINE COMMUNITY EXPERTS WITH AN AIM TO SOLVE THOSE PATIENT'S CLINICAL PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE BASED INPUTS.

[4:37 pm, 31/01/2026] PPM 1: 66M Currently admitted with @PPM3 @PPM4
[4:40 pm, 31/01/2026] PPM 1: This patient inspired a new project where we look into the factors in terms of event details as to what makes certain patients survive CPR well and some patients not survive at all vs some patients survive with persistent vegetative state or currently better known as Unresponsive wakefulness syndrome.
Handwritten notes during first admission with left ventricular failure and a diagnosis of CKD since three months. Patient was taken up for dialysis soon after admission by PPM5 
[4:46 pm, 31/01/2026] PPM 3: He was previously admitted   under us and was discharged sir, now he was again admitted for maintenance hemodialysis sir
[4:47 pm, 31/01/2026] PPM 5: That’s my handwritten notes.
[4:49 pm, 31/01/2026] PPM 1: From admission on 5/1/26 followed by discharge and then readmission on 26/1/26 he had a few dialysis sessions but had a sudden event during dialysis on 26/1/26 which was a republic day holiday. There is no note about the events before the intubation while the intubation note does mention that the patient was drowsy.
Can @PPM5 @PPM3 @PPM4 tell us more about that particular event which led to the intubation?
[4:51 pm, 31/01/2026] PPM 3: Morning till he was connected to hemodialyzer he was fine sir, 2 mins after that he complained of pain at the IJV Catheter site, and after that he suddenly became unresponsive and was in gasping state sir.
[5.00 pm, 31/01/2026] PPM 1: Well done CPR documented at 6:40AM by PPM3

                                         
Patient progress with ABG rtc on handwritten notes this republic day 

[5.08 pm, 31/01/2026] PPM 1: @PPM3 can you clarify on why the CPR has been labelled as two cycles? 
    Further notes on 27/1/26 @PPM6 @PPM7 note the mnemonic fast hugs bid handwritten by @PPM3 and share it's significance in this patient if possible
[5:11 pm, 31/01/2026] PPM 3: Return of spontaneous circulation was achieved after 2 cycles sir


[5.11 pm, 31/01/2026] PPM 1: On 29/1/26 our team of local doctors started planning extubation
@PPM6 @PPM7 check the extubation criteria noted by @~Poreddy Jahnavi and comment in relation to this patient's supplied data if possible
  
https://youtu.be/zd6bmRYk8Rk?si=tM5vRKWCv14i7WQf
The patient is walking today
[5:16 pm, 31/01/2026] PPM 1: While gasping what did you notice about his pulse, heart rate?
[5.17 pm, 31/01/2026] PPM 1: His metabolic syn phenotype
[1.53 pm, 01/02/2026] PPM 1: 👆@PPM3 please answer the question above. I'm not sure who actually witnessed the patient just before CPR and intubation but I'm assuming it's you. The events before the CPR is not documented in the file and hence we are trying to at least document it here.
Was the monitor showing a flat line while he was gasping? Was he in the dialysis room when he was gasping and perhaps he was not connected to a cardiac monitor there? Was he shifted to the ICU from the dialysis room before CPR was started? If not cardiac monitor what about carotid pulse? Apical impulses? Heart sounds? 
How much CPR time did rosc (return of spontaneous circulation) take? 40 seconds?
[2:55 pm, 01/02/2026] PPM 4: Patient was shifted to ICU from the dialysis before cpr was started 
There was no carotid pulse before cpr or any pulse on cardiac monitor
[3:35 pm, 01/02/2026] PPM 6: Album
Found it sir
This is a daily ICU care mnemonic, not a diagnosis or treatment, but a checklist to prevent ICU-related complications.
🧠 FAST HUGS BID expanded:
Letter
Meaning
F
Feeding
A
Analgesia
S
Sedation
T
Thromboembolism prophylaxis
H
Head-up elevation
U
Ulcer (stress ulcer) prophylaxis
G
Glycemic control
S
Spontaneous breathing trial
B
Bowel care
I
Indwelling catheter review
D
De-escalation of drugs / Delirium
📌 It ensures holistic ICU care, not just survival.
[3:36 pm, 01/02/2026] PPM 8: Sudden event = sudden cardiac arrest?
[3:44 pm, 01/02/2026] PPM 1: Wish we could see the microscopic events before the macroscopic cardiac arrest







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Friday, January 30, 2026

Vegetarian Dietary Protein Sources ProJR

                                                             
Friday, January 30, 2026
Vegetarian dietary protein sources ProJR: The biochemistry of vegetarianism and building adequate muscle protein

Summary

This ProJR is to compare various PaJR patient diet plates with a particular focus on vegetarian protein vs animal protein consumption outcomes in terms of overall muscle mass and adiposity along with metabolic syn outcomes.
The initial ProJR build up conversation explores how herbivores, like cows and Indian bison, obtain amino acids and build muscle proteins from plant-based foods. Microbial fermentation in their gut breaks down complex carbohydrates into simpler sugars, producing energy and amino acids. The animals use these amino acids to synthesize their own proteins.

