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Pathoma > Exocrine Pancreas, Gallbladder, and Liver Pathology > Flashcards

Exocrine Pancreas, Gallbladder, and Liver Pathology Flashcards

1
Q

ANNULAR PANCREAS

A

Developmental malformation in which the pancreas forms a ring around the duodenum

risk of duodenal obstruction

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2
Q

ACUTE PANCREATITIS

  • Pathogenesis? $ Which enzyme is most responsible for this disease?*
  • Type of damage that occurs?*
  • Major causes?*
A

Inflammation and hemorrhage of the pancreas

  • Due to autodigestion of pancreatic parenchyma by pancreatic enzymes: Premature activation of trypsin leads to activation of other pancreatic enzymes.
  • liquefactive hemorrhagic necrosis of the pancreas and fat necrosis of the peripancreatic fat
  • Most commonly due to alcohol and gallstones; other causes include trauma,hypercalcemia, hyperlipidemia, drugs, scorpion stings, mumps, and rupture of a
    posterior duodenal ulcer.
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3
Q

ACUTE PANCREATITIS

Clinical features

A
  • Epigastric abdominal pain that radiates to the back.
  • Nausea and vomiting
  • Periumbilical and flank hemorrhage (necrosis spreads into the periumbilical soft tissue and retroperitoneum)
  • Elevated serum lipase and amylase; lipase is more specific for pancreatic damage.
  • Hypocalcemia (calcium is consumed during saponification in fat necrosis)
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4
Q

ACUTE PANCREATITIS

Complications

A
  • Shock -due to peripancreatic hemorrhage and fluid sequestration
  • Pancreatic pseudocyst - formed by fibrous tissue surrounding liquefactive necrosis and pancreatic enzymes
    • Presents as an abdominal mass with persistently elevated serum amylase
      • Rupture is associated with release of enzymes into the abdominal cavity and hemorrhage.
  • Pancreatic abscess - often due toE coli; presents with abdominal pain, high fever, and persistently elevated amylase
  • ** DIC** (enzymes get into blood and activate coagulation enzymes) and ARDS - Chew on alveolar-capillary interface.
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5
Q

CHRONIC PANCREATITIS

Clinical features

A

Fibrosis of pancreatic parenchyma, most often secondary to recurrent acute pancreatitis Most commonly due to alcohol (adults) and cystic fibrosis (children); however, many cases are idiopathic.

  • Epigastric abdominal pain that radiates to the back
  • Pancreatic insufficiency- results in malabsorption with steatorrhea and fatsoluble vitamin deficiencies. Amylase and lipase are not useful serologic markers of chronic pancreatitis.
  • Dystrophic calcification of pancreatic parenchyma on imaging; contrast studies reveal a ‘chain of lakes’ pattern due to dilatation of pancreatic ducts.
  • Secondary diabetes mellitus-late complication due to destruction of islets
  • Increased risk for pancreatic carcinoma
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6
Q

PANCREATIC CARCINOMA

$ Risk factors

Clinical features

Serum tumor marker

Prognosis

A

Adenocarcinoma arising from the pancreatic ducts - Most commonly seen in the elderly (average age is 70 years)

  • $ Major risk factors are smoking and chronic pancreatitis
  • Epigastric abdominal pain and weight loss
  • Obstructive jaundice with pale stools and palpable gallbladder; associated with tumors that arise in the head of the pancreas (most common location)
  • $ Secondary diabetes mellitus; associated with tumors that arise in the body or tail (Thin elderly female presenting with diabetes)
  • Pancreatitis
  • Migratory thrombophlebitis (Trousseau sign); presents as swelling, erythema, and tenderness in the extremities (seen in 10% of patients)
  • Serum tumor marker is CA 19-9

Very poor prognosis;1-year survival is < 10%.

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7
Q

Whipple procedure

A

Treatment for Pancreatic Carcinoma: Surgical resection involves en bloc removal of the head and neck of pancreas,proximal duodenum, and gallbladder

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8
Q

Elderly female presents with diabetes mellitus for the first time. What should be on your differential diagnosis?

A

Pancreatic carcinoma - Tumors that arise in the **body or tail of the pancreas **may be associated with secondary diabetes mellitus.

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9
Q

BILIARY ATRESIA

  • Leads to:*
  • Presentation*
A

Failure to form or early destruction of extrahepatic biliary tree

  • Leads to biliary obstruction within the first 3 months of life.
  • Presents with jaundice and progresses to cirrhosis
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10
Q

CHOLELITHIASIS

Cause

A

GALLSTONES

Solid, round stones in the gallbladder.

