Lecture 41: Complications of End-Stage Liver Disease Flashcards

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
What are the characteristics of hepatic encephalopathy (HE)?
``` Wide ranging altered mental status -subtle behavioral changes -insomnia -delirium, seizures, coma Consider it any patient with MS with evidence of disease ```
26
What is the pathogenesis of hepatic encephalopathy (HE)?
Gut derived neurotoxins  bypass the hepatocytes  lead to cerebral changes Ammonia is one potential neurotoxin (because it is the result of protein catabolism)
27
Why is ammonia a neurotoxin?
Because it is converted to glutamine in astrocytes Glutamine (from ammonia) will cause increased osmolality and astrocyte dysfunction -increases GABA -decreases glutamate
28
What is a cathartic?
A substance that accelerates DEFECATION
29
What is the treatment of for hepatic encephalopathy (HE)?
1. antibiotics (to decrease ammonia generation from colonic bacteria 2. protein restriction to decrease ammonia load 3. Lactulose, a non-absorbed disaccharide
30
What is the mechanism lactulose uses to treat hepatic encephalopathy?
acts as a CATHARTIC and inhibits ammonia production while also decreasing bacterial load Acidifies gut lumen to convert ammonia to NH4+
31
What determines liver transplant candidacy?
MELD score Model for Endstage Liver Disease Excellent predictor of 3 month mortality
32
What is the key point about hepatorenal syndrome?
Hepatorenal syndrome associated with a poor prognosis unless transplantation is performed (transplantation will reverse disease process)
33
What is the definitive treatment for decompensated cirrhosis?
Liver transplantation is the definitive treatment for decompensated cirrhosis, and is associated with an excellent 5 year survival