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Pathology > Pathology of the liver, biliary tract and pancreas > Flashcards

Pathology of the liver, biliary tract and pancreas Flashcards

1
Q

Major characteristics of hepatic failure (3)

A
  1. Hepatic encelopathy
  2. Hepatorenal syndrome
  3. Hemorrhagic diathesis
  4. Hepatopulmonary syndrome
  5. Hepatic cardiomyopathy
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2
Q

Hepatic failure: clinical features

A
  • Jaundice
  • Malabsorption/weight loss
  • Hypoalbuminema
  • Hyperammonemia: decreased urea cycle
  • Hyperestrogenemia: impaire estrogen metabolism
  • Palmar erythema and spider angiomas in the skin
  • Ascites, splenomegaly, gastroesophageal varices: due to portal HTN
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3
Q

Difference in mechanisms of acute and chronic hepatic failure in causing hepatic encelopathy

A

Acute: elevated blood ammonia impairs the neuronal functioning and promotes brain edema

Chronic: altered amino acid metabolism causes deranged neurotransmission

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4
Q

Major alterations that cause liver failure

A
  1. Chronic liver disease: liver cirrhosis
  2. Acute liver disease: associated with hepatic necrosis
  3. Reye syndrome: causes liver failure without necrosis
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5
Q

Types of jaundice (3)

A
  1. Prehepatic: caused by hemolytic anemia - too much hemoglobin is degraded
  2. Hepatic: caused by any liver disease (Criggler-Najjar, Gilbert syndrome, Dubin-Johnson syndrome)
  3. Posthepatic: problems with excretion of bile (gall stones, tumor etc.)
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6
Q

Primary biliary cirrhosis: pathogenesis

A

Autoimmune disorder. Antimitochondrial antibodies target intrahepatic bile ducts, causing inflammation and cholestasis.

Serum ALP and cholesterol are elevated. Hyperbilirubinemia develops later.

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7
Q

Primary sclerosing cholangitis: pathogenesis

A

Autoimmune disease targeting extrahepatic and large intrahepatic bile ducts.

Associated with IBD, especially ulcerative cholitis.

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8
Q

Processes causing formation of cholesterol stones (4)

A
  1. Supersaturation of bile with cholesterol
  2. Nucleation into monohydrate crystals
  3. Stasis in the gallbladder
  4. Mucous hypersecretion traps the crystals
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9
Q

Cholesterol stones: morphology

A

Two types:

  1. Pure cholesterol stones: pale yellow
  2. Cholesterol stones containing calcium carbonate, phosphates and/or bilirubin: grey-white-black
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10
Q

Pigment stones: pathogenesis

A

Presence of unconjugated bilirubin, which can occur with hemolytic anemias and infections of the biliary tree. Precipitates are insoluble calcium bilirubinate salts.

Risk factors - the four Fs:

  • Age (Forty)
  • Gender (Female)
  • Heridetary (Familial)
  • Obesity (Fat)
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11
Q

Differences between black and brown pigment stones

A

Black:

  • Found in sterile GB bile
  • Small; in large quantities
  • Crumble easily
  • Radiopaque

Brown:

  • In infected ducts
  • Occur singly or in small quantities
  • Soft and greasy, due to presence of fatty acids
  • Radiolucent
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12
Q

Circulatory disorders of the liver (3)

A
  1. Impaired flow into the liver: hepatic artery inflow or portal vein obstruction and thrombosis
  2. Impaired flow through the liver
  3. Hepatic vein outflow obstruction
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13
Q

Causes of extrahepatic portal vein obstruction

A
  • Peritoneal sepsis
  • Pancreatitis
  • Tumor
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14
Q

Consequences of portal vein obstruction

A
  • Abdominal pain
  • Ascites
  • Esophageal varices
  • Intestinal congetion
  • Splenomegaly
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15
Q

Symptoms of impaired blood flow through in the liver

A
  • Ascites (cirrhosis)
  • Esophageal varices (cirrhosis)
  • Hepatomegaly
  • Elevated transaminases
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16
Q

Causes of impaired blood flow through the liver

A
  • Cirrhosis (most common)
  • Sickle cell disease
  • DIC (occludes sinusoids)
17
Q

Hepatic manifestations of right-sided heart failure

A

Enlarged, tense and cyanotic liver. Congestion of centrilobular sinusoids. Centrilobular hepatocytes atrophy.

