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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 Overview

A

Inflammation and hemorrhage of pancreas due to auto-digestion of pancreatic parenchyma by pancreatic enzymes - premature activation of trypsin –> activation of other pancreatic enzymes; Results in liquefactive hemorrhagic necrosis and fat necrosis (due to saponification); Most commonly due to alcohol and gallstones; Can be caused by trauma (car accident), hypercalcemia, hyperlipidemia, drugs, scorpion stings, mumps and rupture of posterior duodenal ulcer

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3
Q

Acute Pancreatitis Clinical Features

A

Epigastric abdominal pain radiating to back; Nausea and vomiting; Periumbilical and flank hemorrhage; Elevated serum lipase (more specific) and amylase (can also be found in saliva); hypocalcemia (due to consumption during saponification in fat necrosis (bad prognostic sign)
Complications: shock, pancreatic pseudocyst (fibrous tissue surrounding liquefactive necrosis and pancreatic enzymes), pancreatic abscess (often due to E. Coli), DIC and ARDS (enzymes digest coagulation factors and alveolar-capillary interface)

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4
Q

Pancreatic Pseudocyst

A

Complication of acute pancreatitis; 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 abdominal cavity and hemorrhage

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5
Q

Pancreatic Abscess

A

Often due to E. Coli; presents with abdominal pain, high fever, and persistently elevated amylase

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6
Q

Chronic Pancreatitis

A

Fibrosis of pancreatic parenchyma, most often secondary to recurrent acute pancreatitis (alcohol or CF);
Clinical Features: Epigastric abdominal pain that radiates to back; Pancreatic insufficiency (malabsorption and steatorrhea and fat soluble vitamin deficiencies –> elevated PT and PTT); Dystrophic calcification of pancreatic parenchyma on imaging (chain of lakes pattern due to dilation of pancreatic ducts)
Can result in secondary diabetes mellitus (due to islet destruction)
Increased risk for pancreatic carcinoma
Amylase and lipase are NOT useful serologic markers

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7
Q

Pancreatic Carcinoma

A

Adenocarcinoma from pancreatic ducts; Commonly seen in elderly;
Major risk factors: smoking and chronic pancreatitis
Clinical Features (occur late): epigastric abdominal pain and weight loss, pancreatitis, migratory thrombophlebitis (swelling, erythema and tenderness in extremities)
Tumors in head of pancreas: obstructive jaundice (pale stools and palpable gall bladder) due to conjugated bili not being able to get out
Tumors in body or tail of pancreas: Secondary diabetes mellitus (eg. thin elderly female who develops diabetes)
Serum tumor marker is CA 19-9
Whipple procedure for treatment, but poor prognosis

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8
Q

Whipple Procedure

A

Resection involving en bloc removal of head and neck of pancreas, proximal duodenum and gall bladder; for pancreatic carcinoma

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9
Q

CA 19-9

A

Serum marker for pancreatic carcinoma

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10
Q

Biliary Atresia

A

Failure to form or early destruction of extra-hepatic biliary tree; Leads to biliary obstruction within the first 2 months of life; Presents with jaundice (conjugated bilirubin) and progresses to cirrhosis (due to back pressure into liver)

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11
Q

Cholelithiasis

A

Solid, round stones in gallbladder due to precipitation of cholesterol or bilirubin in bile
Arises with:
1) supersaturation of cholesterol or bilirubin (increased)
2) decreased phospholipid (eg. lecithin) or bile acids, which normally help solubilize cholesterol
3) stasis, which increases bacterial deconjugation of bilirubin –> precipitation
Usu asymptomatic; Complications include biliary colic, acute and chronic cholecystitis, ascending cholangitis, gallstone ileus and gallbladder cancer

