Exam 3: Liver Pathophysiology Flashcards Preview

ARCHIVED: Pathophysiology > Exam 3: Liver Pathophysiology > Flashcards

Flashcards in Exam 3: Liver Pathophysiology Deck (73):
1

Bile flows from the liver into the duodenum when:

Eating - otherwise into the gallbladder

2

Bile is composed of:

Bile acids
Bile salts
Bicarb
Wastes from the liver

3

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

50%

4

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

High in protein

5

The liver is "mushy" because:

Very little structural tissue/basement membrane

6

Proteins synthesized by the liver:

Albumin
Fibrinogen
Prothrombin
Lipoproteins

7

Bile is positively/negatively charged and hydrophilic/hydrophobic:

Negatively
Hydrophobic

8

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

Brain

9

Bridging fibrosis is:

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

10

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

Liver divides into nodules of regenerating hepatocytes surrounded by scar tissue

11

Role of stellate cells in liver injury:

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

12

Activated stellate cells in the liver are called:

Myofibroblasts

13

Lab tests for hepatocyte integrity:

Serum aspartate aminotransferase (AST)

Serum alanine aminotransferase (ALT)

(Old names SGOT, SGPT)

14

Typical AST/ALT values:

< 50

15

Lab tests for biliary tract integrity:

Serum alkaline phophatase (AP/ALP/ALKP)

Serum ɣ-glutamyltransferase (GGT)

16

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

Also found in bone cells

17

Lab tests for serum bilirubin:

Direct (conjugated)
Total (conjugated + unconjugated)

18

Lab tests for hepatocyte functioning:

Serum albumin
Prothrombin time
Serum ammonia

19

Using serum albumin as an indicator of liver functioning:

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

20

Ammonia builds up during liver failure due to:

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

21

Estrogen-related abnormalities in liver disease:

Hypogonadism
Gynecomastia
Palmar erythema
Spider angiomas

22

Blood sugar abnormality in liver disease:

Hypoglycemia; liver no longer making/breaking down glucose

23

Normal liver venous pressure:

10mmHg

24

S/s of hepatic portal hypertension:

Ascites
Esophageal varices
Hemorrhoids
Caput medusae
Splenomegaly

25

Coagulopathy seen in liver failure:

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

26

Life threatening complications of liver failure:

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

27

Normal bilirubin production amount and sources:

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

28

Extrahepatic bilirubin binds to:

Serum albumin, for delivery to the liver and hepatocellular uptake

29

Liver processing of bilirubin:

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

30

Gut processing of conjugated bilirubin:

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

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

31

Three causes of jaundice related to ↑ unconjugated bilirubin:

Excess bilirubin production
Reduced hepatic uptake
Impaired conjugation

32

Two causes of jaundice related to ↑ conjugated bilirubin:

Decreased hepatocellular excretion
Impaired bile flow

33

Pathogenesis of unconjugated bilirubin jaundice:

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

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

34

Pathogenesis of conjugated bilirubin jaundice:

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

Mild jaundice without tissue injury

35

Jaundice tx for hemolytic disease of the newborn:

UV light; skin can conjugate bilirubin under UV

36

Changes seen in parenchyma d/t cholestasis:

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

37

Changes seen in portal tracts d/t cholestasis:

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

38

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

80-90%

39

Special problems r/t hepatic failure:

Hepatic encephalopathy
Hepatorenal syndrome

40

Cirrosis causes hepatic portal hypertension by:

Impairing blood flow through liver via fibrosis/scarring

41

Downstream effects of hepatic portal hypertension:

Ascites
Portosystemic shunts
Splenomegaly

42

Three clinical states of hepatitis:

Carrier/asymptomatic
Acute viral hepatitis
Chronic viral hepatitis

43

Common characteristics of HAV/HEV:

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

HAV-specific characteristics:

Common childhood disease in developing countries; more dangerous in adults

Sporadic infections - associated with oysters and warm-water seafood

45

HEV-specific characteristics:

Endemic and seen in travellers; sporadic infections rare

20% mortality rate in pregnant women

46

Characteristics of HBV, HCV, and HDV:

Can cause carrier state, chronic hepatitis, and cancer

Parenteral transmission

Present in the US

47

HDV-specific trait:

Only survives along with coexisting HBV infection

48

ETOH effect on hepatocytes:

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

49

Relationship between hepatic steatosis and alcoholic hepatitis:

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

50

Incidence of alcoholic liver diseases:

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

51

Physical characteristics of cirrhotic liver and causes:

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

52

The body's only way of eliminating iron is:

Bleeding

53

Hemochromatosis is:

The uncontrolled uptake of iron

54

Demographics and genetic basis of hemochromatosis:

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

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

55

Sequelae of hemochromatosis:

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

56

Bantu siderosis is:

Another primary iron overload condition

57

Three secondary iron overload causes:

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

58

Describe primary biliary cirrhosis:

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

59

Lab abnormalities seen in primary biliary cirrhosis:

Elevated alk phos & cholesterola
Hyperbilirubinemia late in disease

60

Describe secondary biliary cirrhosis:

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

61

Describe primary sclerosing cholangitis:

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

62

Manifestations of hepatic vein outflow obstruction:

Ascites
Hepatomegaly
Abdominal pain
Elevated transaminases
Jaundice

63

Manifestations of impaired intrahepatic blood flow:

Ascites (cirrhosis)
Esophageal varices
Elevated transaminases

64

Manifestations of impaired portal vein inflow:

Ascites
Esophageal varices
Splenomegaly
Intestinal congestion

65

Manifestations of impaired hepatic artery inflow:

Ischemia to bile ducts/parenchyma
Loss of graft in transplant

66

Causes of hepatocellular carcinoma:

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

67

Relationship between HBV and HCC:

Early infection with HBV gives increased risk of HCC

68

Prognosis for HCC:

Mean survival 7 months

69

Risk factors for cholesterol gallstones:

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

70

Risk factors for pigment gallstones:

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

71

Choledocholithiasis is:

Presence of stones in the biliary tree, not the gallbladder

72

Sequelae of choledocholithiasis:

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

73

Major causes of acute pancreatitis:

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