Exocrine Pancreas, Galbladder And Liver Pathology Part I

Front 1

Annular pancreas

Back 1

Developmental malformation in which the pancreas forms a ring around the duodenum; risk of duodenal obstruction

Front 2

Acute pancreatitis

Back 2

Inflammation and hemorrhage of the pancreas due to auto digestion of pancreatic parenchyma by pancreatic enzymes (premature activation of trypsin leads to activation of other pancreatic enzymes); results in liquefactive hemorrhagic necrosis of the pancreas and fat necrosis of the peripancreatic fat

Front 3

Causes of acute pancreatitis

Back 3

• Alcohol and gallstones (most common)
• Trauma
• Hypercalcemia
• Hyperlipidemia
• Drugs
• Scorpion stings
• Mumps
• Rupture of a posterior duodenal ulcer

Front 4

Clinical features of acute pancreatitis

Back 4

1. Epigastric abdo pain that radiates to back

2. Naseau and vomiting

3. Periumbilical and flank hemorrhage (necrosis spreads into periumbilical soft tissue and retroperitoneum)

4. Elevated serum lipase and amylase, lipase is more specific for pancreatic damage

5. Hypocalcemia (Ca2+ consumed during saponification in fat necrosis)

Front 5

Complications of acute pancreatitis

Back 5

1. Shock

2. Pancreatic pseudocyst

3. Pancreatic abscess

4. DIC and ARDS

Front 6

What causes shock in acute pancreatitis?

Back 6

Peripancreatic hemorrhage and fluid sequestration

Front 7

Pancreatic pseudocyst as seen in acute pancreatitis

Back 7

Formed by fibrous tissue surrounding liquefactive necrosis and pancreatic enzymes

• presents as abdo mass with persistently elevated serum amylase
• rupture is associated with release of enzymes into the abdo cavity and hemorrhage

Front 8

Pancreatic abscess

Back 8

often due to E. coli; presents with abdo pain, high fever, and persistently elevated amylase

Front 9

Chronic pancreatitis

Back 9

Fibrosis of pancreatic parenchyma, most often secondary to recurrent acute pancreatitis; most commonly due to alcohol and CF (in children); however many cases are idiopathic

Front 10

Clinical features of chronic pancreatitis

Back 10

1. Epigastric abdo pain that radiates to back

2. Pancreatic insufficiency

3. Secondary diabetes mellitus

4. Increased risk for pancreatic carcinoma

Front 11

What do imaging and contrast studies reveal in chronic pancreatitis?

Back 11

Dystrophic calcification of pancreatic parenchyma on imaging; a 'chain of lakes' pattern due to dilatation of pancreatic ducts

Front 12

Pancreatic carcinoma

Back 12

Adenocarcinoma arising from the pancreatic ducts; most commonly seen in the elderly (average age is 70)

Front 13

Major risk factors for pancreatic carcinoma

Back 13

Smoking and chronic pancreatitis

Front 14

Clinical features of pancreatic carcinoma

Back 14

1. Epigastric abdo pain and weight loss

2. Obstructive jaundice with pale stoles and palpable gallbladder (assoc. w/ tumors in head of pancreas)

3. Secondary DM (assoc. w/tumors in body or tail)

4. Pancreatitis

5. Migratory thrombophlebitis (Trousseau sign)

Front 15

Serum tumor marker for pancreatic carcinoma

Back 15

CA 19-9

Front 16

Trousseau sign

Back 16

Presents as swelling, erythema, and tenderness in extremities (seen in 10% of patients with pancreatic carcinoma)

Front 17

Whipple procedure

Back 17

Surgical resection to treat pancreatic carcinoma; involves en bloc removal of head and neck of pancreas, proximal duodenum, and gallbladder

Front 18

Prognosis of pancreatic carcinoma

Back 18

Very poor; 1-year survival is < 10%

Front 19

Biliary atresia

Back 19

Failure to form or early destruction of extra hepatic biliary tree leading to biliary obstruction within first 2 months of life; presents as jaundice and progresses to cirrhosis

Front 20

Cholelithiasis

Back 20

Gallstones; due to precipitation of cholesterol or bilirubin in bile that arises with (1) supersaturation of cholesterol or bilirubin, (2) decreased phospholipids (e.g., lecithin) or bile acids (these normal increase solubility), or (3) stasis

Front 21

What is the classic example of drug that increases the risk of cholesterol stones?

