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Step 1 Flash Cards > GI day 2 > Flashcards

GI day 2 Flashcards

1
Q

tropical sprue

A

similar findings to celiac sprue, but responds to abx

- cause is unknown, but seen in residents of or recent visitors to the tropics

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2
Q

whipple disease

A
  • infection with tropheryma whippeli, treat with abx
  • PAS + foamy macrophages in intestinal lamina propria
  • Cardiac symptoms, Arthralgias, Neurologic symptoms
  • most often occurs in older men
  • Foamy Whipped cream in a CAN
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3
Q

celiac sprue

A
  • AI mediated intolerance of wheat leading to malabsorption and steatorrhea
  • associated with HLA DQ2 and DQ8
  • findings include anti-endomysial, anti-TTG an anti-gliadin Abs
  • blunting of the villi and lymphocytes in he lamina propria
  • decreased mucosal absorption that primarily affects the dist duo/prox jejunum
  • mod increased risk for malignancy (T cell lymphoma)
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4
Q

disaccharidase deficiency

A
  • most common is lactase deficiency
  • normal appearing villi, osmotic diarrhea
  • lactose tolerance test: positive if administer lactose, get symptoms + glucose rises < 20mg/dL
  • stool pH will also decrease
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5
Q

abetalipoproteinemia

A
  • decreased synthesis of apolipoprotein B –> inability to generate chylomicrons –> decreased secretion of cholesterol and VLDL into blood stream –> fat accumulation in enterocytes (otherwise normal architecture)
  • presents in early childhood with FTT, steatorrhea, acanthocytosis (thorny projections from RBCs), ataxia and night blindness
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6
Q

pancreatic insufficiency

A
  • due to CF, obstructing cancer or chronic pancreatitis
  • ADEK malabsorption
  • increased neutral fat in stool, D-xylose testing normal
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7
Q

crohn disease

A
  • disordered response to bacteria
  • skip lesions, esp affects the terminal ileum
  • transmural inflammation, fistulas, cobblestone mucosa, creeping fat, bowel wall thickening, string sign, linear ulcers, fissures
  • noncaseating granulomas
  • diarrhea may or may not be bloody
  • extraintestinal manifestations: migratory polyarthritis, erythema nodosum, ank spon, pyoderma gangrenosum, apthous ulcers, uveitis, kidney stones
  • treat with corticosteroids, azathioprine, MTX, infilximab, adalimumab
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8
Q

CRC from crohns

A
  • young pts
  • progresses from flat/non-polypoid dysplasia
  • mucinous or signet rings
  • develop early p53 mutations rather than APC
  • distributed within the prox colon
  • multifocal
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9
Q

UC

A
  • AI
  • mucosal and submucosal inflammation only
  • no haustra –> lead pipe appearance on imaging
  • crypt abscesses and ulcers, bleeding, no granulomas
  • malnutrition, sclerosing cholangitis, toxic megacolon, CRC
  • pyoderma gangrenosum, erythema nodosym, ank spon, apthous ulcers, uveitis
  • treat with ASA preps (sulfasalazine), 6-MP, infliximab, colectomy
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10
Q

Zenker diverticulum

A
  • not a true diverticulum
  • cricopharyneal muscle dysfunction due to diminished relaxation leads to increased intraluminal pressure and herniation of the pharyngeal mucosa
  • most common in elderly males, can lead to asp pneumo
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11
Q

meckel diverticulum

A
  • true diverticulum
  • persistence of the vitelline duct that may contain ectopic-acid secreting gastric mucosa and/or pancreatic tissue
  • melena, RLQ pain, intussusception, volvulus, or obstruction near the terminal ileum
  • diagnose with pertechnetate study for uptake by ectopic gastric mucosa
  • this is an example of ectopy, not metaplasia
  • 5 2’s: 2 inches long, 2 feet from the ileocecal valve, 2% of the populaiton, commonly presents at 2 years old, may have 2 types of epithelia
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12
Q

angiodysplasia

A
  • tortuous dilation of vessels –> hematochezia
  • most often found in cecum, terminal ileum, and ascending colon
  • more common in older pts, confirm with angiography
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13
Q

causes of ileus

A
  • abdominal surgery, opiates, hypokalemia, and sepsis
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14
Q

adenomatous polyps

A
  • villous histology more associated with malignancy (tubular less likely to transition)
  • can be asymptomatic, lower GI bleed, partial obstruction, secretory diarrhea (mucus secretion)
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15
Q

hyperplastic polyps

A
  • most common non-neoplastic polyp in the colon (> 50% found in rectosigmoid)
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16
Q

juvenile polyps

A
  • mostly sporadic lesion in children < 5
  • if single, no malignant potential
  • juvenile polyposis syndrome - multiple juvenile polyps in the Gi tract, increased risk of adenocarcinoma
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17
Q

hamartomatous polyps

A

Peutz-Jeghers syndrome

  • AD syndrome featuring multiple nonmalignant hamartomas throughout the GI tract, along with hyperpigmented mouth, lips, hands and genitalia
  • associated with increased risk of CRC and other visceral malignancies
18
Q

reye syndrome

A

hepatoencephalopathy resulting in mitochondrial abnormalities, microvesicular fatt change, hypoglycemia, vomiting, hepatomegaly and coma
- aspirin metabolites decrease b-oxidation by reversible inhibition of mitochondrial enzyme