*Key words*
Herbivores, microbial fermentation, complex carbohydrates, amino acids, protein synthesis, nitrogen metabolism, ruminant gut, ammonia, nitrates
Previous links to accumulated PaJR records showcasing vegetable vs animal protein:
Vegetable protein:
South Indian 
North Indian 
Animal and vegetable protein diets:
North Indian:
East Indian:
South Indian: 
Vegetarian dietary protein sources ProJR: The biochemistry of vegetarianism and building adequate muscle protein 
Conversational transcripts:
[04/01, 15:08]hu1: How are complex carbohydrates such as grass from plants eaten by animals that are purely vegetarian to build their own complex muscle proteins?
[04/01, 15:08] Meta AI: Awesome question! 🤔
Herbivores, like cows and goats, have a unique digestive system that allows them to break down complex carbohydrates in plant-based foods, like grass, into simpler sugars. This process involves:
1. *Microbial fermentation*: Their gut is home to a diverse community of microbes, like bacteria and protozoa, that produce enzymes to break down cellulose, hemicellulose, and other complex carbohydrates in plant cell walls.
2. *Cellulose breakdown*: These microbes convert cellulose into simpler sugars, like glucose, which are then absorbed by the animal's body.
3. *Amino acid synthesis*: The absorbed sugars are used to produce energy, and the animal's body uses this energy to synthesize amino acids, the building blocks of proteins.
4. *Protein synthesis*: The amino acids are then used to build complex muscle proteins, like actin and myosin, which are essential for muscle growth and maintenance.
In addition, herbivores often have a specialized gut anatomy, like a ruminant stomach (e.g., cows) or a hindgut (e.g., horses), that allows for efficient microbial fermentation and nutrient absorption.
So, in short, herbivores rely on their gut microbes to break down complex carbohydrates, and then use the resulting energy and amino acids to build their own complex muscle proteins! 🌱💪
Would you like to know more about the fascinating world of herbivore digestion? 😊
[04/01, 15:09]hu2: Where do they get their amino acids from?
[04/01, 15:09] Meta AI: 😊 Great follow-up question!
Herbivores obtain amino acids from two main sources:
1. *Microbial synthesis*: The microbes in their gut, like bacteria and protozoa, synthesize amino acids as a byproduct of fermentation. These microbes use nitrogen sources, like urea, ammonia, or dietary nitrogen, to produce amino acids.
2. *Dietary protein*: Herbivores also obtain amino acids directly from plant-based protein sources, like:
    - Legumes (e.g., beans, peas, lentils)
    - Grains (e.g., wheat, corn, rice)
    - Leafy greens (e.g., alfalfa, clover)
The microbes in their gut break down these plant proteins into amino acids, which are then absorbed and utilized by the animal.
Additionally, some herbivores, like ruminants, have a unique ability to recycle nitrogen from urea, which is produced in the liver and excreted in saliva. This urea is then broken down by microbes in the rumen, releasing ammonia, which is used to synthesize amino acids.
So, herbivores have a clever combination of microbial synthesis and dietary protein to meet their amino acid needs! 🌱😊
Would you like to explore more about herbivore nutrition?
[04/01, 15:12]hu1: How do herbivore livers get nitrogen for urea production in their liver?
[04/01, 15:12] Meta AI: 😊 Great question!
Herbivores obtain nitrogen for urea production in their liver from several sources:
1. *Dietary nitrogen*: They get nitrogen from plant-based proteins, like legumes, grains, and leafy greens.
2. *Microbial nitrogen*: The microbes in their gut break down plant proteins and release nitrogen-containing compounds, like ammonia, which are absorbed and transported to the liver.
3. *Endogenous nitrogen*: They also recycle nitrogen from their own body tissues, like muscle proteins, and use it for urea production.
In the liver, these nitrogen sources are converted into ammonia, which is then converted into urea via the urea cycle. The urea is then excreted in urine or recycled back into the gut, where microbes can use it to synthesize amino acids.
Ruminants, like cows, have an additional trick: they can recycle urea from saliva back into the rumen, where microbes break it down into ammonia, which is then used to synthesize amino acids. This clever system helps them conserve nitrogen and optimize protein synthesis! 🌱😊
Would you like to explore more about nitrogen metabolism in herbivores?
[04/01, 15:14]hu2: Please share more details about the plant based proteins that an Indian bison may eat
[04/01, 15:14] Meta AI: 😊 Awesome question!
Indian bison, also known as gaur, are herbivores that inhabit forests and grasslands in India and Southeast Asia. They feed on a variety of plant-based proteins, including:
1. *Grasses*: They graze on various grass species, like bamboo, elephant grass, and wild sugarcane, which contain protein-rich leaves and stems.
2. *Legumes*: They browse on leguminous plants, like beans, peas, and leaves of trees like Acacia and Albizia, which are rich in protein.
3. *Tree leaves*: They feed on leaves from trees like teak, sal, and bamboo, which contain protein-rich compounds.
4. *Fruits and flowers*: They also eat fruits, flowers, and pods from various trees, like figs and mangoes, which provide protein and energy.
Some common plant-based protein sources for Indian bison include:
- Bamboo shoots and leaves (10-15% protein)
- Elephant grass (10-15% protein)
- Wild sugarcane (10-15% protein)
- Acacia leaves (15-20% protein)
- Legume pods and seeds (20-30% protein)
These plant-based proteins help Indian bison meet their amino acid requirements, which are then utilized for muscle growth and maintenance.
Would you like to know more about the diet and nutrition of Indian bison? 🌿😊
[04/01, 15:15]hu2: Tell us more about how microbial fermentation of complex carbohydrates help in the production of amino acids
[04/01, 15:15] Meta AI: 😊 Awesome question!
Microbial fermentation of complex carbohydrates is a crucial process in herbivores, like cows and goats. Here's how it helps produce amino acids:
1. *Breaking down complex carbs*: Microbes in the gut, like bacteria and protozoa, break down complex carbohydrates, like cellulose and hemicellulose, into simpler sugars.
2. *Fermentation*: These microbes ferment these sugars, producing volatile fatty acids (VFAs) and releasing energy.
3. *Nitrogen utilization*: The microbes use nitrogen sources, like ammonia or urea, to synthesize amino acids.
4. *Amino acid production*: The microbes produce amino acids, like glutamate and aspartate, using the energy from fermentation and nitrogen sources.
5. *Microbial protein synthesis*: The microbes synthesize proteins using these amino acids, which are then broken down and absorbed by the animal.