Back 21

Cholestryramine (it binds bile acids)

Front 22

How does stasis increase the risk for gallbladder stones?

Back 22

Stasis may lead to an overgrowth of bacteria, which can de-conjugate bilirubin; this form of bilirubin in the bile can lead to stones

Front 23

Cholesterol stones

Back 23

Yellow stones; most common type (90%) of stones, especially in the West; usually radiolucent though some (10%) are radiopaque due to associated calcium

Front 24

Risk factors for cholesterol stones

Back 24

• Age (40s)
• Estrogen (female gender, obesity, multiple pregnancies and oral contraceptives)
• Clofibrate
• Native American ethnicity
• Crohn disease (due to damage in terminal ileum, which leads to decrease in reuptake of bile salts)
• Cirrhosis

Front 25

Bilirubin stones appearance on imaging

Back 25

usually radiopaque

Front 26

Risk factors for bilirubin stones

Back 26

Extravascular hemolysis (increased bilirubin in bile) and biliary tract infection (e.g., E coli, Ascaris lumbricoides, and Clonorchis sinensis)

Front 27

Complications of gallstones

Back 27

• Biliary colic
• Acute and chronic cholescystitis
• Ascending cholangitis
• Gallstone ileus
• Gallbladder cancer

Front 28

Biliary colic

Back 28

• Waxing and waning right upper quadrant pain due to gallbladder contracting against stone lodged in cystic duct
• Symptoms relieved if stone passes
• Common bile duct obstruction may result in acute pancreatitis or obstructive jaundice

Front 29

Acute cholecystitis

Back 29

Acute inflammation of gallbladder wall due to impacted stone in cystic duct resulting in dilatation with pressure ischemia, bacterial overgrowth (E coli), and inflammation

Front 30

How does acute cholecystitis present?

Back 30

• right upper quadrant pain, often radiating to right scapula
• fever with increased WBC count
• nausea, vomiting
• increase serum alkaline phosphatase (from duct damage)

Front 31

Chronic cholecystitis

Back 31

• Due to chemical irritation from longstanding cholelithiasis, with or without superimposed bouts of acute cholecystitis
• characterized by herniation of gallbladder mucosa into muscular wall (Rokitansky-Aschoff sinus)

Front 32

How does chronic cholecystitis present?

Back 32

Vague right upper quadrant pain, especially after eating

Front 33

Porcelain gallbladder

Back 33

Late complication of chronic cholecystitis; shrunken, hard gallbladder due to chronic inflammation, fibrosis, and dystrophic calcification; increased risk for carcinoma (should be removed via cholecystectomy)

Front 34

Ascending cholangitis

Back 34

• Bacterial infection of bile ducts usually due to ascending infection with enteric gram-negative bacteria
• Presents as sepsis, jaundice, and abdo pain
• Increased incidence with choledocholithiasis (stone in biliary duct)

Front 35

Gallstone ileus

Back 35

Gallstone enters and obstruct small bowel due to cholecystitis with fistula formation between gallbladder and small bowel

Front 36

Gallbladder carcinoma

Back 36

• Adenocarcinoma arising from glandular epithelium lining the gallbladder wall
• Gallstones are major risk factor, especially when complicated by porcelain gallbladder

Front 37

Classic presentation of gallbladder carcinoma

Back 37

Cholecystitis in an elderly woman

Front 38

Earliest sign of jaundice

Back 38

Scleral icterus

Front 39

What levels do serum bilirubin have to reach in order for jaundice to occur?