19
Q

alcoholic hepatitis

A
  • swollen and necrotic hepatocytes with neutrophilic infiltration
  • mallory bodes (intracytoplasmic eosinophilic inclusions) are present
20
Q

hepatic encephalopathy

A
  • can be due to decreased NH3 removal (renal failure, diuretics, post-TIPS) or increased production (dietary protein, GI bleed, constipation, infection)
  • treat with lactulose, low-protein diet and rifaximin
  • alpha ketoglutarate is deficient in the brain
21
Q

viral hepatitis

A
  • panlobular lymphocytic infiltrates, ballooning hepatocytes, hepatocyte necrosis/apoptosis
  • round acidophilic Councilman bodies/apoptotic bodies
22
Q

cavernous hemangioma

A
  • most common benign liver tumor, typically at 30-50 years
  • biopsy contraindicated because of risk of hemorrhage, but would show cavernous blood filed spaces with single layer of epithelium
23
Q

hepatic adenoma

A
  • rare, benign liver tumor, often related to OCPs or anabolic steroid use
  • may regress spontaneously or rupture (abdominal pain and shock)
24
Q

angiosarcoma

A
  • malignant tumor of endothelial origin, associated with exposure to arsenic, vinyl chloride
  • express CD31 (PECAM)
25
Q

nutmeg liver

A

due to backup of blood in the liver (Budd Chiari or right sided heart failure)

26
Q

Budd-Chiari syndrome

A

occlusion of the IVC or hepatic veins with centrilobular congestion and necrosis, leading to congestive liver disease (hepatomegaly, ascites, abd pain and liver failure)

  • may develop varices and have visible abdominal and back veins
  • absence of JVD
  • associated with hypercoaguble states, polycythemia vera, pregnancy, HCC
27
Q

Gilbert syndrome

A
  • mildly decreased UDP glucuronosyltransferase conjugation activity leads to decreased bili uptae by hepatocytes
  • asymptomatic or mild jaundice
  • elevated unconjugated bilirubin without overt hemolysis
  • bili will increase with fasting or stress
28
Q

Crigler-Najar syndrome, type I

A
  • absent UDP-glucuronosyltransferase
  • presents in early life, pts die within a few years
  • jaundice, kernicterus, increased unconjugated bili
  • treat with plasmapheresis and phototherapy
  • type II is less severe and responds to phenobarb, which increases liver enzyme synthesis
29
Q

Dubin-Johnson syndrome

A
  • conjugated hyperbilirubinemia due to defective liver excretion
  • grossly black liver, benign
  • high urinary corproporphyrin I levels
30
Q

rotor syndrome

A
  • even milder than Dubin-Johnson and does not have a black liver
31
Q

Wilson disease

A
  • inadequate hepatic Copper excretion (by hepatocute copper transporting ATPase ATP7B gene) and failure of copper to enter circulation and cerulosplasmin
  • copper accumulates int eh liver, brain, cornea, kidneys and joints
  • treat with penicillamine or trientine
  • AR inheritance
  • decreased ceruloplasmin, cirrhosis, corneal deposits, HCC, hemolytic anemia, basal ganglia degeneration, asterixis, dementia, dyskinesia, dysarthria
32
Q

hemochromatosis

A
  • C282Y or H63D mutations in the HFE protein (increased endocytosis of the transferrin receptor)
  • fe absorption increased by 2 mech: increased DMT-1 expression on luminal side, decreased hepcidin synthesis by liver leads to increased ferroportin on basolateral surface
  • associated with HLA A3
  • deposition of hemosiderin –> cirrhosis, diabetes and skin pigmentation
  • results in CHF, testicular atrphy, and increase risk of HCC
  • increased ferritin, increased iron, decreased TIBC, increased transferrin saturation
33
Q

primary biliary cirrhosis

A
  • autoimmune reaction –> lymphocytic infiltrate and granulomas –> destruction of intralobular bile ducts
  • increased serum mitochondrial Abs, associated with other AI conditions (CREST, Sjogren, RA, celiac)
  • middle aged women with insidious onset
  • same mech as graft v. host disease
34
Q

primary sclerosing cholangitis

A
  • unknown cause of concentric “onion skin” bile duct fibrosis –> alternating strictrures and dilation with “beading” of intra and extraheptaic bile ducts on ERCP
  • findings: hypergammaglobulinemia (IgM), associated with UC, can lead to secondary biliary cirrhosis and cholangiocarcinoma
35
Q

black stones

A

due to hemolysis

36
Q

brown stones

A

due to biliary infection

- releases b-glucuronidase into biliary tract by hepatocytes + bacteria

37
Q

causes of acute pancreatitis

A

GET SMASHED

- gallstones, ethanol, trauma, steroids, mumps, AI disease, scorpion sting, hypercalcemia/lipidemia, ERCP, drugs (sulfa)

38
Q

pancreatic pseudocyst

A
  • lined by granulation tissue, not by epithelium, can rupture and hemorrhage
39
Q

Trousseau syndrome

A
  • migratory thrombophlebitis - redness and tenderness on palpation of extremities
  • sign of pancreatic cancer
40
Q

Courvoisier sign

A
  • obstructive jaundice with palpable, non-tender gallbladder

- sign of pancreatic cancer

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