Showing posts with label Hepatobiliary system. Show all posts
Showing posts with label Hepatobiliary system. Show all posts

Sunday, May 16, 2021

Fact of the day - halothane hepatotoxicity


A patient with biliary stones who's undergone laparoscopic cholecystectomy may develop signs of hepatotoxicity between 2 days - three weeks post-op. due to halothane. The mechanism is this anesthetic's biotransformation to reactive metabolites through P450.

At risk category of patients are females more than 40 years of age.
Labs show elevated AST and ALT.
Hepatitis is relatively rare.

Other effects:

- Cardiac arrhythmias

- malignant hyperthermia

- hypertension

That's all

- Jaskunwar Singh

Saturday, May 8, 2021

Friday, May 7, 2021

Simvastatin combination with fibrates in clinical practice


High-yield in clinical practice:

DO NOT combine simvastatin with gemfibrozil (class-X interaction; high risk of acute liver damage and rhabdomyolysis). Inhibition of CYP450 enzyme by gemfibrozil plays the role in increasing levels of simvastatin 2-3x.

Combination of simvastatin with fenofibrate is relatively safer, although close observation and regular monitoring is required (class-C interaction). Serum levels of simvastatin remain unchanged.

- Jaskunwar Singh

Tuesday, March 31, 2020

Acute Liver Failure in a nutshell.

Acute Liver Failure is defined as the acute onset of severe liver injury with encephalopathy and ↓ synthetic function (INR ≥ 1.5 ) in a patient without  cirrhosis or underlying known liver disease.

Acute Liver Failure.

Wednesday, December 18, 2019

Hepatorenal Syndrome: An Overview

Hello good folks! Let's discuss HepatoRenal Syndrome (HRS) in brief.

Cirrhosis + Ascites + Renal Failure = HRS, after excluding other causes of kidney damage.

How common is HRS?
1 in 10 patients of advanced cirrhosis or acute liver failure develop HRS.

How does HRS happen?
Abnormal haemodynamics, that's how. Pathogen, faulty immune system and mesenteric angiogenesis result in splanchnic and systemic vasodilation but renal vasoconstriction. Other factors maybe contributory.

Types and management
Type 1: Rapidly progressive, median survival about 2 weeks. Haemodialysis may be required.

Type 2: Slowly progressive, median survival about 6 months. Transjugular Intrahepatic Portosystemic Shunt (TIPS) maybe required.

Liver and/or kidney transplant maybe considered for both types.

Thanks for reading.
Ashish Singh.

Saturday, November 2, 2019

What's Wrong With My Gallbladder, Doc?

A quick mini-post to help you make a quick diagnosis.

[Please click on the image to enhance it]

Please remember to practise caution as the presentations may overlap.

Thank you for reading.

Ashish Singh

Friday, March 22, 2019

Mnemonic: Incubation Period of Hepatitis

Hey guys, here’s a simple little mnemonic to remember the incubation period of various hepatitis infections.

Rule of 4 to 8:
Hep A - 4 weeks
Hep E - 5 to 6 weeks
Hep C - 7 weeks
Hep B/D - 8 to 12 weeks

Pay attention to the order of Hep infections from 4 to 8.

Why A&E first? That’s because they enter through the mouth (feco-oral mode of transmission) and your mouth is the first part of your GI.

Remember, Hep D co-infects or super-infects Hep B.

- Ashish Singh

Thursday, November 22, 2018

Stones in Crohn's disease

Hello everyone, 

In this post, I'll be talking about the different types of stones seen in Crohn's disease. Let's learn why they form! 

CHOLESTEROL GALLSTONES: Either due to ileal involvement or ileostomy, in Crohn's, enterohepatic circulation of bile acids is perturbed resulting in supersaturation of bile with the cholesterol, altering the delicate composition of bile acids, phospholipids, and cholesterol of 10:3:1 in bile fluid.

CALCIUM BILIRUBINATE GALLSTONES: Due to alteration in colonic flora conjugated bilirubin is converted to unconjugated bilirubin, which along with seepage of excessive unabsorbed bile acids from the ileum, results in enhanced absorption of bilirubin from the colon causing increased concentration in bile.

Usually, calcium in the GI tract forms a complex with oxalate ions resulting in its excretion in stool but in Crohn's due to steatorrhea excessive unabsorbed negatively charged fatty acids bind with calcium, leaving unbound oxalate to be absorbed and subsequently excreted by urine causing nephrolithiasis.

URIC ACID RENAL STONES: Diarrhea in Crohn's causes metabolic acidosis due to decreased bicarbonate absorption or increased excretion from the colon which increases the acidity of tubular fluid. The increased acidity, simultaneous dehydration, hypocitraturia, and hypomagnesemia in such patients precipitate uric acid stones.

