Gi Flashcards Convert

Front 1

1. Can patient wiht T1 esophageal CA have the potential to spread? Why?

2. What stage of esophageal CA can be consider for EMR?

Back 1

1. Yes, because it has rich lymphatics

2. T1sm has 15-30% met so best with surgery. T1m can undergo EMR

Front 2

1. What is the EF cut off for TIPS?

2. What are the 5 major criteria for HRS?

Back 2

1. 50%

1. Presence of liver disease with portal HTN
2. creatinine >1.5,
3. abscence of shock, GI bleed, volume lost
4. No improvement after d/c of diuretics and 1.5L fluid challenge
5. <500mg/dL proteinuria without obstructive uropathy

Front 3

1. After seroconversion, how many patient can have 1 or more revision to HBeAg+?

2. What % of HBV patient also has HCV?

3. What is the treatment rate, complication rate and recurrence for band ligation for hemorrhoids?

4. What are 4 indications for surgical hemorrhoidectomy?

Back 3

1. 4-20%

2. 10-15%

3. 80-90% success, 5-60% complications such as abscess, urinary retention, pelvic floor sepsis, 60% recurrence

4. Too extensive, fail of non-operative management, perference, concurrent need for surgery

Front 4

8 risk factors for HCC in patient with hepatitis B>

Back 4

1. Fmhx
2. age
3. male
4. ESLD
5. hx of revision
6. genotype C
7. precore mutants
8. co-infection.

Front 5

1. Two contraindication for surgical resection of HCC?

2. What is the recurrence of HCC after resection?

3. Which is more effective RFA vs. EtOH ablation for lesion <2cm?

Back 5

1. portal HTN, high bilirubin

2. >70% in 5 years

3. equal.

Front 6

When does acute fatty liver of pregnancy occur?

What is the etiology of AFLP

How do you diagnose it?

Back 6

1. Occurs in the 3rd trimester

2. Maternal deficiency of long channel 3-hydroxyacyl-CoA dehydrogenase leading to low maternal capacitiy to oxidize long chain fatty acid leads to hepatotoxic LCHAD metabolites

3. diagnose with LFT to 1000s, BT<5, biopsy showed microvesicular fatty infiltrate.

Front 7

1. 4 causes of chronic pancreatitis?

2. What is the pathophysiology of pain from chronic pancreatitis?

Back 7

1. Alcohol, hereditary, autoimmune, tropical (SPINK1)

2. inflammation leads to increase pressure build up and ischemia. This also lead to nerve injury and sensitization of the nerve even you remove the inflammation still with pain.

Front 8

What are the 3 indications for EMR for patient with early gastric CA?

Back 8

1. IM well diff CA w/o ulceration or scar

2. IM well diff CA with ulcer/scar <3cm

3. Submucosal <500 micrometer well diff CA <3cm

Front 9

What are the side effects of

IFN?

RBV?

Back 9

IFN: mylosuppression, pancreatitis, flu like symptoms, emotional affects, autoimmune reaction, fatigue, weight lost

RBV: hemolytic anemia, avoid in renal insufficiency and contraindicated in pregnancy.

Front 10

1. When is surgical tx indicated for GIST?

2. which layer does aberrent pancreas appears in

3. What is the EUS appearance of aberrent pancreas

4. Incidence of aberrent pancreas? Where can it be located?

Back 10

1. >3cm with features of malignancy

2. 2,3 or 4th layer

3. hypoechoic or mixed

4. 0.6-14% locate anywhere along the GI tract.

Front 11

1. Rate of HCV transmission from mom to kid is what %?

2. What are the 3 Risk factors for vertical transmission of HCV?

3. When are surgery avoided for choledocholithiasis? when is indictaton for ERCP in pregnancy safe?

Back 11

1. 1-5%

2. IV drug use, HIV+, HCV RNA >10^6

3. Avoid surgery in 1 and 3rd trimester. ERCP indicated if there is ongoing choledocholithiasis

Front 12

1. What are 7 area to look for in doing EUS in patient with mediastinal mass or non-small cell lung CA

2. Which area is difficult to see with EUS while evaluating patient with lung CA?

Back 12

1. Celiac axis, left adrenal, left lobe, periesophageal space, subcarinal space, A/P trunk, paratracheal.

2. Paratracheal LAD (station2)
right lower paratracheal (station 4R)

Front 13

1. What are the 3 fetal complications with intrahepatic cholestasis?

2. What correlate well with high risk of complication?

3. What is the most specific/sensitive marker for ICP/

4. Treatment?

Back 13

1. placental insufficiency, premature birth, fetal death

2. bile acid

3. bile acid

4. Urso 10-15mg/kg

Front 14

What are the 5 layers seen with GI wall? Is it always 5 layers?

Back 14

1-2 mucosa/hyper/hypo
3, submucosal, hyper
4, MP, hypo
5. serosal hyper

Not always 5 layers base on the frequency you use to scan.

Front 15

1. What are some possible treatment for GAVE?

2. Does TIPS help with GAVE?

3. What tamponade balloon can be used for GV bleed?

Back 15

1. Iron/Epo, APC (60-90w@1-2L), estradiol 35ng +Noethridone 1ng

2. No

3. Only Linton tube.

Front 16

How often are anti-SMA present in AIH

2. How often do you seen Anti-LKM in US patients?

3. What condition may give you false positive of anti-LKM

4. Which new antibodies for AIH is very good to assess activity of AIH?

Back 16

1. 87%

2. 4%

3. Hep c

4. Anti-ASGPR (asialoglycoprotein receptor)

Front 17

1. Three conditions when is liver biopsy offer to patient with hemochromatosis?

2. What test can you use to distinguish iron overload due to hemochromatosis vs. EtOH/others

3. What is the stain for hemochromatosis?

Back 17

1. >40years old, ALT, >1000 feritin with liver disease.

2. hepatic iron index

3. Perl's stain

Front 18

1. What is the genetic inheritance for Wilson's? What is the gene defect and how does it lead to liver damage?

2. Why does Wilson disease have low ceruloplasmin level?

Back 18

1. Autosomal recessive/ATP7B which encode a metal-transporting p-Type ATPase which decrease the hepatocellular excretion of copper into bile leads to accumulation of copper in liver.

2. Low copwer incorperation into cereuloplasmin thus liver decrease apoceruloplasmin leads to decrease ceruloplasmin due to reduced 1/2 life of apoceruloplasmin.

Front 19

1. Is there evidence of anti-depressant treatment of functional dyspepsia?

2. What is the clinical approach for patient with dyspepsia?

Back 19

1. No

2. No alarming symptoms then check for H.P. in high risk population and treat. If negative HP then empiric treat with PPI x 4 weeks.

Front 20

1. What are the two genes identified for hemochromatosis?

2. What are the % of homozygous vs. heterozygous hemochromatosis?

3. If left untreated, organ damage occur at what age and iron parenchymal storage?

Back 20

1. C282Y, H63D

2. 90% C282Y homo, 3-5% hetero

3. >40 years or >20g of iron

Front 21

1. Which gene is responsible for Wilson's?

2. When was it discovered?

3. How to differentiate acute viral hepatitis vs. Wilsons?

Back 21

1. ATP7b

2. 1912

3. Wilson's have low ALKP and ALT

Front 22

What are the 12 side effects of the sulfasalazine?

What is the maximine dose of
1. Sulfasalazine
2. Mesalamine
3. Balsalazine
4. Olsalazine

Back 22

Side effects: Acute interstitial nephritis, n/v, oligospermia (sulfasalazine), pancreatitis, hemolytic anemia, pericarditis, hepatotoxicity, HA, pneumonitis, steven johnson's syndrome, drug induced lupus and agranulocytosis.

1. Sulfasalazine 4-6g
2. Mesalamin 2-4.8g
3. Balsalazine 6.75g
4. Olsalazine 1.5-3 gram

Front 23

1. What are the three major ligment of the liver?

2. Which sections of the liver is involved in
Right lobectomy
Right hepatectomy
Left lobectomy
Left hepatectomy

Back 23

1. Round, falciform, coronary

Right lobectomy (4-8)
Right heptectomy (5-8)
Left lobectomy (1-3)
Left heptectomy (1-4)

Front 24

Which liver disease is the only one seen in 1st trimester?

How often does it occur in pregnancy?

name the 5 risk factors for this disease?

Back 24

1. Hyperemesis gravadium

2. 0.3%

3. Hyperthyroidism, psych disease, DM, molar pregnancy, multiple pregnancy

Front 25

IPMN

location?
malignant potential?
EUS feature?
Communicate with PD?
Cytology?
Viscosity?
Amylase? CEA?
M vs. F? Age?
Endoscopic appearance occurs in what %?
On discovery, how many (%) of patient have malignancy?
TX? Prognosis?

Back 25

-HOP>rest, arise from the duct

-high malignant potential

-mural nodules/mass arise from PD or branch

-communicate with PD or side branch, usually PD is dilated

-mucin + cells (columnar or cuboidal)

- high viscosity

- high amylase, variable CEA

- equal sex, usually present in 60s

- 25-50% may have endoscopic appearnce of fish mouth

- 60% malignant and out of it 2/3 is invasive

- Tx is surgery, 75% survival rate at 5 year.

Front 26

1. What is the risk of rebleed in patient with history of GIB who is taking Warfarin?

2. What is the percentage of bleed in patient undergoing polypectomy? ablation? sphincterotomy?

Back 26

1. 30% in 3 years vs. 5% in patient w/o hx of GI bleed

2. polypectomy (1-2.5%), gastric polypectomy (4%), ablation (6%), sphincterotomy (2.5-5%)

Front 27

1. Which antibiotic should be avoided due to risk of cholelithiasis? Why?

2. When can you restart anticoagulation post ERCP with sphincterotomy?

Back 27

1. Ceftriaxone, due to formation of crystals

2. 72 hours.

Front 28

1. What % of patient become chronically infected with HCV?

2. What is the rate of cirrhosis after 20 year of HCV

3. Rate of HCC in patient with cirrhosis?

4. What is the most important clinical information to decided whether tx vs. no treatment?

Back 28

1. 85%
2. 20%
3. 1-4%
4. histologic grade of inflammation.

Front 29

1. What % of patients with atypical chest pain actually have diffuse esophageal spasm?

2. Can DES become achalasia?

3. How do you diagnose it?

Back 29

1. 3-10%

2. 3-5% of DES became achalasia

3. Manometry

Front 30

What is the prevalence of dyspepsia and what is the "true" prevalence after IBS/GERD has been excluded?

2. What are 4 causes of investigated dyspepsia? What % of it has positive findings?

Source?

Back 30

Evidence base on ASGE 2005 review

1. 13% to 3%

2. PUD (5-15%), GERD (erosive esophagitis 5-15%), malignancy (<2%), functional (60%)

Front 31

1. What makes up hemorrhoid tissue?

2. What makes hemorrhoid painful?

3. Is anemia due to hemorrhoid possible?

Back 31

1. Connective tissue cushion surrounding direct AV communicatin of rectal artery with sup/inf and middle rectal vein

2. Thromobsed

3. 0.5/100,000

Front 32

1. What is the test that document significant iron overload in hemochromatosis?

2. What is the screen test for hemochromatosis?

Back 32

1. Hepatic iron index >1.9

2. Fasting Iron Sat >45% + elevated ferritin.

Front 33

1. What are the 2 treatment option for HRS?

2. What are the 3 most common organisme identified in SBP?

3. What is the treatment for SBP?

Back 33

1. Midorine up to 12.5mg TID (increase BP >15) Octreotide (200mcg SQ TID) Albumin 20g IV daily, HD

2. E coli, Klebsiella and strep pna

3. abx for 5 days.

