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STEP 1 Review > GI pathology > Flashcards

GI pathology Flashcards

1
Q

Pleomorphic Adenoma

A

Benign mixed parotid tumor. Presents as a painless mobile mass. Composed of chondromyxoid stroma and epithelium and can recur if incompletely excised. Can transform and cause cranial nerve VII palsies

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2
Q

Warthin tumor

A

Cystic tumor with germinal centers (benign). Common in parotid gland due to embryologic association with parotids.

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3
Q

Mucoepidermoid carcinoma

A

Most common malignant tumor. Has mucinous and squamous components. Presents as a painless, slow growing mass. Commonly involves facial nerve.

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4
Q

Achalasia

A

Failure of LES relaxation due to loss of myenteric plexus. High LES tone and uncoordinated peristalsis leads to progressive dysphagia to solids and liquids. Increased risk of squamous cell carcinoma. Secondary achalasia can arise from chagas disease

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5
Q

Esophagitis

A

Due to candida, HSV-1, or CMV in immunocompromised.

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6
Q

Menetrier Disease

A

Gastric hypertrophy with parietal cell loss. Rugae hypertrophy so looks like brain gyri.

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7
Q

Signs of gastric cancer

A

Leser-trelat sign (keratoses), and acanthosis nigricans.

Also virchow node, sister mary joseph, and krukenberg tumor.

Associated with dermatomyositis.

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8
Q

Sequellae of duodenal ulcers

A

Hypertrophy of brunner glands.

Not cancerous, but type B chronic gastritis is.

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9
Q

Posterior duodenal hemorrgahe

A

Ruptured gastroduodenal artery

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10
Q

Anterior duodenal ulcer complication

A

Perforation with free air under the diaphragm.

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11
Q

Small bowel carcinoids

A

No signs if just in small bowel, however, if met to liver then diarrhea, flushing, palpitation. Can also cause fibrosis of heart valves.

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12
Q

Celiac

A

Associated with DQ2 and DQ8. Autoimmune destruction with intraepithelial lymphocytes. Happens in response to gliadin. Antibodies in response against endomesium transglutaminase and gliadin. Must check IgG because may be IgA deficient. Mostly in duodenum. Moderate increase in risk of lymphoma (EATL). Dermatitis herpetiformis.

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13
Q

Abetalipoproteinemia

A

No B48 so no chylomicrons, no B100 so no VLDL. Decreased secretion of cholesterol/vldl in bloodstream. So accumulatiojn in enterocytes. Also no fat soluble vitamin absorption.

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14
Q

Abetalipoproteinemia

A

No B48 so no chylomicrons, no B100 so no VLDL. Decreased secretion of cholesterol/vldl in bloodstream. So accumulatiojn in enterocytes. Also no fat soluble vitamin absorption.

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15
Q

What liver thing is associated with ulcerative colitis?

A

Primary sclerosis cholangitis.

Lead pipe, also associated with P-ANCA

COLitis = CHOLangitis.

Also associated with colorectal carcinoma.

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16
Q

What part of the Gi tract does crohn’s spare?

A

Rectum

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17
Q

How to check for ectopic gastric mucosa?

A

Pertechnetate uptake

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18
Q

What parts of the colon are involved in volvulus

A

Cecum in kids, sigmoid in elderly

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19
Q

Hirschsprung disease

A

Congenital megacolon due to failure of migration of meissner and auerbach’s plexus. Associated with mutation in RET. THIS IS A FAILURE OF NEURAL CREST CELLS MIGRATION. Diagnosed by retinal suction biopsy. Seen in down.

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20
Q

Angiodysplasia

A

Stress on right side of colon causes bleeds.

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21
Q

Signs of ischemic colitis

A

Postpradial pain.

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22
Q

Juvenile colonic polyps

A

Sporadic lesions in children less than 5 years old. 80% in colon. If multiple, increased risk of adenocarcinoma

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23
Q

Peutz-Jeghers Syndrome

A

Autosomal dominant syndrome features multiple nonmalignant hamartomas throughout GI tract, with hyperpigmented mouth, lips, genitals. Icnreased risk of colorectal carcinoma.

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24
Q

At risk colon

A

Loss of apc, only loss of kras causes adenoma. Then loss of p53 and increased cox can cause carcinoma.

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25
Q

Effects of portal hypertension

A

Esophageal varices leading to hematemesis. Melena from peptic ulcers. Splenomegaly, hepatorenal syndrome, caput medusae, ascites.