Due to precipitation of cholesterol (cholesterol stones) or bilirubin (bilirubin stones) in bile.

  • Arises with (1) supersaturation of cholesterol or bilirubin, (2) decreased phospholipids (e.g., lecithin) or bile acids (normally increase solubility), or (3) stasis - allows deconjugation
  • Drugs like cholestyramine - binds bile acids and decreased bile acids cause precipitation of cholesterol.
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11
Q

Most common type of gallstone?

Risk factors?

A

Cholesterol stones (yellow) are the most common type (90%), especially in the West

  • Usually radiolucent (10% are radiopaque due to associated calcium)
  • Risk factors include age (40s), estrogen (female gender, obesity, multiple pregnancies and oral contraceptives), clofibrate, Native American ethnicity,
    Crohn disease, and cirrhosis.
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12
Q

Bilirubin stones

  • Risk factors*
  • Clinical presentation of all gallstones*
  • Complications*
A

Pigmented, composed of bilirubincomposed of bilirubin

  • Risk factors include extravascular hemolysis from splenic macrophages (increased bilirubin in bile) and biliary tract infection (e.g., E coli, Ascaris lumbricoides, and Clonorchis sinensis)
  • usually asymptomatic
  • Complications include biliary colic, acute and chronic cholecystitis, ascending cholangitis, gallstone ileus, and gallbladder cancer.
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13
Q

Types of gallstones

A
  • Cholesterol stones (yellow) most common type (90%), radiolucent, caused by decreased bile acids, stasis, or supersaturatio of cholesterol.
  • Bilirubin stones (pigmented) made of bilirubin, usually radiopaque, casued by supersaturation of bilirubin, risk factors include: extravascular hemolysis or biliary tract infections.
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14
Q

BILIARY COLIC

  • Cause*
  • Complication*
A

Waxing and waning right upper quadrant pain - Due to the gallbladder contracting against a stone lodged in the cystic duct. Common bile duct obstruction may result in acute pancreatitis or obstructive jaundice.

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15
Q

ACUTE CHOLECYSTITIS

  • Pathogenesis*
  • $ Presentation*
  • Risks if untreated*
A

Acute inflammation of the gallbladder wall

  • Impacted stone in the cystic duct results in dilatation with pressure ischemia,bacterial overgrowth (E coli), and inflammation.
  • Presents with right upper quadrant pain, often radiating to right scapula, fever with increased WBC count, nausea, vomiting, and increased serum alkaline phosphatase (from duct damage)
  • Rupture if untreated
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16
Q

CHRONIC CHOLECYSTITIS

Cause

$ Hallmark

  • Clinical presentation*
  • Late complication*
  • Risks if untreated*
A

Chronic inflammation of the gallbladder

  • Due to chemical irritation from longstanding cholelithiasis +/- bouts of cholecystitis.
  • $ Characterized by herniation of gallbladder mucosa into the muscular wall (Rokitansky-Aschoff sinus)
  • Presents with vague right upper quadrant pain, especially after eating
  • Porcelain gallbladder is a late complication - Shrunken, hard gallbladder due to chronic inflammation, fibrosis, and dystrophic calcification

Increased risk for carcinoma. Treatment is cholecystectomy, especially if porcelain gallbladder is present.

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17
Q

ASCENDING CHOLANGITIS

  • Cause*
  • Presentation*
  • When is there increased incidence of this condition?*
A

Bacterial infection of the bile ducts

  • Usually due to ascending infection with enteric gram-negative bacteria
  • Presents as sepsis (high fever and chills), jaundice, and abdominal pain
  • Increased incidence with choledocholithiasis (stone in biliary ducts)
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18
Q

GALLSTONE ILEUS

Cause?

A

Gallstone enters and obstructs the small bowel - Due to cholecystitis with fistula formation between the gallbladder and small bowel

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19
Q

GALLBLADDER CARCINOMA

  • Major risk factors*
  • Classic presentation*
  • prognosis*
A

_Adenocarcinoma arising from the glandular epithelium that lines the gallbladderwall _

  • Gallstones are a major risk factor, especially when complicated by porcelain gallbladder.
  • Classically presents as cholecystitis in an elderly woman
  • Poor prognosis
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20
Q

A 45 year old man presents with right upper quadrant pain especially after eating. No symptoms in the past. Most likely diagnosis?

