Liver and GB part I covered in Exam II Flashcards

1
Q

liver blood supplies

A

hepatic artery
hepatic portal vein: from GI to the liver
hepatic vein: from liver to inferior vena cava to the heart

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2
Q

bilirubin formation

A

RBCs -> heme -> biliverdin
-> uncong. bilirubin + albumin (in serum) -> conjugation in the liver to produce conjugated bilirubin -> intestinal bacteria -> urobilinogen -> feces and urine

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3
Q

circumstances with an increased urinary urobilinogen excretion

A

Excessive bilirubin production seen in hemolytic anemia

Inefficient hepatic clearance of the absorbed urobilinogen through enterohepatic circulation seen in cirrhosis or hepatitis

Excessive exposure of bilirubin to intestinal bacteria seen in constipation

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4
Q

circumstances with a decreased urinary urobilinogen excretion

A

biliary obstruction seen in tumors

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5
Q

mechanisms to protect against increased bilirubin

A

binding to plasma albumin
rapid uptake
conjugation
clearance

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6
Q

potential health benefit of bilirubin

A

acts as an antioxidant like glutathione

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7
Q

what type of bilirubin (conj or unconj) can be caused by excessive hemolysis

A

unconj bc the conjugation system becomes overwhelmed

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8
Q

what type of bilirubin (conj or unconj) can be caused by abnormalities in the liver

A

it depends: the conj system is normal but clearance is abnormal or vise versa, we might have a mix of conj and unconj

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9
Q

what type of bilirubin (conj or unconj) can be caused by the mechanical obstruction of bile flow after its formation

A

conj

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10
Q

etiologies of increased unconj bilirubin in newborns

A

Increased in number of RBCs

Decreased RBCs’ life span

Decreased bilirubin clearance

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11
Q

what cells send mitotic signals in the liver regeneration

A

Macrophages
Hepatic stellate cells
Liver endothelial cells

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12
Q

etiologies of acute liver failure

A

acetaminophen, HAV, HBV, HCV

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13
Q

clinical characteristics of acute liver failure

A

severe acute liver injury

hepatic encephalopathy

prolonged prothrombin time/INR

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14
Q

pathophys of hepatic encephalopathy in acute liver failure

A

increased ammonia in the systemic circulation that crosses the BBB

in astrocytes, ammonia gets metabolized to glutamate -> astrocyte swelling -> increased ROS -> increased ICP
*watch for brain herniation

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15
Q

pathophys of acetaminophen-induced liver injury

A

acetaminophen overdose: gluthotion storage gets depleted -> it gets metabolized by CYP450 -> formation of free NAPQI -> NAPQI binds to the liver proteins -> cells damage and death

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16
Q

effect of acute alcohol intake with acetaminophen overdose

effect of chronic alcohol intake with acetaminophen overdose

A

no increased risk of hepatotoxicity due to the competition w CYP450

increased risk of hepatotoxicity through depletion of glutathione and increased synthesis and activity of CYP450

17
Q

alcohol metabolism

A

in the liver: acetaldehyde formation by ADH

in the gut: conversion of acetaldehyde to acetate by ALDH

18
Q

Spectrum of alcoholic liver disease

A

alcoholic steatosis -> steotohepatitis -> fibrosis -> cirrhosis