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GIT > Hepatic & Biliary Pathology > Flashcards

Hepatic & Biliary Pathology Flashcards

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1
Q

Causes of Chronic Liver Disease

A
  • nonalcoholic fatty liver disease, viral hepatitis, alcohol, toxins, hereditary disorders, immune mediated disorders, drug reactions
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2
Q

Nonalcoholic Fatty Liver Disease (NAFLD) is associated with __________ and __________.

A
  • obesity and type II diabetes
  • the metabolic syndrome (insulin resistance)
  • HTN and dyslipidemia are also linked
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3
Q

T or F: in viral hepatitis, the viruses do NOT directly injure the liver cells.

A
  • true!

- instead, the immune system targets the infected cells and is responsible for the damage

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4
Q

What are three inherited disorders that can lead to Chronic Liver Disease?

A
  • hemochromatosis
  • Wilson’s disease
  • alpha-1 anti-trypsin deficiency
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5
Q

Compare the duration, symptoms, and hepatic liver enzymes in acute viral hepatitis vs. chronic viral hepatitis.

A
  • acute: less than 6 months duration, jaundice is slightly more common, ALT and AST are in the 1000’s, ALT greater than AST
  • chronic: greater than 6 months duration, jaundice uncommon, ALT and AST are in the 100’s, ALT greater than AST
  • symptoms common to both: malaise, lethargy, RUQ discomfort (symptoms in viral hepatitis are RARE)
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6
Q

Which hepatitis viruses are DNA viruses?

A
  • only HBV

- (all others are RNA viruses)

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7
Q

Which hepatitis viruses can cause chronic hepatitis? How is each transmitted?

A
  • (obviously, all can cause acute hepatitis)
  • A: ssRNA, not chronic, fecal-oral
  • B: dsDNA, chronic, parenteral
  • C: ssRNA, chronic, parenteral
  • D: ssRNA, chronic, requires HBV to be present
  • E: ssRNA, not chronic, fecal-oral
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8
Q

Other than the hepatitis viruses, list three other viruses that are known to cause hepatitis.

A
  • cytomegalovirus, Epstein-Barr virus, herpes virus

- (these viruses are associated with more systemic infections)

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9
Q

What are the top three most common types of hepatitis?

A
  • hep A, then hep C, then hep B
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10
Q

Hepatitis ___ most commonly affects children. Why? What prophylaxis or treatment is there?

A
  • hep A most commonly affects kids because of their hygiene (HAV is spread fecal-orally)
  • there is a hep A vaccine (although the virus is rarely fatal)
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11
Q

How is hepatitis C spread parenterally? What percentage of patients will spontaneously clear the virus? Develop a chronic infection? Develop cirrhosis? What prophylaxis or treatment is there?

A
  • hep C is spread parenterally via blood-to-blood transmission
  • 30% with spontaneously clear the virus, 70% will develop chronic infection, 10% of whom will develop cirrhosis
  • no vaccine, treat with PEGylated interferon and Ribavirin (for genotypes 3, 4, 5, 6; for genotype 1 and 2, replace PEGylated interferon with oral antivirals)
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12
Q

How is hepatitis B spread parenterally? What prophylaxis or treatment is there?

A
  • hep A is spread parenterally via blood, birthing, and baby-making
  • there is a hep B vaccine, treat with PEGylated interferon and nucleoside analogs
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13
Q

T or F: treating hepatitis B and hepatitis C has a 60% cure rate.

A
  • true and false!
  • cure rate for hep C IS 60%
  • cure rate for hep B is very low, the goal of treatment being viral suppression rather than curative
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14
Q

Neonates infected with HBV will most likely develop ACUTE/CHRONIC hepatitis, while infected adults will most likely develop ACUTE/CHRONIC hepatitis.

A
  • neonates w/ HBV: most (90%) will develop chronic hepatitis

- adults w/ HBV: most will develop acute hepatitis and then get better (10% will develop chronic disease)

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15
Q

Which serology marker indicates an ongoing HBV infection? Which indicates an immunity to HBV?

A
  • HBsAg (the HBV surface antigen) indicates an ongoing infection
  • aHBs (anti-HBV surface antigen antibody) indicates immunity
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16
Q

What is Hemochromatosis? What mutation is involved? What causes the damage? When does it typically present?

A
  • an autosomal recessive inherited defect (C282Y mutation of the HFE gene on chromosome 6p) that can lead to chronic liver disease
  • mutations result in excess iron deposition and storage, especially in the liver, pancreas, heart, skin, and gonads
  • iron generates free radicals, which damage these organs
  • typically presents in late adulthood as the accumulation takes a while
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17
Q

What is used to screen for Hemochromatosis? What is the classic triad of symptoms/clinical findings?

