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GI Week 5 - WLB > Liver (Jaundice + Cirrhosis + Tumors) - Pathoma > Flashcards

Liver (Jaundice + Cirrhosis + Tumors) - Pathoma Flashcards

1
Q

What is the earliest sign of jaundice?

A

Scleral Icterus

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2
Q

Why does extravascular hemolysis or ineffective erythropoiesis result in jaundice?

A
  • Excessive destruction of RBCs leads to high levels of unconjugated bilirubin
    • overwhelms the conjugating ability of the liver
    • unconjugated bilirubin spills over into the blood until the liver is able to conjugate it
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3
Q

What are the clinical features in extravascular hemolysis or ineffective erythropoeisis?

A
  • dark urine
    • due to increase in urine urobilinogen
    • UCB is not water soluble and thus is absent from the urine
  • increased risk for pigmented bilirubin gallstones
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4
Q

What is physiologic jaundice of the newborn due to?

A
  • Newborn liver has transiently low UGT activity
    • (UGT= uridine glucuronyl transferase)
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5
Q

What is the potential complication of neonatal jaundice? How does it happen?

A
  • Kernicterus
    • unconjugated bilirubin is fat soluble and can deposit in the basal ganglia
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6
Q

Why does phototherapy work to treat physiologic jaundice of the newborn?

A

it makes unconjugated bilirubin water-soluble

can then leak out in the urine

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7
Q

What syndrome results in jaundice due to autosomal recessive inheritance of mildly lowered UGT activity?

A

Gilbert Syndrome

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8
Q

When is jaundice most prevalent in patients with Gilbert Syndrome?

A
  • During stress
    • severe infection
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9
Q

What syndrome is characterized by a severe decrease or abscence of UGT?

A

Crigler-Najjar Sydrome

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10
Q

What causes death in Crigler-Najjar Syndrome?

A

Kernicterus

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11
Q

What syndrome is characterized by an autosomal recessive inherited deficiency of bilirubin canalicular transport proteins?

A

Dubin-Johnson Syndrome

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12
Q

What are the clinical features of Dubin-Johnson Syndrome?

A

Dark liver → grossly black (benign)

increased Conjugated Bilirubin

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13
Q

What jaundice-causing disease is associated with gallstones, pancreatic carcinoma, cholangiocarcinoma, parasites, and liver flukes?

A

Biliary Tract Obstruction

(a.k.a. obstructive jaundice)

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14
Q

What are the laboratory findings in Biliary Tract Obstruction/Obstructive Jaundice?

A
  • Increased conjugated bilirubin
  • Decreased urine urobilinogen
  • Increased alkaline phosphatase
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15
Q

What are the clinical features of Biliary Tract Obstruction/Obstructive Jaundice?

A
  • Dark urine
    • due to bilirubinuria (conjugated bilirubin is water soluble)
  • Pale stool
    • can’t get bile into the stool
  • Pruritis
    • due to increased plasma bile acids
  • Hypercholesterolemia with xanthomas
  • Steatorrhea with malabsorption of fat-soluble vitamins
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16
Q

What jaundice-causing disease results in increased conjugated and unconjugated bilirubin in the blood and results in dark urine?

A

Viral hepatitis

(inflammation damages both the hepatocytes (UB) and small bile ductules (CB))

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17
Q

What is cirrhosis?

A
  • End-stage liver damage
  • Characterized by disruption of normal hepatic parenchyma by
    • broad bands of fibrosis
    • regenerative nodules of hepatocytes
18
Q

What is the fibrosis in cirrhosis mediated by?

A
  • Stellate cells
    • fibrosis is mediated by TGF-beta from stellate cells
    • lie beneath the endothelial cells that line the sinusoids
19
Q

What four sequelae are due to portal hypertension in cirrhosis?

A
  • Ascites
  • Congestive splenomegaly/hypersplenism
    • consumes RBCs and platelets
  • Portosystemic shunts
    • esophageal varices
    • caput medusae
  • Hepatorenal syndrome
20
Q

What sequelae are due to decreased detoxification in cirrhosis?

