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.

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