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12
Q

Cholesterol Gallstones

A

Most common in West; Yellow in color; Radiolucent usu;
Risk Factors: age (40s), estrogen leading to increased HMG CoA reductase activity and increased lipoprotein receprots on hepatocytes (female gender, obesity, multiple pregnancies, OCPs), clofibrate (increases HMG CoA reductase –> decreased lipids and decreased conversion of cholesterol to bile acids –> increase precipitation), Native American ethnicity, Crohn Disease (terminal ileum damage –> decreased reuptake of bile salts/acids –> decreased solubalization of cholesterol) and cirrhosis (decreased production of bile salts)

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13
Q

Bilirubin Gallstones

A

Pigmented (black); Usu. radiopaque;
Risk Factors: extravascular hemolysis (increased bilirubin), and biliary tract infection (E. Coli, Ascaris lumbricoides, Clonorchis sinensis)

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14
Q

Biliary Colic

A

Waxing and waning RUQ pain due to gallbladder contracting against a stone lodged in cystic duct;
Common bile duct obstruction may result in acute pancreatitis or obstructive jaundice
Symptoms subside if stone passes

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15
Q

Acute Cholecystitis

A

Acute inflammation of gallbladder wall; Impacted stone in cystic duct results in dilatation with pressure ischemia, bacterial overgrowth (E. Coli) and inflammation;
Presents with: RUQ pain often radiating to scapula, fever with increased WBC count, nausea, vomiting, increased serum alkaline phosphatase (duct damage)
Risk of rupture if left untreated

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16
Q

Chronic Cholecystitis

A

Chronic gallbladder inflammation due to chemical irritation from longstanding cholelithiasis with or without bouts of acute cholecystitis; Characterized by herniation of gallbladder mucosa into the muscular wall (Rokitansky-Aschoff sinus)
Presents with: vague RUQ pain (esp. after eating)
Porcelain gallbladder is a late complication
Tx. is cholecystectomy (esp. if porcelain bladder present)

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17
Q

Porcelain Bladder

A

Late complication of chronic cholecystitis; Shrunken, hard gallbladder due to chronic inflammation, fibrosis and dystrophic calcification of walls; Increased risk for carcinoma

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18
Q

Rokitansky-Aschoff Sinus

A

Herniation of gallbladder mucosa into the muscular wall due to chronic cholecystitis

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19
Q

Ascending Cholangitis

A

Bacterial infection of bile ducts; Usu due to ascending infection with enteric gram neg. bacteria; Presents as sepsis (high fever and chills), jaundice and abdominal pain; Increased incidence with choledocholithiasis (stone in biliary duct that prevents bile from washing bacteria away)

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20
Q

Gallstone Ileus

A

Gallstone enters and obstructs small bowel due to cholecystitis with fistula formation btw. the gallbladder and small bowel

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21
Q

Gallbladder Carcinoma

A

Adenocarcinoma arising from glandular epithelium that lines walls; Gallstones are major risk factor (esp. when complicated by porcelain gallbladder); Classically presents as cholecystitis in an elderly woman (as opposed to the usu. 40 yo - female); poor prognosis

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22
Q

Jaundice

A

Yellow discoloration of skin; Earliest sign is scleral icterus; Due to increase in serum bilirubin (usu > 2.5mg/dL)
Arises with disturbances in bilirubin metabolism - extravascular hemolysis, ineffective erythropoiesis, physiologic jaundice of newborn, Gilbert syndrome, Crigler-Najjar syndrome, Dubin-Johnson syndrome, biliary tract obstruction, viral hepatitis

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23
Q

Normal Bilirubin Metabolism

A

1) RBCs are consumed by macrophages of the RES
2) Protoporphyrin (from heme) is converted to UCB
3) Albumin carriers UCB to the liver, where it is transported inside hepatocytes via specific transporters
4) Uridine glucuronyl transferase (UGT) in hepatocytes conjugates bilirubin
5) Conjugated bilirubin (CB) is transferred to bile canaliculi to bile ducts to form bile
6) Bile is stored in gallbladder
7) Bile is released into the small bowel to aid in digestion (triggered by CCK from duodenum)
8) Intestinal flora convert CB to urobilinogen, which is oxidized to stercobilin (makes stools brown) and urobilin (partially reabsorbed into blood and filtered by kidney, making urine yellow)

