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Pathology > Liver and Biliary > Flashcards

Liver and Biliary Flashcards

1
Q

How is the liver connected to the intestine and the great vessels?

A

The liver is connected to the gallbladder on the inferior side. Also at the hilus is the dual blood supply

  • hepatic artery: arterial oxygenated
  • portal vein: venous rich nutrient
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2
Q

Which cells form liver lobules?

A

hepatocytes are arranged into lobules

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3
Q

What are the main functions of the liver?

A
  • *Excretory:** bile
  • *Metabolic:** processing factory for food
  • *Storage:** carbs/lipids
  • *Synthetic:** major plasma proteins (except immunoglobulins)
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4
Q

What are the consequences of portal hypertension?

A
  1. formation of varicosities d/t increased pressure
  2. chronic passive congestion in the spleen (portal vein connects)
  3. transudation of fluid >> ascites
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5
Q

How is bilirubin formed and excreted?

A

Senescent RBCs are taken up by phagocytic cells of the spleen and kupffer cells of the liver. Within these cells, hgb is degraded to heme and globin.

Heme loses the iron and is transformed into yellow pigment = bilirubin. Bilirubin is then bound in the blood by albumin = unconjugated. Unconjugated which is not water soluble is taken up by liver cells and conjugated to glucuronide. Bilirubin bound to glucuronide = water soluble. Bacteria not used in the intestine is converted by bacteria to urobilinogen.

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6
Q

Which enzymes are released into the circulation from damaged liver cells?

A

AST and ALT are ubiquitous enzymes that are elevated in blood after liver injury (and also other organs).

Alkaline phosphatase is used as marker for bile duct obstruction.

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7
Q

What are three principal forms of jaundice and what causes each of them?

A
  • *Prehepatic:** unconjugated, usually due to excessive bilirubin formation secondary to hemolysis
  • malaria, Gilbert’s disease*

Hepatic: mixed conjugated, unconjugated, can be caused by acute or chronic hepatitis, hepatotoxicity, cirrhosis, drug-induced hepatitis and alcoholic liver disease. Cell necrosis reduces the liver’s ability to metabolize and excrete bilirubin** **

**Posthepatic: **conjugated, disturbance in excretion, usually (gallstones) at the level of the common bile duct.

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8
Q

Compare the biochemical laboratory findings in prehepatic, hepatic, and posthepatic jaundice.

A

unconjugated >> does NOT cross BBB, does not filter in urine

conjugated >> excreted in urine

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9
Q

What are the causes of viral hepatitis?

A

Hepatitis A, B, C, D, E

Hepatotropic viruses: mono, epstein-barr, herpes, CMV

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10
Q

Compare viral hepatitis A with viral hepatitis B and C.

A

Hepatitis A and C and RNA viruses; Hepatitis B is aDNA virus.

Hep A is F/O, while B and C are Par/Sex.

Hep A is NOT associated with a carrier state. Hep B and C are.

A vaccine is available for A and B. NOT for C.

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11
Q

Explain the signficance of serologic tests for the diagnosis of hepatitis.

A

HBsAg: surface antigen

released early, can be detected 1 week after onset
Persists only in patient who develop CHRONIC

HBcAg: core antigen

Antibodies appear in all infected persons
IGM first, IgG later

HBeAg: e antigen

Appears early, but disappears during ICTERIC stage

*presence in CHRONIC is a marker of INFECTIVITY

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12
Q

Compare the findings in acute and chronic hepatitis.

A

In hepatitis B there is a preicteric, icteric, and convalescent phase:
Preicteric: weakness, N/V, mild enlargement/tenderness of liver, rash, dark urine
* the more profound jaundice = more likely recovery
mild jaundice = likely transition to chronic

Chronic = intralobular inflammation, portal tract inflammation, disruption of lobular architecture secondary to aggresive inflammation and fibrosis

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13
Q

What is cirrhosis, and how does this disease present clinically?

A

= chronic liver disease characterized by loss of normal liver structure and function

irreversible and incurable

  • coma
  • thin hair
  • facial telangiectasia
  • jaundice
  • parotid bland enlargement
  • spider nevi
  • muscle wasting, gynecomastia
  • HSM
  • caput medusa
  • ascites
  • palmar erythema
  • absent of reduced pubic hair, small testes
  • edema, purpura
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14
Q

What are the common causes of cirrhosis?

A

Alcohol abuse

Hepatitis B and C

Hereditary metabolic diseases

  • Hemochromatosis
  • Wilson’s disease
  • Alpha antitrypsin

Autoimmune disease

  • biliary cirrhosis
  • primary sclerosing cholangitis
  • autoimmune hepatitis

drug use

biliary obstruction

  • cystic fibrosis
  • gallstones

or cryptogeneic

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15
Q

Compare portal and biliary cirrhosis.

A

portal >> results from liver cell necrosis followed by ingrowth of fibrous tissue from the portal tracts

fibrous scars increase, incirciling remaining liver parenchyma and inhibiting ability to regenerate.

biliary >> results from diseases of the biliary tree, primary or secondary

primary = autoimmune disease

secondary = develops after prolonged, partial or complete obstruction of bile flow

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16
Q

Describe the gross and microscopic features of a cirrhotic liver.

A

Alcoholic cirrhosis: fatty, yellow, enlarged

Other forms: shrinks

Histology: liver cells arranged into nodules, separated by dense connective tissue

  • if fat: alcoholic
  • mallory’s hyaline: alcoholic
  • cytoplasmic granules: alpha AT deficiency
  • iron: hemochromatosis
17
Q

Why are some cirrhotic livers yellow and some others are rusty brown.

