Gi

Front 1

best diagnostic test for diverticulitis in the acute setting?

Back 1

Abdo CT

Front 2

Acute pancreatitis:
1. MCC in woman, in man
2.labs
3. potential complications

Back 2

1. woman = gallstone, man=ROH
2.high amylase and lipase
3. exhudative left-sided pleural effusion, abdo compt synd,intraabdo hemorr, shock, diabetes, pancreatic pseudocyst, abdo pseudoaneurysm

Front 3

Achalasia:
1. presentation
2.1st thing you do in pt. >60yo ad w/ assoc.d wt. loss?
3. imaging shows?
4. causes

Back 3

1. can't swallow solids or liquids + regurgitation
2. endoscopy to make sure it is achalasia and not pseudoachalasia (2ndary to neoplasm at GE jnxn)
3. dilated esoph with bird beak tapering at distal end.
4. idiopathic (MC), chagas, amyoidosis, sarcoidosis, or other systemic dz

Front 4

Pt with persistently normal liver enzymes on multiple occasions but his PCR for HCV RNA is positive. what do you do?

Back 4

yearly follow ups labs.
studies show pt.s's with chronic hep C with persistently normal lver enzymes on multpile occasions have minimal histo abnormalities. and so don't need interferon or antiviral drugs

Front 5

Pt w/ dyspepsia (=epigastric pain, postprandial fullness, early satiety with abdo burning, nausea, and/or bloating)
What do you do for:
1. pt.>55 yrs w/ dyspepsia
2. pt. of any age with alarm symptoms
3. what are alarm symptoms
4.what do you in pt.s <55 and w/o alarm symptoms

Back 5

1.. upper endoscopy
2.same as above
3.unexplained wt. loss, persistent vomiting, dysphagia, GI blood loss, odynophagia, FHx of GI CA
4. H. pylori serology test, or empiric PPI

Front 6

1.how does hepatorenal syndrome happen?
2. Tx

Back 6

1.severe liver dz ->systemic hypoperfusion & prerenal failure (absence of blood or protein on UA makes intrinsic renal dz less likely) -> hepatorenal synd.
2.midodrine and octreotide and TIPS if this doesn't help

Front 7

hepatocellular carcinoma
1.initial test
2. next
3. next

Back 7

1. check serum for AFP tumor marker
2. CT or MRI bc hepat CA isn't excluded by normal AFP and if AFP is elevated the CT or MRI is needed to detect the lesion
3. Bx if above imaging showed lesion

Front 8

*HY*
what is the most important pathogenic factor in the development of zenker's div?
Dx
Tx?

Back 8

-upper esophageal sphincter dysfnxn and esophageal dysmotility.
-barium study (ie contrast esophagogram)
-excision and cricopharyngeal myotomy

Front 9

Hepatic adenoma:
1. Assoc.d w/
2. histology
3. but don't normally bx bc:
4. tx

Back 9

1. OCP, anabolic ster, DM
2. enlarged hepatocytes containing lipids and glycogen.
3.Don't bx bc can ->rupture and bleeding
4. Qx resxn

Front 10

Acute pancreatitis complications:

Back 10

-hypoTN (intravasc vol. loss) <- systemic vasodil <- vascular endothelial injury
-pseudocyst
-severe retroperitoneal hemorrhage

Front 11

origin of post cholecystectomy pain

Back 11

1 of 3 reasons:
1. common bile duct stone (^alk phos or biliary tree dil. next step ERCP to confirm and treat through stone removal)
2. sphincter of oddi dysfnxn (same as above except ERCP to dx and Tx thru sphincterotomy)
3. functional causes (normal LFTs and no biliary tree dilation. Tx w/ analgesics)

Front 12

elderly pt. w/ iron def. anemia and negative occult blood test. what do you do?

Back 12

MCC of Fe def anemia in elderly pt. is GI blood loss. next step in eval is colonoscopy.
a single negative occult blood test does not exclude the possibility of GI bleeding.

Front 13

Porcelain gallbladder:
1. dxed by
2. assoc.d with >ed risk of?
3. Tx

Back 13

1. abdo imaging (usually by accident)
2. gallbladder carcinoma
3. Qxical rsxn

Front 14

Pancreatic laceration
1. cause
2. if untreated what complication can happen?
3. Tx for complication

Back 14

caused by blunt trauma can be missed by CT during 1st 6 hours following trauma
2. can be complicated by retroperitoneal abscess or pseudocyst
3. perQ drainage cath, Cx, and Qxical debridement

Front 15

Dubin Johnson syndrome
1. biliruben
2. when does it manifest
3. Dx
4. Confirmatory Dx
5. Tx

Back 15

1. has conjugated hyperbilirubinemia (not assoc.d w/ hemolysis)
2. after trigger: illness, pregs, OCP
3. at least a 50% fraction of direct bili .
4. D-J has >80% urinary coproporphyrin I (normal people have >80% copro III)
5. No Tx, benign condition

Front 16

Carcinoid synd. will have what kind of vit def and why?