A
  • transferrin saturation (if greater than 0.45 –> indicative of hemochromatosis)
  • classic triad: cirrhosis (liver), diabetes (pancreas), and bronze skin
  • (also: cardiac arrhythmia and gonadal dysfunction)
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18
Q

What is Wilsons’ Disease? What mutation is involved? When does it typically present?

A
  • an autosomal recessive inherited defect that can lead to chronic liver disease
  • mutations in ATP7B gene (chromosome 13) coding for ATP-mediated hepatocyte copper transport result in excess copper accumulation (in liver, brain, cornea, kidneys, and joints), resulting in acute liver failure, cirrhosis, and neurological disease
  • copper fails to enter the circulation as ceruloplasmin
  • presents in childhood, unlike hemochromatosis
  • much more rare than hemochromatosis
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19
Q

Which phenotype is responsible for alpha-1 anti-trypsin deficiency?

A
  • a recessive PiZ/PiZ phenotype
  • (normal allele is PiM)
  • (note that only 10% of patients will develop liver disease; emphysema is much more common)
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20
Q

Give three examples of immune disorders that can cause chronic liver disease.

A
  • autoimmune hepatitis (AIH)
  • primary biliary cirrhosis (PBC)
  • primary sclerosing cholangitis (PSC)
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21
Q

Autoimmune Hepatitis (AIH) usually involves elevated ____ levels. What do we use to treat it?

A
  • AIH usually has elevated IgG levels

- treat with prednisone

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22
Q

Primary Biliary Cirrhosis (PBC) usually involves elevated ____ levels. What do we use to treat it? What is targeted in this autoimmune disorder?

A
  • PBC usually has elevated IgM levels
  • treat with ursodeoxycholic acid
  • targets the mitochondria of intrahepatic/intralobular bile ducts (granulomatous destruction)
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23
Q

What is meant by “impaired synthetic function” and “decompensated liver disease”?

A
  • impaired synthetic function: abnormalities in prothrombin time and serum albumin
  • decompensated liver disease: issues w/ fluid accumulation, ascites, edema, and encephalopathy
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24
Q

Why does liver disease cause encephalopathy? What are the 4 grades of encephalopathy?

A
  • in severe liver disease, blood is shunted past the liver, so many toxins in the blood are unable to be cleared; when this toxic blood enters the brain/nervous system = impaired consciousness
  • grade 1: sleep inversion –> grade 2: asterixis –> grade 3: progression into a coma –> grade 4: coma
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25
Q

3 Major Life-Threatening Complications of Cirrhosis

A
  • variceal hemorrhages, spontaneous bacterial peritonitis, and hepatocellular carcinoma
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26
Q

How can we differentiate between ascites due to portal hypertension or due to another cause?

A
  • ascites in portal hypertension: albumin gradient increases, but total protein is decreased
  • ascites in another setting: albumin gradient increases, and total protein increases
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27
Q

What is Spontaneous Bacterial Peritonitis (SBP)?

A
  • infection of the ascitic fluid

- it is very dangerous and often asymptomatic

28
Q

Why are patients with varices commonly given antibiotics?

A
  • it’s used as a prophylaxis against sepsis if the varices rupture (variceal rupture is often associated with sepsis)
29
Q

What are the main causes of cirrhosis in the Western world? What about worldwide?

A
  • western world: alcoholic and metabolic liver disease

- worldwide: viral hepatitis B and C

30
Q

4 Main Biliary Diseases (and the age group they most commonly affect)

A
  • primary biliary cirrhosis (PBC): adults (female)
  • primary sclerosing cholangitis (PSC): adults (male)
  • congenital biliary atresia: infants/neonates
  • bile duct obstruction: all ages
31
Q

Congenital Biliary Atresia

A
  • failure of the common bile duct to develop normally, leading to complete obstruction of the biliary tract –> rapid cirrhosis occurs
  • elevated CONJUGATED bilirubin in neonates (neonatal jaundice/cholestasis)
32
Q

What is the most common liver malignancy? Why?