-Kirtan Patolia

Wednesday, November 1, 2017

MELD score mnemonic

Hello everyone!

Model for End-Stage Liver Disease (MELD) The Model for End-Stage Liver Disease (MELD) is a reliable measure of mortality risk in patients with end-stage liver disease. It is used as a disease severity index to help prioritize allocation of organs for transplant.

MELD uses the patient's values for serum bilirubin, serum creatinine, and the international normalized ratio for prothrombin time (INR) to predict survival. Sodium was recently added to improve predictive value.

Wednesday, July 26, 2017

Acute Pancreatitis - Mnemonic

Hello Awesomites!
Here's a Mnemonic on the causes of Acute Pancreatitis.
The mnemonic is- GET SMASHED

G- Gall Stones
E- Ethanol (Alcohol consumption)
T- Trauma
S- Steroids
M- Mumps
A- Autoimmune
S- Scorpion stings
H- Hyperlipidemia /Hypercalcemia
E- ERCP (Iatrogenic)
D- Drugs

I hope that this is useful for you guys.
Thank you.

MD Mobarak Hussain (Maahii)

Saturday, June 10, 2017

Jaundice Syndromes : Mnemonic

Hey everyone. Just a short post on how to remember the Jaundice Syndromes.


Remember :
(As in the CGI special effects in movies.)

C - Criggler Najjar Syndrome
G - Gilbert Syndrome
I  - Indirect Jaundice ( Unconjugated Bilirubin).

So this would make Dublin Johnson and Rotor Syndromes Direct Jaundice.

Another useful fact :
All are inherited as Autosomal recessive trait except Gilbert and Criggler Najjar 1.

Hope this helped !
Happy studying.
~ A.P.Burkholderia

Monday, May 22, 2017

Fact of the day: Marchiafava-Bignami disease

Marchiafava-Bignami disease is a rare disorder of demyelination or necrosis of the corpus callosum and adjacent subcortical white matter that occurs predominantly in malnourished alcoholics. Dementia, spasticity, dysarthria, and inability to walk may present as an acute, subacute or chronic condition.

Lesions appear as hypodense areas in portions of the corpus callosum on CT and as discrete or confluent areas of decreased T1 signal and increased T2 signal on MRI. Alcohol abusers without liver disease, amnesia, or cognitive dysfunction show thinning of the corpus callosum at autopsy and on MRI, suggesting that alcohol or malnutrition damages the corpus callosum commonly in the absence of the necrotic lesions of Marchiafava-Bignami disease.

Interesting, isn't it?

Wednesday, May 10, 2017

Acalculous cholecystitis notes


Let's learn about Acalculous cholecystitis today. These are my step 2 CK notes, made from UpToDate.

What is acalculous cholecystitis?

Acalculous cholecystitis is an acute necroinflammatory disease of the gallbladder with a multifactorial pathogenesis. It is typically seen in patients who are hospitalized and critically ill.

Clinical features:
In critically ill patients, the appearance of unexplained fever, leukocytosis, or vague abdominal discomfort may be the only sign of acalculous cholecystitis. Patients may also have jaundice or a right upper quadrant mass. Laboratory test abnormalities may include a leukocytosis or abnormal liver tests, but they are nonspecific.

Diagnosis: USG.

Advantages of ultrasonography are that it is noninvasive, can be done at the bedside, and has good sensitivity and specificity for diagnosing acalculous cholecystitis. In addition, ultrasonography may reveal alternative diagnoses (such as calculous cholecystitis). Thickening of the gallbladder wall is the most reliable feature seen in patients with acalculous cholecystitis.

Ultrasonographic features:
●Absence of gallstones or sludge
●Thickening of the gallbladder wall (>3 mm)
●Pericholecystic fluid
●Striated gallbladder
●A positive Murphy's sign induced by the ultrasound probe (may be absent in patients who are obtunded or sedated)
●Mucosal sloughing
●Gallbladder distension (>5 cm).

In patients with acalculous cholecystitis, we recommend the initiation of broad spectrum antibiotics as soon as blood cultures have been drawn.

Infection with enteric pathogens, including E. coli, E. faecalis, Klebsiella, Pseudomonas, Proteus species, and Bacteroides is common.

Preferred surgery: Cholecystostomy rather than cholecystectomy.


Cholecystostomy is effective and is less invasive than cholecystectomy. (especially in critically ill patients.)

However, cholecystectomy should be performed if there are findings suggesting gallbladder necrosis, emphysematous cholecystitis, or perforation. Cholecystectomy is also a reasonable alternative in patients who are good surgical candidates.

That's all!

Wednesday, February 8, 2017

Alcohol and Drug Interactions: 4th Part

Hii friends...

