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Flashcards in GI day 2 Deck (40):

tropical sprue

similar findings to celiac sprue, but responds to abx
- cause is unknown, but seen in residents of or recent visitors to the tropics


whipple disease

- 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


celiac sprue

- 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)


disaccharidase deficiency

- 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



- 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


pancreatic insufficiency

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


crohn disease

- 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


CRC from crohns

- 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



- 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


Zenker diverticulum

- 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


meckel diverticulum

- 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



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


causes of ileus

- abdominal surgery, opiates, hypokalemia, and sepsis


adenomatous polyps

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


hyperplastic polyps

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


juvenile polyps

- 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


hamartomatous polyps

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


reye syndrome

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


alcoholic hepatitis

- swollen and necrotic hepatocytes with neutrophilic infiltration
- mallory bodes (intracytoplasmic eosinophilic inclusions) are present


hepatic encephalopathy

- 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


viral hepatitis

- panlobular lymphocytic infiltrates, ballooning hepatocytes, hepatocyte necrosis/apoptosis
- round acidophilic Councilman bodies/apoptotic bodies


cavernous hemangioma

- 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


hepatic adenoma

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



- malignant tumor of endothelial origin, associated with exposure to arsenic, vinyl chloride
- express CD31 (PECAM)


nutmeg liver

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


Budd-Chiari syndrome

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


Gilbert syndrome

- 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


Crigler-Najar syndrome, type I

- 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


Dubin-Johnson syndrome

- conjugated hyperbilirubinemia due to defective liver excretion
- grossly black liver, benign
- high urinary corproporphyrin I levels


rotor syndrome

- even milder than Dubin-Johnson and does not have a black liver


Wilson disease

- 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



- 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


primary biliary cirrhosis

- 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


primary sclerosing cholangitis

- 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


black stones

due to hemolysis


brown stones

due to biliary infection
- releases b-glucuronidase into biliary tract by hepatocytes + bacteria


causes of acute pancreatitis

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


pancreatic pseudocyst

- lined by granulation tissue, not by epithelium, can rupture and hemorrhage


Trousseau syndrome

- migratory thrombophlebitis - redness and tenderness on palpation of extremities
- sign of pancreatic cancer


Courvoisier sign

- obstructive jaundice with palpable, non-tender gallbladder
- sign of pancreatic cancer