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ARCHIVED: Pathophysiology > Exam 3: Liver Pathophysiology > Flashcards

Exam 3: Liver Pathophysiology Flashcards

1
Q

Bile flows from the liver into the duodenum when:

A

Eating - otherwise into the gallbladder

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2
Q

Bile is composed of:

A

Bile acids
Bile salts
Bicarb
Wastes from the liver

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3
Q

Liver produces ___% of the body’s daily lymph:

A

50%

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4
Q

Liver lymph differs from the rest of the body’s in this way:

A

High in protein

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5
Q

The liver is “mushy” because:

A

Very little structural tissue/basement membrane

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6
Q

Proteins synthesized by the liver:

A

Albumin
Fibrinogen
Prothrombin
Lipoproteins

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7
Q

Bile is positively/negatively charged and hydrophilic/hydrophobic:

A

Negatively

Hydrophobic

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8
Q

25% of the body’s cholesterol is in this organ:

A

Brain

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9
Q

Bridging fibrosis is:

A

A reversible (early on) linking of regions of the liver by fibrous strands; caused by inflammation

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10
Q

This occurs in the liver when fibrosis continues to develop along with parenchymal injury:

A

Liver divides into nodules of regenerating hepatocytes surrounded by scar tissue

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11
Q

Role of stellate cells in liver injury:

A

With inflammation, stellate cells lay down dense extracellular collagen matrix (causing fibrosis)

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12
Q

Activated stellate cells in the liver are called:

A

Myofibroblasts

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13
Q

Lab tests for hepatocyte integrity:

A

Serum aspartate aminotransferase (AST)

Serum alanine aminotransferase (ALT)

(Old names SGOT, SGPT)

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14
Q

Typical AST/ALT values:

A

< 50

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15
Q

Lab tests for biliary tract integrity:

A

Serum alkaline phophatase (AP/ALP/ALKP)

Serum ɣ-glutamyltransferase (GGT)

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16
Q

Alk phophatase not a reliable indicator for biliary disease by itself because:

A

Also found in bone cells

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17
Q

Lab tests for serum bilirubin:

A

Direct (conjugated)

Total (conjugated + unconjugated)

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18
Q

Lab tests for hepatocyte functioning:

A

Serum albumin
Prothrombin time
Serum ammonia

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19
Q

Using serum albumin as an indicator of liver functioning:

A

If serum albumin is ↓ and total protein is too, liver is not working well

If serum albumin is ↓ but total protein is okay, liver is okay - it only makes enough albumin to bring oncotic pressure up to normal

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20
Q

Ammonia builds up during liver failure due to:

A

Inability to metabolize/digest nitrogenous byproducts from gut bacteria via the urea cycle

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21
Q

Estrogen-related abnormalities in liver disease:

A

Hypogonadism
Gynecomastia
Palmar erythema
Spider angiomas

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22
Q

Blood sugar abnormality in liver disease:

A

Hypoglycemia; liver no longer making/breaking down glucose

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23
Q

Normal liver venous pressure:

A

10mmHg

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24
Q

S/s of hepatic portal hypertension:

A 
Ascites
Esophageal varices
Hemorrhoids
Caput medusae
Splenomegaly
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25
Q

Coagulopathy seen in liver failure:

A

Impaired clotting and clot breakdown; liver makes both clotting factors and plasminogen

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26
Q

Life threatening complications of liver failure:

A 
Multiple organ failure
Coagulopathy
Hepatic encephalopathy
Hepatorenal syndrome
Varices rupture
Hepatocellular carcinoma
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27
Q

Normal bilirubin production amount and sources:

A

0.2 - 0.3 g/day
Primary source: breakdown of senescent erythrocytes
Minor source: degradation of tissue heme-containing proteins

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28
Q

Extrahepatic bilirubin binds to:

A

Serum albumin, for delivery to the liver and hepatocellular uptake

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29
Q

Liver processing of bilirubin:

A

Glucoronidation into bilirubin monoglucuronides/diglucuronides (conjugated bilirubin), which are excreted into bile

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30
Q

Gut processing of conjugated bilirubin:

A

Gut bacteria deconjugate bilirubin and degrade it to urobilinogens + pigment residues

Most excreted into feces, some reabsorption/re-excretion into bile

31
Q

Three causes of jaundice related to ↑ unconjugated bilirubin:

A

Excess bilirubin production
Reduced hepatic uptake
Impaired conjugation

32
Q

Two causes of jaundice related to ↑ conjugated bilirubin:

A

Decreased hepatocellular excretion

Impaired bile flow

33
Q

Pathogenesis of unconjugated bilirubin jaundice:

A

Fraction tightly bound to albumin is insoluble, so not excreted by kidney

Unbound fraction diffuses into tissues (esp. brain) and produces toxic injury

34
Q

Pathogenesis of conjugated bilirubin jaundice:

A

Soluble in water, weak albumin binding, so excreted by kidney

Mild jaundice without tissue injury

35
Q

Jaundice tx for hemolytic disease of the newborn:

A

UV light; skin can conjugate bilirubin under UV

36
Q

Changes seen in parenchyma d/t cholestasis:

A

Enlargement of bile canaliculi
Apoptosis of hepatocytes
Bile uptake by Kupffer cells

37
Q

Changes seen in portal tracts d/t cholestasis:

A 
Bile duct proliferation
Edema
Bile pigment retention
Neutrophilic inflammation
Toxic degeneration of neighboring hepatocytes
38
Q

