Aims:
- Identify cirrhosis based on blood tests-
- Understand why platelets are low in #cirrhosis
- Describe the plt’s role in the #cirrhotic#coagulopathy
The hepatologist's dream:
identify patients with cirrhosis before complications like HCC and variceal bleeding.
Enter the platelet count
Shout out to JAMA's Rational Clin Exam Series & Udell et al's big beautiful systematic review ncbi.nlm.nih.gov/pubmed/22357834
Platelets are low in #cirrhosis.
We can use this to our advantage - even sparing biopsies.
Be like Britain:
Even in their guidelines for the evaluation of elevated ALT, the brits make a plea for looking at platelet-based scores the minute you realize ALT abnormal (ncbi.nlm.nih.gov/pmc/articles/P…)
Temporarily: super cool 1966 study from Aster (Fig 1)
-Radiolabel platelets
-inject epi(!)
-radiotracer shifts spleen to blood ncbi.nlm.nih.gov/pmc/articles/P…
2. Cirrhosis is a pro-inflammatory state which is bad for platelets
Endotoxin from the gut circulates, stimulating immune responses.
As total IgG 🔼, so does anti-platelet antibodies (Fig1)
Reduced spleen volume 🔽 anti-plt IgG (Fig2)
Reduced endotoxin may 🔼plts (Fig3)
Wild?
3. The hormone for platelet growth - thrombopoetin (TPO) - comes from, you guessed it, the liver
Fig 1: replace the liver, 🔼TPO, 🔼platelets
Fig 2: TPO levels and plts by stage of fibrosis
Fig 3: 🔼TPO activity, raise plts
Act 3:
So what does this have to do with the cirrhotic coagulopathy?
Platelets rule!
The platelet is the MVP of the first phase of hemostasis:
Need it to stick, aggregrate, and activate on the vessel wall.
It even catalyzes the coag cascade!(Fig 1)
In cirrhosis, thrombin generation is preserved, independent of INR, until plts are superlow(Fig2)
Platelets are quantitatively AND qualitatively defective in cirrhosis
1. Cirrhosis 🔽 platelet adhesion (fig 1) 2. Cirrhosis 🔽 platelet aggregation in response to stimulus (fig 2-3) 3. Cirrhosis platelets 🔽activation (they are metabolically "exhausted")(Fig4)
Well I hope you enjoyed this platelet rich tweetorial. And I hope it helps you identify #cirrhosis.
Despite all this coagulopathy talk, some parting words.
None of this should stop you from:
Fig1: Doing that para
Fig2: Banding that varix
Fig3: Placing that central line
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Hepatology is awesome, exciting, but also humbling.
Nowhere is that clearer than HRS, a true unmet need for patients with ascites
Aims 1. What 2. Why 3. How to prevent/treat 4. ❤️ #cirrhosis physiology
What: 1. Ascites trashes QOL & is deadly enough to merit mention in the bible(Fig1) 2. Ascites physiology damages other organs; Austin Flint said it 1st (Fig2) 3. HRS is the knockout punch of portal hypertension. What begins as elevated portal mmHg and ascites ends as HRS(Fig3)
What: 1. HRS is not rare in pts w/ascites (Fig1) 2. HRS is deadly (Fig2) 3. For a definition of terms, check out the Ascites Club (that's a thing!)
ref: gut.bmj.com/content/gutjnl…
or see my review: amjmed.com/article/S0002-… (Fig3)
Hepatic encephalopathy in the hospital (An ode to #lactulose):
A brief #livertwitter#tweetorial
Aims: 1. Share the greatest t-shirt ever made 2. Rule out infection! 3. Laxation now! But how?
1. This shirt, made by a patient, reminds us:
▶️HE is horrible, unpredictable
▶️Preventing HE is hard
▶️Dont be quick 2 label pts as 'noncompliant' - there's more to the story
▶️Our patients are awesome. Hepatology is the best
Aims
Try to answer this question while also showing 1) Ammonia levels dont matter 2) U should not restrict protein in patients with HE
Keywords: "ammonia hypothesis", sarcopenia
First, a poll:
Does Ammonia cause hepatic encephalopathy?
How did NH3 get involved with #HE in the first place?
Step 1: In 1877 Eck develops the first successful vascular anastamosis, a portocaval shunt. ncbi.nlm.nih.gov/pubmed/9186464
Step2: Pavlov improves it
Step3: Dogs get goofy after eating meat:"Meat stupor"
Step4: What's up with meat!?