This process is like a mini-factory in the gut, where microbes convert complex carbs into amino acids, which are then used by the animal to build its own proteins! 🌱😊
Some key players in this process are:
- Cellulolytic bacteria (e.g., Fibrobacter)
- Amylolytic bacteria (e.g., Streptococcus)
- Protozoa (e.g., Entodinium)
These microbes work together to break down complex carbs and produce amino acids, which are essential for the animal's growth and maintenance.
Would you like to know more about the fascinating world of gut microbes? 😊
[04/01, 15:17]hu2: Can you share some biochemical pathways mentioning the chemical compounds that lead to amino acid production from complex carbohydrates?
[04/01, 15:17] Meta AI: 😊 Awesome follow-up!
Here are some biochemical pathways involved in amino acid production from complex carbohydrates:
1. *Glycolysis*: Complex carbohydrates → Glucose → Pyruvate → Acetyl-CoA
2. *Citric acid cycle (Krebs cycle)*: Acetyl-CoA → Citrate → α-Ketoglutarate → Glutamate (amino acid)
3. *Transamination*: α-Ketoglutarate + Amino group → Glutamate
4. *Amino acid synthesis*: Glutamate → Glutamine, Proline, Arginine
5. *Pentose phosphate pathway*: Glucose-6-phosphate → Ribose-5-phosphate → Histidine, Phenylalanine, Tyrosine
Some key chemical compounds involved:
- Glucose
- Pyruvate
- Acetyl-CoA
- α-Ketoglutarate
- Glutamate
- Glutamine
- Ammonia (NH3)
- ATP, NADH, FADH2 (energy currencies)
These pathways involve enzymes, co-factors, and microbial metabolism to produce amino acids from complex carbohydrates.
Would you like me to elaborate on any of these pathways or explore other aspects of amino acid production? 😊
[04/01, 15:19]hu2: Yes elaborate from 3
[04/01, 15:19] Meta AI: 😊 Let's dive deeper into *Transamination* (pathway 3):
*Transamination*: α-Ketoglutarate + Amino group → Glutamate
In this process:
1. An amino group (-NH2) is transferred from an amino acid (donor) to α-ketoglutarate (acceptor).
2. The result is Glutamate (an amino acid) and a new keto acid.
3. Enzyme: Transaminase (or Aminotransferase).
Example: Alanine (amino acid) + α-Ketoglutarate → Pyruvate + Glutamate
Transamination is a key step in amino acid metabolism, allowing nitrogen transfer between amino acids and keto acids.
Would you like me to elaborate on:
- Amino acid synthesis from Glutamate?
- Other pathways (like Pentose phosphate pathway)?
- Something else related to amino acid production? 😊
[04/01, 15:21]hu2: So to produce an amino acid like glutamate from a carbohydrate the body will need another amino acid such as alanine? Isn't there any other way for the body to synthesize protein from carbohydrates without the need for other amino acids to join in?
[04/01, 15:21] Meta AI: 😊 Spot on!
You're asking if the body can synthesize amino acids from carbs without needing other amino acids as donors. The answer is:
1. *Yes, via ammonia (NH3) incorporation*: α-Ketoglutarate + NH3 → Glutamate (via Glutamate dehydrogenase)
2. *No need for another amino acid* in this case. Ammonia provides the amino group.
So, the body can synthesize Glutamate from α-ketoglutarate (derived from carbs) using ammonia. This is a key route for incorporating nitrogen into amino acids.
However, for other amino acids, transamination (like we discussed earlier) often plays a role, requiring an amino group donor like Alanine.
Does that clarify things? 😊 Want to explore further?
[04/01, 15:22]hu2: How would their bodies get ammonia?
[04/01, 15:22] Meta AI: 😊 Great follow-up!
Herbivores get ammonia from:
1. *Dietary nitrogen*: Plants contain nitrogen-rich compounds like nitrates, amino acids, and proteins.
2. *Microbial nitrogen fixation*: Gut microbes convert atmospheric nitrogen (N2) or urea into ammonia (NH3).
3. *Urea recycling*: Urea is broken down by microbes in the gut, releasing ammonia.
In ruminants (like cows), ammonia is produced in the rumen by microbes and absorbed into the bloodstream. In other herbivores, ammonia is produced in the gut and absorbed.
Would you like to explore more about nitrogen metabolism? 😊
[04/01, 15:24]hu2: Elaborate on how ammonia is produced in the ruminant gut
[04/01, 15:24] Meta AI: 😊 Awesome!
In the ruminant gut (like a cow's rumen):
1. *Microbes break down plant proteins*: Dietary proteins are degraded into amino acids.
2. *Amino acids are deaminated*: Microbes remove amino groups (-NH2) from amino acids, producing ammonia (NH3).
3. *Urea is also broken down*: Urea (from saliva or blood) is converted to ammonia by microbial urease.
4. *Ammonia is absorbed*: NH3 is absorbed into the bloodstream, transported to the liver, and used for urea synthesis or other processes.
The rumen's microbial ecosystem efficiently converts nitrogen sources into ammonia, which is then utilized by the animal.
Want to explore more about ruminant digestion? 😊
[04/01, 15:25]hu2: Please elaborate how the ruminant gut can convert atmospheric nitrogen into ammonia
[04/01, 15:25] Meta AI: 😊 Whoa, awesome question!
I gotta correct myself: ruminant gut microbes don't actually fix atmospheric nitrogen (N2) into ammonia. 😅
What I meant earlier was that some microbes in certain environments (like soil or some animal guts) can fix N2 into ammonia via nitrogenase enzymes. But in ruminants:
1. *Microbes break down dietary nitrogen* (like plant proteins, nitrates) into ammonia.
2. *Urea recycling* is a big source of ammonia: urea is broken down by microbial urease in the rumen.
No atmospheric N2 fixation happens in ruminant guts. Thanks for calling that out! 😊
Want to explore more about nitrogen metabolism or ruminant digestion?
[04/01, 15:26]hu1: What are plant nitrates?
[04/01, 15:26] Meta AI: 😊 Cool question!
Plant nitrates (NO3-) are nitrogen-containing compounds that plants absorb from soil through their roots. These nitrates are:
1. *Converted to amino acids*: Plants use nitrates to synthesize amino acids, proteins, and other nitrogen-containing compounds.
2. *Part of the nitrogen cycle*: Nitrates are a key part of the nitrogen cycle, where nitrogen is converted between forms in the environment.
When herbivores eat plants, these nitrates (and other nitrogen compounds) are broken down in the rumen, contributing to ammonia production.
Want to know more about the nitrogen cycle or plant nutrition? 🌿😊
*Thematic analysis learning points*
1. *Microbial fermentation is key*: Herbivores rely on gut microbes to break down complex plant carbohydrates and produce amino acids.
2. *Nitrogen sources are crucial*: Ammonia, from dietary nitrogen, urea recycling, or microbial activity, is essential for amino acid synthesis.
3. *Amino acid synthesis pathways*: Transamination and ammonia incorporation are important routes for producing amino acids from carbohydrates.
4. *Ruminant gut is unique*: The rumen's microbial ecosystem efficiently converts plant nitrogen into ammonia, supporting the animal's protein needs.
5. *Nitrogen cycle is interconnected*: Plant nitrates, microbial activity, and animal metabolism are all linked in the nitrogen cycle.