A

Chronic cholecystitis - inflammation of the gallbladder most likely due to chemical irritation from longstanding cholelithiasis

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21
Q

An elderly woman presents with right upper quadrant pain, especially after eating. What should be on your differential diagnosis?

A

Presentation of cholecystitis in an elderly woman should be highly suscpective of gallbladder carcinoma - adenocarcinoma arising from the glandular epithelium that lines the gallbladder.

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22
Q

Most common cause of RUQ

A

Cholecystitis

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23
Q

Cholelithiasis

A

Gallstones

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24
Q

Cholecystitis

A

Inflammation/infection of the gall bladder

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25
Q

Cholangitis

A

Inflammation/infection of the biliary tree

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26
Q

Choledocholithiasis

A

Gallstones in the bile ducts

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27
Q

Reynolds Pentad

A

Charcot’s triad (Jaundice, Fever, RUQ) + Hypotension and altered mental status. for (osbtructive cholangitis)

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28
Q

Gold standard for diagnosing gallstones

A

RUQ ultrasound

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29
Q

Hallmark of cholecystitis

A

Positive Murphy’s sign - inspiratory arrest on deep palpation due to pain

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30
Q

Bilirubin

  • How removed from blood?*
  • Types?*
A

Yellow bile pigment that is a product of heme metabolism

  • Removed from blood by liver, conjugated with glucuronate (to make it water soluble), and excreted in bile
  • Direct - conjugated with glucuronic acid, water soluble
  • Indirect - unconjugated, water INSOLUBLE
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31
Q

JAUNDICE

A

Yellow discoloration of the skin, earliest sign is scleral icterus (yellow discoloration of the sclera)

  • Due to elevated total serum bilirubin, usually > 2.5 mg/dL
  • 3 Causes:
    1. Direct hepatocelluar injury
    2. Obstruction to bile flow
    3. Hemolysis
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32
Q

Normal bilirubin metabolism

A
  1. RBCs are consumed by macrophages of the reticuloendothelial system.
  2. Protoporphyrin (from heme) is converted to unconjugated bilirubin (UCB).
  3. Albumin carries UCB to the liver.
  4. Uridine glucuronyl transferase (UGT) in hepatocytes conjugates bilirubin.
  5. Conjugated bilirubin (CB) is transferred to bile canaliculi to form bile, which is stored in the gallbladder.
  6. Bile is released into the small bowel to aid in digestion.
  7. Intestinal flora convert CB to urobilinogen, which makes the stool brown. Urobilinogen is also partially reabsorbed into the blood and filtered by the kidney, making the urine yellow.
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33
Q

Jaundice caused by Extravascular hemolysis or ineffective erythropoiesis

Etiology

Lab findings

Clinical features

A
  • High levels of UCB overwhelm the conjugating ability of the liver
  • Increased UCB
  • $ Dark urine due to increased urine urobilinogen (NOT due to UCB because UCB is not water soluble and, thus, is absent from urine)
  • Urine biliruben is Absent (acholuria)
  • Increased risk for pigmented bilirubin gallstones
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34
Q

Physiologic jaundice of the newborn

  • Etiology*
  • Lab findings*
  • Clinical manifestations*
  • Treatement*
A

Newborn liver has transiently low UGT activity.

  • Increased UCB
  • UCB is fat soluble and can deposit in the basal ganglia (kernicterus) leading to neurological deficits and death.
  • Treatment is phototherapy (makes UCB water soluble). Does not conjugate UCB, only makes it water soluble.
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35
Q

Crigler-Najjar syndrome

Labs

Manifestations

A
  • Absence of UGT
  • Increased UCB
  • Kernicterus; usually fatal
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36
Q

Gilbert syndrome

Labs

Manifestations

A
  • Mildly low UGT activity; autosomal recessive
  • Increased UCB
  • Jaundice during stress (e.g., severe infection); otherwise, not clinically significant
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37
Q

Dubin-Johnson syndrome

  • Labs*
  • Clinical manifestation*
A

Deficiency of bilirubin canalicular transport protein; autosomal recessive

  • Increased CB
  • Liver is dark; otherwise, not clinically significant
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38
Q

Biliary tract obstruction (obstructive jaundice)

  • Etiology*
  • Labs*
  • Clinical manifestation*
A

Associated with gallstones, pancreatic carcinoma, cholangiocarcinoma, parasites, and liver fluke (Clonorchis sinensis)

  • Increased CB (anything in bile will leak into blood), Decreased Urine urobiliniogen and increased alkaline phosphatase
  • Dark urine (due to bilirubinuria) and **pale stool (can’t put bile into bowel) **
  • Pruritus due to increased plasma bile acids
  • Hypercholesterolemia with xanthomas
  • Steatorrhea with malabsorption of fat-soluble vitamins (can’t put bile into bowel)
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39
Q

Jaundice due to Viral hepatitis

A

Inflammation disrupts hepatocytes and small bile ductules.