Back 16

Niacin def bc. of >ed formation of serotonin from tryptophan

Front 17

conditions where one may have an >ed BUN w/o an > in creatinine?

Back 17

1. Prerenal renal failure
2. GI bleeding (bacterial breakdown of Hgb in GI tract with resultant urea absorption)
3. Steroid administration

Front 18

Niacin def.
how does it manifest

Back 18

pellagra = diarrhea, dermatitis, dementia, and death

Front 19

what is and when do you hear abdo succussion splash?

Back 19

splash heard in stomach if gastric material retained for >3hrs.
happens in Hx of acid ingestion , pyloric stricture and obstrxn from gastric CA

Front 20

angiodysplasia
1. =
2. best initial dx
3. gold standard dx
4. associated w/

Back 20

1. common cause of intermittent and occult lower
GI bleeding in pt.s >65
2. colonoscopy
3. angiography
4.aortic stenosis = systolic ejxn at right 2nd intercostal

Front 21

Digoxin toxicity

Back 21

w/ concurrent verapamil bc. verapamil <es the renal CL of dig.
SEs = GI (MC), and Vtach

Front 22

Crigler-Najjar type 2
1. path phys
2. dangerous?

Back 22

1. auto rec. disorder of bili metab. liver enzymes are normal
2. no. but may need periodic administration of phenobarb or clofibrate to reduce serum bilirubin levels

Front 23

Gilbert's syndrome
1. path phys
2. dangerous?

Back 23

1. <ed UDP glucuronyl transferase - so >ed uncongugated bili
2. benign

Front 24

Crigler-Najjar type 1
1. path phys
2 dangerous?

Back 24

1. auto rec. really high indirect bili. liver enzymes and histo are normal
2. severe jaundice and kernicterus (Nod yer head)
Tx. phototherapy, or plasmapheresis - short term therapy. liver transplant is only curative option

Front 25

chronic hep C
1. extrahepatic sequelae
2. how do liver enzymes present

Back 25

1. arthralgias (w/ false-pos rheumatoid factor or ANA Ab), cryoglobulinemia, porphyria cutanea tarda, and glomerulonephritis
2. transient elevations of AST and ALT

Front 26

Ischemic colitis
1.when to suspect it?
2. most comon segments of colon involved:

Back 26

1. after Qxery, HypOTN, atherosclerotic dz, abdo pain followed by bloody diarrhea
2. watershed zones:
(1) splenic flexure - SMA's terminal branches
(2) recto-sigmoid jnxn -IMA's terminal branches

Front 27

Non-alcoholic fatty liver dz.
1. Pt. description
2. mechanism behind dz.

Back 27

1. obesity and DM type2
2. insulin resistence -> >ed lipolysis -> >ed fat accum. in hepatocytes

Front 28

GI malignancy:
1-4. reasons you know the pt. has it
2. next step

Back 28

1.microcytic anemia (from occult GI bleed)
2.firm hepatomegally
3. liver enzymes suggestive of cholestatic dz ( ^alk phos, and slightly elevated AST and ALT)
2. Abdo CT with contrast

Front 29

Nonalcoholic steatohepatitis (NASH)
1. clinical manifestation
2. leading causes

Back 29

1. obese, DM, hyperTGs
2. asymptomatic, hepatomegaly, ^ ALT and ASTs

Front 30

Pt. w/ pancreatitis 2ndary to gallstones:
ERCP vs cholecystectomy

Back 30

ERCP: pt.s w/ severe biliary pancreatitis (also used in Dx of chronic pancreatitis, Dx of ampullary CAs, and need for bile duct exploration

Cholecystectomy:
symptomatic gallstones w/ resolved acute pancreatitis and stable enough for Qx

Front 31

gastric malignancy. what's the next step in management?

Back 31

CT to evaluate the extent of the dz.
do it b4 Qx = therapy

Front 32

Hepatic hydrothorax
1 Tx
2. what is it?

Back 32

1. initial = salt rstrxn + diuretics
if refractory = TIPS
2. trasudative pleural effusion from cirrhosis w/o pulm or heart cause

Front 33

when is the liver damage from alcoholism irreversible ?

Back 33

w/ true cirrhosis = regenerative nodules
Reversible with ROH cessation: Fatty liver (steatosis), ROH hepatitis, and early fibrosis

Front 34

ascending cholangitis
1. how do you clinically dx
2. usual causes
3. labs show
4.1st imaging study
5. Tx
6. if persists inspite of #5, what do you do?