A
  • metastases are the most common (especially from colon, pancreas, lungs, and breasts)
  • because the liver receives a ton of blood from many different organs
33
Q

3 Patterns of Injury that can Cause Liver Failure

A
  • acute liver failure with massive hepatic necrosis (drugs, hepatitis)
  • chronic liver disease (most common; cirrhosis usually involved)
  • hepatic dysfunction without overt necrosis (least common; hepatocytes are viable but non-functional)
34
Q

5 Major Clinical Features of Hepatic Failure (due to chronic liver disease)

A
  • jaundice, hypoalbuminemia, palmar erythema, spider angiomas, hyperestrogenemia (hypogonadism and gynecomastia in men)
  • (in acute liver failure, patients may be jaundiced w/ encephalopathy)
35
Q

Jaundice in the eyes is known as:

A
  • sclerae icterus
36
Q

What is Cholestasis?

A
  • the retention of bilirubin and other bile solutes (bile salts and cholesterol)
  • manifests as pruritis and xantholasma
37
Q

What is Cirrhosis?

A
  • cirrhosis is a diffuse process characterized by fibrosis and the conversion of normal liver architecture into abnormal nodules
38
Q

What are the three main characteristics of a cirrhotic liver?

A
  • diffuse involvement, bridging fibrous septa, and parenchymal nodules
39
Q

What are the main symptoms of cirrhosis? What do most cirrhotic patients die from?

A
  • symptoms are non-specific: weight-loss, fatigue, anorexia (loss of appetite)
  • death due to liver failure, portal HTN, HCC
40
Q

What causes the portal hypertension in liver failure?

A
  • increased resistance to portal blood flow, mainly at the sinusoids, results in the hypertension
41
Q

What type of shunt can develop with portal hypertension? What 4 areas are at risk?

A
  • portosystemic shunts can develop wherever the systemic and portal circulations share capillary beds
  • can occur around and within the rectum (hemorrhoids), at the cardioesophageal junction (esophageal varices), in the retroperitoneum, and at the falciform ligament of the liver
42
Q

Caput Medusae

A
  • abdominal wall collaterals that develop in response to portal hypertension
43
Q

What is the predominant cell infiltrate in acute hepatitis? What about in chronic?

A
  • in BOTH types, the infiltrate is mainly mononuclear (T-cell mediated immune response)
  • (this differs to normal acute inflammation being neutrophilic in nature)
44
Q

What is a ground-glass cell?

A
  • a hepatocyte with HBsAg in its cytoplasm; this cell morphology is seen in hepatitis B
  • it occurs when the viral genome that encodes HBsAg is integrated into the host cell’s DNA
45
Q

Why does hepatitis D require HBV?

A
  • because it is replicative defective and requires encapsulation by HBsAg in order to replicate
46
Q

What unique morphology is seen in histology of hepatitis C?

A
  • fatty change

- (it often resembles alcoholic/non-alcoholic steatosis)

47
Q

List the stages of acute viral hepatitis.

A
  • incubation period –> symptomatic pre-icteric phase (malaise, fatigue, anorexia) –> symptomatic icteric phase (jaundice) –> convalescence
48
Q

Which three drugs have toxic effects that mimic hepatitis?

A
  • acetaminophen, isoniazid (used to treat TB), and some toxins
49
Q

What serology finding lets you know a patient is immune to hepatitis B via vaccination? What about immune due to a previous exposure?

A
  • vaccine: HBsAg neg, aHBc neg, aHBs pos

- previous infection: HBsAg neg, aHBc pos, aHBs pos

50
Q

Major diagnostic use for ALP, GGT, AST, and ALT.

A
  • ALP = alkaline phosphatase; obstructive hepatobiliary diseases, HCC, bone disease
  • GGT = gamma-glutamyl transpeptidase; similar to ALP but without bone disease, associated with alcohol
  • AST + ALT = aminotransferases; when AST is greater than ALT: alcoholic hepatitis (but neither will be greater than 300); when ALT is greater than ALT: viral hepatitis (acute is in the 1000s, chronic in the 100s)
51
Q

Major diagnostic use for amylase, lipase, ceruloplasmin, and transferrin.

A
  • amylase: acute pancreatitis, mumps
  • lipase: acute pancreatitis (the most specific!)
  • ceruloplasmin: decreases in Wilson’s disease
  • transferrin: increases in hemochromatosis
52
Q

What is Reye Syndrome? What is it highly associated with? What are the symptoms?

A
  • rare, often fatal childhood hepatoencephalopathy associated with viral infection treated with aspirin
  • symptoms: hypoglycemia, nausea, vomiting, coma
53
Q

Where does steatosis and fibrosis usually begin?

A
  • both begin in the centrilobular hepatocytes (zone III)
54
Q

What is a Mallory-Denk body? What pathology is it associated with? What does it look like on histology?