A

Initally virally infected livers appear normal and have a smooth surface on gross examintaiton. In such livers, the signs of liver cell injury can be seen only microscopically. Alcohol abuse leads to fatty transformation of the liver, which appears yellow.

18
Q

What is the pathogenesis of ascites and splenomegaly in chronic liver disease?

A

Backpressure in brances of the portal vein results in the transudation of fluid from the serosal surfaces of the intestines, liver, and peritoneal surfaces lining the abdominal cavity. REduced oncotic pressure of the plasma secondary to hypoalbuminemia facilitates the passage of fluids from the circulation to the abdominal cavity. This results in relative hypovolemia, which triggers the release of aldosterone from the adrenal cortex. Aldosterone causes sodium and water retention >> anuria = hepatorenal syndrome.

19
Q

What is the pathogenesis of hepatic encephalopathy, and how does it present clinically?

A

= clouded mentation and neurologic symptoms

*thought to be caused by ammonia. Shows edema and altered astrocytes. *

20
Q

What is hepatorenal syndrome?

A

REduced oncotic pressure of the plasma secondary to hypoalbuminemia facilitates the passage of fluids from the circulation to the abdominal cavity. This results in relative hypovolemia, which triggers the release of aldosterone from the adrenal cortex. Aldosterone causes sodium and water retention >> anuria = hepatorenal syndrome.

21
Q

Which endocrine abnormalities are found in patients with cirrhosis?

A

Sex hormones: impotence, gynecomastia, anovluation

Abn Vit D: osteodystrophy

Abn metabolism of thyroid hormones: hypothyroidism

22
Q

Why do patients with cirrhosis bleed?

A

Decreased synthesis of coagulation proteins.

23
Q

Compare predictable and unpredictable liver injury caused by drugs.

A

predictable = dose related

eg. tylenol (necrosis, >15g), tetracycline (fatty changes)

unpredictable = those without obvious explanation

eg. halothane (viral like), chlorpromazine (cholestasis), methyldopa (chronic), phenybutazone (granuloma), estrogens (tumor), isoniazid (mild hepatitis)

24
Q

How does alcohol affect the liver?

A

Fatty liver: increases fatty acid sythesis, decreased oxidation, decreased export of lipoproteins, dose dependent fatty changes

**alcoholic hepatitis: **fever, leukocytosis, abd pain, jaundice. Focal necrosis of liver cells associted with leukocytic infiltrates and bile stasis. OFten contain eosinophilic aggregates of intermediate cyoskeletal filamens = mallory’s hyaline.

cirrhosis

25
Q

What is Gilbert’s disease?

A

Autosomal dominant disorder

  • intermittent jaundice
  • after puberty
  • males
  • unconjugated hyperbilirubinemia
26
Q

Compare hereditary hemochromatosis and Wilson’s disease.

A
  • both autosomal recessive
  • hemochromatosis = iron, pigmentary cirrhosis, bronze diabetes
  • wilson’s = copper, cirrhosis, eyes and brain
27
Q

How does alpha 1 antitrypsin deficiency affect the liver?

A

Autosomal recessive

  • accumulates in the form of cytoplasmic globules
  • >> cholestasis, chronic hepatitis
28
Q

What is autoimmune hepatitis?

A
  • affects young women
  • serology: high Ig, ANA
  • inflammatory infiltrates of plasma cells and lymphocytes
29
Q

Compare primary biliary cirrhosis and primary sclerosing cholangitis.

A
  • *Primary biliary cirrhosis**
  • destruction of intrahepatic bile ducts and progression >> cirrhosis
  • type IV hypersensitivity?
  • antibodies to mitochondria
  • women
  • fatigue, itching, jaundice
  • xanthomas = infiltrates of macrophages full of lipids
  • *Primary sclerosing cholangitis**
  • destruction of intra and extra hepatic ducts
  • cell mediated
  • segmental, beaded appearance
  • often have Crohn’s, UC
30
Q

How do bacteria protozoa, and parasites infect the liver?

A

Infections can reach the liver through the bile ducts, blood flowing from hepatic artery/portal vein, wounds, extension from adjacent abdominal organs.

  • Typically bacterial resistant: pylphlebitic abcess, ascending cholangitis, e coli, proteus, strep fecalis
31
Q

What is the difference between cholangitic and pylephlebitic abscesses?

A

Cholangitic: mostly assoc with biliary obstruction
Pylephlebitic: entry from portal vein

32
Q

Compare cholesterol stones with pigmentary gallstones.

A

Cholesterol stones = supersaturated bile, decreased bile acids, lecithin, solitary

Pigmentary = calcium bilirubinate, multiple

33
Q

What is the pathogenesis of cholecystitis?

A

Gallstones may mechanically injure the mucosa.

  • cause chronic inflammation
  • obstruction >> mecrosis
  • inflamed serosa >> adhesion >> fistula
34
Q

List the most important primary tumors of the hepatobiliary tract.

A

Hepatocellular carcinomas = most important

35
Q

Compare hepatocellcular carcinoma with cholangiocarcinoma.

A

Hepatocellular:

Cholangiocarcinoma:

36
Q

Compare cholangiocarcinoma with gallbladder carcinoma.

A
37
Q

Compare the pathology of primary and metastatic liver tumors.

A

Metastatic = typically multiples, nodules, central softened or indented necrotic areas

38
Q

What are the indications for liver transplantation?

A
  • all forms of cirrhosis
  • acute liver necrosis
  • metabolic disorders (wilson’s, at deficiency, hemochromatosis)

Pathology (16 decks)

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