Cirrhosis PP Week 4 Flashcards

1
Q

what is cirrhosis

A

Late stage of progressive hepatic fibrosis: characterized by distortion of the hepatic architecture
– formation of regenerative nodules
– considered to be irreversible in its advanced stages, at
which point the only option may be liver transplantation

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2
Q

In earlier stages of cirrhosis

A

specific treatments aimed at the underlying cause of liver disease may improve or even reverse cirrhosis

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3
Q

major complications of decompensated cirrhosis

A

Variceal hemorrhage, Ascites, Spontaneous

bacterial peritonitis, Hepatic encephalopathy, Hepatocellular carcinoma, Hepatorenalsyndrome, Hepatopulmonarysyndrome

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4
Q

Risk factors for decompensation include

A

bleeding, alcohol intake, infection, medications, dehydration, constipation, obesity, portal vein thrombosis, cardiomyopathy (**= these complications alone are not considered to have decompensated cirrhosis)

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5
Q

many of the complications of cirrhosis are the result of portal hypertension, which

A

increased pressure within the venous portal system. It can lead to the formation of: venous
collaterals (varices), Circulatory abnormalities, Vascular abnormalities, Functional abnormalities biochemical
abnormalities (All contribute to the pathogenesis of ascites and other complications)

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6
Q

stages of hepatic encephalopathy

A

stage 1- personality changes
stage 2- lethargy, tremors, muscle twitching
stage 3- combative, violent
stage 4- coma

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7
Q

how does liver disease lead to varices

A
  1. increased in intrahepatic vascular resistance d/t the architectual distortion and deficiency of nitric oxide
  2. portal htn from inc. intrhepatic resistance (decreased outflow and splanchnic arterial vasodilation (increased inflow)
  3. varices form in the esophagus and stomach by dilation of preexisting vessels and by active angiogenesis. they increase in size with severity of portal htn and can rupture and bleed when the pressure exceeds a maximal point
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8
Q

spontaneous bacterial peritonitis evaluation

A

do a tap- look at PMN, if greater than 250 assume bacterial peritonitis- start broad spectrum such as cefoxatime and also give albumin (on day 1 and day 3 if serum creatinine is greater than 1 and BUN greater than 30)

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9
Q

SBP

A

common but treatable complication of decompensated cirrhosis, its the translocation of bacteria and endotoxins from GI tract to peritoneal fluid, facilitated by impaired defensive mechanisms in cirrhotic patients

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10
Q

hepatorenal syndrome caused by

A

cirrhosis–> portal hypertension–> severe renal constriction–> hepatorenal syndorome.

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11
Q

hepatorenal syndrome easily recognized features

A

low mean arterial BP less than 80, hyponatremia, urinary sodium retention (low urinary sodium concentration), oliguria

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12
Q

treatment for hepatorenal syndrome

A

IV albumin, vasocontrictors i.e. midodrine plus octreotide, IV terlipressin

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13
Q

portal htn gastropathy

A

effects of portal htn- hematemesis/ melena (from esophogeal variceles), dilated abdominal veins (caput medusa), splenomegaly, ascites

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14
Q

hepatic hydrothorax

A

transudative pleural effusion usually greater than 500ml, aims of therapy is relieve sx and to prevent pulmonary complications (tx- duretics, lasix/ spironolactone)

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