Increased CB (small bile ducturles damaged causing increased bilirubin in urinedark urine) and UCB (destoryed hepatocytes decreases conjugating ability)

Urine urobilinogen is normal or decreased.

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40
Q

$ HEV infection in a pregant woman

A

HEV infection .in pregnant women is associated with fulminant hepatitis (liver failure with massive liver necrosis).

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41
Q

Where is HEV commonly acquired from?

A

Contaminated water or undercooked seafood

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42
Q

Describe the dependence of HDV on HBV for infection

A

HDV is dependent on HBV for infection;

$ Superinfection upon existing HBV is more severe than coinfection (infection with HBV aJld HDV at the same time)

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43
Q

What defines the chronic state of HBV infection?

A

+ HBsAG (presence > 6 + months defines the chronic state

  • Presence of HBeAg or HBV DNA indicates infectivity.
  • IgG to HBcAB and NEGATIVE IgG to HBsAB (lost the battle)
44
Q

What determines a resolved HBV infection?

A
  • NEGATIVE HBsAG
  • NEGATIVE HBeAG or HBV DNA
  • Positive HBcAB (indicating previous infection)
  • IgG POSITIVE to HBsAB (protective, indicating the patient has won the battle)
45
Q

VIRAL HEPATITIS

  • Causes*
  • Presentation*
  • Compare acute vs. chronic*
A

Inflammation of liver parenchyma, usually due to hepatitis virus other causes include EBV and CMV.

  • Hepatitis virus causes acute hepatitis, which may progress to chronic hepatitis
  • Acute hepatitis presents as jaundice (mixed CB and UCB) with dark urine (due to CB), fever, malaise, nausea, and elevated liver enzymes (ALT > AST).
    • Lobules and portal tracts inflammed with apoptosis of hepatocytes
    • Some cases asymptomatic
    • Symptoms < 6 month
  • Chronic hepatitis symptoms > 6 months
    • Inflammation mainly portal tract, risk of cirrhosis.
46
Q

CIRRHOSIS

$ What mediates fibrosis?

Describe the conditions it causes and what each state results in

A

End-stage liver damage characterized by disruption of the normal hepatic parenchyma by bands of fibrosis and regenerative nodules of hepatocytes.

$ Fibrosis is mediated by TGF-beta from stellate cells which lie beneath the endothelial cells that line the sinusoids.

1. Portal hypertension leads to:

  • Ascites (fluid in the peritoneal cavit y)
  • Congestive splenomegaly/hypersplenism
  • Portosystemic shunts
  • Hepatorenal syndrome

2. Decreased detoxification

  • Mental status changes, asterixis, and eventual coma (due to inc serum ammonia); metabolic, hence reversible
  • Gynecomastia, spider angiomata, and palmar erythema due to hyperestrinism
  • Jaundice

3. Decreased protein synthesis leads to

  • Hypoalbuminemia with edema
  • Coagulopathy due to decreased synthesis of clotting factors; degree of
    deficiency is followed by PT.
47
Q

ALCOHOL-RELATED LIVER DISEASE

Fatty liver

Alcoholic Hepatitis

Etiology

$ Hallmark seen in histology

Cirrhosis

A

Damage to hepatic parenchyma due to consumption of alcohol - Most common cause of liver disease in the West

  • Fatty liver - resolves with abstinence
  • Alcoholic hepatitis results from chemical injury to hepatocytes; generally seen with
    binge drinking
    • Acetaldehyde (metabolite of alcohol) mediates damage
    • $ Characterized by swelling of hepatocytes with formation of Mallory bodies (damaged cytokeratin filaments, necrosis, and acute inflammation
    • painful hepatomegaly
    • AST > ALT
  • Cirrhosis is a complication of long-term, chronic alcohol-induced liver damage; occurs in 10-20% of alcoholics
48
Q