Front 34

1. Which layer is usually for lipoma and how does it appear on EUS?

2. How does carcinoid appear on EUS? Which layer?

3. Rectal carcinoid represt what % of all GI carcinoid?

4. What is the EUS criteria for EMR treatment of carcinoid?

Back 34

1. 3rd, hyperechoic

2. 2-3 layer, mildly hypoechoic and homogeneous

3. 20%

4. Confined within the 3rd layer and <2cm.

Front 35

1. How many % of patient with EV will bleed in 2 years?

2. What is the best clinical predictor for bleeding and what % risk for each?

3. What is the % of patient re-bleed within 6 weeks?

Back 35

1. 25%

2. EV size. <5mm=7% @ 2 year and >5mm = 30% @ 2 year

3. 1/3

Front 36

1. What are the 5 test that you can send to rule out 2nd peritonitis?

2. What is the sensitivity for AFB smear/culture for ascites fluid?

3. What is the chance that ascites fluid grow organism if +SBP by cell count?

Back 36

1. CEA>5, ALKP>240, glucose, LDH, total protein.

2. 0% smear, 50% culture

3. 50% if you wait, and 80% if you inoculate immediately during paracentesis.

Front 37

1. How do you monitor patient with post CRC resection?

2. What is the recurrence of CRC at anastomosis? base on?

3. Why is there difference between colon CA vs. rectal CA? How do you monitor them?

Back 37

1. Need peri or preop colonoscopy to rule out synchronous lesions then 1 year post surgery, then 3 year then every 5 years.

2. 2-4%, AGA guideline 2006

3. Increase local recurrence rate for rectal cancer, therefore you need Q3-6 months surviellence.

Front 38

1. Which type of chronic liver disease has best post transplant survival which doesnt?

2. What is the survival rate for re-transplant?

Back 38

1. Best:Alcohol, cholestatics. Worse: hemchromatosis,

2. 20% less then inital transplant.

Front 39

1. What EUS finding suggest duplication cyst?

2. If you see a mediastinal cyst, what is the most likely cause.

3. Which layer do you see varices in? What is the echotexture?

Back 39

1. Contain all 3 or 5 layers

2. Bronchogenic cyst

3. Submucosal, anechoic tubular feature.

Front 40

How to treat hemochromatosis and monitor it?

1. What is the most common complication due to hemochromatosis?

2. What should patient NOT take

3. HCC accout for what % of death in patient with Hfe?

Back 40

Phlebotomy 1 units/Q0.5-1week until ferritin <50ng/mL (check after 10-12 phlebotomy)

1. Arrhythemias
2. Vitamin C
3. 30%

Front 41

1. How often does IBD patient have PSC?

2. What is the peak age of incidence for PSC?

3. Is there a possible genetic componenet to PSC? Why?

Back 41

1. 2-8%

2. 40s

3. Yes according to twin studies

Front 42

1. What are 3 treatment option medically for GERD?

2. What are 4 types of symptoms which can happen post surgery for GERD?

3. What is the success rate for surgery in well chosen patient with GERD?

4. How does PPI work?

Back 42

1. PPI, h2 blocker, Baclofen

2. Gas/bloating, diarrhea, dyspepsia, dysphagia

3. 80-90%

4. It gets taken up by parietal cells and irreversibly complex with H/K+ ATPase.

Front 43

1. Where does AST come from other than liver? (6 locations)

2. Which clotting factors are made by liver?

Back 43

1. kidney, brain, muscles, RBC, pancreas, heart muscles

2. all but factor 8

Front 44

1. How to determine whether patient is diuretic resistant or not?

2. What is the general guideline for giving albumin during paracentesis?

3. Maximum diuretic that you can give is?

Back 44

1. Give 80mg IV lasix then measure then measure the urine sodium, if >50mmol then sensitive to diuretic

2. After 5 liters given 8grams per extra liter taken out

3. 400 aldactone, 160 lasix

Front 45

1. What demographic data is Barrett's associated with?

2. Barrett's are diagnosed on average what % of patient's

3. Cancer risk for Barrett's are?

Back 45

1. male, white, age, GERD

2. 3.5-7%

4. Annal rate of 0.5%

Front 46

1. Is it good to restage with EUS after chemoradiation treatment of esophageal CA? why or why not?

2. What 5 particular areas to exam for esophageal CA using EUS?

Back 46

1. No, because the treatment can lead to inflammation/necrosis which is difficult to differentiate CA vs. other.

2.
liver,
CAX,
periesophageal area above aortic arch,
note relation of CA to carina, invasion into diaphragm.

Front 47

1. when does flare typically occurs with IFN on HBV treatment? How often does it occur?

2. When does flare typically occur in patient with HBV and immunosuppression therapy?

Back 47

1. 1/3 patient treated occur during 2-3rd month of treatment.

2. On withdrawal of therapy

Front 48

1. How effective is sitz bath+bran vs. 2% hydrocortisone cream in treatment of hemorrhoid?

2. How effective is nitropaste in treatment of hemorrhoid? Dosage? side effect? Effectiveness?

Back 48

1. Jensen 1986
Sitz+10g Bran BID x 3 week vs.2% cream x 3 week
87-82% healing rate.

2. 2% glyceral TID x 8 weeks
side effect: headache in >50%, initial study more effective but studies in 2001 shows 55% resolution, 33% drop out due to headache.

Front 49

1. What are the 2 danger for hepB+HIV co-infection?

2. Define anti-viral resistance?

Back 49

1. Severe hepatitis can flare in patient with low CD4 count and starts on HARRT therapy (immunoconstiutional syndrome)

Pt with only anti-HBc but no hepBsAg can have increase DNA due to immunosuppression and hepatonecrosis.

2. >1 log increase in HBV DNA

Front 50

1. How often does H. Pylori cause duodenal ulcer? what about gastric ulcer?

2. What is the diagnostic criteria for functional dyspepsia? What are the 3 suspect causes of this?

Back 50

1. DU:90%, GU:70%

2. >3months of dyspepsia in which there are no structural finding.
1. 25-40% gastroparesis
2. 40% fundal accomondation problem
3. h. pylori?

Front 51

What are the two typical symptoms of gastric NHL?

Secondary gastric NHL account for what % of the gastric lymphoma? Where does it mostly occur and which part of the stomach does it typically infiltrate?

Back 51

1. Abdominal pain, vomiting

2. 20-60%
Occur mostly in fundus and duodenum
Infiltrate mostly in the body and antrum.

Front 52

What are some bridging therpay for Wilson patient with fulminant failure?

Back 52

plasmaphresis which protects the kidney

Front 53

Who should have 3 year follow up colonoscopy? (3) How about 5 year? (2) Base on which referrence?

Back 53

1. >2 adenoma, >1cm adenoma, and adenoma with villous histology/HGD

2. 1-2 <1cm adenoma
No family hx of CRC

AGA recommendations 2006

Front 54

How do you manage patient with HBV with HepBeAg negative?

Referrence?

Back 54

If ALT>2x + DNA >20,000 then treat

If ALT = 1-2x and DNA between 2000-20000 then Q3month ALT and DNA, if persistently elevated, then treat

ALT=1 and DNA <2000, Q3 months ALT

Lok AASLD recommendation

Front 55

Where does the periesophageal vein drain?

Where does distal esophagus drain?

How much % patient with ESLD have EV? How fast do they develop in patient with ESLD but no EV?

Back 55

1. azygous vein

2. coronary vein to the portal vein

3. 40% pt with ESLD have it, 5% per/year in patien twith ESLD but no EV

Front 56

1. How long can botox last for tx for achalasia? what is the response rate?

2. What is the response rate for myotomy?

3. What is the increase CA risk for achalasia?

Back 56

1. drop LES in 60-75% but sx returns in 3-12 months.

2. 90%

3. 2-7% with increase esophageal CA risk

Front 57

1. What are the surgical treatment for chronic pancreatitis?

2. Why drainage vs. resection?

Back 57

Complete drainage: Modified Puestow (down side is that patient still with pain at head of pancrease)

Extend drainage: Frey's which core out the HOP + drainage

Resection: Whipple

Drainage remove inflammatory mass at the HOP which improves pain

Front 58

How does tylenol cause hepatotoxicity?

What is the indication for transplant?

What is the Tx? Oral and IV dosage?

Back 58

1. It normally gets met to aulfate + glucoronide but 8% gets through and breakdown by p450 system which form NAPQI that is a free radical. Normally NAPQI is conjugated with glututhione and form mercapturate but if there is a low glututhione, then NAPQI build up and become toxic

Kings criteria: if pH<7.3 OR PT>100 (INR>6.3), creatinine >3.4, +PSE

PO Mucomyst: 140mg/kg x 1 + 70mg/kg x 17 dose at Q4 interval

IV: 150mg/kg/ 1 hour follow by 50mg/kg for 4 hours follow by 100mg/kg for 16 hours.

Front 59

What are the treatment for anal fissure? 5 pharmacologic tx?

Back 59

1. Sitz bath
2. Topical nitro
3. Dilt. cream
4. Botox
5. Bethanechol topcial

Front 60

1.What is the accuracy of EUS in T staging and N staging for esophageal CA?

2. What improves the N staging? What accuracy can it get? and sensitivity?

3. What is EUS sen/spec for LAD in esophageal CA?

Back 60

1. T:85%, N:77%

2. EUS with FNA, sen:83%, Spec:93% and Accuracy:87%

3. EUS sens: 71%, spec:79% and accuracy:74%

Front 61

What is the condition where gallstone causes gastric outlet obstruction?

Back 61

Bouveret's syndrome

Front 62

What is he colorectal cancer risk for patient with ulcerative colitis? What is the % increase risk and what is the screening recommendations?

Back 62

Screen 8-10 years after diagnosis of colitis.

Increase risk of CA at 0.5-1% cummulative year.

Yearly screen

Front 63

1. At what level in esophagus do smooth muscle take over?

2. Which nerve innervate smooth muscle vs. striated muscle/UES?

3. Clues that tells you that there might be UES disorder? How do you assess this?

Back 63

1. 22-24cm

2. CN10=smooth, CN9+10 controls UES/striated muscle

3. Regurgiate liquid early (can assess by video swallow)

Front 64

1. What clinical outcome can occur with HBsAg mutation?

2. What is a potential cause with lamuvidine resistance?

Back 64

1. Can lead to virus escape vaccintation due to change in surface antigen epitope

2. DNA polymerase mutation (YMDD mutant) can rarely lead to serious hepatitis.

Front 65

1. What are 3 findings on cross sectional CT/MRI you can see for patient with AI pancreatitis? (3)

2. How do you treat AIP?

3. What should you use to montior for response?

Back 65

1. sausage like pancreas with enhanced peripheral rim and low attenuating mass in HOP

2. 40mg Prednisone x 1 week follow by taper of daily dose by 5mg/wk

3. CT 2-4 weeks after treatment.

2.