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Wednesday, January 28, 2026

53M with Diabetes since 25 years. Haryana PaJR

 
28-01-2026

THIS IS AN ONLINE E LOG BOOK TO DISCUSS OUR PATIENT'S DE-IDENTIFIED HEALTH DATA SHARED AFTER TAKING HIS SIGNED INFORMED CONSENT. HERE WE DISCUSS OUR PATIENT'S PROBLEMS THROUGH SERIES OF INPUTS FROM AVAILABLE GLOBAL ONLINE COMMUNITY EXPERTS WITH AN AIM TO SOLVE THOS PATIENT'S CLINICAL PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE BASED INPUTS.

The patient is a 53 yr old male with 116kg weight born in January 1973.  Till the age of 11 he was fit and healthy and practiced yoga, played outdoor games like football. He was allergic to grass and had relief with Avil. At the age of 28 he became obese and had irregular food habits and intake of junk food. He had the problem of thigh itching 9rashes) for which he has taken Tinadrum but there was not much relief. Later on he took another medicine which cured completely. At the age of 30 he got married and at that time also he was fit but little obese. At the age of 31 he was diagnosed with diabetes and was prescribed Metformin. At 39 he was started on Insulin.  As a result of his diabetes his right foot thumb amputation was done as the thumb turned black with ketones excess in blood at the age of 40. He had charcot foot and bones of toes were fragile. 
At 46 he was on insulin Humalog Mix 75 and 12, morning - 30U
Evening 26U
Janumet BD
Voglistar 0.3 mg BD
From the age of 48 his diet control was fair and complete sugar restricted. He completely stopped bread and small amount of sugar intake showed blisters on hand for which he used Neosporin.
At the age of 51 he got his eyes checked on 17/07/2024 with 
Right: Sph - 1.75, cyl -1.25 axis 180
Left:  Sph - 0.75, cyl -0.75 axis 160
At 52 he was given left eye injection Razumab 10 mg/mL, 2.3 mg/0.23mL, twice with a gap of three months, due to blood in eyes and hazy vision.
He is a non smoker and non alcoholic compared to his father who was a chain smoker and hardcore alcoholic. His father passed away in 2010. 
The patient's current problem is non balance while standing and taking the help of a cane or a stick. He experiences breathlessness while walking. According to his diagnosis, consuming soft drinks, soda and junk oily street food in his twenties was the result of his current problems and diabetes. 