NONALCOHOLIC FATTY LIVER DISEASE

A

Fatty change, hepatitis, and/or cirrhosis that develop without exposure to alcohol (or other known insult)

  • Associated with obesity
  • Diagnosis of exclusion; ALT > AST
49
Q

HEMOCHROMATOSIS

  • What causes tissue damage?*
  • 2 types?*
A

Excess body iron leading to deposition in tissues (hemosiderosis) and organ damage (hemochromatosis)

  • Tissue damage is mediated by generation of free radicals.
  • Due to autosomal recessive defect in iron absorption (primary) or chronic
    transfusions (secondary)
50
Q

hemosiderosis

A

Accumulation of hemosiderin in tissue, particularly in the liver and spleen. SEE hemochromatosis SYN haemosiderosis [hemosiderin + -osis, condition]

51
Q

hemosiderin

A
  • A yellow or brown protein produced by phagocytic digestion of hematin; found in most tissues, but especially in the liver; at higher levels, it stains blue with Perls Prussian blue stain.
52
Q

What causes Primary hemochromatosis?

Clinical presentation

Labs

Liver biopsy - What is seen and what agent is used? Why?

Risks

A

autosomal recessive defect in iron absorption

  • Primary hemochromatosis is due to mutations in the HFE gene, usually C282Y (cysteine is replaced by tyrosine at amino acid 282).
  • Presents in late adulthood: Classic triad is cirrhosis, secondary diabetes mellitus, and bronze skin; other
    findings include cardiac arrhythmias and gonadal dysfunction (due to testicular
    atrophy).
  • Labs show increased ferritin, decreased TIBC, increased serum iron, and increased %saturation
  • Liver biopsy reveals accumulation of brown pigment in hepatocytes
  • Prussian blue stain distinguishes iron (blue) from lipofuscin - Brown pigment granules representing lipid-containing residues of lysosomal digestion and considered one of the aging or “wear-and-tear” pigments; found in liver, kidney, heart muscle, and ganglion cells.
  • Increased risk for hepatocellular carcinoma
53
Q

WILSON DISEASE

  • Pathogenesis*
  • Presentation*
  • Labs*
  • Risks*
  • Treatment*
A

Autosomal recessive defect (ATP7B gene) in ATP mediated hepatocyte copper transport = lack of copper transport into bile and lack of copper incorporation into ceruloplasmin.

  • Copper builds up in hepatocytes, leaks into serum, and deposits in tissues.
  • Copper-mediated production of hydroxyl free radicals leads to tissue damage

Presentation:

  • Cirrhosis
  • Neurologic manifestations (behavioral changes, dementia, chorea, and
    Parkinsonian symptoms due to deposition of copper in basal ganglia)
  • Kayser-Fleisher rings in the cornea

Labs

  • Increased urinary copper,decreased serum ceruloplasmin, and i copper on liver biopsy.

Increased risk of hepatocellular carcinoma

D-penicillamine (chelates copper).

54
Q

PRIMARY BILIARY CIRRHOSIS

Labs

A

Autoimmune granulomatous destruction of intrahepatic bile ducts

  • Classically arises in women (average age is 40 years)
  • Associated with other autoimmune diseases

$ antimitochondrial antibody is present.

obstructive jaundice, cirrhosis late

55
Q

PRIMARY SCLEROSING CHOLANGITIS

Labs

$ Associations

Presents

Risks

A

Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts

  • Periductal fibrosis with an _‘onion-skin’ appearance _
  • Uninvolved regions are dilated resulting in a “beaded” appearance on contrast imaging.

$ Associated with ulcerative colitis; p-ANCA is often positive.

Presents with obstructive jaundice; cirrhosis is a late complication.

Increased risk for cholangiocarcinoma

56
Q

REYE SYNDROME

$ Pathogenesis

Presentation

A

Fulminant liver failure and encephalopathy in children with viral illness who take aspirin.

$ mitochondrial damage of hepatocytes

hypoglycemia, elevated liver enzymes, and nausea with vomiting; may progress to coma and death

57
Q

HEPATIC ADENOMA

$ Associations?

