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GI Week 4 > Lecture 41: Complications of End-Stage Liver Disease > Flashcards

Lecture 41: Complications of End-Stage Liver Disease Flashcards

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1
Q

What is the difference between compensated and decompensated cirrhosis?

A

Former = cirrhosis is present but liver functioning well…asymptomatic
Latter = end-stage liver disease, cirrhosis present and liver is NOT functioning well
-symptomatic, indication for liver transplantation

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2
Q

What is portal hypertension due to?

A

Pressure = R x Q (resistance x blood flow)

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3
Q

Does cirrhosis mean endstage liver disease?

A

No it does not

You can have cirrhosis and not have ESLD

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4
Q

How can you tell if ascites is due to infection vs. cirrhosis?

A

Use the Serum albumin ascites gradient (SAAG)
Serum albumin – Ascites albumin = SAAG
If SAAG > 1.1 mg/dL, then cirrhosis and portal hypertension
If SAAG < 1.1 mg/dL, then infection or cancer

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5
Q

What are the major complications of portal hypertension (ESLD)?

A
  1. Ascites
  2. Gastroesophageal varices
  3. Spontaneous bacterial peritonitis
  4. Portosystemic Encephalopathy
  5. Hepatorenal syndrome
    Key point: Nitric oxide leads to activation of vasoconstrictors (like RAA system) which leads to impaired sodium excretion
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6
Q

What are causes of ascites?

A
  1. malignancy
  2. TB
  3. Cirrhosis
  4. Congenital heart failure
  5. starvation
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7
Q

What is the treatment for ascites?

A
  1. low salt diet
  2. diuretics (spironolactone)
  3. large volume paracentesis
  4. TIPS (transjugular intrahepatic portosystemic shunting
    REFER FOR LIVER TRANSPLANT NINJAAA
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8
Q

What are the different degrees of survival in ascites?

A
  1. average = 2 years
  2. refractory ascites = unresponsive to diuretics and requires large volume paracentesis (6 months)
  3. hepatorenal syndrome = 6 weeks survival
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9
Q

What is hepatorenal syndrome?

A

Acute renal insufficiency in the setting of end-stage liver disease WITHOUT an alternative diagnosis

  • no improvement after stopping diuretics/IV replacement
  • look for alternative explanation such as infection, etc
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10
Q

What is the pathophys of hepatorenal syndrome?

A

Dysregulation of vasoactive hormones
TOO MUCH VASOCONSTRICTION
Associated with refractory ascites
Requires transplant but only have 6 weeks

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11
Q

What are the key characteristics of spontaneous bacterial peritonitis?

A

When ascites becomes infected
Presentation can be insidious
>250 PMN is diagnostic
Infection is ONLY 1 organism
If you have >1, that means you have perforated bowel
SAAG > 1.1 because you HAVE TO HAVE PORTAL HYPERTENSION
Remember, SAAG <1.1 means there is INFECTION that causes ascites, but it does NOT mean there is bacteria present in the ascites…Nahmean?

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12
Q

What are the symptoms of SBP (spontaneous bacterial peritonitis)?

A
  1. fever
  2. abdominal pain
  3. mental confusion
  4. renal failure
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13
Q

What are the most common organisms in spontaneous bacterial peritonitis (SBP)?

A
  1. E. coli
  2. Klebiellla
  3. Streptococcus
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14
Q

What is the treatment for SBP?

A
  1. antibiotics
  2. give IV albumin to protect kidneys from renal failure
  3. Need antibiotics to prevent recurrence
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15
Q

What is the quintessential complication of portal hypertension?

A

Varices
Blood is trying to find an easier route back to heart
Esophageal and gastric varices

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16
Q

What do cherry red spots mean?

A

It means that shit bled already so you need to keep an eye out for rebleeding varices

17
Q

What does size of varices tell you?

A

Larger varices = more likely to bleed

18
Q

What is the pathophysiology for non-selective beta blocker treatment for esophageal varices?

A

NON-SELECTIVE beta blocker like propranolol or nadolol
Beta2 is inhibited, thereby allowing for unopposed alpha adrenergic response
Alpha adrenergic response = vasoconstriction of SPLANCHNIC vessels = DECREASED portal inflow = DECREASED portal pressure

19
Q

What are the treatments for esophageal varices?

A
  1. non-selective beta blockers (propranolol and nadolol)
  2. Octreotide (splanchnic vasoconstrictor)
  3. Band ligations
  4. TIPS
  5. Mechanical tamponade
20
Q

Why don’t Beta1 blockers work for esophageal varices?

A

Because Beta 2 is still working, thereby you don’t get vasoconstriction

21
Q

What is a mechanical tamponade?

A

Used a balloon to block the bleeding (like placing gauze over bleeding wound)

22
Q

What are the key characteristics of varices?

A
  1. present in many cirrhotics (up to 81%)
    1/3 will bleed in a given year
    Mortality from initial bleed = 40%
23
Q

What is TIPS?

A

Transjugular Intrahepatic Portosystemic Shunting
Surgical procedure that links the portal vein to the HEPATIC VEIN to decrease resistance and thereby decrease portal hypertension

24
Q

How do you prevent rebleeds?

A
  1. follow-up endoscopies with banding

2. NON-selective beta-blockers

25
Q

What are the characteristics of hepatic encephalopathy (HE)?

A 
Wide ranging altered mental status
	-subtle behavioral changes
	-insomnia
	-delirium, seizures, coma
Consider it any patient with MS with evidence of disease
26
Q

What is the pathogenesis of hepatic encephalopathy (HE)?

A

Gut derived neurotoxins  bypass the hepatocytes  lead to cerebral changes
Ammonia is one potential neurotoxin (because it is the result of protein catabolism)

27
Q

Why is ammonia a neurotoxin?

A

Because it is converted to glutamine in astrocytes
Glutamine (from ammonia) will cause increased osmolality and astrocyte dysfunction
-increases GABA
-decreases glutamate

28
Q

What is a cathartic?

A

A substance that accelerates DEFECATION

29
Q

What is the treatment of for hepatic encephalopathy (HE)?

A
  1. antibiotics (to decrease ammonia generation from colonic bacteria
  2. protein restriction to decrease ammonia load
  3. Lactulose, a non-absorbed disaccharide
30
Q

What is the mechanism lactulose uses to treat hepatic encephalopathy?

A

acts as a CATHARTIC and inhibits ammonia production while also decreasing bacterial load
Acidifies gut lumen to convert ammonia to NH4+

31
Q

What determines liver transplant candidacy?

A

MELD score
Model for Endstage Liver Disease
Excellent predictor of 3 month mortality

32
Q

What is the key point about hepatorenal syndrome?

A

Hepatorenal syndrome associated with a poor prognosis unless transplantation is performed (transplantation will reverse disease process)

33
Q

What is the definitive treatment for decompensated cirrhosis?

A

Liver transplantation is the definitive treatment for decompensated cirrhosis, and is associated with an excellent 5 year survival

GI Week 4 (12 decks)

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