Front 66

1. What is the most common sx of autoimmune pancreatitis?

2. What are the 2 other auto antibodies frequently seen with AIP?

Back 66

1. 63% jaundice, 35% pain

2. Anti-lactoferrin, anti-carbonic anhydrase II

Front 67

1. What is the % for mom with +EAg and +EAB that can trasmit HBV to their child?

2. Define chronic hepatitis B infection.

3. How does HBV replicate?

Back 67

1. EAG+=60-90%, EAB+ 10-20%

2. HBsAG+>6 months or >20,000IU with abnormal LFT

3. use RNA intermediate

Front 68

1. What is MALToma compose of interms of cell type

2. This type of tumor arise from organs with or without lymphoid tissues? If not how did they get it?

3. What is the 3 most common chromosomal breakage?

Back 68

1. Small B cell lymphocytes with centrocytic immunocytic appearance

2. MALToma can develop from organ w/o lymphoid tissue due to infection or autoimmune process

3. Trisomy 3, 18

Front 69

1. What is the genetic mutation causing hereditary pancreatitis?

2. What are the 2 type of autoimmun pancreatitis? In terms of histology, labs, epidemiology?

Back 69

1. PRSS1 on chromosome 7

2.
periductal lymphoplastic infiltrate rich in IgG4+ plasma cell. Mostly in Asian country, older female, high IgG4 and is associated with other autoimmune organs

Ductal epithelial granuocytic infiltration leading to damage and obliteration. They are typically younger, European, low IgG4 and is associated with IBD

Chari, Mayo, 2009 AJC

Front 70

1. How many % of patient with HBV get polyarteritis nodosa? How about % of patient with PAN has HBV?

2. What is the characteristic finding on pathology for HBV infection? Why?

Back 70

1. <1%, 30% pt with PAN has HBV

2. Ground glass appearance, HBsAG deposit in the hepatocyte's ER.

Front 71

1. What is Milan criteria?

2. What is the UCSF criteria?

Back 71

1. No one lesion >5cm and no more then total of 3 lesions with each <3cm

2. No single lesion >6.5cm or 3 lesions each <4.5cm with total of <8cm.

Front 72

1. How long should anticoagulation be avoided after biliary sphincterotomy

2. Do patient need routine abx for ERCP?

3. Do patient need abx after cholangioscopy?

Back 72

1. 72 hours

2. No

3. Yes

Front 73

1. What are the 2 most common chemo. agent use for TACE?

2. What is the #1 contra-indication for TACE? Why?

3. What are the survival rate post OLT at year 1, 3 and 5?

4. When patient should be consider for transplant?

Back 73

1. adriamycin + cisplatin

2. Portal vein thrombosis due to lack of blood supply to the TACE area

3. 1:88, 3:80% and 5:75%

4. 15

Front 74

What are the rebleeding risk base on the following stigmata?

1. Active arterial bleed
2. non-bleeding visible vessel
3. non-bleeding clot
4. ulcer oozing
5. flat spot
6. clean base ulcer?

Referrence?

Back 74

1. 99%
2. up to 50%
3. 30-35%
4. 10-27%
5. <8%
6. <3%

ASGE guideline

Front 75

1. What is the majro diagnostic criteria for PSC?

2. How often can you see "small duct" PSC?

3. Do small duct PSC progress to large duct?

Back 75

1. cholangiogram

2. 2%

3. usually do not progress

Front 76

What are the two strategies to treat AIH relapse? How effective is each one of them?

Back 76

1. Indefinite low predisone strategy. Lower steroid by 2.5mg/month until the lowest reach with stable LFT (87% managed with 10 or less)

2. Increase AZA to 2mg/kg daily and prednisone withdraw at 2.5mg/month untile completely gone.

Front 77

Which 4 condition would you consider NOT treating patient for HCV?

AT what histological grade would you consider treatment?

Back 77

1. ESLD, severe uncontrolled psych disease, substance/etoh abuse, low WBC/plt

2. METAVIR >F2

Front 78

How do you manage patient with HBeAg+?

Back 78

ALT>2xULN: Q1-3 montha LAT and if persistent elevated then tx or HBV DNA>20,000

ALT (1-2xULN) then Q3 month ALT and Q6 months EAG, consider bx if age >40

3. ALT<1, Q3-6 months ALT and HepBeAG.

Front 79

What is the accuracy of EUS for posterior mediastinal mass?

Back 79

90%

Front 80

What accout for most primary posterior mediastinal mass? What percent is malignant. What about 2nd most common?

Back 80

Neurogenic tumor
10-20% are malignant
2nd most common is congenital cyst.

Front 81

What is the second most common cause of jaundice in pregnant woman?

Back 81

Intrahepatic cholestasis of pregnancy.

Front 82

What is the prevalence of Wilson's disease

Back 82

30 out of 1 million

Front 83

What is the classic clinical presentation for Wilson's disease

Back 83

age 5-40
low ceruloplasmin
+KF ring

Front 84

What makes up the KF ring. What type of Wilson's patient has KF ring

Back 84

copper deposit in the decemt membrane
Always (>95%) has neurological complaints.

Front 85

How often are diverticular bleed stop bleeding

Back 85

70-80%

Front 86

What is the rebleeding rate for diverticular bleed?

What is the chance of a third bleed after a second diverticular bleed.

Back 86

22-38%

50%

Front 87

Define mod, mild, severe disease in UC

Back 87

Mod: <4BM
Mild: >4BM with minor signs of toxicity
Severe: >6 BM, fever, anorexia
Fulminant: >10 bloody BM

Front 88

Treatment of intrahepatic cholestasis of pregnancy?

What is the diagnostic lab test for it?

What is the lab value correlate with fetal complication in intrahepatic cholestasis of pregnancy

Back 88

Urso 10-15mg/kg

Bile acid >10 or >100 ULN.

Bile acid level in mother.

Front 89

What is the morphological feature of a malignant lymph node

Back 89

>1cm, round and homogenous

Front 90

What is the sensitivity, specificity, PPV and NPV for EUS alone in diagnosing metastatic esophageal lymph nodes

Back 90

Sen: 79%
Spec: 71%
PPV: 79%
PV: 75%

Front 91

What is the test and range to document significant iron overload in hemochromatosis? What is the screen test for hemochromatosis

Back 91

Hepatic iron index >1.9 mmol/gm.year

Trasferin saturation (fasting) >45% and increase ferritin.

Front 92

When do steatorrhea occurs How often do patient with chronic pancreatitis get it?

Back 92

<10% of pancreatic secretion
50-80% of patients eventually get it

Front 93

What are the 3 stool tests you can do to check for pancreatic function

Back 93

stool fat
decrease stool chymotrypsin
decrease stool elastase

Front 94

What type of patients needs EGD for variceal surveillance? Is there a different guideline for patient with cholestatic disease?

Back 94

Normal
Childs A (plt<140), portal pressure >13
Childs B and C

Cholestatics
Plt<200

ASGE practice guideline 2005

Front 95

What is the risk for use of steroid in pregnancy?

What are 2 type of amino acids that are missing in ELSD patients?

Back 95

cleft palate, adrenal insufficiency

Branch chained amino acid, aromatic amino acid

Front 96

What are 3 common substance commonly missing in patients with ESLD

Back 96

Mg, Zn and folic acid

Front 97

World wide what is the most common esophageal cancer?

What type of cancer is usually in the upper 1/3 of esophagus and what types in the distal 1/3. Where are the rare esophageal tumors usually found.

Back 97

SqCCa

upper 1/3: SqCCa
lower 1/3: adenocarcinoma

Rare esophageal tumors are usually found in the lower esophagus.

Front 98

How to diagnose IBS by Rome III criteria

Back 98

6 months of continuous or recurrent:
1. abdominal pain relief with defecation
2. Disturbed bowel pattern at 25% of time consist of either change frequency, consistency, passage of mucous, distention
3. no change in constitutional symptoms.

Front 99

How often should variceal surveillance be conducted?

Back 99

No varix: 3 years
small: 1-2 years

Front 100

What is the vessel connection which forms rectal varix? caput medusae, retroperitoneal varix

Back 100

rectal varix: IMV to pudendal
caput: vestigal umbilical vein connect to the portal vein
retroperitoneal: central communicate with ovarian/iliac vein.

Front 101

How accurate is T staging for gastric cancer? Which stage is less accurate?

Back 101

Average 83%, less accurate in T2 disease due to difficult to differentiate T2 vs. T3 invasion

Front 102

Primary extra-nodal lymphoma account for what % of disease? Most commonly in which 4 organs?

Back 102

20%
stomach, duodenum, skin and brain

Front 103

How do you classify hemorrhoids?

Back 103

Banov
1. bleed but no prolapse
2. prolapse but reduce spontaneously
3. prolapse need manuel reduction
4. prolapse can't be reduced

Front 104

How is bilirubin made?

Back 104

RBC gets break down in the endoreticular system in spleen to heme. Heme + heme oxygenase = bilverdin. Bilverdin + bilverdin reductase = bilirubin 9A + UGT = conjungated bilirubin.

Front 105

What are 2 tests recommended prior to having anti-reflux surgery?

Back 105

pH and manometery

Front 106

Difference between Barrett's and intestinal metaplasia of cardia?

Back 106

Normal Z line in patient with intestinal metaplasia of cardia. Barrett's usually have abnormal Z line

Front 107

What is the definition of long vs. short segment Barrett's

Back 107

<3cm is short.

Front 108

When are the most common relapse occur for HCV treatment?

How can you tell if someone may fail therapy during treatment?

Which race respond poorly even with 48 weeks of HCV therapy?

Back 108

1. 12 weeks post treatment

2. No EVR (> 2log decrease in HCV RNA) after 12 weeks

3. african american

Front 109

What does the pathology of autoimmune pancreatitis look like?

What are the 5 organs that can be involved in autoimmune pancreatitis

Back 109

1. Collar like periductal infiltrative composed of lymphocytes and plasma cells
2. Gall bladder, bile duct, kidney, lungs, salivary glands

Front 110

Mucinous cystadenoma/carcinoma
1. location
2. malignant potential?
3. EUS appearance?
4. Communication with PD?
5. Vascularity?
6. Cytology?
7. Viscosity?
8. Amylase, CEA other markers
9. Male vs. female predominance?
10. treatment

Back 110

1. body/tail of pancreas
2. high malignant potential
3. EUS shows macrocystic (>2cm cysts) with nodular papillary projection and calcification rim.
4. Rarely communicate with PD
5. High vascularity
6. Cytology shows columnar/cuboidal cells with mucin + cells
7. High viscosity
8. low amylase, high CEA
9. common in young/middle age female
10. treat with surgery.

Front 111

1. What are the medical treatment for hemorrhoids?

2. What is the best non-operative management of hemorrhoids?

Back 111

1. topical, steroids if there is peri-anal inflammation.

2. Best non-operative management is base on symptoms.

Front 112

How is sclerotherapy performed for treatment of hemorrhoids?