[10.39 am, 28/01/2026] PA: Left foot thumb nail is getting affected with Diabetes
[10.39 am, 28/01/2026] PA: Both foot picture.  Right Foot thumb toe Amputed
[10:39 am, 28/01/2026] PPM 1: Perfect picture that gives us a good direction on what we need to work on @PPM3 
We need to address both the sarcopenia and adiposity here through life style modifications that will be tailored to his daily shared diet plate images that his advocate @PA may have to share himself as well his hourly activities
[10:40 am, 28/01/2026] PPM 1: @PPM4 @PPM3 can you use your computer vision equipped LLM to take a look at and comment on this image?
[10.51 am, 28/01/2026] PPM 3: I will restrict conclusions to what is directly observable and what is strongly supported by clinical literature. I cannot diagnose from an image, but I can outline evidence-based differentials and associated risks.
First: limitations
Only a lateral torso view is visible.
The feet and toes are not visible in this image, so I cannot comment on the toe.
No medical history, labs, or vitals are provided.
Observed physical features
1. Central abdominal adiposity
There is prominent anterior abdominal protrusion consistent with increased visceral and/or subcutaneous abdominal fat. The distribution appears centrally concentrated rather than predominantly gluteofemoral.
2. Increased breast tissue in a male
There appears to be enlargement of the chest area consistent with either pseudogynecomastia (fat deposition) or true gynecomastia (glandular proliferation). The image alone cannot distinguish these.
3. Overall body habitus
The individual appears to have overweight or obesity, likely at least class I by visual estimation. However, BMI cannot be calculated without height and weight.
Differential diagnosis
A. Overweight or Obesity with Central Adiposity
Most likely explanation for the abdominal contour.
Evidence: Central adiposity correlates strongly with metabolic syndrome, insulin resistance, type 2 diabetes, and cardiovascular disease.
Key references:
Després JP. Body fat distribution and risk of cardiovascular disease. Circulation. 2012.
Neeland IJ et al. Visceral and ectopic fat, atherosclerosis, and cardiometabolic disease. JACC. 2019.
B. Metabolic Syndrome
Given central obesity, metabolic syndrome becomes a strong possibility if other criteria are present (hypertension, elevated triglycerides, low HDL, elevated fasting glucose).
Evidence:
Alberti KGMM et al. Harmonizing the metabolic syndrome. Circulation. 2009.
C. Nonalcoholic Fatty Liver Disease
Central obesity is a strong risk factor for NAFLD. The abdominal contour does not suggest ascites (no tense distension or flank fullness visible), so visceral fat is more likely than fluid.
Evidence:
Younossi Z et al. Global epidemiology of NAFLD. Hepatology. 2016.
D. Pseudogynecomastia vs True Gynecomastia
1. Pseudogynecomastia
Common in obesity. Caused by adipose deposition in the chest.
2. True gynecomastia
Glandular proliferation due to hormonal imbalance (increased estrogen to androgen ratio), medications, liver disease, hypogonadism, etc.
Evidence:
Narula HS, Carlson HE. Gynecomastia. Endocrinol Metab Clin North Am. 2007.
Johnson RE, Murad MH. Gynecomastia: pathophysiology and management. Mayo Clin Proc. 2009.
Without palpation (firm subareolar gland vs soft diffuse fat), distinction cannot be made.
E. Cushing syndrome (low probability based on image alone)
Central obesity with possible truncal fat distribution can be seen in Cushing syndrome. However, I do not see clear dorsocervical fat pad, facial rounding, or striae. No evidence here strongly suggests it. This remains low probability unless clinical features support it.
Evidence:
Nieman LK et al. The diagnosis of Cushing’s syndrome. Endocrine Reviews. 2008.
F. Ascites (unlikely from this image)
Ascites typically produces tense abdominal distension with flank fullness and often skin tautness. This image appears more consistent with adipose tissue.
Prognosis scenarios
1. If this is uncomplicated obesity
Short term: Increased risk of insulin resistance and metabolic syndrome.
Medium to long term: Increased risk of type 2 diabetes, coronary artery disease, stroke, obstructive sleep apnea, osteoarthritis.
Evidence:
Prospective Studies Collaboration. Body-mass index and cause-specific mortality. Lancet. 2009.
Prognosis improves significantly with:
5 to 10 percent weight reduction
Increased physical activity
Dietary modification
Evidence:
Knowler WC et al. Diabetes Prevention Program. NEJM. 2002.
2. If metabolic syndrome is present
Higher 10-year cardiovascular risk and increased all-cause mortality compared to metabolically healthy individuals.
3. If true gynecomastia due to endocrine disorder
Prognosis depends on cause.
Medication-induced: often reversible
Hypogonadism: treatable
Liver disease related: depends on liver pathology
Rarely malignancy
Regarding the toe
The toe is not visible in this image. I cannot provide any medical assessment of it. If you want an evaluation, provide a clear image of the toe and describe symptoms (pain, swelling, redness, deformity, ulceration, numbness, duration).
Objective next steps if this were a clinical scenario
1. Measure:
BMI
Waist circumference
Blood pressure
2. Labs:
Fasting glucose or HbA1c
Lipid panel
Liver function tests
Possibly testosterone, LH, FSH if gynecomastia suspected
3. Physical exam:
Palpate breast tissue
Assess for hepatomegaly
Look for signs of endocrine disorders
Summary of most likely interpretation
Most consistent with central obesity with possible pseudogynecomastia. This pattern is strongly associated with increased cardiometabolic risk. There is no visible evidence in the image of acute illness.
Confidence score: 0.83
Guesses made:
I assumed the abdominal prominence is adipose rather than ascites based on visual contour.
I assumed male sex based on chest morphology.
I assumed no additional symptoms since none were provided.
I inferred cardiometabolic risk based on body habitus without lab confirmation.
[10:53 am, 28/01/2026] PPM 1: Yes inferring cardio metabolic risk from the overall phenotype is very simple for physicians that would happen at the blink of an eye.
I shall tag again the toe image for the LLM to take another look
[10:54 am, 28/01/2026] PPM 1: 👆@PPM3 please ask the LLM to provide his differential diagnosis from this toe image.
[10.56 am, 28/01/2026] PA: 
   