A

Benign tumor of hepatocytes - Associated with oral contraceptive use; regresses upon cessation of drug

  • Risk of rupture and intraperitoneal bleeding, especially during pregnancy - Tumors are subcapsular and grow with exposure to estrogen
58
Q

HEPATOCELLULAR CARCINOMA

$ Risk factors

When typically detected

Serum marker

A

Malignant tumor of hepatocytes

Risk factors include
1. Chronic hepatitis (e.g., HBV and HCV)
2. Cirrhosis (e.g., alcohol, nonalcoholic fatty liver disease, hemochromatosis,
Wilson disease, and AIAT deficiency)
3. $ Aflatoxins derived from Aspergillus (induce p53 mutations)

Increased risk for Budd-Chiari syndrome

  1. Liver infarction secondary to hepatic vein obstruction
  2. Presents with painful hepatomegaly and ascites

Tumors are often detected late because symptoms are masked by cirrhosis; poor prognosis

Serum tumor marker is alpha-fetoprotein - elevated in 70% of cases with HCC.

59
Q

METASTASIS TO LIVER

Sources

Results in:

How is it clinically detected?

A

More common than primary liver tumors; most common sources include colon, pancreas, lung, and breast carcinomas.

Results in multiple nodules in the liver

Clinically may be detected as hepatomegaly with a nodular free edge of the liver

60
Q

Most common cause of jaundice? #2?

A
  1. Viral hepatitis
  2. Gilbert’s disease: 2nd most common cause of jaundice; fasting unconjugated hyperbilirubinemia
61
Q

Phases of acute hepatitis?

What occurs during the prodrome?

A
  • prodrome, jaundice, recovery
  • Fever, painful hepatomegaly, Transaminases: peak before jaundice
62
Q

What causes color of stool and urine

A

Urobilin: color of stool and urine - Intestinal bacteria convert CB to urobilinogen (UBG). UBG is spontaneously oxidi/.ed to urobilin.

63
Q

Why is AST>ALT in alcoholic hepatitis?

A

AST is located in the mitochondria, and alcohol is a mitochondrial poison

64
Q

ALT

A

Serum alanine transaminase

Specific enzyme for liver cell necrosis
Present in the cytosol
ALT > AST: viral hepatitis

65
Q

AST

A

Serum aspartate transaminase

Present in mitochondria
Alcohol damages mitochondria: AST > ALT indicates alcoholic hepatitis

66
Q

most common viral cause of jaundice

A

HAV

67
Q

Most common blood-borne infection in the U.S.

A

HCV? CMV?

68
Q

Most common main indication for liver transplantation in U.S.

A

Hepatitis C

69
Q

Gold standard to diagnose HCV?

A

IICA’ RNA using polymerase chain reaction

70
Q

Most common cause of a liver abscess worldwide

Most common cause of liver abscess in US?

A

Amebiasis due to Entamoeba histolytica

Ascending cholangitis - *Escherichia coli -> *Tx: percutaneous drainage; metronidazole + ceftriaxone

71
Q

Autoimmune hepatitis: Markers?

A

+ serum ANA
+ anti-smooth muscle antibodies

72
Q

Neonatal hepatitis:

A

multifactorial; biopsy shows multinucleated giant cells

73
Q

Most common cause of fulminant hepatic failure?

Fulminant hepatic failure: labs?

A

Viral hepatitis

acetaminophen most common drug cause

Decreased transaminases, increased PT
and ammonia

74
Q

Poliosis hepatis

A

Sinusoidal dilation due to blood - caused by anabolic steroids. Bartonella henselae

75
Q

Most common cause of hepatic vein thrombosis

A

Polycythemia vera (40%)

Hypercoagulablc state (20% of cases)

Hepatocellular carcinoma (<5% of cases)

76
Q

Vcno-occlusive disease of the liver

A

Complication of bone marrow transplantation - Collagen develops around the central veins

77
Q

Hematobilia

A

Blood in the bile in patients with trauma to the liver

78
Q

Intrahepatic fibrosis due to these drugs:

Intrahepatic cholestasis due to these drugs:

A

methotrexate, amiodarone

OCP. anabolic steroids, estrogen from pregnancy can also induce cholestasis.

79
Q

Vinyl chloride, arsenic, thorium dioxide

A

Angiosarcoma

80
Q

Cholangiocarcinoma

A

Thorium dioxide

81
Q

Vinyl chloride, aflatoxln (due to Aspergillus mold)

vs.