Success rate?
Complication rate?
Recurrence rate?

Back 112

Use for 1st and 2nd degree Banov.
Inject 5mL of phenol oil or hypertonic saline
90% tx rate
70% pain, abscess, urinary retentiion
30% recurrance after 4 years

Front 113

What are 7 associated disorder which can be found with PBC?

Back 113

1 Thyroid disease
2. SICCA
3. CREST
4. Raynaud
5. RF (25%)
6. Celiac disease
7. IBD

Front 114

In evaluating the large gastric fold which layer of the gastric mucosa does the following involves:

1. H. Pylori
2. Menetrier
3. Large Rugae
4. Varix
5. Anisakiasis
6. malignancy

Back 114

1. mucosa/SM
2. Mucosa/hyperechoic
3. Mucosa
4. submucosa
5. all 4 layers
6. SM

Front 115

How does H. Pylor cause damage of the stomach?

Back 115

It lives in the antrum and destroy D cells which lead to unopposed gastrin production

Front 116

What are the 6 signs to look for in patients with Wilson's disease induced fulminant liver failure?

Back 116

1. Female>male
2. Normal ALKKP
3. Coomb's negative hemolytic anemia
4. Coagulopathy not corrected by vitamin K
5. Rapid progress to renal failure
6. Modest rise of ALT/AST (<2000)

Front 117

What are the gastrinoma triangle?

What % of gastrinoma is malignant?

Back 117

3rd portion of duodenum, gallbladder, midbody of pancreas

60%

Front 118

What is lunulae ceruleae

Back 118

bluish discoloration at the base of finger nails. (WD)

Front 119

What is the current treatment strategy of gastric non-hodgkin lymphoma?

1. Surgery?
2. Chemotherapy? % in remission, survival and complication?
3. Radiation?

Back 119

1. No surgery due to high M&amp;M
2. Chemo with CHOP shows remission in 81% and survival of 71%. Complication (bleeding 0.3%), 80-100% survival if used in combination with surgery or radiation.

3. Radiation is not standard of treatment but promising result.

Front 120

What is the risk of developing ESLD within 5 years without treatment in patient with chronic HBV? What about risk of hepatoma in 5 years?

Back 120

8-20%
9-14%

Front 121

What tumors are involved in MEN1. What mutation cause this?

Back 121

parathyroids
pancreas (gastrinoma, islet cell tumor)
pituitiary tumor

Autosomal dominant, MEN gene on chromosome 11

Front 122

How often does HCC associated with HBV without ESLD?

When do you start screening patient with chronic HBV for HCC?

Back 122

30-50%

Age>35 or ESLD

Front 123

How long can it take H. Pylori serology to decrase after treatment?

Back 123

6-12 months

Front 124

How does sucralfate work? How do you give it and why? What type of patients should NOT have sucralfate?

Back 124

complex sulfate polysaccharride bind with alumin to prevent acute/chronic ulceration without affecting the release of gastrin or pepsin. It is usually given before meal (need pH<3.5) and should be avoided in patient with renal failure.

Front 125

What type of risk does woman with autoimmune hepatitis has during pregnancy?

Back 125

1. prematurity
2. low birthweight
3. increase fetal lost

Front 126

What are the 3 absolute indication for treatment of AIH?

What are the 3 most common cause of treatment withdrawn in patient with AIH?

Back 126

1. AST >10xULN
2. AST>5xULN + globulin >2xUNL
3. Bridging necrosis or multi-acinar necrosis

1. obesity
2. brittle DM
3. vertebral compression fx.

Front 127

What is the Rutgeert's anastomotic score? Which score indicate no escalating treatment after surgery for IBD?

Back 127

0=no inflammation
1=<5 aphthous ulcers
2=>5 aphthous ulcer with normal mucosa inbetween, or skip lesion of large lesion or lesion confer to anastomosis
3=diffuse aphthous ileitis with inflammed mucosa.
4=diffuse inflammation with large ulcer, nodularity or narrowing

0-1 will not need escalating treatment

Front 128

What are 2 factors that indicate risk for liver failure and the possibility of needing OLT for AIH?

Back 128

In ability to enter remission after 4 years

Persistent elevated bilirubin after 2 weeks of treatment

Front 129

How often does de Novo AIH occurs? What is one known risk factor?

What % of AIH children suffer treatment failure?

Back 129

2.5-3.5%. Cyclosporin use is a risk factor

5-15%

Front 130

How effective is using diltiazem in treatment of anal fissure? What is the dosage?

Back 130

2% diltiazem DIB for 9 weeks
Jonas et al. showed 65% healing rate but no comparsion to sitz and bran treatment.

Front 131

What are two surgical option for treatment of anal fissure?

Back 131

sphincterotomy and anal dilation

Front 132

What is the sen/spec/accuracy for differentiate malignant vs. non-malignant GIST? Literature source?

Back 132

With FNA
Sen: 67%
Spec: 100%
Accuracy: 91%

Without FNA
Sen: 83%
Spec:77%
Accuracy: 78%

Hawes

Front 133

What is the most common mesenchymal tumor of the esophagus? stomach and small bowel?

Back 133

Esophagus: leiomyoma
stomach and small bowel: GIST

Front 134

If 2 out of 4 findings is suggestive of malginancy what is the sensitivity of true malignancy for GIST?

Back 134

80-100%

Front 135

What are the three theories behind chronic pancreatitis?

What are the 3 genetic component to chronic pancreatitis?

Back 135

Ductal obstruction
Metabolic toxicity
Necrosis leading to fibrosis

Partial CFTR expresssion (Cystic fibrosis)
PRSS1 (resistent to inactiveation of typsin)
SPINK1(mutlation to gene inhibits trypsin)

Front 136

What do you look for on EUS in patient suspect of non-hodgkin lymphoma? Accuracy rate and sensitivity rate?

Back 136

Submucosal/mucosal thickening
Sen: 89%
Spec: 97%
Accuracy: 95%

Front 137

What is the normal gastric wall thickness?

Back 137

0.8-3.6mm thick.

Front 138

MALToma regress with H. Pylori treatment in what % of patients? What stage of the MALToma tend to regress and which tend not to?

Back 138

50-60% regress
Stage T1m, T1sm regress, T2-T4 typically does not

Front 139

How long does it typically take for MALToma to regress? is it okay for patient to wait if biopsy continue to show MALToma but EUS is negative?

Back 139

18 months to enter remission
Its okay if biopsy is positive but EUS is negative.

Front 140

When does HELLP syndrome typically occur?

How do you diagnose it?

What is the dreaded complication of HELLP syndrome?

Back 140

1. 27-36 week of gestation to post partum

2. Need hemolysis, elevated LFT and dropping plt

3. hepatic rupture.

Front 141

When do you typically see hepatitis surface Ag positivity. How about Hep BcAB IgM+

What is the typical incubation period for HBV?

How many viral copies = 1 IU?

Back 141

1. HepsAg (2-10wks), HBcAb IgM 4-6 months after acute episode.

2. weeks to 6 months (up to 2-3 months)

3. 5 copies

Front 142

What is the rate of bleed for + tag RBC scan?

How fast of bleed is needed to show up on angiogram?

Back 142

0.1mL/min

0.5-1mL/min

ASGE recommendations.

Front 143

What are the 4 parenchymal abnormalities and 5 ductal abnormalities seen on EUS for chronic pancreatitis?

Back 143

parenchyma
1. hyperechoic stranding
2. lobulation
3. hyperechoic foci.
4. cyst

Ductal
1. hyperechoic ductal wall
2. stone
3. main PD dilation
4. irregularity
5. dilated side braches.

Front 144

1. How do you intrepret secretin test?

2. What is systemic mastocytosis?

3. How to differentiate antral G-cell hyperplasia vs. ZE syndrome?

Back 144

1. ZE patients will have increase gastrin by >200mcg/mL

2. mast cell infiltrate all organ leads to increase histamine release

3. ZE with secretin test will have >200mcg/mL gastrin where as mastocytosis will have less.

Front 145

Patient with AIH treatment should improve serological markers in how many weeks. How about histologic findings?

Back 145

serologic = within 2 wks
historlogic = 3-6 months

Front 146

1. When do you start AZA treatment in patient with ulcerative colitis?

2. When to think start U.C. patients with CSA?

Back 146

Mod-severe UC flare (2mg/kg)

Severe colitis refractory of IV steroid (7-10days) 4mg/kg/day

Front 147

How many % of AIH patient enter remission first 18 months?

Define remission for AIH (3 criteria) and the two possible course of action?

Back 147

65%

Remission
1. nl LFT, nl globulin level
2. no symptoms
3. normal hepatic tissue

course of action
1. withdrawn steroid over 6 weeks.
2. stop AZA

Front 148

Which type of drug induces mucosal healing in patient with IBD?

How many biopsies do you need minimally for CRC surviellence in patient with IBD? What detection rate can you get with that many biopsy?

What is the odds radio for CRC in IBD patient with low grade dysplasia?

Back 148

1. anti-metabolites or IFX

2. >33 to have 90% detection rate

3. 9X

Front 149

1. Who is the first to describe PSC (when) and who conceptualized PSC (when?)

2. What is the risk of cholangiocarcinoma in patient with PSC?

3. How often is IBD find in patient with PSC?

4. Sex dominance for PSC?

Back 149

1. Hoffman (1867), Thorpe (1967)

2. 6-20%

3. 2/3

4. Male dominant.

Front 150

1. What % of all GI malignancy compose of MALToma?

2. How frequently is MALToma associated with H. Pylori?

3. What immunostains are useful for MALTomas

Back 150

1. 3-5%

2. 90%

3. CD20+, CD21+, CD35+, IgM+

Front 151

1. Which 2 HLA types are associated with AIH?

2. Patient with anti-LKM+, mucosal candidiasis and multiple endocrine organ failure has ?

3. What 3 factors are associated with higher risk of drug related complication in treating AIH?

Back 151

1. HLA D3 and D4

2. Autoimmune polyendocrineopathy candidiasis ectodermal dystropahy

3. Age, post menopausal and presence of ESLD

Front 152

What are 8 things to check for EUS in patient with non-Hodgkin lymphoma

Back 152

1. layer of origin/wall thickness
2. mucosal appearance
3. Mucosal defect?
4. Depth of penetration of focal mass
5. LAD
6. Check Cax
7. Liver hilum/liver
8. Gastrohepatic ligament.

Front 153

1. Is viral hepatitis an indication for discouragement for breastfeeding?

2. When is peri-natal transmission of HBV the highest?

3. How does HBV transmitted to kids

Back 153

1. NO

2. Pt mom with acute hepatitis with +E antigen in 3rd trimester (50-80%)

3. Transmit during delivery NOT transplacentally.

Front 154

1. What is the risk rate of post ERCP pancreatitis as per ASGE 2003?

2. What are the risk factors for causing post ERCP pancreatitis?

Back 154

1. 1-7%

2. Young age (<60), injection of PD, SOD disease, difficult duct for cannulation.

Front 155

How does Trientine work?
1. Side effect
2. Dosage?
3. How do you monitor?
4. How do you adjust for pregnancy
5. What can't be given together with the drug.