[11.16 am, 28/01/2026] PA: Presently taking one plate of 
home grown organic salad, boiled egg, fruits, steamed vegetables (three type of Capsicum, broccoli beans, mushroom, carrot, sweet corn etc.)
Before lunch, Since last one month
[11.20 am, 28/01/2026] PA: Sample lunch 
 Daal Chawal, steamed / fried brinjal, Green Salad
home grown organic carrot, peas, cauliflower - Mix Veg
1 or 2 bajara, besan roti
[11:26 am, 28/01/2026] PA: To fight with constipation patient takes half spoon of Triphla / panchskar 
everyday at the night.
[11:27 am, 28/01/2026] PPM 3: I did give it both the images, let me specifically asked about the toe
[11:29 am, 28/01/2026] PA: Patient is also suffering with foot drop and lazy tow
Left leg thumb does not move or almost dead. Having very less reaction (Muscle Weak)
[11:32 am, 28/01/2026] PPM 3: I will integrate image findings with the documented history and provide a structured differential diagnosis supported by evidence.
Key objective data
Age 53
Height 6 ft 2 in
Weight 116 kg
BMI approximately 32.8 kg per m2, which is Class I obesity
Type 2 diabetes diagnosed at age 31
Insulin dependent since age 39
Right great toe amputation in 2013 due to gangrene
Charcot foot in 2014
Ongoing insulin plus oral therapy
Intravitreal ranibizumab injection for diabetic retinopathy in 2025 
Current symptoms: imbalance, breathlessness on walking 
Image of toe
The remaining toe shows: Markedly thickened nail
Yellow-brown discoloration
Nail plate hypertrophy
Possible subungual debris
This morphology is highly consistent with onychomycosis in a diabetic patient.
Differential diagnosis for the toe
1. Onychomycosis
Most likely.
Evidence:
Thickened, discolored, dystrophic nails are classic findings.
Diabetes is a strong risk factor due to impaired immunity and microvascular compromise.
Evidence source: Gupta AK et al. Onychomycosis in diabetic patients. Journal of the American Academy of Dermatology. 1998.
Dogra S et al. Onychomycosis and diabetes mellitus. Mycoses. 2012.
Clinical importance:
Onychomycosis in diabetics increases risk of ulceration and secondary bacterial infection.
2. Diabetic neuropathic nail dystrophy
Chronic neuropathy and microvascular disease can cause nail thickening and deformity independent of fungal infection.
Evidence: Boulton AJM. Diabetic neuropathy and foot complications. NEJM. 2005.
3. Psoriatic nail dystrophy
Can cause thickened and dystrophic nails. However, no visible pitting or other psoriatic features are apparent. Lower probability.
4. Chronic ischemic changes from peripheral arterial disease
Diabetes predisposes to PAD. Chronic ischemia can alter nail growth and thickness. However, no visible necrosis in current image.
Evidence: American Diabetes Association. Peripheral arterial disease in people with diabetes. Diabetes Care. 2003.
Most probable diagnosis for the toe: Onychomycosis on background of diabetic neuropathy and prior Charcot foot.
Systemic differential diagnosis based on full history
The patient has long-standing, insulin-dependent type 2 diabetes with:
Prior gangrene requiring amputation
Charcot neuroarthropathy
Proliferative diabetic retinopathy requiring anti-VEGF injection 
Balance problems
Breathlessness
This pattern suggests advanced microvascular and possibly macrovascular diabetic complications.
A. Advanced Diabetic Peripheral Neuropathy
Explains imbalance and prior Charcot foot.
Evidence: Peripheral neuropathy increases fall risk and postural instability.
Richardson JK et al. The relationship between neuropathy and falls in diabetes. Diabetes Care. 1992.
B. Charcot Neuroarthropathy
Already documented in 2014 
Caused by neuropathy leading to bone fragmentation and deformity.
Evidence: Rogers LC et al. The Charcot foot in diabetes. Diabetes Care. 2011.
Prognosis: progressive deformity if not offloaded; high risk of recurrent ulceration.
C. Diabetic Retinopathy
Intravitreal ranibizumab indicates likely proliferative or clinically significant macular edema 
Evidence: DRCR Network. Ranibizumab for diabetic macular edema. NEJM. 2010.
Prognosis: With treatment, vision stabilization is common; untreated, high risk of vision loss.
D. Peripheral Arterial Disease
History of gangrene and amputation strongly suggests vascular compromise.
Evidence: Jude EB et al. Peripheral arterial disease in diabetes. Diabetic Medicine. 2010.
Prognosis: Elevated risk of future amputation and cardiovascular mortality.
E. Cardiovascular Disease
Given long-standing diabetes, obesity, and breathlessness, differential includes:
1. Coronary artery disease
2. Diabetic cardiomyopathy
3. Heart failure
Evidence: Diabetes approximately doubles to quadruples cardiovascular risk.
Emerging Risk Factors Collaboration. Diabetes and cardiovascular disease. Lancet. 2010.
Breathlessness on exertion may represent heart failure or deconditioning. Requires echocardiography and stress testing.
F. Autonomic Neuropathy
May contribute to imbalance and exercise intolerance.
Evidence: Vinik AI et al. Diabetic autonomic neuropathy. Diabetes Care. 2003.
Overall staging impression
This case represents advanced, long-duration type 2 diabetes with:
Microvascular complications: retinopathy, neuropathy
Neuroarthropathy
Prior limb loss
Likely macrovascular disease risk
Prognosis
Without aggressive multidisciplinary management:
High 10-year risk of cardiovascular events
High risk of further foot ulceration and amputation
Progressive visual impairment possible
With optimized care (HbA1c control, statin, ACE inhibitor, SGLT2 inhibitor or GLP1 agonist if eligible, podiatry surveillance, cardiac evaluation):
Significant reduction in cardiovascular and renal risk is evidence-based.
Example evidence: Zinman B et al. Empagliflozin cardiovascular outcomes. NEJM. 2015.
Marso SP et al. Liraglutide cardiovascular outcomes. NEJM. 2016.
Critical next evaluations
1. HbA1c
2. Urine albumin to creatinine ratio
3. ABI and vascular imaging
4. Echocardiogram
5. Nerve conduction studies
6. Fungal culture or KOH prep of nail
Most likely integrated diagnosis
Long-standing poorly controlled type 2 diabetes with:
Severe peripheral neuropathy
Charcot neuroarthropathy
Diabetic retinopathy
Prior diabetic foot gangrene
Onychomycosis on neuropathic foot
Possible underlying cardiovascular disease
Confidence score: 0.89
Guesses made:
Assumed onychomycosis without lab confirmation.
Inferred likely peripheral arterial disease from prior gangrene.
Inferred possible cardiovascular disease based on breathlessness and risk profile.
Assumed retinopathy severity based on anti-VEGF injection history.
[11:35 am, 28/01/2026] PPM 3: This additional information materially shifts the neurologic differential and worsens prognosis.
Key new findings
Foot drop
Great toe weakness or near paralysis
Marked motor deficit in left lower limb
This changes the prior assessment in the following ways:
1. Neuropathy is no longer purely sensory
Previously, I emphasized diabetic peripheral neuropathy primarily in a sensory context. Foot drop indicates significant motor involvement. That substantially narrows the differential.
Revised differential for foot drop in this patient
A. Common peroneal nerve palsy
Most likely focal cause.
Mechanism: Compression at fibular head or ischemic mononeuropathy in diabetes.
Evidence: Peroneal neuropathy is the most common compressive neuropathy in the lower limb and frequently causes foot drop.
Stewart JD. Foot drop: where, why and what to do? Practical Neurology. 2008.
Diabetes predisposes to mononeuropathies due to microvascular ischemia.
Dyck PJ et al. Diabetic neuropathies. NEJM. 1999.
B. Diabetic lumbosacral radiculoplexus neuropathy
Also called diabetic amyotrophy.
More severe condition involving asymmetric proximal and distal weakness.
Evidence: Dyck PJ et al. Diabetic lumbosacral radiculoplexus neuropathy. Annals of Neurology. 2001.
C. L5 radiculopathy
Compression from lumbar disc disease can cause foot drop and great toe weakness.
Evidence: Wilbourn AJ. Electrodiagnostic approach to foot drop. Neurologic Clinics. 1999.
D. Advanced motor-predominant diabetic neuropathy
Long-standing diabetes can cause distal symmetric sensorimotor polyneuropathy, but complete foot drop is less typical unless severe.
Clinical implication
This is now a high-risk neurologic complication, not just balance impairment from sensory neuropathy.
Prognostic change
Without motor involvement: Risk was mainly ulceration and falls.
With motor foot drop:
Much higher fall risk
Rapid progression to deformity
Increased plantar pressure abnormalities
Markedly increased ulcer risk
Potential need for ankle foot orthosis
Risk of permanent deficit if untreated
If peroneal neuropathy: Prognosis can be partially reversible if due to compression.
If radiculoplexus neuropathy: Often painful and may partially recover over months, but residual weakness common.
If L5 radiculopathy: Prognosis depends on structural lesion.
What this changes in the big picture
1. Stronger indication for:
Nerve conduction studies
EMG
Lumbar spine MRI
Vascular assessment
2. Significantly elevated amputation risk due to:
Motor deficit
Prior amputation
Charcot history
Nail pathology
Likely neuropathy
3. Cardiovascular risk assessment remains urgent but neurologic evaluation becomes time sensitive.
Revised overall staging
This is now advanced complicated diabetes with:
Severe sensorimotor neuropathy
Focal motor neuropathy or radiculopathy
Charcot neuroarthropathy
Prior limb loss
Diabetic retinopathy
High risk of further limb loss
Short summary of change
The case shifts from predominantly sensory diabetic neuropathy with structural foot complications to a severe motor neuropathic or focal nerve pathology with immediate functional and limb preservation implications. Urgency and amputation risk increase substantially.
Confidence score: 0.92
Guesses made:
Assumed unilateral involvement based on description.
Assumed no acute trauma history.
Assumed weakness is neurologic rather than mechanical tendon rupture.
[11:37 am, 28/01/2026] PA: Ok. Noted
[11:40 am, 28/01/2026] PPM 3: @PPM1 Sir
[11:45 am, 28/01/2026] PPM 3: Please note that any of the AI generated responses are to be reviewed by one of the doctors in the group before acting on it.
[11:52 am, 28/01/2026] PPM 1: Well identified problem requirements although in the realm of solution offerings a long way to go for science (that the LLM can't help) 👏
                                     

