Complications of End Stage Liver Disease Flashcards

1
Q

Portal venous system pressure calculation

A

vascular resistance (r) X blood flow (q)

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2
Q

Two capillary beds of the portal venous system

A

splanchnic capillaries and hepatic sinusoids

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3
Q

Hallmarks of end stage liver disease

A

collateral dilation and splenomegaly due to portal hypertension

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4
Q

Major complications of portal hypertension (5)

A

ascites, gastroesophageal varices, spontaneous bacterial peritonitis, portosystemic encephalopathy, hepatorenal syndrome

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5
Q

Pathophysiology of ascites

A

portal hypertension –> baroreceptor activation and neurohormonal alterations (NO) resulting in arterial vasodilation –> drop in blood volume/pressure–> altered renal perfusion –> sodium retention –> intra and extravascular volume overload

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6
Q

Etiologies of ascites

A

cirrhosis > malignancy > CHF > TB > other

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7
Q

SAAG

A

serum album - albumin in ascites fluid

if >1.1 indicates portal hypertension (cirrhosis, CHF)

if <1.1 indicates other etiology (infection, cancer)

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8
Q

Tx of ascites

A

low salt, diuretics (spironolactone, furosemide), paracentesis, TIPS

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9
Q

Survival of ascites

A

2 year

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10
Q

Survival of refractory ascites

A

treatment unresponsive –> 6 months

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11
Q

Survival of hepatorenal syndrome

A

6 weeks

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12
Q

Acute renal insufficiency in the setting of end stage liver disease w/o alternative explanation.

A

hepatorenal syndrome –> no improvement after stopping diuretics, giving iv fluid –> dialysis, liver transplant

due to too much vasoconstriction

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13
Q

Dx of spontaneous bacterial peritonitis

A

SAAG>1.1, >250 PMN in ascites fluid, 1 organism only

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14
Q

Most common organisms in bacterial peritonitis

A

e coli, strep, klebsiella

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15
Q

What are the factors that influence bleed risk for varices?

A

large size, cherry red spots

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16
Q

Tx of large varices

A

propanolol or nadolol (non-selective beta blockers) to prevent bleeding –> 50% reduction in risk for first bleed

17
Q

Why do we give non-selective vs selective beta blockers for varices?

A
  1. beta 2 inhibition in splanchnic capillaries leads to unopposed alpha adrenergic vasoconstriction which reduces inflow of blood to liver (if use a beta 1 blocker, this effect won’t occur) –> beta 2 inhibition is mediated by non-specific blockers
  2. octreotide (splanchnic vasoconstricter)
  3. blood transfusion
  4. antibiotics
  5. band ligation
  6. tips
  7. mechanical tamponade
18
Q

Prevention of rebleeding of varices

A

follow up endoscopies, banding, beta blockers

19
Q

Pathogenesis of hepatic encephalopathy

A

gut derived neurotoxins –> absorbed and bypass hepatocytes causing cerebral changes
*bacteria catabolize ammonia which is converted to glutamine –> astrocyte dysfunction // increased GABA, reduced glutamate activity

20
Q

Marker of hepatic encephalopathy

A

ammonia

21
Q

Precipitants of hepatic encephalopathy

A

tranquilizers, GI hemorrhage, dietary protein, azotemia

22
Q

Tx of hepatic encephalopathy

A

tx underlying cause, bleeding, constipation, infection, avoid sedatives, lactulose, antibiotics

23
Q

MOA lactulose

A

cathartic, decreases bacterial load and inhibits intestinal ammonia production

24
Q

MELD

A

score based on creatinine, bilirubin, INR (6-40) predicts 3 month mortality

25
Q

Definitive treatment for decompensated cirrhosis

A

liver transplant