Back 155

Promote copper excretion by kidney
1. aplastic anemia, gastritis, worsen neurological symptoms.
2. 750-150mg/day in 2-3 doses
3. Monitor 24 hour urine copper excretion (goal is 200-500)

Can't be given with iron due to it can chelate iron.

Pregnancy: reduce dosage by 25-50% during pregnancy and surgery.

Front 156

How do you diagnose nutcracker esophagus?

How do you treat it?

Back 156

1. >180mmHg contraction which has normal propagation and LES relax normally.

2. Treat diltazem (60-90mg TID), myotomy and treat GERD as it can occasionally trigger Nutcracker.

Front 157

Which genotype of HBV are more severe and link to HCC?

Which mutant can cause more severe infection and how does it work?

Back 157

Aa, Ba, C, D

Precore mutant leading to anti-HBe+ chronic hepatitis B. Base pair mismatch leads to prevent formation of HBeAg

Front 158

How does pancreatic enzmes thought to help with chronic pancreatitis? How much? Non-enteric or enteric coated?

How good is endoscopic therapy for chronic pancreatitis?

Back 158

1. CCK releasing peptide in duodenum denatured by pancreatic trypsin but in chronic pancreatitis, the CCK is high due to lack of degraded CCK releasing peptide, so pancreatic enzyme help degrades it. Use Viokase8 6tabs QID. Non-enteric coated.

2. Rosch 2007
57% improvement with pain after stent and median of 4 ERCP. 20% complications.

Front 159

Pancreatic pseudocyst
1. location?
2. malignant potential?
3. EUS features?
4. communicate with PD?
5. Cytology?
6. viscosity?
7. Amylase, CEA level?

Back 159

1. anywhere
2. EUS shows unilocular, anechoic but can have echogenic material inside.
3. No malignant potential
4. sometime communicate with PD
5. cytology show inflammatory cells/debris
6. low viscosity
7. high amylase and low CEA (except when it is infected, in high case, CEA maybe high).

Front 160

How to manage HBeAg+ with normal ALT level?

How about HBeAg+ with elevated ALT?

Back 160

1. Q3 months LFT x 1 year then Q 6 months

2. liver biopsy

Front 161

Do you need to continue perform surviellence of HBV/HCV patients even after treatment? Literature support?

Back 161

Yes, AASLD

Front 162

What is the AFP level for diagnosis of HCC w/o biopsy? What is the recommendation if the lesion is less then 2cm?

Back 162

200

recommend biopsy if <2cm

Front 163

What type of problem does Wilson's patient has?
1. neruologically
2. hematologically
3. ophthalmalogically
4. nephrolog?
5. Bones?

Back 163

1. dystonia, mask faceis, movement disorder
2. hemolysis leads to gallstone
3. KF ring
4. Fanconi, hematuria, stones
5. Arthritis, osteoporosis, rickett's

Front 164

What is 1 and 5 year Lamuvidine resistance rate?

What about Adefovir?

Entecavir?

Back 164

LMV: 1 year (14-32%), 5 year (60-70%)

Adefovir: 1 year (0%), 5 year s(30%)

Entecavir: <1% in 2 years

Front 165

How does nitrate thought to work to decresae varices? How about beta blockers?

Back 165

Nitrate: decrese intraheaptic pressure

beta-blocker: decresae portal venous resistance

Front 166

Where are the 4 sites of varices?

Back 166

1. rectal, umbilical, esophageal/gastric and retroperitoneal.

Front 167

What percentage of AIH patients relapse?

Can all AIH pateints eventually have normal histology?

Back 167

1. 20-100% depend on histologic finding.

2. No

Front 168

1. What are the two form of chronic gastritis?

2. What is the cause of type A gastritis?

3. What two symptoms can type A gastritis leads to?

4. What are 4 conditions that type A gastritis associated with?

Back 168

1. A&B
2. associated with anti-IF antibody and anti-parital cell antibdoy.
3. achlorhydria which leads to high gastrin, anemia (b12 and IDA)

4. polyps, cancer, lymphoma and endocrine tumors.

Front 169

What do you do if you have AIH treatment failure? (2 things) and how often do you get treatment failure?

Why is biopsy perferred prior to stop therapy?

Define relapse of AIH (2)

Back 169

1. Prednisone 60mg/daily, Prednisone 30mg + AZA 150mg/daily. 9% gets treatment failure

2. Interface hepatitis can be seen in 55% of patients with normal LFT and globulins.

3. LFT>3xULN, and/or increase IgG to >2g/dL

Front 170

What is the GI complication rate post CABG? What percentage of this is GI bleeding?

What is the mortality rate in patient with GI complications

Back 170

0.5-5% GI complication (includes ulcer, bleed, ileus etc...) 17% UGIB, 14% colonic bleed. (31% bleed)

12-21%

Front 171

What are the 6 pre-operative risk factors for GI bleed in cardiac surgery?

What are the 2 intra-operative risk factors that leads to GI complications in patient underwent cardiac surgery?

What about 2 post operative risk factors?

Back 171

1. Age>75, hx of CHF, hx of renal dysfunction, prior CV surgery, concurrent valve procedure, urgent procedure.

2. Bypass time >100min, circulatory failure

3. being on HD, being on balloon pump.

J Am Coll Surgery 2007

Front 172

What is the % of patient on ASA causes GI bleed? What % is major? What is the RR?

Literature support?

Back 172

3% bleed and 1% was major. RR = 2. No difference between low and high dose.

CAPRIE, CURE study

Front 173

What is the % of patient on plavix causes GI bleed? What % is major? What is the RR?

Literature support?

Back 173

2% bleed, 1% major. RR=2

MATCH, CAPRIE study

Front 174

What is the % of patient on ASA + Plavix lead to major GI bleed? RR?

Literature support?

Back 174

1-2% and RR =4

Base on CURE, CREDO, MATCH study

Front 175

What is the RR for GI bleed in patient patient on Warfarin? How about ASA + Warfarin?

Back 175

RR= 2 for warfarin
RR= 7 for ASA+warfarin

Delaney CMAJ 2007.

Front 176

What is the EGD risk for patient having MI? Does the "severity" of MI matter?

Back 176

1-10%, risk mostly involve cardiovascular/pulmonary risk and severity of MI doesn't seems to matter.

Retrospective data.

Front 177

What is the sensitivity rate of ultrasound in detecting choledocholithiasis?

What is it a good test for? What is the NPV and PPV?

Back 177

30-90%, technique is highly operator dependent.

Good rule out test if patient has normal bilirubin and ALKP

NPV 95%, but PPV is only 35% if there is abnormal test.

Front 178

What is the sen, spec of MRCP in setting of choledocholithiasis?

Back 178

Sen: 80-100%
spec: 85-100%

Front 179

What are the structures for major papilla?

Back 179

Prepuce, ostium, papillary mound and the frenulum

Front 180

70-80% of gallbladder stones in the US are composed of cholesterol. What is the composition of primary common bile duct stones?

Back 180

Brown pigment stones. Common bile duct are almost always associated with ascending cholangitis and colonization of the bile by enteric organisms.

Front 181

What diseases are frequently associated with black pigment stone formation?

Back 181

Chronic hemolysis and cirrhosis.

Front 182

What is the prevalence of gallstones in the US?

Back 182

Approx 10%. They're 2-3 times more common in women than men. Pima Indians are at highest risk of developing them in the US. A genetic influence is noted in gallstone formation. Pigment stones account for 10-25% of all gallstones in the US.

Front 183

Distal ileal diseases are recognized risk factors for the development of gallstones. What is the most common problem resulting in lithogenic bile in these diseases?

Back 183

The loss of specific bile acid receptors in the distal ileum resuts in excessive bile salt excretion and a diminshed bile acid pool.

Front 184

Ursodeoxycholic acid (UDCA) is a tertiary bile acid. What is the percentage of UDCA in the human bile acid pool?

Back 184

2-4%. The bile acid poor becomes enriched up to 40% with UDCA conjugates during UDCA treatment, however there is little change in total bile acid secretion.

Front 185

Describe the pathophysiogical mechanisms resulting in gallstone formation in the following groups: the elderly, the obese, the pregnant, those receiving clofibrate, and those receiving parenteral nutrition.

Back 185

Elderly - increased biliary cholesterol saturation.
Obese - increased 3-hydroxy-3-methyl glutaryl-CoA reductase activity.
Pregnant - increased biliary cholesterol saturation and impaired gallbladder motility.
Clofibrate therapy - decreased 7-alpha-hydroxylase activity with decreased bile salt production.
Parenteral nutrition - gallbladder stasis.

Front 186

What are common conditions associated with the development of gallbladder sludge?

Back 186

Spinal cord injuries, prolonged parenteral nutrition and fasting and prolonged treatment with octreotide may cause gallbladder stasis-induced gallbladder sludge. Ceftriaxone may also result in the formation of sludge. GB sludge may cause actute cholecystitis and acute pancreatitis.

Front 187

What is the rate of development of biliary pain per yr in patients with previously asymptomatic gallstones?

Back 187

2% per year for 5 yrs (study from Michigan). A recent Italian study reported 12%, 17%, and 20% at 2, 4, and 10 years. Therefore, prophylactic cholecystectomy is not indicated in an otherwise healthy person with asymptomatic gallstones.

Front 188

What patients with asymptomatic gallstones woudl you recommend prophylactic cholecystectomy?

Back 188

Those awaiting lung transplantation, patients with porcelain gallbladder and young women of American Indian ancestry. The last two conditions are associated with a high prevalence of gallbladder carcinoma.

Front 189

What is the overall sensitivity of abdominal ultrasonography for the detection of gallstones?

Back 189

95% for stones that are larger than 2 mm in diameter. In contrast, it's only ~50% for common bile duct stones.

Front 190

What is Mirizzi's syndrome?

Back 190

A rare complication of gallstones in which a stone becomes impacted in the neck of gallbladder of the cystic duct and extrinsically compresses the commmon bile duct resulting in jaundice. Preoperating diagnosis of this syndrome is important in order to avoid bile duct injury. This syndrome is rare, occurring in approx 1% of all patients undergoing cholecystectomy.

Front 191

What is the most common location of a bowel obstruction in patients with gallstones ileus?

Back 191

Distal ileum where the lumen is the narrowest. Majority are women and older than 70 years. Recurrent gallstone ileus may occur in approx 5% of pateints and a search should be made for an add'l stone during surgery.

Front 192

Acalculous cholecystitis may occur in patients, especially the elderly and those with AIDS, with seriously injury or illness and after major complicated surgeries. What is the cause of it?

Back 192

The etiology is unknown but possibilities include biliary/gallbladder stasis resulting from long-standing fasting, alterations in gallbladder flow, especially in elderly patients with peripheral vascular disease, prostaglandins and endotoxins. Gangrene, empyema and performation of gallbladder more commonly complicate the course of acalculous cholecystitis than acute calculous cholecystitis.

Front 193

When is cholecystectomy indicated in a patient with a gallbladder polyp?

Back 193

Polyps of 10-18mm raise the question of cancer arising within an adenoma and should be removed as long as the patient is a candidate. Open cholecystectomy and consideration of more radical surgery is indicated in patients with gallbladder polypoid lesions larger than 18mm.

