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STEP 1 Pathoma > Chapter 11 > Flashcards

Chapter 11 Flashcards

1
Q

Describe acute pancreatitis

A

Inflammation and hemorrhage of the pancreas due to autodigestion of pancreatic parenchyma by premature activation of trypsin resulting in LIQUEFACTIVE hemorrhagic necrosis of the pancreas and fat necrosis of the peripancreatic fat

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2
Q

What are the most common causes of acute pancreatitis?

A

alcohol and gallstones

other causes include trauma, hypercalcemia, hyperlipidemia, drug, scopion stings, mumps, and rupture of a posterior duodenal ulcer

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3
Q

What are the clinical features of acute pancreatitis?

A

Epigastric abdominal pain that radiates to the back

N/V

Periumbilical and flank hemorrhage (necrosis spreads into the periumbilical soft tissue and retoperitoneum)

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

What are the complications of acute pancreatitis?

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 persistnely elevated serum amylase)

Pancreatic abscess often due to E. Coli that presents with abdominal pain, high fever, and persistently elevated amylase

DIC and ARDS

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5
Q

Describe chronic pancreatitis

A

Fibrosis of pancreatic parenchyma, most often secondary to recurrent acute pancreatitis and most commonly due to alcohol in adults and cystic fibrosis in children

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6
Q

What are the classical features of chronic pancreatitis?

A

Epigastric abdominal pain that radiates to the back

Pancreatic insufficiency- results in malabsorption with steatorrhea and fat0soluble vitamin deficiencies. Amylase and lipase are not useful serologic markers of chronic pancreatitis

Dystrophic calcification of pancreatic parenchyma on imaging; constrast studies reveal a ‘chain of lakes’ pattern due to dilation of pancreatic ducts

Secondary diabetes mellitus as a late complication due to destruction of islets

Increased risk of pancreatic carcinoma

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7
Q

Pancreatic carcinoma

A

Adenocarcinoma arising from the pancreatic ducts most commonly seen in the elderly (70+ yo)

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8
Q

What are the major risk factors for Pancreatic carcinoma?

A

Smoking and chronic pancreatitis

NOTE: Very poor prognosis overall

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9
Q

How might Pancreatic carcinoma present?

A

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

Pancreatitis

Migratory thrombophlebitis (Trousseau syndrome)- presents as swelling, erythema, and tenderness in the extremities (seen in 10% of pts.)

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10
Q

What is the main serum marker for Pancreatic carcinoma?

A

CA19-9

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11
Q

What is a Whipple procedure?

A

Removal of the head and neck of the pancreas, proximal duodenum, and gallbladder

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12
Q

What is biliary atresia?

A

Failure to form or early destruction of the extrahrpatic biliary tree leading to biliary obstruction within the first 2 yrs of life and presenting with jaundice, progressing to cirrhosis

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13
Q

What is a cholelithiasis?

A

A gallstone, typically due to precipitation of cholesterol (cholesterol stones) or billirubin in bile that arises:

1) supersaturation of cholesterol or billirubin
2) decreased phospholipids (e.g. lecithin) or bile acids (normally increase solubility)
3) stasis

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14
Q

What are the most common types of stones?

A

Cholesterol stones (90%), especially in the west

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15
Q

Describe Cholesterol stones

A

These are usually radiolucent (10% are radiopaque due to associated calcium)

Risk factors include age (40s), estrogen (female, obesity, multiple pregnancies, and oral contraceptives), clofibrate, Native Americans, Crohn disease, and cirrhosis

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16
Q

Describe Bilirubin stones

A

Usually radiopaque

Risk factors include extravascular hemolysis (increased bilirubin in bile) and biliary tract infections (e.g. E. Coli, Ascaris lumbricoides, and Clonorchis sinensis)

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17
Q

What is Ascaris lumbricoides?

A

a common roudnworm that infects 25% of the world’s population, esp. in areas of poor sanitation (fecal-oral transmission)- infects the biliary tract, increasing the risk of gallstones

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18
Q

What is Clonorchis sinensis endemic?

A

China, Korea, and Vietnam (Chinese liver fluke)- ifnects the biliary tract, increasing the risk for gallstones, cholangitis, and cholangiocarcinoma

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19
Q

What is biliary colic?

A

Waxing and waning RUQ pain due to the gallbladder contracting against a stone lodged in the CYSTIC DUCT. Symptoms typically pass as the stone dislodges

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20
Q

Describe acute cholecystitis

A

Acute inflammation of the gallbladder wall due to a chronically lodged stone

presents with RUQ pain, often radiating to the right scapula, fever with increased WBC count, vomiting, and elevated serum alk phos from duct damage

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21
Q

What is ascending cholangitis?

A

Bacterial infection of the bile ducts usually due to ascending infection with enteric gram-neg bacteria

Presents as sepsis (high fever and chills), jaundice, and abdominal pain

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22
Q

What is gallstone ileus?

A

When a gallstone enters and obstructs the small bowel

23
Q

What causes jaundice?

A

Yellow discoloration of the skin due to elevated serum bilirubin (usually >2.5mg/dL)

24
Q

Briefly explain bilirubin metabolism

A

RBCs are consumed by macrophages of the RES, where protoporphyrin from heme is converted to unconjugated bilirubin, which is carried by albumin to the liver. Uridine glucuronyl transferase (UGT) in hepatocytes conjugates bilirubin.

Conjugated bilirubin is transferred to bile canaliculi to form bile, which is stored in the gallbladder. Bile is released into the small bowel to aid in digestion.

Intestinal flora convert CB to urobilinogen, which is oxidized to stercobilin (makes stool brown) and urobilin (makes urine yellow)

25
Q

What are some common causes of jaundice?