A
  • Mental status changes, asterixis, and coma
  • Gynecomastia, Spider angiomata, Palmar erythema
    • liver cannot remove estrogen from blood
  • Jaundice
21
Q

What three sequelae are due to decreased protein synthesis in cirrhosis?

A
  • Hypoalbuminemia
  • Edema
  • Coagulopathy
    • both PT and PTT increased
22
Q

What are the three classic patterns of injury in Alcohol-Related Liver Disease?

A
  • Fatty liver
    • reversible heavy, greasy liver
  • Alcoholic hepatitis
    • direct chemical injury to hepatocytes mediated by acetaldehyde
  • Cirrhosis
    • chronic alcohol-induced liver damage
23
Q

In what disease are Mallory Bodies found? What are they?

A
  • Found in Alcoholic Hepatitis
    • consist of damaged intermediate filaments within the hepatocytes
24
Q

What is the helpful laboratory finding in Non-Alcoholic Fatty Liver Disease?

A

ALT > AST

25
Q

What iron-related disease can lead to cirrhosis?

A

Hemochromatosis

26
Q

What is primary hemochromatosis due to?

A

mutations in the HFE gene

(most commonly C282Y > H63D)

27
Q

What is secondary hemochromatosis due to?

A
  • Complication of chronic transfusion therapy
    • iron constantly recycled
    • no way to get rid of excess iron
    • builds up in tissues → hemosiderosis
28
Q

What is the symptom triad of Secondary Hemochromatosis?

A

cirrhosis + 2° diabetes mellitus + bronze skin

(cardiac arrhythmia and gonadal dysfunction also possible)

29
Q

What is the key finding on biopsy in Hemochromatosis?

A

Brown pigment in hepatocytes

(Prussian blue stain distinguishes iron (blue) from lipofuscin)

30
Q

What is Wilson Disease?

A
  • Autosomal recessive defect in ATP7B gene that involved in ATP-mediated hepatocyte copper transport
  • Results in lack of copper transport into bile and lack of copper incorporation into ceruloplasm
31
Q

What is the clinical manifestation of Wilson Disease?

A
  • Presents in childhood or before age 40
  • Cirrhosis
  • Neurologic manifestations (like psychopathy in House)
  • Kayser-Fleisher rings in cornea
  • Increased risk of hepatocellular carcinoma
32
Q

What cirrhosis-causing disease involves autoimmune granulomatous destruction of intrahepatic bile ducts and usually arises in women around age 40 who present with obstructive jaundice?

A

Primary Biliary Cirrhosis

33
Q

What antibody is present in Primary Biliary Cirrhosis?

A

Anti-Mitochondrial Antibody

34
Q

What disease is characterized by inflammation and fibrosis of intrahepatic and extrahepatic bile ducts resulting in periductal fibrosis with an “onion-skin” appearance?

A

Primary Sclerosing Cholangitis

35
Q

What is Primary Sclerosing Cholangitis associated with?

A
  • Ulcerative colitis
  • (+) p-ANCA
  • middle-aged men
  • increased risk for cholangiocarcinoma
36
Q

What kind of damage is seen in Reye Syndrome?

A
  • Fulminant liver failure and encephalopathy
    • likely related to mitochondrial damage of hepatocytes
37
Q

Is a hepatic adenoma benign or malignant?

A

Benign tumor of hepatocytes

38
Q

Hepatic adenomas are associated with the use of what two things?

A
  • Oral contraceptives
  • Anabolic steroids
39
Q

What is the risk/complication with hepatic adenomas?

A

Rupture and intraperitoneal hemorrhage

(especially during pregnancy)

40
Q

What are the risk factors for Hepatocellular Carcinoma?

A
  • Chronic hepatitis
  • Cirrhosis
  • Aflatoxins related to Aspergillus
    • induce p53 mutations
41
Q

What syndrome is presents with painful hepatomegaly and ascites, and is characterized by liver infarction secondary to hepatic vein obstruction (HCC, hypercoagulopathy, postpartum states, etc.)?

A

Budd-Chiari Syndrome

42
Q

What is a helpful serum tumor marker in HCC

A

Alpha-fetoprotein

GI Week 5 - WLB (16 decks)

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