Front 194

A 56 yr old man presents for evaluation of jaundice. He had been well until 3 wks ago when he noticed the onset of mild mid-epigastric paing which resolved spontaneously. His past medical and surgical histories were unremarkable. He reported an 8lb weight loss which he blamed on lack of appetite. Examination was notable only for jaundice and icteric conjuctivae. Lab tests reveleased a total bilirubin of 8.6 mg/dl and an alkaline phosphatase of 565 IU/L. Aminotransferases were only slightly elevated. Amylase and lipase were normal. An abdominal ultrasound demonstrated dilated intra- and extra-hepatic bile ducts. What is the most appropriate test?

Back 194

Endoscopic retrograde cholangiopancreatography. In this case, several gallstones were successfully removed after performing a sphincterotomy.

Front 195

A 42 yr old man with no previous health problems presented with a 2 day history of servere intermittent epigastric pain radiating to his back with associated nausea and vomiting. He denied alcohol abuse, prior pancreatitis or gallstones. He lost 35 lbs over the last 4 months and attributed the loss to intentional dieting and exercise. On examination he was febrile, jaundiced and tender to palpation over the epigastrium. Lab testing revealed a leukocyte count of 19,000 with a left shift, alkaline phosphatase of 650 IU/L, bilirubin of 4.8 mg/dl and amylase of 2,500 IU/L. An abdominal ultrasound showed some sludge in the gallbladder but was otherwise normal. What is the most appropriate therapy?

Back 195

Endoscopic retrograde cholangiography w/sphincterotomy and stone extraction are the most appropriate in the setting of acute gallstone-related cholangitis and severe pancreatitis. If he was hemodynamically unstable or had a concomitant coagulopathy, a nasobiliary stent could be placed to decrease the duration of the procedure and obviate the need for sphincterotomy, at least temporarily. Of course, intravenous antibiotics and other supportive measures are also necessary.

Front 196

T/F: Prophylactic cholecystectomy is recommended in the mgmt of asymptomatic cholelithiasis.

What are the exceptions to the above practice?

Back 196

False. Since almost all patients with cholelithiasis develop symptoms before they develop complications, there is no evidence to support prophylactic treatment in the management of asymptomatic gallstones. 2/3 of patients with gallstones are asymptomatic. The annual rate of conversion from aymptomatic to symptomatic disease with biliary pain is only 1-4%. Patients with symptoms of gallstone disease have a 50% risk/year to reexperience biliary colic and their annual rate to develope biliary complications of 1-2%.

Calcified gallbladder, children with gallstones, patients with sickle cell disease, the morbidly obese and American Indians. The risk of malignancy in calcified gallbladders exceeds 25%.

Front 197

What ethnic group might benefit from prophylactic cholecystectomy for asymptomatic gallstones?

Back 197

American Indians appear to have rate of gallstone-associated gallbladder cancer that is sufficiently high to justify proph. cholec.

Front 198

T/F: Prophylactic cholecystectomy is justified in diabetics.

Back 198

False. Diabetics seem to be prone to developing both gallstones and gallstone-related complications. It's suggested that diabetics have a high morbidity and mortality when undergoing emergency operations for gallstones. However these perceptions have not been borne out when confounding variables such as hyperlipidemia, obesity, cardiovascular disease and renal insufficiency are taken into account.

Front 199

In the era of laparoscopic cholecystectomy, what are the indications for conventional open cholecystectomy?

Back 199

Open cholec. shoudl be reserved to patients with suspected cancer of the gallbladder, cases of severe acute or chronic inflammation, liver cirrhosis with portal hypertension, pregnancy, severe upper abdominal adhesions following previous surgery and in patients with biliary disease.

Front 200

What are some absolute contraindications to laparoscopic cholecystectomy?

What are the exceptions to the above practice?

Back 200

Inability to tolerate general anesthesia, uncontrolled coagulopathy, suspected cancer of the gallbladder, liver cirrhosis with portal hypertension and cholecystoenteric fistulas.

Calcified gallbladder, children with gallstones, patients with sickle cell disease, the morbidly obese and American Indians. The risk of malignancy in calcified gallbladders exceeds 25%.

Front 201

What are some relative contraindications to laparoscopic cholecystectomy?

Back 201

Morbid obesity, cardiopulmonary diseases, Mirizzi's syndrome, empyema of the gallbladder, a contracted gallbladder, pregnancy, severe acute or chronic inflammationof the gallbladder and patients who have previously undergone upper abdominal surgery.

Front 202

What ethnic group might benefit from prophylactic cholecystectomy for asymptomatic gallstones?

Back 202

American Indians appear to have rate of gallstone-associated gallbladder cancer that is sufficiently high to justify proph. cholec.

Front 203

T/F: Prophylactic cholecystectomy is justified in diabetics.

Back 203

False. Diabetics seem to be prone to developing both gallstones and gallstone-related complications. It's suggested that diabetics have a high morbidity and mortality when undergoing emergency operations for gallstones. However these perceptions have not been borne out when confounding variables such as hyperlipidemia, obesity, cardiovascular disease and renal insufficiency are taken into account.

Front 204

What is the false positive rate of detecting common bile duct (CBD) stones with intraoperative cholangiogram?

Back 204

3-4%

Front 205

What factors predict the presence of CBD stones?

Back 205

4 independent predictors of CBD stones are 1) age greater than 55 years, 2) elevated bilirubin over 1.7 mg/dl, 3) dilated CBD (>6mm) on ultrasonography, and 4) suspected or detected CBD stone on ultrasonography.

Front 206

What is the Strasberg's classification of bile duct injuries?

Back 206

Type A - injuries to minor ducts without loss of continuity of biliary tree
Type B - injuries to abberant right hepatic bile duct with duct occlusion
Type C - injuries to aberrant right hepatic bile duct with transection
Type D - lateral injuries that involve the main ducts and can progress to Type E injuries
Type E - injuries to the main duct with complete obstruction

Front 207

In primary sclerosing cholangitis, how often is the pancreatic duct involved?

Back 207

10-15%

Front 208

What % of patients have concomitant gallstones in the gallbladder and the common bile duct?

Back 208

15%

Front 209

Cholangitis is found in what % of patients with malignant strictures?

Back 209

10-15%

Front 210

How do you use urinary copper excretion to diagnose Wilson's disease in 2 ways

What is the best way to diagnose Wilson's disease? What is the down side of using this method?

What is the normal daily hepatic copper weight?

Back 210

1. Base 24 hr urinary excretion >100mcg in symptomatic patients and >1600 mcg copper excreted if given 500mg of D-pencillium at beginning and 12 hours during collection.

2. Hepatic copper >=250 mcg/g.day weight

3. <50mcg

Front 211

1. What % of patient with ESLD develop ascites in 10 years?

2. Without treatment, how many patient with ascites die in 2 years.

3. How much fluid must be present before you can detect shifting dullness?

4. What is the complication rate for paracentesis.

Back 211

1. 50%

2. 50%

3. 1.5L

4. <1/1000

Front 212

1. What are the 4 favorable clinical predictors in treatment of HCV?

2, Does treatment of HCV affect the histologic grading?

3. What is consider "cure" of HCV?

Back 212

1. <wt, EVR (>=2log reduction in viral load after 12wks), younger patient, HCV RNA <2 millions

2. Yes

3. SVR 2 years after treatment

Front 213

1. Why don't we use hot biopsy forcep to remove polyp?

2. Why hasn't USA being more aggressive with small flat polyps?

3. How to manage patient with >2cm polyp?

Back 213

1. 29% incomplete remove rate and high risk for perforation.

2. low % HGD with polyp <5mm, no increase risk of CRC if patient only has small polyp, and no increase risk of polyps missed during US national polyp study

3. Q3-6 months until complete removed

Front 214

1. What is the risk of death in patient with GI bleed due to variceal bleed? 1 wk vs. 6 wks.

2. What is the data behind non-selective beta blocker for primary prophylaxis. NNT to prevent bleed and death?

3. What blood level should patient be resuscitated at after variceal bleed?

Back 214

1. 1wk 5-8%, 6 wk 20-30%

2. NNT=10 for bleed and 22 for death
Abraczinskas, Hepatology in 2001

3. Hct;25-30%

Front 215

1. What are the number cut off for HPS in terms of contra-indication? What about screen test to obtain exceptions?

2. What is the BMI cut off for OLT?

Back 215

1. PaO2 <50 or less with MAA>20% shunt, PaO2<60 on RA gets you the exception

2. 40

Front 216

1. How is acute fatty liver of pregnancy different then patient with HELP?

2. Management of acute fatty liver of pregnancy?

3. Recovery possibilities

Back 216

1. AFLP has more liver failure and PSE. Also less hypoglycemia, renal failure. Occurs more in Nulliparous female.

2. Termination of pregnancy

3. Can occur in days vs. month but usually complete recovery

Front 217

1. How often can you except maternal/fetal problems in patient with ESLD who gets pregnant?

2. What is the main risk for mom? At what time during the pregnancy?

3. What are the only 2 drugs okay in pregnancy?

Back 217

1. 50%

2. Variceal bleed (20-35%) especially during 2nd week and labor time

3. octreotide and actigall

Front 218

1. Do you need abx for patients with any cardiac problem who need procedures?

2. Is ABX needed if Bile duct obstruction in abscence of cholangitis and if ERCP is unable to drain completely?

3. ERCP for patient with PD communicate to pseudocyst?

Back 218

1. No

2. Yes

3. Yes

Front 219

What is the cause of anal fissure? Where does it usually occur?

Back 219

Increase resting anal pressure leads to decrease perfusion of anaoderm lead to poor perfusion and ischemic damage. Usually occur in the posterior midline. 25% female can be in the anterior midline and 8% male i the anterior aspect. 3% of all patient can have both

Front 220

Serous cystadenoma
1. Location
2. Malignant potential
3. EUS features
4. Communicate with PD?
5. Vascularity?
6. Cytology?
7. viscosity?
8. amylase, CEA level?
9. Male more or female?
10.Tx?

Back 220

1. body/tail > HOP
2. very low malignant potential.
3. EUS with multiple small cysts, honey comb, with central calcification/fibrosis
4. Rarely communicate with PD
5. Very vascular
6. Glycogen cuboidal cells
7. low viscosity
8. low CEA and amylase
9. more female
10.tx with surgery if symptomatic

Front 221

GIST
1. arise from which layer?
2. Hyper/hypo or anechoic
3. What is the sen/spec/accuracy using EUS in diagnosis?
4. Which cell is the precursor of GIST
5. Which stain positive for GIST
6. What % malignant GIST?
7. Which 4 findings are suggestive of GIST?

Back 221

1. arise from the MM or MP layer
2. Appears hypoechoic
3. Sen 95%, spec 72%, accuracy 87%
4. Arise from the interstitial cells of Cajal
5. Express c-kit (CD117), CD34 and desmin negative.
6. 10-30% of GIST is malignant
7. irregular boarder, echogenic foci, >4cm and anechoic space.

Front 222

What are the 4 conditions that you would consider treating patient with HBV infection?