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26
Q

Effects of liver cell failure

A

Hepatic encephalopathy, scleral icterus, musty breath, spider nevi (from estrogen), gynecomastia (from estrogen), jaundice, testicular atrophy (from estrogen), asterixis, bleeding tendency (due to decreased synthesis of coag factors increased prothrombin time), edema (from decreased albumin).

27
Q

Cirrhosis

A

Diffuse fibrous bands separating nodules of regenerating hepatocytes. Increased risk of HCC. Caused by stellate cells that produce TGF beta. Caused by alcohol, hepatitis. biliary disease, hemochromatosis

28
Q

Most sensitive marker for acute pancreatitis?

A

Lipase

29
Q

Reye syndrome

A

Rare fatal childhood hepatoencaphalopathy. Causes mitochondrial abnormalities, fatty liver, hypoglycemia, vomiting, hepatomegaly, coma. Associated with viral infection (like VZV or influenza) treated with aspirin.

Aspirin metabolites decrease beta oxidation of fatty acids due to inhibition of mitochondrial enzymes.

30
Q

Alcoholic hepatic steatosis

A

Increased NADH causes accumulation of Fatty acids inside cells. Reversible with alcohol cessation.

31
Q

Alcoholic hepatitis

A

Caused by direct damage to hepatocytes by acetaldehyde. Increases AST. Necrotic and swollen hepatocytes with mallory’s hyaline (collections of damaged intermediate filaments).

32
Q

Alcoholic cirrhosis

A

Final irreversible form. Micronodular irregularly shrunken liver. Sclerosis mostly around central vein in zone III, has manifestations of chronic liver disease (jaundice, hypoalbuminemia)

33
Q

NAFLD

A

Metabolic syndrome and insulin resistance causes fatty infiltration of hepatocytes. This causes ballooning necrosis. Can cause cirrhosis and HCC.

34
Q

Things that exacerbate hepatic encephalopathy

A

Increased NH3 production from protein intake, GI bleed, constipation, infection. Decreased NH3 clearance due to renal failure, diuretics, TIPS.

Treat with lactulose which generates NH4 in intestine.

Can also treat with rifaximin(kills intestinal bacteria).

35
Q

Rifaximin

A

Can treat hepatic encephalopathy by killing bacteria.

36
Q

Hepatocellular carcinoma

A

Most common malignant tumor in adults, associated with hepatitis B and C, wilson disease, hemochromatosis, a1at deficiency, alcoholic cirrhosis, and aflatoxin. Can lead to budd chiari syndrome.

Causes tender hepatomegaly, ascites, and anorexia. Spreads hematogenously.

37
Q

Cavernous hemangioma

A

Most common benign liver tumor. Occurs at 30-50. Don’t biopsy because there is a risk of hemorrhage.

38
Q

Hepatic adenoma

A

Benign liver tumor that is rare. Caused by increased estrogen. Can rupture because it’s right below the capsule.

39
Q

Angiosarcoma

A

Malignant endothelial tumor, associated with arsenic or vinyl chloride.

40
Q

Nutmeg liver

A

Painful liver due to heart failure/budd chirari syndrome. Centrilobular congestion and necrosis can occur

41
Q

Budd-Chiari syndrome

A

Occlusion of IVC or hepatic veins with centrilobular congestion and necrosis. Leads to congestive liver disease.

42
Q

A1AT deficiency

A

Misfolded gene product accumulates in the ER of hepatocytes (PAS + globules in liver). Trait is codominant because PIMZ and PIZZ are different.

43
Q

What levels does jaundice occur

A

> 2.5

44
Q

Why is the color of urine dark in unconjugated hyperbilirubinemia

A

Because urine urobilinogen increases.

45
Q

How to treat crigler-najjar type II

A

Less severe and responds to phenobarbital.

46
Q

Worst hereditary hyperbilirubinemia?

A

Crigler Najjar type I causes kernicterus. NO UGT transferase activity.

47
Q

Difference between Dubin Johnson syndrome and Rotor?

A

Rotor doesn’t have a black liver.

48
Q

Symptoms of biliary tract obstruction

A

Dark urine due to conjugated bilirubinemia, pruritis due to bile acids in blood, hypercholesterolemia, increased alk phos, steatorrhea due to lack of absorption

49
Q

Wilson Disease

A

Defect in ATP7b which causes ineffective copper secretion into bile. Builds up in tissues like basal ganglia causing neurologic symptoms, cirrhosis, Kayser-Fleisher rings. HCC carcinoma.