Vinyl chloride, arsenic, thorium dioxide

A

Hepatocellular carcinoma

Angiosarcoma (Arsenic)

82
Q

Isomazid (caused by toxic metabolite), halothane, acetaminophen, methyldopa

A

Acute hepatitis

83
Q

Cause of jaundice in newborns

A

Extrahepatic biliary atresia

84
Q

ERCP diagnostic:
‘beading” of bile ducts

A

Primary sclerosing cholangitis (PSC)

85
Q

Factors precipitating encephalopathy

A
  1. Increased protein (most important)
  2. Alkalosis keeps ammonia in NH3 state
  3. Sedatives
  4. Portosystemic shunts
86
Q

TIPS

A

Transjugular intrahepatic portosystemic shunt (TIPS) - Ireduces portal vein pressure: connects portal vein with hepatic vein

87
Q

Serum albumin and ascitic fluid albumin

A

Ascites—liver vs. peritoneal’ serum albumin - ascitic fluid
albumin; >1.1 g/dL liver origin, <1.1 ug/dl peritoneal origin

88
Q

Primary Biliary cirrhosis (PBC)

Pathogenesis

findings

Clinical presentation

A

Granulomatous autoimmune destruction of bile ducts in portal triads

Environmental insult affecting mitochondrial proteins triggering CD8 T-cell destruction of intralobular bile duct epithelium

Autoantibodies (antimitochondrial antibodies) develop against the mitochondria

pruritus before jaundice, jaundice late

89
Q

Hemosiderosis

A

acquired iron overload disease

90
Q

Hemochromatosis

Features

Best screen

follow up

Screen relatives?

A

“bronze diabetes” (Type 1 DM)

malabsorption, restrictive cardiomyopathy, infertility

% saturation best screen

Serum ferritin: used to
follow therapy

HFE gene testing for C282Y mutation

91
Q

Metabolic state in cirrhosis

A

Decreased gluconeogenesis, Hypoglycemic, decreased glycogen stores, lactic acidosis, hyponatremia, hypokalemia.

92
Q

most common Liver cancer

A

Metastasis - Lung most common primary

93
Q

Biggest risk factor for HCC

A

Postnecrotic cirrhosisHBV/HCV most common risk factors

94
Q

Characteristic finding in HCC

A

Characteristic finding is the presence of bile in neoplastic cells.

95
Q

Most Common cause of cholangiocarcinoma

A

Primary sclerosing cholangitis (US)

96
Q

Courvoisier’s sign

A

Palpable gallbladder

97
Q

Treatment cholecystitis;

A

Cholecystectomy (laparoscope preferred) ERCP with sphincterotomy to extract stone in CBD

Meperidine for pain, Do not use morphine - Contracts the sphincter of Oddi and worsens pain

98
Q

excellent newborn screen for cystic fibrosis

A

Serum immunoreactive trypsin

99
Q

Pancreatic cancer mets site?

A
  • left supraclavicular node (Virchow),
  • periumbilical (sister mary Joseph’s) (Both also occur in stomach cancer)
100
Q

Gene mutation in Pancreatic cancer?

A
  • Association with K-RAS gene mutation
  • Mutation of suppressor genes (TP16 and TP53)
101
Q

Stages of Acute Cholecystitis

A
  1. Stone lodges in cystic duct; midepigastric colicky pain
  2. Stone impacts in cystic duct; pain shift to RUQ (dull, continuous aching); radiation to right scapular shoulder
  3. Bacterial invasion GB wall; + Murphy sign; subsides if stone falls out (90% subside over 37 days)
  4. Perforation - wall tension from BG distension compress lumen of intramural vessels - gangrenous necrosis
102
Q

Grey Turner sign:

Cullen’s sign:

A

flank hemorrhage seen in acute pancreatitis

periumbilical hemorrhage

103
Q

Persistent increase in scrum amylase:

A

consider pancreatic pseudocyst - Collection of digested pancreatic tissue around pancreas

104
Q

Most common cause of Acute pancreatitis

A

#1 Gallstones and #2 Ethanol. “GET SMASHHED” HIV drugs that cause pancreatitis are your NRTI’s - didanosine, zalcitabine, stavudine. and the PI - Ritonavir.

  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune
  • Scorpion
  • Hypercalcemia
  • Hypertriglyceridemia (>1000)
  • ERCP
  • Drugs (sulfa, NRTIs)
105
Q

Typical presentation of patient with pancreatic insufficiency

Treatment

A

Diarrhea; Steatorrhea; Weight loss; Weakness; Vitamin deficiencies (ADEK)

Tx: Limit fat intake; Replace pancreatic enzymes.

Pathoma (8 decks)

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