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24
Q

Jaundice due to Extravascular Hemoloysis or Ineffective Erythropoiesis

A

High levels of UCB overwhelm the conjugation ability of liver –> Increased UCB
Dark urine due to increased urine urobilinogen
Increased risk for pigmented bilirubin gallstones

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25
Q

Physiologic Jaundice of the Newborn

A

Newborn liver has transiently low UGT activity –> increased UCB; UCB deposits in basal ganglia (kernicterus) leading to neurological deficits; Treatment is phototherapy which makes UCB water soluble (DOESN’T conjugate it)

26
Q

Gilbert Syndrome

A

AR condition; Mildly low UGT activity –> increased UCB –> jaundice during stress (eg. severe infection); otherwise not clinically significant; Can decrease bilirubin concentration with phenobarbital

27
Q

Crigler-Najjar Syndrome Type I

A

Mutation in UGT1A1 gene –> Absence of UGT —> really increased UCB –> kernicterus –> death in children unless liver transplant is done; >20 mg/dL of unconjugated bilirubin in serum
Type II is a milder form where some UGT is still present and bilirubin concentrations can be decreased with phenobarbital

28
Q

Dubin-Johnson Syndrome

A

Deficiency of bilirubin canalicular transport protein (due to AR MRP2 mutation) –> impaired export of conjugated bili –> increased CB; Liver is dark/black, but otherwise clinically insignificant; Estrogens can cause further increase in bilirubin levels and should be avoided
Rotor syndrome is similar but lacks the liver discoloration

29
Q

Biliary Tract Obstruction (Obstructive Jaundice)

A

Associated with gallstones, pancreatic carcinoma, cholangiocarcinoma, parasites and liver fluke (Clonorchis sinesis) –> increased CB, decreased urine urobilinogen and increased alkaline phosphatase;
Dark urine (due to bilirubinuria) and pale stools
Pruritis due to increased plasma bile acids
Hypercholesterolemia with xanthomas
Steatorrhea with malabsorption of fat-soluble vitamins

30
Q

Viral Hepatitis-Associated Jaundice

A

Inflammation disrupts hepatocyte and small bile ductules –> increase in both UCB and CB; Dark urine due to increased urine bilirubin; Urine urobilinogen is normal or decreased because this depends on amount of CB being deconjugated in the duodenum

31
Q

HAV

A

Fecal-oral transmission
Commonly acquired in travelers
Acute hepatitis with no chronic state
Anti-virus IgM marks active infection; Anti-virus IgG is protective and its presence indicates prior infection or immunization

32
Q

HEV

A

Fecal-oral transmission
Commonly acquired from contaminated water or undercooked seafood
Acute hepatitis with no chronic state; In pregnant women is associated with fulminant hepatitis (liver failure with massive necrosis)
Anti-virus IgM marks active infection; Anti-virus IgG is protective and its presence indicates prior infection

33
Q

HDV

A

Dependent on HBV for infection; Superinfection upon existing HBV is more severe than co-infection with both HBV and HDV at same time

34
Q

HBV

A 
Parenteral transmission (eg. childbirth, unprotected intercourse, IV drug use and needle sticks)
Results in acute hepatitis --> chronic disease occurs in 20% of cases (or 90% of those infected by M-to-C transmission)
35
Q

HBsAg

A

First serologic marker to rise; found on surface of HBV; indicates HBV infection; disappears when infection resolves; present in cases of chronic hepatitis (>6 months)

36
Q

Anti-HBs

A

IgG antibody to HBsAg, indicates immunity to HBV (either through infection or prior exposure)