18
Q

Hepatic manifestations of left-sided heart failure

A

Can cause hepatic hypoperfusion and hypoxia. Hepatocytes undergo ischemic necrosis.

19
Q

Causes of obstruction of the hepatic vein

A
  • Hepatic vein thrombosis (Budd-Chiari syndrome): thrombosis of two or more hepatic veins
  • Sinusoidal obstruction syndrome: caused by toxic injury to sinusoidal epithelium
20
Q

Hepatitis A

A
  • Benign, self-limiting
  • Causes acute hepatitis, never becomes chronic
  • Fecal-oral transmission
21
Q

Hepatitis B

A
  • Pareneteral transmission (blood and body fluids)

Stages:

  1. Acute (IgM)
  2. Window (non-progressive)
  3. Resolved
  4. Chronic (IgG)
  5. Immunization
22
Q

Hepatitis C

A
  • Pareneteral transmission
  • Acute; often becomes chronic
  • No vaccination
23
Q

Chronic hepatitis: etiology

A
  • Wilson disease: inherited disorder where copper deposits
  • alpha1-antitrypsin deficiency
  • Chronic alcoholism
  • Drugs
  • Autoimmunity
24
Q

Forms of alcoholic liver disease (3)

A
  1. Hepatic steatosis
  2. Alcoholic hepatitis
  3. Cirrhosis
25
Q

What are Mallory bodies?

A

Eosinophilic cytoplasmic inclusions in degenerating hepatocytes. Appear in cases of alcoholic hepatitis.

26
Q

Hemochromatosis

A

AR disorder characterized by excess iron storage. Mutation in the HFE-gene leading to impaired function of hepcidin which inhibits iron absorption. Iron is toxic to tissues.

Clinically: abdominal pain, hepatomegaly, diabetes mellitus.

27
Q

Wilson disease

A

AR disorder of copper metabolism, in which copper deposits in mainly the liver, eyes and brain. Mutation in a gene encoding an ATPase metal ion transporter. Commonly presents as acute or chronic liver failure.

28
Q

α1-antitrypsin deficiency

A

AR disorder marked by abnormally low AAT levels. AAT works to inhibit proteases as sites of inflammation. Can cause emphysema in the lungs.

29
Q

Cirrhosis: pathogenesis

A
  • Hepatocellular death
  • Regeneration
  • Progressive fibrosis
  • Vascular changes
30
Q

Tumor-like lesions of the liver (3 types of nodules)

A
  1. Focal nodular hyperplasia: response to vascular injury causing parenchymal atrophy
  2. Macroregenerative nodules: appear in cirrhotic livers
  3. Dysplastic nodules: proliferative hepatocytes
31
Q

Benign tumors of the liver

A
  • Hepatic cavernous hemangioma
32
Q

Hepatocellular cc: etiology

A
  • HBV/HCV
  • Aflatoxin exposure
  • Chronic alcoholism/cirrhosis
33
Q

Classification of cholecystitis

A
  • Acute (calculous) cholecytitis: usually due to obstruction by gallstones
  • Acute non-calculous cholecystitis: associated with infections, autoimmune vasculitis and trauma
  • Chronic cholecystitis
34
Q

Complications of cholecystitis

A
  • Bacterial superinfection
  • Gallbladder perforation
  • Gallbladder rupture
  • Biliary enteric fistula
35
Q

Acute pancreatitis: pathogenesis

A

Inappropriate activation of pancreatic enzymes, due to:

  • Pancreatic duct obstruction
  • Primary acinar injury
  • Defective intracellular transport of proenzymes within acinar cells
36
Q

Chronic pancreatitis: pathogenesis

A
  • Ductal obstruction
  • Toxic-metabolic
  • Oxidative stress
  • Necrosis fibrosis
37
Q

Types of chronic pancreatitis (3)

A
  1. Chronic autoimmune pancreatitis
  2. Chronic obstructive pancreatitis: periductal fibrosis, ductal dilation
  3. Chronic fibrotizing pancreatits (most common): seen in chronic alcoholic patients

Pathology (14 decks)

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