Liver Failure Flashcards

1
Q

When does hepatic failure occur?

A
  • when 80-90% of the functional capacity of the liver is lost
  • 80% mortality w/o transplant
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2
Q

What is acute hepatic failure defined as?

A
  • occurring w/in 26 weeks (6 months) of some initial injury
  • occurs in absence of preexisting liver dz
  • is associated with encephalopathy and coagulopathy
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3
Q

What are the main causes of acute liver failure? (mnemonic)

A

ABCDEF

  • Acetominophen, Hepatitis A, Autoimmune hepatitis
  • Hepatitis B
  • Hepatitis C, Cryptogenic
  • Drugs/toxins/ hepatitis D
  • Hepatitis E, esoteric causes (Wilson’s dz, Budd-chiari)
  • Fatty change of the microvesicular type (fatty liver of pregnancy, valproate, tetracycline, Reye syndrome)
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4
Q

What are the morphological changes of acute hepatic failure?

A
  • massive hepatic necrosis leading to broad regions of parenchymal loss surrounding areas of regenerating hepatocytes
  • small shrunken liver
  • diffuse microvesicular steatosis (diffuse poisoning of liver cells w/o obvious cell death and parenchymal collapse)
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5
Q

What are the clinical signs of acute hepatic failure?

A
  • N/V, jaundice that progresses to life-threatening encephalopathy and coagulation defects
  • moderate increase in liver transaminases
  • hepatomegaly (and eventual shrunken liver)
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6
Q

In acute hepatic failure, what is a decline in serum transaminases indicative of?

A

Fewer viable hepatocytes, NOT recovery!

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7
Q

What is indicative of a poor prognosis in acute hepatic failure?

A
  • decrease in liver enzymes (indicates few remaining hepatocytes)
  • worsening jaundice
  • coagulopathy
  • encephalopathy
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8
Q

What are the possible consequences of acute hepatic failure? (7)

A
  • jaundice and icterus
  • cholestasis
  • hepatic encephalopathy (due to increased serum ammonia) leading to:
  • – rigidity and hyperreflexia
  • – asterixis (CHARACTERISTIC)
  • coagulopathy
  • DIC
  • portal HTN
  • hepatorenal syndrome (a form of renal failure in ppl w/liver failure whose kidneys are otherwise normal)
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9
Q

How is chronic liver failure defined?

A
  • it is associated with cirrhosis, though not mutually exclusive
  • is associated with hepatitis B and C, NAFLD, alcoholic fatty liver dz
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10
Q

What are the ultimate causes of death in chronic liver failure?

A
  • hepatic encephalopathy
  • bleeding from esophageal varices
  • bacterial infections
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11
Q

How is cirrhosis defined?

A
  • diffuse transformation of the entire liver into regenerative parenchymal nodules surrounded by fibrous bands and variable degrees of vascular (portosystemic) shunting)
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12
Q

What are the Child-Pugh classifications of cirrhosis and what is it for?

A
  • the classifications help monitor the decline of the patients on the path to chronic liver failure
  • Class A: well compensated
  • Class B: partially decompensated
  • Class c: decompensated
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13
Q

What are clinical symptoms of cirrhosis? Do you always see them?

A
  • don’t always see symptoms, ~40% of patients

Symptoms:

  • jaundice + pruritis
  • hypoalbuminemia –> systemic edema
  • hyperammonemia
  • fetor hepaticus: mercaptan formation
  • hyperestrogenemia due to impaired metabolism can lead to palmar erythema, spider angiomata, hypogonadism, gynecomastia (males)
  • increased risk of developing hepatocellular carcinoma
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14
Q

What are prehepatic causes of portal HTN?

A
  • obstructive thrombosis
  • narrowing of portal v. before entering the liver
  • massive splenomegaly w/increased splenic blood flow
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15
Q

What are posthepatic causes of portal HTN?

A
  • severe right heart failure
  • constrictive pericarditis
  • hepatic v. outflow obstruction
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16
Q

What are intrahepatic causes of portal HTN?

A
  • usually CIRRHOSIS
  • shistosomiasis
  • massive fatty change
  • diffuse fibrosing granulomatous dz (like sarcoidosis)
  • increased resistance to portal flow (at lvl of sinusoids)
  • increased portal venous flow due to hyperdynamic circulation
17
Q

What are clinical consequences of portal HTN?

A
  • ascites
  • portosystemic shunt formation
  • congestive splenomegaly
  • hepatic encephalopathy
18
Q

What is ascites?

A
  • excess fluid in the peritoneal cavity
19
Q

What is the composition of ascites fluid?

A
  • serous fluid (< 3gm/dl albumin)
  • neutrophils (suggests infection)
  • blood (suggests disseminated intraabdominal cxr
20
Q

What are the mechanisms that lead to ascites?

A
  • sinusoidal HTN: drives fluid into Space of Disse which is drained by lymphatics (space beneath endothelial cells)
  • percolation of hepatic lymph in peritoneal cavity: thoracic duct can’t keep up, fluid leaks out
  • splanchnic vasodilation: causes systemic hypotension -> vasoconstriction –> RAAS activation –> Na+ retention –> increased perfusion pressure –> transudation into abd. cavity
21
Q

What are portosystemic shunts? Examples of some?

A
  • flow that’s reversed from the portal into systemic circulation where there are shared capillary beds
  • esophageal varices
  • caput medusa (dilated subq veins from umbilicus to rib margins)
  • hemorrhoids (rectum)
22
Q

What is hepatopulmonary syndrome? Symptoms of?

A
  • hypoxia + dyspnea due to ventilation/perfusion (V/Q) mismatch from rapid blood flow through dilated vessels w/decreased time for diffusion
  • exacerbated in upright position due to gravity
  • improves in recumbent position
23
Q

What is portopulmonary HTN? Symptoms of?

A
  • excessive pulmonary vasoconstriction and vascular remodeling w/concomitant portal HTN
  • it’s when you have pulmonary arterial HTN in liver dz and portal HTN
  • dsypnea on exertion and clubbing
24
Q

What is acute-on-chronic liver failure?

A
  • it’s when ppl w/stable, well-compensated chronic liver dz develop sudden signs of acute liver failure
  • they commonly have established cirrhosis and extensive vascular shunting
  • there are significant amounts of parenchyma w/borderline vascular supply that are vulnerable to superimposed insults