37
Q

HBcAg

A

Antigen associated with core of HBV

38
Q

Anti-HBc

A

Antibody to HBcAg; IgM = acute/recent infection (only thing that can be measured in window period); IgG = prior exposure or chronic infection

39
Q

HBeAg

A

different antigenic determinant of HBV core; indicates active viral replication and therefore high transmissibility; if this is positive mother is very likely to transmit to child

40
Q

Anti-HBe

A

antibody to HBeAg, indicating low transmissability

41
Q

Immunization against HBV

A

Will only show IgG against HBsAg; will NOT have IgG against HBcAg

42
Q

HCV

A

Parenteral transmission (eg. IV drug use, unprotected intercourse); Risk from transfusion used to exist, but blood is now screened; Results in acute hepatitis that usu. progresses to chronic disease; HCV-RNA test confirms infection; decreased RNA levels indicates recovery, while persistence indicates chronic disease

43
Q

Viral Hepatitis

A

Inflammation of liver parenchyma; Usu due to hepatitis virus, but could also be due to EBV or CMV

44
Q

Acute Hepatitis

A

Presents as jaundice (mixed CB and UCB) with dark urine (due to CB), fever, malaise, nausea and elevated LFTs (ALT>AST)
Inflammation involves lobules of liver and portal tracts, and is characterized by apoptosis of hepatocytes due to CD8+ mediated cytotoxic killing
Some cases may be asymptomatic with elevated liver enzymes
Symptoms last <6 months

45
Q

Chronic Hepatitis

A

Characterized by symptoms that last > 6 months

Inflammation predominantly involves the portal tract (not lobules); Risk of progression to cirrhosis

46
Q

Cirrhosis

A

End-stage liver damage characterized by disruption of 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
Clinical Features:
1) Portal HTN –> Ascites, congestive splenomegaly/hypersplenism (consumption of RBCs and platelets), portosystemic shunts (esophageal varices, hemorrhoids, caput medusae), hepatorenal syndrome (rapidly developing renal failure secondary to cirrhosis)
2) Decreased detoxification leading to (a) mental status changes, asterixis and eventually coma (increased serum ammonia); (b) gynecomastia, spider angiomata and palmar erythema due to increased estrogen levels;
3) Jaundice
4) Decreased protein synthesis –> hypoalbunimia with edema, coagulopathy due to decreased synthesis of clotting factors (follow with PT)

47
Q

Alcohol-Related Fatty Liver

A

Damage to hepatic parenchyma due to accumulation of fat in hepatocytes; Results in heavy, greasy liver that resolves with abstinence

48
Q

Alcoholic Hepatitis

A

Results from chemical injury to hepatocytes; Generally seen with binge drinking; Acetaldehyde (alcohol metabolite) mediates damage; Characterized by swelling of hepatocytes with formation of Mallory bodies (damaged cytokeratin filaments), necrosis and acute inflammation;
Presents with painful hepatomegaly and elevated liver enzymes (AST>ALT)

49
Q

Mallory Bodies

A

Damaged cytokeratin/intermediate filaments within the hepatocytes cytoplasm due to alcoholic hepatitis or alcoholic cirrhosis; Mallory bodies are highly eosinophilic and thus appear pink on H&E stain. The bodies themselves are made up of intermediate cytokeratin 8&18 filament proteins that have been ubiquinated, or bound by other proteins such as heat shock proteins, or p62;
They are also a recognized feature of Wilson’s disease, primary biliary cirrhosis,, non-alcoholic cirrhosis, hepatocellular carcinoma and morbid obesity

50
Q

Nonalcoholic Fatty Liver Disease

A

Fatty change, hepatitis and/or cirrhosis that develop without exposure to alcohol or other known insults
Associated with obesity
Diagnosis of exclusion
ALT > AST