Back 34

1. charcot's triad = fever, severe jaundice, RUQ abdo pain.
Reynold's pentad = charcot's triad + hypOTN, and confusion
2. infxn in CBD (common bile duct) <- CBD stone or stricture
3. leukocytosis and ^LFTs
4. US
5. supportive care and broad spec abx (80% will clear up this way)
6. if persists in spite of #5, ERCP

Front 35

Familial colonic polyposis (FAP)
1. inheritence, gene
2. risk of CA
3. Tx
4. how to Dx

Back 35

1.AD, APC gene
2. 100%
3. tx. proctocolectomy
4. colonoscopy shows 100s of adenomatous polyps

Front 37

sprue

Back 37

-all show blunting of villi in s. bowel, malabsorption esp B12 and folic a.
- tropical: if history of endemica area
- celiac: if (+) FHx

Front 38

drugs causing pancreatitis

Back 38

(AAIIDS)
1. AIDS - Didanosine, pentamidine
2. Abx - metronidazole, Tetracyclines
3. IBD - sulphasalazine, 5-ASA
4. immunosuppresive agents - azathioprine, L-asparaginase
5. diuretics - furosemide, thiazides
6. Seizure drug or bipolar- valproic acid

Front 39

hypercoagulability:
1. in younger person
2. in older person

Back 39

1. genetic defect
2. malignancy; particularly visceral adenocarcinomas (gastric, pancreatic, and ovarian)

Front 40

celiac dz clinical features

Back 40

1, foul smelling floating stool
2. loss of muscle mass or subQ tissue
3. pallor - iron def anemia
4 bone pain- osteomalacia
5. easy bruising - vit K def
6. hyperkeratosis - vit A def.

Front 41

Most common serious complication of peptic ulcer dz:

Back 41

hemorrhage.

Front 42

*HY*
how do you test for C. dif

Back 42

cytotoxin assay of stool

Front 43

Most sensitive and specific test to dx pancreatitis

Back 43

fecal elastase

Front 44

1.Potentially lethal complication of IBD
2. what do you do if you suspect it
3. Tx

Back 44

1. toxic megacolon
2. initial test is abdo XR (colon dilated > 6cm)
3. initial tx: conservative = bowel rest, NG tube, steroids, Abx for 2ndary infxn
severe cases not responding to conserv. mg then ermergency colectomy and end-ileostomy

Front 45

In pt. w/ ZE synd:
1. what is explanation for impaired fat absorption?
2. Best step in Dx?
3. if #2 is nondxic what do you do?

Back 45

1.fat malabs <- pancreatic enzyme inactivation <- >ed stomach acid prdxn
2. fasting gastrin serum levels > 1000 pg/mL is diagnostic
3. secretin stim. test

Front 46

*HY*
which polyps are dangerous?

Back 46

villous adenoma, sessile adenoma, and size > 2.5 cm
(yperplastic polyps are non-neoplastic and don't need further work-up)

Front 47

pt. w/ cirrhosis + ascites + fever (or change in MS)
1. likely Dx
2. next step
3. MC orgs
4. Tx

Back 47

1. SBP
2. paracentesis (do this b4 abx)
3. E. coli, Klebsiella
4. 3rd gen cephalos

Front 48

*HY*
pt. from developing country or rocky mnt.s w/ malabsorption.
1.Dx
2.Tx
3. pathophys

Back 48

1.Giardiasis
2. metro
3. adhesive disks and malabsorption

Front 49

portal hypertension:
labs
Tx

Back 49

- >ed NH4, SAAG value > 1.1 (serum albumin - ascites albumin), >ed WBC
- salt rstrxn, diuretics, IV abx, lactulose, neomycin, low protein diet (the previous 3 for hepatic encephalopathy), vasopressin, TIPS

Front 50

SAAG
-acronym for
- definition
- calculation
- important causes of high SAAG

Back 50

- Serum-Ascites albumin gradient.
- calculation to determine cause of ascites.
- serum albumin- albumin ascites albumin
- high protein (> 2.5): HF, Budd Chiari syndrome
- low protein (<2.5) cirrhosis of the liver

Front 51

spontaneous bacterial peritonitis
- cause
- what does paracentesis show?

Back 51

- systemic infxn + comorbid portal HTN
- PMNs >250/microL, glucose < 50 mg/dL, and LDH > normal serum LDH

Front 52

Portal HTN of neoplastic etiology
- lab values

Back 52

very high albumin and
LDH equal to 60% serum LDH

Front 53

Mallory bodies

Back 53

- ROHic hepatitis
- Wilson's Dz
- PBC

Front 54

Wilson's dz:
- best initial test
- most accurate test

Back 54

- slit lamp
- abnormally high Cu urine excretion after penicillamine taken

Front 55

Hepatic mass found on CT. what do you do?

Back 55

Don't Bx! bc. of hypervascularity -> hemorrhage
so, larger tumor can be resected or embolized to prevent rupture

Front 56

tumor marker for hepatoma (ie malignant hepatocellular carcinoma

Back 56

alpha fetoprotein