Back 222

1. HepBEAg+ with DNA>20,000
2. HepBEAg- with DNA >2000
3. Decompensated HBV Cirrhosis
4. HBV Cirrhosis with DNA >2000

Front 223

What are the evidence behind prophylactic treatment of EV
beta-blocker vs. EBL

What is the pro and cons. What is the literature support?

Back 223

Tripathi Euro Journal of Gastro Hep 2007

Meta-analysis included patient without history of bleed or treatment of EV. G2-3 EV, +stigmata

Pool RR favor EBL with NNT of 13
No difference in mortality
Adverse event favor EBL NNT of 10
No difference in bleeding related mortality
con= wide confidence intervals.

Front 224

1. What is the prevalence of autoimmune pancreatitis in patient with chronic pancreatitis? Base on what literature?

2. What is the most common age and sex distribution for autoimmune pancreatitis

3. What 3 diseases is autoimmune pancreatitis commonly associated with?

Back 224

1. 5-6% base on Finkelberg 2006 NEJM

2. >50 years and 2X man > female

3. RA, Sjogren and IBD.

Front 225

1. Does any pharmacological drug help with post ERCP pancreatitis

2. What is the rate of hemorrhage with ERCP

3. What is the rate of perforation during ERCP?

Back 225

1. No

2. 0.76-2%

3. 0.3-0.6%

Front 226

What should patient do if they are on warfarin and need a high risk procedure? If patient is high risk, when can heparin be started?

Back 226

They should stop Warfarin 3-5 days prior to procedure. Heparin can be started 2-6 hours after the procedure.

Front 227

How do you define TPN induced cholestasis? What are the 3 categories that was thought to be the cause of TPN induced cholestasis?

Back 227

TPN induced cholestasis is defined as patient being on TPN with increase conjugated bilirubin >2mg/dL +/- abnormal LFT.

Causes of the TPN-IC
1. loss physiological enteral intake due to decrease enterocyte growth hormone and hypoplasia
2. Toxicity of TPN components
3. Underlying disease

Front 228

1. What are the 7 causes of GERD?

2. What cause the wheezing and coughing in patient with reflux.

3. What are the 3 most common finding of EGD for patient with GERD

Back 228

1. Decrease or weak LES, hiatal hernia, increase acid production, poor acid clearance, OSA, TLESR, delay emptying

2. Vagal medicated refluxing respond to acid in distal esophagus.

3. 10% benign stricture, 4% Barrett's and 50% no findings.

Front 229

1. Can you get KF ring in other liver disease? If so, which one?

2. How are ceruloplasmin related to apoceruloplasmin and holoceruloplasmin?

3. What are the 6 markers you can check for Wilson's?

Back 229

1. Yes, cholestatic disease.

2. Apo = circulating form of ceruloplasmin without copper. Holo = + copper

3. Lower ceruloplasmin, low uric acid, lower serum copper level, Urinary copper > 100mcg, Hepatic copper concentration >250, MRI to r/o neurological involvement.

Front 230

How to calculate NNT and absolute risk reduction?

Back 230

Absolute risk reduction is equal to % of bad outcome (placebo) - % bad outcome (treatment group)

NNT = 1/ ARR

Front 231

How does NSAIDs damage gastric lining

Back 231

It block the production of prostaglandin which help increase protective layer of gastric lining, increase mucosal blood flow and increase restitution of the gastric lining.

Front 232

1. How is anal fissure in IBD different? How do you treat this disease?

2. Estimate how many % of patient with Crohn's disease have anal fissure?

Back 232

1. Usually around midline and multiple. Treat by treating the underlying disease

2. 25-30%

Front 233

1. According to study, what percentage of patient die with 6 months of dx of autoimmune hepatitis without treatment?

2. What 2 serological marker identify patient with early mortality for AIH?

3. Can AIH occur post OLT?

Back 233

1. 40%

2. 10X> normal LFT or 5x>normal LFT + 2x > normal globulins

3. Yes

Front 234

1. How are the ulcers in colon differ in patient with UC vs. Crohn's

2. How often due you find granuloma in Crohn's disease in biopsy vs. surgical biopsy?

3. What can be used to predict need for early escalating in therapy in patient post surgery for Crohn's

Back 234

1. sharp demarcation colitis in UC and deep, stellate, linear or serpiginous ulcers seen in patient with Crohn's

2. 30% biopsy and 50% in surgical specimen

3. Endoscopic appearance of ileo-colonic anastomosis 6 months post surgery using Rutgeert's score.

Front 235

What is the life cycle of Entameba Histolytica. How does it pass to human? What is the clinical manifestation? How do you diagnose it?

Back 235

Exist in 2 forms cyst (infectious) transmitted via oral-fecal route. cyst migrate to small intestine and develop into Trophozoite which invade into the intestine, liver, lung, heart.

Manifest in intestine leads to chronic non-bloody diarrhea, wt loss and abdominal pain

In lung, cause effusion, empyema

In liver leads to abscess

In CV leads to pericardium effusion

In Brain leads to brain abscess.

Dx with serology, aspirate

Front 236

What are the low risk condition in patient and their absolute risk of an embolic events if their anticoagulant is stopped for 4-7 days

Back 236

Hx of DVT, PAfib, bioprothesis, mechanical valves with aortic position. If no anticoagulation for 4-7 days, their risk of embolic event is 1-2/1000 patients.

Front 237

1. What are 2 conditions when AST>ALT

2. What is the 1/2 life for albumin

3. How much albumin hepatocytes make in 1 day

Back 237

1. EtOH use and Wilson's

2. 20 days

3. 10 grams

Front 238

1. What are some contraindication for FNA

2. What is the risk of perforation, bleeding, infection and pancreatitis for EUS

3. What is the echoendoscope's diameter?

Back 238

1. INR>1.5 or Plt<50K

2. perforation: 0.4%, bleeding 0.4-1.3% (6% if FNA done) , infection 0.3% (9% if cyst), pancreatitis: 0.3-2%

3. 13mm

Front 239

How does D-pencillumine work
1. side effects
2. dosage
3. monitoring
4. 2 important "notes"

Back 239

function as copper chelating moiety leads to urinary excretion of copper.

Side effect: worsen neurological symptoms, rash, lupus like reaction, aplastic anemia, leukopenia, thrombocytopenia, renal failure.

dosage: 250-500mg/day

monitor: Monitor urine copper excretion

Note: take it 1hr before meals and take Pyrodoxin 25-50mg/day

Front 240

1. What is the risk of perforation for EGD and cardiopulmonary complications?

2. What should be done if patient needs H. Pylori stool/breath test done?

3. Treatment for documented functional dyspepsia?

Back 240

1. 1:4000 perforation, 1:2600 CV event

2. stop PPI for 2 weeks

3. PPI for 2-8 wks with NNT=9. Eradicate H. Pylori, NNT=17
AGA technical review 2005

Front 241

1. What is the preventative treatment for Hep B + mom who are pregnant? How effective is it?

2. What are the 8 genotype of HBV. Which are the most popular?

Back 241

1. HBIG and vaccination. 95% effective

2. A: 35%, B:22%, C:31%, D:10%, E-G:2%

Front 242

1. What area is the distal esophagus base on American Thoracic society classification.

2. What about subcarinal

3. AP window?

4. What is the distance from the incisors are the antrum expected?

Back 242

1. 8

2. 7

3. 4L/5

4. 35cm

Front 243

1. What is the accuracy for Post. mediastinal mass?

2. What account for most primary posterior mediastinal mass? What is its malignant rate? What about the 2nd?

Back 243

1. 90%

2. Neurogenic tumor (75%) of which 10-20% are malignant. Congenital cyst (10-15%)

Front 244

1. What is second in cause of jaundice in pregnant women?

2. When does this disease typically occur?

3. What is the suspected mechanism of injury?

4. What gene predispose this problem?

Back 244

1. intrahepatic cholestasis of pregnancy

2. 2nd half of pregnancy

3. Multifactorial mostly related to abnormal biliary transport across canalicular membrane.

4. MDR3

Front 245

What is the current recommendation for treatment for HCV patients with genotype 1, 2, 3 and 4.

1. What is the data (literature)
2. What is the response rate
3. Tx duration
4. Amount of HCV RNA matter?

Back 245

Base on Hadziyannis 2004 (AIM)

genotype 1&4, PEG-IFN2a + wt based RBV
48wks: 52%SVR vs 24wks: 42%
however, if HCV RNA <2 million then 65%

Genotype 2 &3. PEG-IFN2a + fix RBV (800mg) for 24 wks
80% SVR, no difference between wt base or 48 wks treatment.

Front 246

What are the 4 zones that gastroesophageal varices resides? where do these veins drain? Which zone bleed easily and why?

Back 246

Gastric zone (2-3cm below GEJ, drain to short gastric/left gastric vein)

Palisade zone (2-3cm proximal into esophagus)

Perforating zone (proximal to palisade zone)

truncal zone (proximal to perforating zone)

Palisade bleed more due to lack of perforating vein.

Front 247

What is the Sarin classification?

Published date, articles?
classification?
How is it used? Which bleed more?

Back 247

Sarin et al. Hepatology 1992

Used to classify GV
1. GOV1:extend 2-5cm below GEj with conjunction to EV
2. GOV2:extend into fundus and continuity with EV
3. IGV1: isolated GV in fundus, not continuous with EV
4. IGV2: any where else

GOV2 and IGV1 bleed the most

Front 248

What is the normal pancreatic duct size at head, body and tail?

Back 248

HOP:4mm, body of pancreas: 3mm, tail of pancreas: 2mm

Front 249

What is HVPG? How do you calculate it? What is the free HV pressure and how is it related to IVC?

Back 249

Wedge HVP - FHVP

Should be within 2mmHg

Front 250

What are the recommended preventative tx for PBC? How to mange patient who are contemplating pregnancy?

Back 250

1. screen for varcies Q3 years EGD
2. osteoporosis (1500Ca, 1000u of vit D, Q2 year DEXA and HRT)
3. fat soluable vitamin

Hold therapy until last trimester

Front 251

what causes achalasia? What is the pathophysiology? The cause? Percentage patient has chest pain and regurgitation? What are the 4 treatment methods?

Back 251

Reduced non-adrenergic/non-cholinergic inhibitory ganglion cells caused by Chaga, Zoster or genetic problem.

1/3 has chest pain, and 60-90% has regurgitation

TX with drugs such as nifedipine, nitrate and viagra, Botox, dilation and myotomy

Front 252

Granular cell tumor
1. which EUS layers
2. EUS appearance
3. What compose it?
4. Is it benign or malignant?

Back 252

2-3rd layer homogenous mass with smooth border

Rare lesions of neural deviation

2-3% malignant

Front 253

What is the sump syndrome?

Back 253

It is a complication of choledochoduodenostomy in which food debris accumulates in the bypassed segment of the native biliary tree. Recurrent episodes of pain or cholangitis may occur. These episodes may effectively be treated by endoscopic sphincterotomy of the native ampulla with removal of the debris.

Front 254

1. What marker was used to identify mucinous cyst? which study and what is the accuracy rate?

2. How can you use CA 19-9 to help you differentiate?

3. How is CA 72-4 helpful?

Back 254

1. CEA >192 mcg/mL with 79% accuracy. Brugge 2004

2. >50,000U/mL 81% specific

3. Distinguish mucinous cystadenoma vs. other. 94-98% specific.

Front 255

List all treatment for HCV and how it works, its dosage?