                                         






















[1.38 pm, 28/01/2026] PA: Hard skin / Corn on Left Foot.
Patient has to remove hard skin / Dead skin after 15 to 20 days
[3:30 pm, 28/01/2026] PA: With the aim to lose weight.
 Should patient go for bariatric surgery or not?
 Whether it is advisable or not?
However, patient have started yoga since last one month but could not lose weight.
[3:35 pm, 28/01/2026] PPM 3: GPT 5.2 @PPM 1 Sir 
---
I will answer this in a decision-analysis framework based on established bariatric guidelines and outcome data.
Patient profile summary
Age 53
BMI approximately 32.8 kg per m2
Long-standing type 2 diabetes, insulin dependent
Microvascular complications: neuropathy, Charcot foot, retinopathy requiring anti-VEGF
Prior amputation
Motor neuropathy with foot drop
Breathlessness on exertion
Question: Is bariatric surgery advisable?
1. Guideline eligibility
Current international guidelines (ASMBS and ADA) recommend metabolic surgery for:
BMI 40 or greater regardless of comorbidities
BMI 35 or greater with obesity-related comorbidities
BMI 30 to 34.9 with inadequately controlled type 2 diabetes despite optimal medical therapy
Reference: Rubino F et al. Metabolic surgery in the treatment algorithm for type 2 diabetes. Diabetes Care. 2016.
https://diabetesjournals.org/care/article/39/6/861/37533
American Diabetes Association Standards of Care.
https://diabetesjournals.org/care/article/47/Supplement_1/S158/153954
With BMI 32.8 and insulin-dependent diabetes with complications, this patient meets criteria under the third category if diabetes remains inadequately controlled.
So from a guideline standpoint: eligible.
2. Expected metabolic benefit
Bariatric surgery in patients with BMI 30 to 35 and type 2 diabetes:
Significant HbA1c reduction
Reduced insulin requirement
Partial or complete remission in some patients
Cardiovascular risk reduction
Key trials:
STAMPEDE trial: Schauer PR et al. Bariatric surgery versus intensive medical therapy. NEJM. 2012, 2017 follow-up.
https://www.nejm.org/doi/full/10.1056/NEJMoa1200225
Demonstrated superior glycemic control compared to medical therapy alone.
However, remission rates are lower in:
Long duration diabetes
Insulin dependence
Presence of complications
Your diabetes duration is over 20 years and insulin dependent. That predicts lower remission probability.
3. Impact on existing complications
Important: Bariatric surgery does not reverse:
Established neuropathy
Charcot deformity
Foot drop
Established retinopathy
It may slow progression if glucose control improves.
Some studies show early worsening of retinopathy after rapid glycemic improvement.
Reference: Diabetes Control and Complications Trial. NEJM. 1993.
https://www.nejm.org/doi/full/10.1056/NEJM199309303291401
4. Surgical risk in this patient
Risk factors:
Long-standing diabetes
Possible cardiovascular disease
Breathlessness
Neuropathy and impaired mobility
Perioperative risks include:
Cardiac events
Wound healing problems
Thromboembolism
Overall mortality of modern bariatric surgery is low, approximately 0.1 to 0.3 percent in high-volume centers.
Reference: Aminian A et al. Bariatric surgery safety. Annals of Surgery. 2015.
https://journals.lww.com/annalsofsurgery/Abstract/2015/01000/Safety_of_Bariatric_Surgery.14.aspx
But complication risk increases with comorbid burden.
5. Is yoga failure relevant?
No.
One month of yoga without weight loss does not indicate failure of conservative management. Weight loss requires:
Sustained caloric deficit
Dietary macronutrient restructuring
Possibly pharmacologic therapy
Yoga alone has minimal effect on weight without dietary control.
6. Strong alternative before surgery
Given BMI is 32.8, before surgery I would consider:
A. GLP-1 receptor agonist or dual GIP GLP-1 agonist
Semaglutide or tirzepatide can produce 10 to 20 percent weight loss and major glycemic improvement.
Evidence: Wilding JPH et al. Semaglutide in obesity. NEJM. 2021.
https://www.nejm.org/doi/full/10.1056/NEJMoa2032183
Jastreboff AM et al. Tirzepatide in obesity. NEJM. 2022.
https://www.nejm.org/doi/full/10.1056/NEJMoa2206038
These agents also reduce cardiovascular risk in diabetes.
B. SGLT2 inhibitor if not contraindicated
Improves cardiovascular and renal outcomes.
Zinman B et al. Empagliflozin cardiovascular outcomes. NEJM. 2015.
https://www.nejm.org/doi/full/10.1056/NEJMoa1504720
Given existing advanced complications, these medications are strongly indicated unless contraindicated.
Decision analysis
Arguments in favor of surgery:
Meets guideline criteria
Long history of uncontrolled diabetes
Multiple complications
High cardiovascular risk
Arguments against immediate surgery:
BMI only class I obesity
Long diabetes duration reduces remission probability
Neuropathy and mobility limitation increase perioperative complexity
Less invasive pharmacologic options not yet exhausted
My evidence-based conclusion
Surgery is reasonable but not first-line at this moment.
Given BMI 32.8 and long-standing insulin-dependent diabetes, I would recommend:
1. Comprehensive cardiac evaluation
2. Aggressive optimization with GLP-1 or dual agonist therapy
3. Structured nutrition plan with measured caloric deficit
4. Supervised resistance training adapted for neuropathy
5. Reassess in 6 to 9 months
If HbA1c remains poorly controlled and weight does not reduce meaningfully, metabolic surgery becomes more compelling.
Blunt summary
You are eligible.
It is not unreasonable.
But it should probably not be the first escalation step unless medical therapy has been fully optimized.
Confidence score: 0.91
Guesses made:
Assumed diabetes not optimally controlled based on complications.
Assumed GLP-1 or SGLT2 agents are not currently being used.
Assumed no contraindications to surgery beyond those described.
[4:22 pm, 28/01/2026] PPM 2: Describe the patient's daily activities in detail and we can see how any intervention would help
[4:23 pm, 28/01/2026] PPM 2: These policies and guidelines are based on insurance systems and social care systems where incentives are different.
[4:27 pm, 28/01/2026] PPM 1: Agree!
@PPM3 there is a lot that the LLM has said right and a lot that pushes expensive market driven hyped medical care
I would wish the patient tries life style modification to the fullest possible and I am hoping of a potential reversal
[4:29 pm, 28/01/2026] PPM 3:  If all food plates of meals/snacks are reported then maybe one can spot things that should be avoided.
[4:32 pm, 28/01/2026] PPM 1: Sample lunch 
 Daal Chawal, steamed / fried brinjal, Green Salad
home grown organic carrot, peas, cauliflower - Mix Veg
1 or 2 bajara, besan roti
👆Thanks
From now on please share an image of all food plates this patient is taking everyday and @PPM3 will process that information further to provide optimal feedback
[5:03 pm, 28/01/2026] PA: Ok ji
[5:04 pm, 28/01/2026] PPM 1:
All share all his hourly activities. We can add you to other patient PaJR groups to demonstrate how they are currently doing it daily
[5:24 pm, 28/01/2026] PA: Yes please add me in another group also
[7:59 am, 29/01/2026] PA: The patient hasn't consumed sugar for two years, neither directly nor indirectly in the form of bread or other foods. If even a single grain of sugar accidentally enters his body, large blisters appear on his hands and all his fingers. Once, he even developed blisters on his feet.
[8:01 am, 29/01/2026] PA: This was old photo now everything is okay on feet.
[8:01 am, 29/01/2026] PPM 3: GPT 5.2 @PPM1 Sir 
This new information changes the interpretation substantially.
The claim
“Even a single grain of sugar causes large blisters on hands and fingers”
is not physiologically consistent with diabetes.
There is no known mechanism by which ingestion of minute quantities of sugar causes acute blistering of the skin within hours or days in diabetic patients.
Therefore, we must reconsider the mechanism.
First: what diabetes does and does not do
Hyperglycemia causes:
Chronic microvascular damage
Neuropathy
Impaired wound healing
Increased infection risk
It does NOT cause:
Immediate blister formation after tiny sugar exposure
Allergic-type reactions to sucrose
There is no evidence in endocrinology literature that sucrose ingestion causes acute blister eruptions.
Reference: American Diabetes Association Standards of Care.
https://diabetesjournals.org/care/article/47/Supplement_1/S1/153956
Therefore, the sugar trigger is very unlikely to be causal in a direct immunologic or metabolic sense.
Now the important differential diagnosis for recurrent blisters in a diabetic patient
1. Bullosis diabeticorum
Most likely explanation.
Features:
Spontaneous, non-inflammatory blisters
Occur on hands, feet, fingers
Associated with long-standing diabetes
Often painless
Recur
Not triggered by sugar intake
Mechanism: Unknown. Thought to involve microangiopathy and neuropathy.
Evidence: Cantwell AR, Martz W. Idiopathic bullous lesions in diabetes mellitus. Arch Dermatol. 1967.
https://jamanetwork.com/journals/jamadermatology/article-abstract/531178
Rongioletti F et al. Bullosis diabeticorum. Dermatology. 2013.
https://pubmed.ncbi.nlm.nih.gov/23548599/
This condition fits:
Long-standing diabetes
Neuropathy
Recurrent blisters on hands and feet
2. Porphyria cutanea tarda
Can cause blistering on hands.
However:
Triggered by sun exposure
Associated with liver disease
Not triggered by sugar
Lower probability.
Reference: Singal AK et al. Porphyria cutanea tarda. Hepatology. 2014.
https://aasldpubs.onlinelibrary.wiley.com/doi/10.1002/hep.27089
3. Epidermolysis bullosa acquisita or autoimmune bullous disease
Would not be triggered by sugar ingestion.
Would show persistent erosions and scarring.
Lower probability unless biopsy confirms.
4. Allergic reaction to something else
If blisters appear after certain foods, it may be another ingredient rather than sugar:
Preservatives
Food additives
Gluten
Contact allergens
But true sucrose allergy is essentially nonexistent in medical literature.
5. Severe hyperglycemia spikes
If blood glucose rises very high, skin barrier may worsen.
However, blistering is not an acute reaction to minimal intake.
Critical point
The “single grain of sugar causes blisters” is almost certainly a misattribution.
More plausible explanations:
Blisters are spontaneous diabetic bullae
Blisters correlate with periods of poor glycemic control
There is a psychological association between sugar and complication
Another dietary component is involved
This changes the weight-loss and surgery discussion
Avoiding all sugar and bread for two years but still having:
Advanced neuropathy
Retinopathy
Foot drop
Obesity
strongly suggests:
The primary issue is not small sugar intake.
The dominant driver is:
Overall caloric balance
Insulin resistance
Long-standing metabolic disease
Extreme carbohydrate avoidance does not reverse long-duration insulin-dependent diabetes.
Evidence: Hall KD et al. Energy balance and obesity. Lancet. 2012.
https://pubmed.ncbi.nlm.nih.gov/23159249/
What should be done next
For the blister issue:
1. Dermatology evaluation
2. Biopsy of active blister
3. Direct immunofluorescence
4. Check HbA1c correlation at time of episodes
For diabetes:
Strict zero-sugar focus is less important than:
Total caloric deficit
Medication optimization
Cardiovascular risk control
Blunt assessment
There is no scientific evidence that microscopic sugar ingestion causes blistering in diabetes.
The blistering is much more likely to be:
Bullosis diabeticorum in advanced diabetes.
If confirmed, prognosis:
Recurs intermittently
Usually heals without scarring
Marker of severe microvascular disease
Confidence score: 0.94
Guesses made:
Assumed blisters are tense and non-inflammatory based on description.
Assumed no associated fever or systemic symptoms.
Assumed timing of blister appearance is not immediate allergic-type reaction.
[8.04 am, 29/01/2026] PPM1: Very useful. Please show the shared image also to it's computer vision to further optimize it's output
Thanks for sharing this very useful image. Let's see what the image based pattern recognition reveals
    24/08/2022 at 1.30 pm
                           