Back 39

Usually above 2.5 mg/dL

Front 40

Extravascular hemolysis or ineffective erythropoiesis

Back 40

• High levels of UCB overwhelm the conjugating ability of the liver
• ↑ UCB
• Dark urine due to ↑ urine urobilinogen
• Increased risk for pigmented bilirubin gallstones

Front 41

Physiologic jaundice of the newborn

Back 41

• Newborn liver has transiently low UGT activity
• ↑ UCB (can lead to kernicterus)
• Treatment is phototherapy

Front 42

Kernicterus

Back 42

Due to high levels of bilirubin: UCB is fat soluble and can deposit in the basal ganglia, leading to neurological deficits and death

Front 43

Gilbert syndrome

Back 43

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

Front 44

Crigler-Najjar Syndrome

Back 44

• Absence of UGT
• ↑ UCB
• Kernicterus; usually fatal

Front 45

Dubin-Johnson syndrome

Back 45

• Deficiency of bilirubin canalicular transport protein; autosomal recessive
• ↑ CB
• Liver is dark (otherwise not clinically significant)
• Similar to rotor syndrome but in rotor syndrome liver is not dark

Front 46

Biliary tract obstruction (obstructive jaundice)

Back 46

• Associated with gallstones, pancreatic carcinoma, cholangiocarcinoma, parasites, and liver fluke (Clonorchis sinensis)
• ↑ CB, ↑ alkaline phosphatase, ↓ urine urobilinogen
• Dark urine and pale stool
• Pruritus due to ↑ plasma bile acids
• Hypercholesterolemia with xanthomas
• Steatorrhea with malabsorption of fat-soluble vitamins

Front 47

Viral hepatitis

Back 47

• Inflammation disrupts hepatocytes and small bile ductules
• ↑ in both CB and UCB
• Dark urine due to ↑ urine bilirubin; urine urobilinogen is normal or decreased

Front 48

HAV and HEV mode of transmission

Back 48

• Fecal-oral
• HAV is commonly acquired by travelers
• HEV is commonly acquired from contaminated or undercooked seafood

Front 49

What is HEV in pregnant women associated with?

Back 49

Fulminant hepatitis (liver failure with massive liver necrosis)

Front 50

Type of hepatitis and serum markers for HAV and HEV

Back 50

Acute hepatitis; no chronic state

• Anti-virus IgM marks active infection
• Anti-virus IgG is protective, and its presence indicates prior infection or immunization

Front 51

HBV mode of transmission

Back 51

Parenteral transmission (e.g., childbirth, unprotected intercourse, IV drug abuse, and needle stick)

Front 52

HBV disease course

Back 52

Results in acute hepatitis, chronic disease occurs in 20% of cases

Front 53

HCV mode of transmission and disease course

Back 53

• Parenteral transmission
• Results in acute hepatitis; chronic disease occurs in most cases

Front 54

Serum markers HCV

Back 54

• HCV-RNA test confirms infection
• Decreased RNA levels indicate recovery; persistence indicates chronic disease

Front 55

HDV

Back 55

Dependent on HBV for infection; superinfection upon existing HBV is more severe than confection (infection with both at the same time)

Front 56

Which is the first serologic marker to rise in HBV infection?

Back 56

HBsAG (presence > 6 months defines chronic state)

Front 57

What are the markers for infection with acute HBV?

Back 57

HBsAG, HBeAG and HBV DNA, IgM

Front 58

Which marker indicates resolved HBV infection?

Back 58

HBcAB (IgG) and HBsAB (IgG protective)

Front 59

Other viral causes of hepatitis

Back 59

EBV, CMV

Front 60

How does acute hepatitis present?

Back 60

• Jaundice (mixed CB/UCB) with dark urine, fever, malaise, nausea, and elevated liver enzymes (ALT > AST)
• Inflammation involves liver lobules and portal tracts and is characterized by apoptosis of hepatocytes
• Some cases may be asymptomatic with elevated liver enzymes
• Symptoms last < 6 mo

Front 61

What characterizes chronic hepatitis?

Back 61

• Symptoms that last > 6 months
• Inflammation predominantly involves portal tract
• Risk of progression to cirrhosis