This is the last post in the series: Alcohol and Drug Interactions. The previous posts in this series were Disulfiram-like Reaction2nd Part, and 3rd Part.

With Warfarin

1. Binge drinking- Leads to inhibition of warfarin metabolism by CYP450 enzyme system. So it can precipitate warfarin toxicity with increased bleeding tendency in the body.

2. Chronic Alcohol consumption- Leads to induction of CYP450 enzyme system, so increases metabolism of Warfarin in the liver. So higher than usual dose of warfarin is needed to exert appropriate anticoagulant action in the patient.

With Opioids

Alcohol increases the sedative effects and also increases the risk of respiratory depression. It also attenuates cough reflex and gag reflex, so the patients have a higher risk of getting food stuck in their respiratory tract, remember Cafe Coronary.


1. NSAIDs have been implicated in an increased risk of ulcers and gastrointestinal bleeding in elderly
people. Alcohol may exacerbate that risk by enhancing the ability of these medications to damage the
stomach mucosa.

2. Alcohol also potentiates the antiplatelet actions of Aspirin, hence increase the risk of bleeding in the patients.

3. Intake of alcohol with acetaminophen can increase the risk of acetaminophen-related toxic effects
on the liver. Acetaminophen breakdown by CYP2E1 (and possibly CYP3A) results in the formation of a toxic product(NABQI) that can cause potentially life-threatening liver damage. As mentioned earlier, heavy alcohol use enhances CYP2E1 activity. In turn, enhanced CYP2E1 activity increases
the formation of the toxic acetaminophen product. In people who drink heavily or who are fasting
(which also increases CYP2E1 activity), liver injury may occur at doses as low as 2 to 4 grams per day.

That concludes this series. I hope it will help you to guide your patients towards drinking alcohol more judiciously. :p


Alcohol and drug interactions: 3rd part

Hey, guys.....

This is the third post in the series, Alcohol and drug interactions. The other posts are Disulfiram-like Reaction2nd Part and 4th Part.

With Antihistaminics

Alcohol increases the risk of sedation, drowsiness and falls, especially in the elderly population and with the 1st gen antihistaminics.

With Barbiturates and Benzodiazepines

Alcohol acts synergistically with them to increase their sedative effects and memory-impairing effects( This memory-impairing effect is misused in Date Rape drug, Flunitrazepam(Rohypnol)). Besides it also inhibits their metabolism in the liver, hence, increasing the drug's levels in the blood.

With H2-Receptor Antagonists

These agents(eg., Cimetidine, Ranitidine) inhibit the action of Alcohol dehydrogenase(ADH) present in gastric mucosa.  Cimetidine may also increase the rate of gastric emptying hence increasing the absorption of alcohol. So both of these effects contribute to increasing the Blood Alcohol levels.

With Muscle Relaxants

Several muscle relaxants (e.g., carisoprodol, cyclobenzaprine, and baclofen), when taken with alcohol, may produce a certain narcotic-like reaction that includes extreme weakness,
dizziness, agitation, euphoria, and confusion. For example, carisoprodol is a commonly abused and readily available prescription medication that is sold as a street drug. Its metabolism in the liver generates an anxiety-reducing agent that was previously marketed as a controlled substance (meprobamate). The mixture of carisoprodol with beer is popular among street abusers for creating a quick state of euphoria.

That's all!


Alcohol and Drug Interactions: 2nd part

Hey guys,

This is a continuation of the previous post on Disulfiram-like Reaction.

Let us start with a basic info. Pharmacokinetic drug interactions with alcohol are only seen in heavy drinkers whereas Pharmacodynamic drug interactions can be seen in moderate drinkers and even after a single episode of drinking. 

With Antibiotics

As already mentioned, the Disulfiram-like reaction can occur with Isoniazid, Cefotetan, Cefamandole, Cefoperazone, Chloramphenicol, Sulfamethoxazole, Sulfisoxazole.

Besides patients on Isoniazid should abstain from drinking alcohol since isoniazid is hepatotoxic and the liver damage can be exacerbated by concurrent alcohol consumption

With Antidepressants

1. With TCAs: Alcohol increases the sedative action of TCAs, especially Amitriptyline, Doxepin etc.
Alcohol also impairs the first-pass metabolism of Amitriptyline in the liver causing increased bioavailability of the drug. Excessive increase in levels of TCAs in the blood can precipitate convulsions and cardiac arrhythmias.

2. Among SSRIs, all are relatively safer with alcohol; the safest being Fluoxetine.

3. With MAOIs(eg., Phenelzine, Tranylcypromine): There can be severe high BP(cheese reaction) if taken together with red wine which contains Tyramine.

That's all! :)
Do go through the subsequent posts in this series, 3rd Part and 4th Part.