A
  • a tangle of intermediate filaments in the cytoplasm of degenerating hepatocytes
  • found in steatohepatitis (alcoholic fatty liver and NAFLD)
  • look for a twisted rope abnormality in the cytoplasm of the cell
55
Q

What is meant by the “chicken-wire fence” pattern?

A
  • associated with hepatic fibrosis (due to alcoholic fatty liver and NAFLD)
  • fibrosis begins at the centrilobular hepatocytes (zone III), first sclerosing the central vein and then spreading out to the sinusoids = chicken-wire fence
56
Q

What percent of heavy drinkers will develop alcoholic steatosis? Alcoholic hepatitis? Alcoholic cirrhosis?

A
  • 90-100% will develop steatosis (reversible)
  • 10-35% will develop hepatitis
  • 8-20% will develop cirrhosis (irreversible)
57
Q

What other liver pathology is a major accelerating factor of liver disease in alcoholics?

A
  • hepatitis C
58
Q

What is the most common primary malignant tumor of the liver? What is is associated with? Are there any serum markers?

A
  • hepatocellular carcinoma (HCC)
  • associated with HBV, HCV, cirrhosis, Wilson disease, hemochromatosis, a1AT deficiency, aflatoxins from Aspergillus spp.
  • in Oz, 70% of cases are due to chronic HCV
  • serum marker: alpha-fetoprotein (AFP)
59
Q

What percentage of patients with alpha-1 anti-trypsin deficiency present with hepatic involvement?

A
  • only 10-20% (emphysema is a much more common ailment)
60
Q

What’s a secondary cause of Hemochromatosis?

A
  • chronic blood transfusions
  • (ex: in patients with beta-thalassemia, they have non-functional Hb and require chronic transfusions. each transfusion is essentially bringing in iron into the body, as RBCs are an iron reservoir)
61
Q

Primary Sclerosing Cholangitis (PSC) usually involves elevated ____. What is targeted in this autoimmune disorder? What pathology is it associated with?

A
  • IgM antibodies are involved and elevated
  • targets both intra- and extrahepatic bile ducts (fibrotic destruction –> onion skin appearance)
  • associated with ulcerative colitis
62
Q

In hemochromatosis, affected hepatocytes will have a brown pigment from iron accumulation - what else gives hepatocytes a similar color? What can be used to distinguish between these on histo?

A
  • lipofuscin also gives a brown color similar to iron (it’s basically from old cells being broken down)
  • distinguish with a Prussian blue stain (if it’s iron, it will stain blue)
63
Q

What is colelithiasis? What are the general causes? What are the two types of stones? What are four main risk factors?

A
  • gallstones; precipitation of cholesterol and/or bilirubin in bile
  • due to stasis, excess cholesterol or bilirubin, and/or decreased bile acids
  • 2 types of stones: cholesterol stones (more common, yellow, radio-lucent) and bilirubin stones (black, radio-opaque)
  • risk factors are the 4 F’s: female (estrogen activates HMG CoA reductase, which makes cholesterol), fat (obesity), fertile (pregnant0, forties (age)
64
Q

What are the major symptoms/complications of colelithiasis?

A
  • biliary colic pain: waxing and waning pain in the RUQ (when the gallbladder is contracting against the stones)
  • cholecystitis: due to elevated pressures; RUQ pain that radiates to the right scapula, fever, nausea)
  • ascending cholangitis: bacterial infection of bile ducts via stasis
  • acute pancreatitis
  • gallstone ileus: stone enters the small bowel, causing an obstruction
  • fistula between gallbladder and small intestine
  • gallbladder carcinoma
65
Q

Long-standing cholelithiasis can result in cholecystitis, which can progress to chronic cholecystitis. What is the hallmark morphology of chronic cholecystitis? What complication can result?

A
  • Rokitansky-Aschoff sinus formation: mucosal outpouchings found in the smooth muscle of the gallbladder wall
  • can result in calcification of the gallbladder due to the chronic time frame = “porcelain gallbladder”
66
Q

What percent of cholecystitis is due to cholelithiasis? What percent of patients with cholelithiasis will also have choledocholithiasis?

A
  • 90% of cases of cholecystitis is due to gallstones (cholelithiasis)
  • 15% of patients with cholelithiasis also have choledocholithiasis (biliary tract stones)
67
Q

What is the triad of symptoms associated with acute cholangitis? The pentad of symptoms associated with suppurative ascending cholangitis?

A
  • acute: Carchot triad; RUQ pain, fever, jaundice
  • suppurative: Reynold pentad: the triad + mental status changes and hypotension
  • (cholangitis is infection of the biliary ducts)

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