51
Q

Hemochromatosis

A

Excess body iron leading to deposition in tissues (hemosiderosis) and organ damage; Tissue damage is mediated by formation of free radicals;
Primary disease is due to mutations in the HFE gene (usu. C282Y cysteine replaced by tyrosine at AA 282) -> increased iron uptake
Clinical Presentation: Presents in late adulthood with cirrhosis, secondary diabetes mellitus and bronze skin; Can also present with cardiomyopathy, cardiac arrhythmias and gonadal dysfunction (due to testicular atrophy)
Labs: increased ferritin, decreased TIBC, increased serum iron, and increased % saturation
Liver biopsy reveals accumulation of brown pigment in hepatocytes (need to use prussian blue stain to distinguish from lipofuscin)
Increased risk of hepatocellular carcinoma
Treatment is phlebotomy

52
Q

Lipofuscin

A

Brown pigment that is a by-product of turnover (wear and tear) of peroxidized lipids; Sign of cellular aging; Commonly present in hepatocytes; can be distinguished from iron because iron stains blue on prussian blue stain

53
Q

Wilson Disease

A

AR defect in ATP7B in ATP-mediated hepatocyte copper transport –> lack of copper transport into bile and lack of copper incorporation into ceruloplasmin (key copper carrying molecule)
Copper builds up in hepatocytes and leaks into serum and deposits in tissues –> hydroxyl free radical production –> tissue damage
Presents in childhood with: cirrhosis, neurological manifestations (behavioral changes, dementia, chorea and Parkinsonian symptoms due to deposition in basal ganglia), Kayser-Fleisher rings in cornea
Labs: increased urinary copper, decreased serum ceruloplasmin, increased copper on liver biopsy
Increased risk of hepatocellular carcinoma
Treatment it D-penicillamine (chelator)

54
Q

Primary Biliary Cirrhosis

A

Autoimmune granulomatous destruction of intrahepatic bile ducts; Classically arises in women (40 yo); associated with other autoimmune diseases; Etiology unk; Antimitochondrial antibody is present; Presents with features of obstructive jaundice; Cirrhosis is a late complication

55
Q

Antimitochondrial Antibody

A

Primary Biliary Cirrhosis

56
Q

Primary Sclerosing Cholangitis

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”/string of pearls appearance on contrast; Etiology is unk., but associated with Ulcerative Colitis (pANCA is usu. +); Presents with obstructive jaundice; Cirrhosis is a late complication; Increased risk for cholangiocarcinoma

57
Q

Reye Syndrome

A

Fulminant liver failure and encephalopathy in children with viral illness who take asprin; Likely related to mitochondrial damage of hepatocytes; Presents with hypoglycemia, elevated liver enzymes, nausea, vomiting and may progress to coma and death
* Kawasaki disease is the only time you should give asprin to children

58
Q

Hepatic Adenoma

A

Benign tumor of hepatocytes; Associated with OCPs
Risk of rupture and intraperitoneal bleeding, esp. during pregnancy; Tumors are subcapsular and grow with exposure to estrogen

59
Q

Hepatocellular Carcinoma

A

Malignant tumor of hepatocytes;
Risk factors include: chronic hep (B, C), cirrhosis, Aflatoxins (derived from Aspergillus - induce p53 mutations); Increased risk for Budd-Chiari syndrome; Tumors often detected late because symptoms are masked by cirrhosis;
Serum marker is alpha-fetoprotein

60
Q

Alpha-fetoprotein

A

nonspecific serum marker for hepatocellular carcinoma and yolk sac tumors; prenatal screening: increased =neural tube defect, decreased = Down’s

61
Q

Budd-Chiari Syndrome

A

Liver infarction secondary to hepatic vein obstruction; Presents with painful hepatomegaly and ascites

62
Q

Metastasis to Liver

A

More common than primary liver tumors; Most common sources include colon, pancreas, lung and breast carcinomas
Results in multiple nodules in liver
Clinically may be detected as hepatomegaly with nodular free edge of liver

Pathoma (8 decks)

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