A

Extravascular hemolysis or ineffective erythropoiesis

Physiologic jaundice of the newborn

Gilbert Syndrome

Crigler-Najjar syndrome

Dubin-Johnson Syndrome

Biliary tract obstruction
Viral Hepatitis

26
Q

How does Extravascular hemolysis or ineffective erythropoiesis cause jaundice?

A

High levels of UCB overwhelm the conjugating ability of the liver (will produce dark urine due to increased urine urobilinogen (UCB is not water solublt, and this is absent from urine)

27
Q

How does Physiologic newborn cause jaundice?

A

Newborn livers have transiently low UGT activity (UCB is fat soluble and can deposit in the basal ganglia (kernicterus) leadig to neurological deficits and death

Tx is phototherapy (makes UCB water soluble)

28
Q

How are Hep A and E transmitted?

A

Fecal-oral transmission

NOTE: Both are NOT associated with a chronic state, but HEV is pregnant women is associated with fulminant hepatitis

29
Q

How is Hep B transmitted?

A

Parenteral trnasmission (e.g. childbirth, unprotected intercourse, IVDU, and needle stick)

Results in acute hep, but chronic disease can occur in 20% of cases

30
Q

How would acute HBV present in labs?

A

HBsAg positive (first marker to rise)

HBeAG and HBV DNA positive

HbcAg-IgM

31
Q

How would resolved HBV present in labs?

A

HBcAG- IgG

HBsAG- IgG (protective)

32
Q

How would chronic HBV present in labs?

A

HBsAG positive

HbcAB- IgG

HBeAG and HBV DNA- may be positive or negative depending on infectivity

33
Q

How would immunizayion against HBV present in labs?

A

ONLY HBsAB IgG

34
Q

Describe liver cirrhosis

A

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

The fibrosis is mediated by TGF-B from stellate cells which lie beneath the endothelial cells that line the sinusoids

35
Q

What are the clinical features of cirrhosis?

A

Portal HTN leads to ascites, congestive splenomegaly/hypersplenism, and portosystemic shunts (esophageal varices, hemorrhoids, and caput medusae)

Hepatorenal syndrome (rapidly developing renal failure secondary to cirrhosis)

36
Q

What is this?

A

Caput medusae

37
Q

Decreased liver detox arising from liver cirrhosis results in:

A

Mental status changes, asterixis, an eventual coma (all due to elevated serum ammonia); metabolic, hence reversible

Gynecomastia, spider angiomata, and palmar erythema due to hyperstrinism

jaundice

38
Q

Decreased protein synthesis arising from liver cirrhosis results in:

A

Hypoalbuminemia with edema

Coagulopathy due to decreased synthesis of clotting factors

39
Q

Fatty liver

A

Mallory bodies (alcohol)- swelling of hepatocytes with damaged cytokeratin filaments

40
Q

What is hemochromatosis?

A

Excess body iron leading to deposition in tissue (hemosiderosis) and organ damage (hemochromatosis)- tissue damage is mediated by free radicals

Due to AR defect in iron absorption (primary) or chronic transfusions (secondary)

41
Q

What causes primary hemochormatosis?

A

mutation of HFE gene, usually C282Y (cysteine replaced by tyrosine)

42
Q

How does primary hemochromatosis present?

A

Typically presents in adulthood with a classic triad of cirrhosis, secondary DM, and bronze skin

Other findings include dilated cardiomyopathy, cardiac arryhthmias, and gonadal dysfunction (due to testicular atrophy)

Increased risk of HCC

43
Q

What are the lab findings of primary hemochromatosis?

A

elevated ferritin, serum iron, and % saturation

decreased TIBC

44
Q

How can iron be ID’d in tissue?

A

Prussian blue stain- distinguishes iron from lipofuschin, which is a brown pigment that is a by-product from the turnover (‘wear and tear’) of peroxidized lipids

45
Q

How is hemochromatosis tx?

A

Phlebotomy

46
Q

What causes Wilson disease?

A

AR defect in ATP7B gene in ATP-mediated hepatocyte copper transport that results in lack of copper transport into ile and alck of copper incorporation into ceruloplasmin

Copper builds up in hepatocytes, leaks into serum, and deposits in tissue where copper-mediated production of hydroxyl free radicals lead to tissue damage

47
Q

How does Wilson disease present?

A

Presents in childhood with cirrhosis, neurologic manifestations (behavioral changes, dementia, chorea, and Parkinsonian symptoms due to deposition of copper in basal ganglia)

Kayser-Flesicher rings in the cornea

48
Q

What are the lab findings of Wilson Disease?

A

Elevated uriary copper

decreased serum ceruloplasmin

elevated copper on liver biopsy

increased risk of HCC

49
Q

How is Wilson Disease tx?

A

Penicillamine (chelates copper)

50
Q

What is primary biliary cirrhosis?

A

Autoimmune granulomatous destruction of intrahepatic bile ducts classically seen in women around 40 yo

Etiology is unknown

cirrhosis is a late complication

51
Q

Describe primary sclerosing cholangitis

A

Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts causing periductal fibrosis with an ‘onion-skin’ appearance

Increased risk of cholangiosarcoma

52
Q

What is Reye Syndrome?

A

Fulminant liver failure and encephalopathy in children with viral illness who take aspirin likely due to mitochondrial dmaage of hepatocytes

Pts present with hypglycemia, elevated liver enzymes, and nausea wih vomiting- may progress to coma/death

53
Q

What is the serum marker for HCC?

A

Alpha-fetoprotein

54
Q

METS to the liver are more common than primaries. What are the most common sources?

A

Colon, pancreas, lung, and breast carcinomas

STEP 1 Pathoma (18 decks)

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