GI - Pathology (Liver Part I: Cirrhosis & other conditions) Flashcards

Pg. 360-361 in First Aid 2014 Sections include: -Cirrhosis and portal hypertension -Serum markers of liver and pancreas pathology -Reye syndrome -Alcoholic liver disease -Non-alcoholic fatty liver disease -Hepatic encephalopathy

1
Q

What are 8 signs/symptoms of cirrhosis that result from effects of portal hypertension?

A

(1) Esophageal varices => (2) Hematemesis => (3) Peptic ulcer disease, (4) Melena (from esophageal varices and/or peptic ulcer disease), (5) Splenomegaly, (6) Caput medusae/Ascites, (7) Portal hypertensive gastropathy (8) Anorectal ascites

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2
Q

What are 11 signs/symptoms of cirrhosis that result from effects of liver cell failure?

A

(1) Hepatic encephalopathy (2) Scleral icterus (3) Fetor hepaticus (breath smells musty) (4) Spider nevi (5) Gynecomastia (6) Jaundice (7) Testicular atrophy (8) Liver “flap” = asterixis (coarse hand tremor) (9) Bleeding tendency (decreased clotting factors, increased prothrombin time) (10) Anemia (11) Ankle edema

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3
Q

Of the 11 signs/symptoms of cirrhosis that result from effects of liver cell failure, which 3 are due to increased estrogen?

A

(1) Spider nevi (2) Gynecomastia (3) Testicular atrophy

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4
Q

What gross/histological features define cirrhosis?

A

Diffuse fibrosis and nodular regeneration destroys normal architecture of liver

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5
Q

What risk does cirrhosis increase?

A

Increased risk for hepatocellular carcinoma (HCC)

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6
Q

What are 4 etiologies of cirrhosis?

A

(1) Alcohol (60-70%) (2) Viral hepatitis (3) Biliary disease (4) Hemochromatosis

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7
Q

What is a vascular consequence of cirrhosis, and why? Give 2 examples of this.

A

Portosystemic shunts partially alleviate portal hypertension: (1) Esophageal varices (2) Caput medusae

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8
Q

Name 6 serum markers of liver and pancreas pathology.

A

(1) Alkaline phosphatase (ALP) (2) Aminotransferases (AST and ALT) (often called “liver enzymes”) (3) Amylase (4) Ceruloplasmin (5) gamma-glutamyl transpeptidase (GGT) (6) Lipase

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9
Q

What are 3 major diagnostic uses for alkaline phosphatase (ALP)?

A

(1) Obstructive hepatobiliary disease (2) HCC (3) Bone disease

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10
Q

What are 2 major diagnostic uses for Aminotransferases (AST and ALT) (often called “liver enzymes”)?

A

(1) Viral hepatitis (ALT > AST) (2) Alcoholic hepatitis (AST > ALT)

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11
Q

What are 2 major diagnostic uses for Amylase?

A

(1) Acute pancreatitis (2) Mumps

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12
Q

What is the major diagnostic use for Ceruloplasmin?

A

Decreased in Wilson disease

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13
Q

What is the major diagnostic use of gamma-glutamyl transpeptidase (GGT)? With what condition is it associated?

A

Increase in various liver and biliary diseases (just as ALP can), but NOT in bone disease; Associated with alcohol use

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14
Q

What is the major diagnostic use for Lipase?

A

Acute pancreatitis (most specific)

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15
Q

What is Reye syndrome, and in what patient population does it occur?

A

Rare, often fatal childhood hepatoencephalopathy

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16
Q

What are 6 clinical findings associated with Reye syndrome?

A

Findings: (1) mitrochondrial abnormalities, (2) fatty liver (microvesicular fatty change), (3) hypoglycemia, (4) vomiting, (5) hepatomegaly, (6) coma.

17
Q

What preceding exposures are associated with Reye syndrome?

A

Associated with viral infection (especially VZV and influenza B) that has been treated with aspirin.

18
Q

What is the mechanism of damage in Reye syndrome?

A

Mechanism: aspirin metabolites decreased Beta-oxidation by reversible inhibition of mitochondrial enzyme

19
Q

What is the general rule for Aspirin use in children? What is the exception?

A

Avoid aspirin in children, except in those with Kawasaki disease

20
Q

What are 3 types of alcoholic liver disease?

A

(1) Hepatic steatosis (2) Alcoholic hepatitis (3) Alcoholic cirrhosis

21
Q

What kind of change does hepatic steatosis lead to, and what causes it?

A

Reversible change with moderate alcoholic intake

22
Q

What is the key histologic finding in hepatic steatosis? How may it be reversed?

A

Macrovesicular fatty change (see hepatocytes filled with clear fat droplets) that may be reversible with alcohol cessation

23
Q

What causes alcoholic hepatitis?

A

Requires sustained, long-term consumption

24
Q

What are 2 major histologic findings in alcoholic hepatitis?

A

(1) Swollen and necrotic hepatocytes with neutrophilic infiltration. (2) Mallory bodies (intracytoplasmic eosinophilic inclusions) are present.

25
Q

Of ALT and AST, which is greater in alcoholic hepatitis? What is their ratio?

A

AST > ALT (ratio usually > 1.5); Think: “make toAST with alcohol”

26
Q

What is the final and irreversible form of alcoholic liver disease?

A

Alcoholic cirrhosis

27
Q

What is the major histologic description of alcoholic cirrhosis?

A

Micronodular, irregularly shrunken liver with “hobnail” appearance. Sclerosis around central vein (zone III).

28
Q

What vascular structure is sclerosed in liver cirrhosis, and in what zone of the liver is this?

A

Sclerosis around central vein (zone III).

29
Q

What defines the manifestations of alcoholic cirrhosis?

A

Has manifestations of chronic liver disease (e.g., jaundice, hypoalbuminemia)

30
Q

What is the pathophysiology and resultant histologic finding of non-alcoholic fatty liver disease? How does it relate to alcohol use?

A

Metabolic syndrome (insulin resistance) => fatty infiltration of hepatocytes => cellular “ballooning” and eventual necrosis. Independent of alcohol use.

31
Q

What are 2 conditions that may result from non-alcoholic fatty disease?

A

May cause cirrhosis and HCC

32
Q

Of ALT and AST, which is greater in non-alcoholic fatty liver disease?

A

ALT > AST; Think: “L = aLt & Lipids”

33
Q

Briefly give the pathogenesis of hepatic encephalopathy.

A

Cirrhosis => portosystemic shunts => decreased NH3 metabolism => neuropsychiatric dysfunction

34
Q

What is the spectrum of symptoms/signs defining hepatic encephalopathy?

A

Spectrum from disorientation/asterixis (mild) to difficult arousal or coma (severe)

35
Q

What are 2 triggers of hepatic encephalopathy? Give at least 3 examples in which each occur.

A

Triggers: (1) Increased NH3 production (due to dietary protein, GI bleed, constipation, infection) (2) Decreased NH3 removal (due to renal failure, diuretics, post-TIPS)

36
Q

What are the treatments for hepatic encephalopathy?

A

Treatment: Lactulose (increased NH4+ generation), Low-protein diet, and Rifaximin (kills intestinal bacteria)