🧵 Why every Gastroenterologist & Hepatologist should be comfortable prescribing for Alcohol Use Disorder (AUD) in CLD patients : a thread 🧵 1/ Abstinence is the only disease-modifying therapy for alcohol-related liver disease (ALD).
There is no antifibrotic, no disease-specific drug, no transplant workaround that compensates for continued alcohol use.

I’m a Gastroenterology SR.
Here Are 10 Questions That Expose the ‘Gut Health’ Myth.
A must read thread 🧵 1/ You keep saying “good gut health,” but could you please define what gut health actually means in clinical terms?
What are your measurable parameters ? microbial diversity? stool frequency? SCFA output? mucosal immunity markers?
Because in evidence-based gastroenterology, there’s no standardized biomarker for so-called “gut health.”

🧵 For everyone arguing about protein :- whether for or against: a thread 🧵 1/ Core Idea: Muscle Protein Synthesis (MPS) is not linear

•Most people imagine: the more protein I eat, the more muscle I build.
•Wrong. MPS is saturable.
•It follows a dose–response curve:
•Small protein → small rise.
•20–25 g high-quality protein → maximum rise.
•Beyond that → no further muscle gain in that meal.
•This upper limit is called the “MPS ceiling”.

🧵 ALT vs AST :- Significance of zonation in interpreting patterns of enzyme elevations
A thread 🧵- 1/ The puzzle:
Every physician knows ALT & AST go up in liver disease.
But why ALT sometimes > AST… and other times AST > ALT?
The secret lies in liver zonation.

How to take “Alcohol History” in Liver Disease (for students & residents)
🧵
Disclaimer: This is my method of history taking. You can modify it as per your needs. 1. Start with the type of alcohol

Ask: What do you usually drink : whisky, rum, vodka, beer, wine, arrack, or country liquor?

A special thread 🧵

My understanding of Hepatic encephalopathy (HE)–nutrition–muscle–ammonia in Cirrhotics
#MedTwitter 1/n Simple picture :-

•Ammonia is produced in the gut and must be detoxified.

•The LIVER is the main detox organ (urea cycle); MUSCLE is the backup (converts ammonia to glutamine via glutamine synthetase).

•In cirrhosis, liver capacity falls → the muscle has to help more. If muscle is lost (sarcopenia), ammonia rises and HE worsens.

Coconut Oil in Chronic Pancreatitis: My Evidence based take 🧵
1/ I do not routinely advise coconut oil in chronic pancreatitis (CP).
Optimize PERT and keep a normal-fat diet.
Consider MCT oil (C8/C10) only if steatorrhea persists despite adequate PERT.
Coconut oil ≠ MCT therapy. 2/ Why normal fat with PERT?
Modern guidance: avoid very-low-fat diets;
dose PERT with meals/snacks and titrate. When PERT is adequate, fat restriction is unnecessary.

Starbucks Diarrhea: It’s not just the caffeine. 🧵
Ever wonder why your patient gets sudden post-coffee urgency or loose stools?
It’s not IBS. And it’s not just caffeine.
Let’s break it down. 🧵 - Caffeine is a colonic stimulant, yes.
•It increases colonic motor activity via adenosine receptor antagonism.
•But interestingly, decaf can also cause diarrhea.
Why? Because there’s more to coffee than caffeine.

🧵 Understanding ALBUMIN in Liver disease : What matters is not just Quantity but QUALITY
A thread 🧵 : 1/
Human Serum Albumin (HSA) is widely used in patients with cirrhosis ( for ascites, spontaneous bacterial peritonitis (SBP), & hepatorenal syndrome)
But what many do not know is:
There are different types of albumin in the blood, and not all of them are functional.

Basics of Acute Pancreatitis & Atlanta Classification terminology - a thread 🧵

1/14
The Atlanta Classification was first proposed in 1992 to standardize terminology in AP
over time, some terms became confusing hence, it was revised in 2012 to reflect better understanding . 2/14
Despite the revision, radiology reports still often misuse terms.
One of the most misused?
‘Pseudocyst’ = incorrectly applied to many pancreatic collections, leading to mismanagement.

Standardized terminology matters. Here’s how:

A patient presented today with cholestatic liver injury after 2 months of taking these herbal formulations. 📸⬇️

Among the ingredients, case reports have linked the following to hepatotoxicity:
✅ Tinospora cordifolia (Guduchi) – Immune-mediated cholestatic hepatitis
✅ Commiphora wightii (Guggul) – Cholestatic liver injury
✅ Withania somnifera (Ashwagandha) – DILI with cholestatic pattern

1/n
Stepwise clinical interpretation of pH-Impedance for Gastroenterology trainees : A thread 🧵

pH-impedance isn’t just about reading software outputs . It’s about understanding reflux physiology and applying it clinically. Let’s go step by step. 2/
Step 1: How Impedance detects bolus movement
•The catheter has multiple impedance sensors along its length.
•Impedance (Z) = Electrical resistance to flow.
•Conductivity (σ) = How well current flows (inverse of impedance).

Thread 🧵: Managenent of Diabetic Ketoacidosis (DKA) & Hyperosmolar Hyperglycemic State (HHS)

This SOP is based on how I used to treat DKA - a condition I loved to manage. You may actually find this very useful in clinical practice.

Let’s begin! 🧵 1️⃣ Triad of DKA:
•Hyperglycemia
•Acidosis
•Ketosis

C/F:
•Dry skin/mucous membranes
•⬇️JVP
•Kussmaul breathing (deep, rapid respiration)
•⬇️mental function
•Nausea, vomiting, anorexia
•Acute abdominal pain
•Weakness, lethargy
•Polyuria,polydipsia

🧵 Standard Operating Procedure for Organophosphorus (OP) Poisoning management ,

Step 1: Confirm the Diagnosis
1️⃣ History & Clinical Suspicion
2️⃣ Serum Butyryl Cholinesterase Activity
3️⃣ RBC Acetylcholinesterase Activity Clinical Presentation:
☠️ Muscarinic Symptoms – Bronchospasm, bronchorrhea, miosis, lacrimation, urination, diarrhea,hypotension, bradycardia, salivation,vomiting.

☠️ Nicotinic Symptoms – Tachycardia, mydriasis, hypertension, sweating, muscle weakness, paralysis, fasciculations.

Thread 🧵 : Hypoglycemia in Alcoholism

1/
Hypoglycemia in alcoholism = 🚫 gluconeogenesis
Key :- Ethanol metabolism → ↑NADH/NAD⁺ ratio disrupts gluconeogenesis

Let’s understand :- 2/
Pathway:
Ethanol → Acetaldehyde (via alcohol dehydrogenase) → Acetate (via acetaldehyde dehydrogenase)

➡️ Both steps consume NAD⁺ and generate NADH