% of liver function that must be lost for hepatic failure to occur:

A

80-90%

39
Q

Special problems r/t hepatic failure:

A

Hepatic encephalopathy

Hepatorenal syndrome

40
Q

Cirrosis causes hepatic portal hypertension by:

A

Impairing blood flow through liver via fibrosis/scarring

41
Q

Downstream effects of hepatic portal hypertension:

A

Ascites
Portosystemic shunts
Splenomegaly

42
Q

Three clinical states of hepatitis:

A

Carrier/asymptomatic
Acute viral hepatitis
Chronic viral hepatitis

43
Q

Common characteristics of HAV/HEV:

A 
Self-limiting
2-8 week incubation
Acute only - no carrier or chronic states
Do not cause cancer
Fecal-oral transmission
Not common in US
44
Q

HAV-specific characteristics:

A

Common childhood disease in developing countries; more dangerous in adults

Sporadic infections - associated with oysters and warm-water seafood

45
Q

HEV-specific characteristics:

A

Endemic and seen in travellers; sporadic infections rare

20% mortality rate in pregnant women

46
Q

Characteristics of HBV, HCV, and HDV:

A

Can cause carrier state, chronic hepatitis, and cancer

Parenteral transmission

Present in the US

47
Q

HDV-specific trait:

A

Only survives along with coexisting HBV infection

48
Q

ETOH effect on hepatocytes:

A

Can no longer incorporate fatty acids into lipoproteins for export –> hepatic steatosis (fatty liver)

49
Q

Relationship between hepatic steatosis and alcoholic hepatitis:

A

Steatosis can turn into hepatisis with severe exposure; abstinence can have hepatitis revert to steatosis

50
Q

Incidence of alcoholic liver diseases:

A

Hepatic steatosis: 90-100%
Alcoholic hepatitis: 10-35%
Cirrhosis: 8-20%

51
Q

Physical characteristics of cirrhotic liver and causes:

A

Nodularity from fibrous scarring
Greenish tint from bile
Yellowish tint from bilirubin

52
Q

The body’s only way of eliminating iron is:

A

Bleeding

53
Q

Hemochromatosis is:

A

The uncontrolled uptake of iron

54
Q

Demographics and genetic basis of hemochromatosis:

A

Mostly males (5-7:1) in their 50s or older

Autosomal recessive, affecting 0.5% of people
10% are heterozygous carriers

55
Q

Sequelae of hemochromatosis:

A

Cirrhosis (100%)
DM (75-80%)
Skin pigmentation (75-80%)

56
Q

Bantu siderosis is:

A

Another primary iron overload condition

57
Q

Three secondary iron overload causes:

A
  1. Transfusion (0.25 gm/unit)
  2. β-thalassemia
  3. Sideroblastic anemia
58
Q

Describe primary biliary cirrhosis:

A

Destruction (often fatal) of intrahepatic bile ducts, most commonly with antimitochondrial antibodies present

59
Q

Lab abnormalities seen in primary biliary cirrhosis:

A

Elevated alk phos & cholesterola

Hyperbilirubinemia late in disease

60
Q

Describe secondary biliary cirrhosis:

A 
Obstruction of the extrahepatic biliary tract due to:
Gallstones
Biliary atresia
Malignancy (biliary tree/pancreas)
Surgical strictures
61
Q

Describe primary sclerosing cholangitis:

A

Destruction of intra- and extrahepatic bile ducts
Associated with ulcerative colitis (develops 2nd) but no antimitochondrial antibodies
Elevated alk phos

62
Q

Manifestations of hepatic vein outflow obstruction:

A 
Ascites
Hepatomegaly
Abdominal pain
Elevated transaminases
Jaundice
63
Q

Manifestations of impaired intrahepatic blood flow:

A

Ascites (cirrhosis)
Esophageal varices
Elevated transaminases

64
Q

Manifestations of impaired portal vein inflow:

A

Ascites
Esophageal varices
Splenomegaly
Intestinal congestion

65
Q

Manifestations of impaired hepatic artery inflow:

A

Ischemia to bile ducts/parenchyma

Loss of graft in transplant

66
Q

Causes of hepatocellular carcinoma:

A 
HBV
Chronic liver disease (HCV, ETOH)
Aflatoxin (from peanuts)
Tyrosinemia
Cirrhosis
67
Q

Relationship between HBV and HCC:

A

Early infection with HBV gives increased risk of HCC

68
Q

Prognosis for HCC:

A

Mean survival 7 months

69
Q

Risk factors for cholesterol gallstones:

A 
Fair (or Native American)
Forty (older)
Female
Fertile
Fat
Gallbladder stasis
Hyperlipidemia
70
Q

Risk factors for pigment gallstones:

A

Chronic hemolytic syndrome
Biliary infection
GI disorders (Crohn’s)
Asian descent

71
Q

Choledocholithiasis is:

A

Presence of stones in the biliary tree, not the gallbladder

72
Q

Sequelae of choledocholithiasis:

A 
Biliary obstruction
Pancreatitis
Cholangitis
Hepatic abscess
Chronic liver disease/biliary cirrhosis
Acute calculous cholecystitis
73
Q

Major causes of acute pancreatitis:

A 
IGETS
Idiopathic (most common)
Gallstones (2nd most common)
Ethanol
Trauma
Steroids

ARCHIVED: Pathophysiology (18 decks)

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