Exam 3: Liver Pathophysiology Flashcards

(73 cards)

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
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 ```