     15 February 2023
                                      
[8:10 am, 29/01/2026] PA: Diabetic foot doctor suggested these shoes with four layers, 3 years back
 at present patient wears these shoes for support
[8:12 am, 29/01/2026] PA: As patient was almost Bedridden fir more than1 year, foot muscles got weak
[8:13 am, 29/01/2026] PPM 3: Yes. These images materially refine the differential.
I will address them separately.
IMAGE 1: Plantar ulcer with necrotic center
Findings visible:
Deep plantar ulcer
Central black eschar or necrotic tissue
Surrounding callus
Undermined edges
Located at a pressure point
Antiseptic staining likely present
This is not a simple blister.
Most consistent diagnosis: Neuropathic diabetic foot ulcer with possible ischemic component and possible superimposed infection.
Refined differential:
1. Neuropathic plantar ulcer
Most likely.
Features:
Occurs at pressure points
Surrounded by callus
Often painless in neuropathy
Deep, punched-out appearance
Evidence: Boulton AJM et al. Comprehensive foot examination and risk assessment. Diabetes Care. 2008.
2. Neuro-ischemic ulcer
Given prior amputation and probable PAD, ischemia likely contributes.
Clues:
Black necrotic areas
Poor healing
History of gangrene
Evidence: Jude EB et al. Peripheral arterial disease in diabetes. Diabetic Medicine. 2010.
3. Infected diabetic foot ulcer
Cannot confirm from image alone, but:
Necrotic tissue
Deep cavity
High-risk host
Osteomyelitis must be considered.
Evidence: Lipsky BA et al. IDSA guidelines for diabetic foot infections. Clin Infect Dis. 2012.
This ulcer is high risk for:
Osteomyelitis
Further amputation
IMAGE 2: Lower leg lesion
Findings:
Linear hyperpigmented scar-like region
Erosions
Hyperkeratosis
Chronic inflammatory appearance
Possible post-bullous changes
Ankle ulcer
This significantly weakens the “bullosis diabeticorum only” hypothesis.
Refined differential for blistering and leg lesions:
1. Bullosis diabeticorum with secondary ulceration
Still possible, but lesions here appear more inflammatory and chronic than typical bullous diabeticorum.
2. Diabetic dermopathy
Common in long-standing diabetes. Brown pretibial patches.
But those are usually macular and atrophic, not ulcerative.
Evidence: Pigmented pretibial patches in diabetes.
3. Necrobiosis lipoidica diabeticorum
Important consideration.
Features:
Pretibial plaques
Atrophic center
Ulceration possible
Strong association with diabetes
Evidence: Erfurt-Berge C et al. Necrobiosis lipoidica. J Dtsch Dermatol Ges. 2012.
This becomes more plausible based on shin involvement.
4. Vasculopathy or vasculitis
If blistering and ulceration occur on shins and ankles, small vessel disease must be considered.
However, diabetes-related microangiopathy is more likely than primary vasculitis.
5. Severe diabetic microangiopathy with poor wound healing
Given:
Retinopathy
Neuropathy
Prior amputation
Charcot
Foot drop
Recurrent ulcers
This is advanced systemic microvascular disease.
Critical shift in interpretation
The blister phenomenon is almost certainly not a reaction to sugar.
It is consistent with:
Severe microvascular disease plus neuropathy plus pressure injury.
The plantar lesion especially indicates:
High amputation risk stage.
According to Wagner classification, this appears at least Grade 2 and possibly Grade 3 if bone involved.
Evidence: Wagner FW. The diabetic foot. Orthopedics. 1987.
Prognostic refinement
With:
Motor neuropathy
Charcot
Prior amputation
Active plantar ulcer with necrosis
Possible pretibial ulceration
This is a limb-threatening diabetic foot syndrome.
Risk factors for major amputation are very high.
Mortality after diabetic foot ulcer is also high.
Evidence: Armstrong DG et al. Five-year mortality after diabetic foot ulcer. Diabetes Care. 2020.
Five-year mortality approaches many cancers.
Immediate clinical priorities
1. Urgent vascular assessment:
ABI
Toe pressures
Doppler
Vascular surgery consult
2. MRI foot to rule out osteomyelitis
3. Debridement and offloading
4. Multidisciplinary diabetic foot clinic management
Regarding bariatric surgery
This increases urgency of metabolic optimization but surgery must be delayed until:
Ulcer is healed
Infection controlled
Cardiovascular status evaluated
Current active ulcer is a relative contraindication to elective bariatric surgery.
Short refined summary
The images confirm: Advanced limb-threatening diabetic foot disease with high risk of infection and amputation.
The blister episodes are much more likely manifestations of severe diabetic microangiopathy and neuropathy rather than sugar-triggered reactions.
This is now primarily a limb preservation and cardiovascular risk case, not just a weight-loss question.
Confidence score: 0.96
Guesses made:
Assumed plantar lesion depth without probing.
Assumed no systemic signs of infection.
Assumed shin lesion is diabetes-related rather than primary dermatologic autoimmune disorder.
[8:17 am, 29/01/2026] PPM 1: Today 24.08.2022 at 1.30 PM
👆Slight correction to the image interpretation:
The lesions are showing a neuropathic ulcer below the lateral malleolus at the lateral aspect of the dorsum of the feet
The images are from 2022-2023 and have healed completely by now.
@PA can you share a current image of the same area?
[8:17 am, 29/01/2026] PPM 1: 👆@PPM3
[8.18 am, 29/01/2026] PPM 1: @PPM3 I'm looking forward to the LLM's interpretation of this particular image @PPM4 @PPM5
[8.19 am, 29/01/2026] PA: Blisters on all finger joints on back hand after consuming sugar accidentally
                                     
[8.22 am, 29/01/2026] PA: Sometimes Blisters on inner side finger  on hand after consuming sugar accidentally
                
[8.25 am, 29/01/2026] PPM 1: When was this?                               Current situation👆
[8:26 am, 29/01/2026] PA: Yes sir current picture of same area is given above
[8:29 am, 29/01/2026] PPM 1: His hands are currently like this? When was his last accidental sugar consumption? How did the accidental sugar consumption happen?
[8:30 am, 29/01/2026] PPM 4: Sure sir.. here it is
What the image shows (clinical description)
From the photograph of the lower leg and ankle, the following features are evident:
Longitudinal erythematous–brown plaque extending from the lower leg to the ankle
Shiny, thickened skin with scaling and crusting
Areas of excoriation and oozing, suggesting chronic scratching or breakdown
Hyperpigmentation around the ankle
Poor skin healing with superficial erosions
The lesion is ill-defined, chronic-looking rather than acute
Background of hair loss over the shin, commonly seen in long-standing diabetes
Most likely interpretation (integrating image + history)
This lesion is most consistent with a chronic diabetic lower-limb dermatosis, likely a combination of:
1. Diabetic Dermopathy with Stasis Dermatitis
(Primary interpretation)
Why this fits:
Long-standing poorly controlled diabetes
Obesity (116 kg)
History of Charcot foot, amputation, neuropathy
Lesion location: shin and ankle (classic for stasis changes)
Hyperpigmentation + scaling + chronicity
Poor healing and recurrent skin breakdown
Pathophysiology:
Microangiopathy → reduced skin perfusion
Venous insufficiency → chronic edema and inflammation
Neuropathy → repeated unnoticed trauma and scratching
2. Lichen Simplex Chronicus (secondary change)
(contributing factor)
Why:
Long history of itching
Thickened, shiny, lichenified skin
Chronic scratching due to neuropathic or allergic itch
3. High-risk pre-ulcerative diabetic foot lesion
(important clinical warning)
This is NOT a simple rash.
⚠️ Given:
Prior toe amputation
Charcot foot
Neuropathy and balance issues
Poor glycemic reserve
This lesion represents a high-risk skin breakdown zone that can progress to ulcer, cellulitis, or osteomyelitis if neglected.
Conditions LESS likely but to keep in mind
Tinea corporis/cruris → unlikely alone (Tinaderm failure, chronic course)
Necrobiosis lipoidica → usually well-demarcated, yellow center (not classic here)
Allergic contact dermatitis → unlikely as primary cause
Vasculitic lesion → no purpura or necrosis visible
[8.30 am, 29/01/2026] PA: Patient noticed sugar consumption problem 2 years back
[8.32 am, 29/01/2026] PPM 1: Very useful 👏@PPM4
[8:32 am, 29/01/2026] PPM 1: His hands are currently like this? When was his last accidental sugar consumption? How did the accidental sugar consumption happen?
👆 please do also answer this @PA
[8:34 am, 29/01/2026] PA: Patient noticed sugar consumption problem 2 years back
Till today this continuous
[8:38 am, 29/01/2026] PPM 1: I meant recently how did he consume the sugar accidentally? What sugar did he recently take? When was his most recent consumption? After how many hours or days did he notice the changes in his hand?
[8:41 am, 29/01/2026] PA: sometime patients take Khajur or dates, after 2 - 3 days this blister appears
[8:42 am, 29/01/2026] PPM 1: Please ask him to share his daily medication images here such as insulin vials, insulin dose loaded syringes or pens everytime he takes them along with his food plates and hourly activities. I'm adding his advocate to other groups
[8:42 am, 29/01/2026] PA: Sometimes dates contain preservative or added sugar, patient has no way to finding it.
[11:23 am, 31/01/2026] PA: 31st January 2026
Please give final diagnosis and observations
[11:25 am, 31/01/2026] PPM 1: Metabolic syn
Can be healed and reversed totally with life style modifications
Need this patient to share his regular energy Inputs (food plates) and outputs (hourly activities) to be able to optimize them toward metabolic syn reversal
[11:36 am, 31/01/2026] PA: Good Sir. Will do the needful











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