Autosomal recessive on chromosome 13.

50
Q

Hemochromatosis

A

HFE mutation makes body think that there’s no iron so hepcidin decreases and ferroportins increase. More iron brought in causes cirrhosis, secondary diabetes, skin pigmentation. Can cause CHF, testicular atrophy. Findings include increased ferritin, decreased TIBC, increased iron. Can also be secondary to transfusions in thalassemia major Genetic version associated with HLAA3. Treat with phlebotomy, desferasirox, or desferoxamine

51
Q

Primary biliary cirrhosis

A

Intrahepatic duct fibrosis due to autoimmune attack. More common in women. Causes granulomas and lymphocytic infiltrate. Presents with pruritis, jaundice, dark urine, lights tools. Marked by serum anti-mitochondrial antibodies. Associated with CREST, sjogrens, RA celiac.

52
Q

Primary sclerosis cholangitis

A

Seen with UC, onion skinning of intra and extrahepatic bile ducts. Alternating strictures and dilatiations leads to beaded appearance. Associated with hyper IgM, can predispose to cholangiocarcinoma, associated with p-anca.

53
Q

Gallstones

A

Due to increased cholesterol (decreased 7 alpha hydroylase) or bilirubin, or decreased bile salts/phosphatidylcholine

Can be cholesterol- radiolucent, fat 40 female fertile, chrohn’s disease, CLOFIBRATE, estrogen (due to an increase in HMG coa reductase), rapid weight loss, cholestyramine (loss of bile acids)

Pigment stones - due to extravascular hemolysis or brown for infection (e.coli, ascaris, chlonorchis)

54
Q

Biliary colic

A

Stone in cystic duct, after meal there is cck contracting the gall bladder. Can be painless in diabetics

55
Q

Cholangitis

A

Jaundice, fever, RUQ pain.

Caused by biliary tree obstuction (choledocolithiasis) and ascending invaders

56
Q

Cholecystitis

A

Due to cholelithiasis causing infection. Rarely ischemia or primary infection (CMV). Presents with RUQ with radiation to scapula. Diagnose with murphy’s sign.

57
Q

What can cause primary infection of gallbladder?

A

CMV

58
Q

Porcelain gallbladder

A

Due to chronic cholecystitis, calcified must be removed to prevent gallbladder carcinoma (adenocarcinoma of gallbladder wall)

59
Q

Gallbladder carcinoma

A

Adenocarcinoma of gallbladder wall. Presents as cholecystitis in elderly. Can arise from porcelain gallbladder or recurrent gallstones. Poor prognosis

60
Q

Acute pancreatitis

A

Activation of pancreatic enzymes (trypsin first) causes autodigestion of the pancreas. Liquifactive and fat necrosis ensue.

Gallstones, ethanol (contract sphincter of oddi), trauma, scorpion bite, mumps, autoimmune disease, steroids, hypercalcemia (general activator of enzymes), hypertriglyceridemia, ercp, drugs (sulfa, opioids).

Causes epigastric pain that radiates to the back, anorexia, nausea, vomiting.

Labs include increased amylase, increased lipase (more specific), hypocalcemia if very severe.

61
Q

Complications of acute pancreatitis?

A

ARDS, DIC, hypocalcemia

Pseudocyst formation (lined by fibrous and granulation tissue) which can rupture/hemorrhage.

62
Q

Chronic pancreatitis

A

Due to recurrent acute pancreatitis so seen in CF and alcoholics. Slower emptying increases time for activation of enzymes. Presents with pancreatic insufficiency causing fat malabsorption, DM, increased risk of pancreatic adenocarcinoma. Calcifications of pancreas. Amylase and lipase may not be elevated because most of pancreas has been destroyed

63
Q

Pancreatic adenocarcinoma

A

Horrible prognosis, tumor arising from pancreatic ducts, mostly metastasized at presentation. Tumors common in pancreatic head leading to obstructive jaundice. Associated with Ca 19-9 (can be associated with CEA but less specific).

Caused by tobacco use, chronic pancreatitis, age, jewish-african american males, diabetes.

Presents with pale stools, abdominal pain radiating to the back, MIGRATORY THROMBOPHLEBITIS.

May also have virchow’s node.

Palpable nontender gallbladder

TREAT WITH WHIPPLE PROCEDURE (en block resection of head/neck of pancreas, gallbladder, and duodenum.

64
Q

Which malignancy has trousseau syndrome?

A

Pancreatic

STEP 1 Review (21 decks)

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