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
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
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)
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
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
6
Q
pancreatic insufficiency
A
- due to CF, obstructing cancer or chronic pancreatitis
- ADEK malabsorption
- increased neutral fat in stool, D-xylose testing normal
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
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
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
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
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
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
13
Q
causes of ileus
A
- abdominal surgery, opiates, hypokalemia, and sepsis
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)
15
Q
hyperplastic polyps
A
- most common non-neoplastic polyp in the colon (> 50% found in rectosigmoid)
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
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