Back 255

IFN-alpha (3x10^6 units, TID x 6 months)

IFN-alpha 2 a (180mcg/qwk, 1/2 life is 80 hrs)

IFN-alpha 2 b (1.5mcg/kg/qwk, 1/2 life is 40hrs)

Ribavirin
800 mg (<65kg)
1000mg (65-85kg)
1200mg (85-105kg)
1400mg (105-125kg)

Front 256

1. Of all polyps what percentage is tubular adenoma? TVA? VA? Base on what evidence?

2. How many % pt with adenoma have HGD? How many % has carcinoma in situ

3. What is colonoscopy accuracy in polyp detection

4. What is the % of patient with synchronous polyp in patient with adenoma?

Back 256

1. 70-85% adenoma, 10-25% TVA, <5% VA. ACG guideline 2000

2. 5-7% HGD, 3-5% CIS

3. 94%

4. 30-50%

Front 257

1. Why tissue appear hyper-echoic on EUS?

2. How does reflection occurs?

3. How many % of neuoendocrine tumor lack somatostatin receptors?

Back 257

1. Because these tissue scatter ultrasound beam. Tissue have different impedance value or smaller then the wavelength the US waves

2. Occurs between 2 media of different acoustic impedance

3. 20%

Front 258

1. How often does malignant polyp penetrate into the lymph nodes?

2. How to manage patient with malignant polyp?

Back 258

1. Only 10% penetrate the MM layer but they were all poorly differentiated

2. Make sure it is completely excised without penetration. Q3 months evaluation until it is clear, then q5 years surveillance

Front 259

1. What is the recommendation for dysplasia associated lesion/mass (DALM).

2. In patient with colonic stricture, what is the goal of balloon dilation? (in term of size) and complication rate?

Back 259

1. colectomy

2. serial dilation to 15-20mm. 0-11% complication rate (perforation)

Front 260

What are the 5 cells commonly seen in liver and their function?

Back 260

1. hepatocytes
2. cholangiocytes
3. Ito or stellate cells (store vitamin A and can change to form fibroblast)
4. Kupfer cells
5. endothelial cells

Front 261

Duplication cyst
1. Where can you find it?
2. Which part of the body is less commonly seen?
3. Malignant potential?
4. Symptoms?

Back 261

1. All along GI tract
2. Less commonly seen in the stomach
3. Can have malignant potential
4. Can cause symptoms such as dysphagia, pain or pancreatitis

Front 262

Inflammatory polyp
1. Which layers are involved
2. What does it appear on EUS?

Back 262

1. mucosal or submucosal layer
2. hypo or mix echoic.

Front 263

1. Patient with ascites, how many % of them have ascites not from the ESLD?

2. Do patient with low SAAG ascites respond to diuretics?

3. How much mmol does body excret Na? What # of mmol is 2grams of sodium?

Back 263

1. 15%

2. No, except nephrotic syndrome

3. 10mmol by sweat, 88mmol = 2grams of sodium

Front 264

1. What enzyme can change during pregnancy?

2. What is the gene and function in patient with familial intrahepatic cholestasis?

3. What are 3 fetal complications possible for ICP?

Back 264

1. ALKP, globulin, ceruloplasmin

2. MDR3 gene

3. placental insufficiency, premature labor, sudden fetal death.

Front 265

1. What regimen is used to prevent SBP in patient with GI bleed

2. Who should receive prophylaxis for SBP?

Back 265

1. 7 days BID of norfloxacin or bactrium

2. Hx of SBP, ascites protein <1g/dL, bilirubin >2.5mg/dL

Front 266

What is BRIC?

How are they present with? What are the lab finding for BRIC? What is the pathophysiology of this disease?

Back 266

Benign recurrent intrahepatic cholestasis present with abdominal pain.

Lab shows elevated ALKP, LFT except for normal GGT

Caused by genetic usually missing functional gene on chromosome 18q (BRIC I)

Front 267

How do you define T staging for gastric CA with EUS?

Back 267

T1= in the mucosa/submucosa
T2= in MP/serosa but not breaking the layers
T3= Breaking serosa
T4= invading adjacent organ

Front 268

1. In general what % of pancreatic cysts are pseudocysts? Neoplastic? and congenital?

2. Which is better in study the accuracy of cystic lesion? EUS vs. cytology? Base on which study?

Back 268

1. 80-90% = pseudocyst, 5-10% neoplastic, 5-10% congenital

2. Bragge 2004
EUS with FNA revealed that 59% accuracy base on cytology and 51% with EUS alone.

Front 269

What are the 5 classification for ascites fluid infection?

Back 269

1. SBP (+ culture and >250PMN)
2. Monomicrobial non-neutrocytic bacterioascites (+culture, -PMN)
3. Culture negative neutrocytic ascites
4. secondary bacterial peritonitis
5. polymicrobial bacterioascites

Front 270

1. How often do you encounter gastric submucosal lesions?

2. What is the overlay zone and transition zone?

Back 270

1. 0.36%

2. Overlay zone (not touch the lesion show which layer overlaying it). Transition zone (show which layer merge into the lesion)

Front 271

1. How is a random spot urine lytes help determine whether patient is compliant with sodium restriction.

2. What is the amount of sodium in mmol that we aim for to treat ascites? why?

Back 271

1. If Na>K then 24 hr sodium excretion >78mmol/day with 90% accuracy

2. 88mmol = 2g Na.
10mmol = natural loss thus >78mmol/day

Front 272

How does zinc work to treat Wilson's disease?

1. side effect
2. dosage
3. pregnancy changes?

Back 272

Interfere intestinal uptake of copper. intestinal protein bind zinc rather copper since zinc also enter GI tract via salivary/gastric secretion leading to negative balance.

Side effect: pancreatitis, gastritis, worsen neurological symptoms

Dosage 150mg/day divided into TID
No changes in pregnancy

Front 273

T/F: A physical examination finding of a decrease in anal sphincter pressure while the patient is straining is usually sufficient to rule out the diagnosis of pelvic floor dyssynergia.

Back 273

True. However the finding of an increase in anal sphincter pressure on digital rectal exam during straining is not reliable enough and further studies are indicated.

Front 274

1. Approximately what percentage of inpatient patients are affected by C. diff while on antibiotics?

2. How many percentage of patients will experience relapse in symptoms after successful initial therapy and when do they typically occur?

Back 274

1. 20%

2. 15-30% in first few weeks

Front 275

1. Does infants get C. diff despite colonizing 70-80% of infant's (up to 12-18 months)colon? why?

2. What type of C. diff is associated with 3 fold higher mortality rate? What are the two major characteristics that makes this possible?

Back 275

1. They lack receptors for the c. diff toxin

2. NAP1/027 strain which is fluoroquinolone resistant and produce higher level of toxin.

Front 276

1. What is the first line regimen for C. Diff?

2. What is the treatment regimen for Vancomycin?

Back 276

1. Flagyl 500mg PO TID for 14 days treats >90% of patients.


2. 125mg PO QID Vancomycin for 10-14 days.

Front 277

1. Does IV or PO formulation of flagyl matters in terms of treating C. Diff? why?

2. What is the side effect in long term Flagyl use?

Back 277

1. No, both form result in distribution of all tissues and fluids.

2. Peripheral neuropathy, vertigo and rarely ataxia can be seen with patient >1 months of flagyl use.

Front 278

1. Why can you only use PO vancomycin to treat C. diff?

2. Do side effects such as red man syndrome, ototoxicity and nephrotoxicity from Vancomycin cause problems in patient taking it PO?

Back 278

1. Because the IV form is not excreted into the colonic lumen and due to its large molecular weight, it gets completely pass into the colon.

2. No

Front 279

1. What is the first line therapy in pregnant women and children <10 years of age infected with C. diff?

2. What are the scoring system which characterize "severe" c. diff? Referrence?

Back 279

1. Vancomycin

2. > 2 points:
1 points: age > 60, temp >101F, albumin <2.5, WBC>15k
2 points: pseudomembraneous colits at colonoscopy or ICu patients

Zar et al. clin infect disease 2007.

Front 280

1. What is consider a fulminant c. diff infection? (6 conditions)

2. What is the fatality rate?

3. What is the recommended treatment?

4. What about those with peritonitis/mega colon but not a good surgical candidate... what can be used to treat it?

Back 280

1. presence of toxic megacolon, peritonitis, albumin <2.5, renal failure, respiratory distress, hemodynamic instability.

2. >2%

3. PO vancomycin and IV flagyl.

4. Pooled human immunoglobulin (200-500mg/kg/day)

Front 281

1. What is the 2 most common cause of recurrent C. diff?

2. How do you treat first recurrence?

3. How do you treat second recurrence?

Back 281

1. repeat ingestion of c. diff. and the other is incomplete eradication.

2. treat with initial antibiotic course 14 days.

3. Tapered pulse dose oral vancomycin
125mg QID x 1 week, then BID for 1 week, then QD for 1 week, then QOD for 1 week then every third day for 2 weeks. Also consider probiotic therapy starts 2 weeks prior to finish therapy

Front 282

1. What are 2 other alternative antibiotics for C. diff?

2. What is the only probiotic that showed to improve c. diff symptoms?

Back 282

1. rifaximin and nitazoxanide

2. Saccharomyces boulardii

Front 283

1. What is alpha one anti-trypsin? What does this protein do?

2. What gene encodes it?

3. What is the estimated prevalence of AAT deficiency?

Back 283

1. It is a serine protease inhibitor which is highly effective inhibitor of neutrophil elastase.

2. SERPINA1 or A.K.A. PI

3. 1 per 3000-5000 persons

Front 284

1. What does the Z protein do in the patient suspect with alpha-1 antitrypsin deficiency?

2. What are the three inherited genetic variants of alpha-1 antitrypsin leads to liver disease?

3. Is measuring the level of alpha 1 antitrypsin accurate in evaluating whether it is deficient? Why?

Back 284

1. It form polymers that trap AAT within the rough endoplasmic reticulum of hepatocytes thus reduce level of circulating AAT in blood stream.

2. ZZ, MZ and SZ.

3. No, it is an acute phase reactant therefore it may not be accurate.

Front 285

1. What are two less common manifestation of severe alpha-1 antitrypsin deficiency?

2. What is the therapy for AAT deficiency? is it effective for liver disease?

Back 285

1. necrotizing panniculitis, vasculitis primary anti-proteinase 3 positive vasculitis (Wegener's)

2. AAT augmentation therpay may slow the rate of decline in lung disease but no liver disease.

Front 286

1. What is the most common type of gastric lymphoma?

2. How do you stage it?

Back 286

1. B cell in origin with NHL and diffuse histiocytic type the most common.

2. Sage I: stomach, II: localized involvement of abdominal lymph node, III: both side of diaphragm, IV: disseminated.

Front 287

What is the 5 year survival for gastric lymphoma?

Back 287

50%

Front 288

1. What level of sympathetic innervate stomach to small bowel?

2. Which "plexus" is responsible for motility of the gut? Where is it located?

3. Which plexus control absorption, secretion and mucosal blood flow?

Back 288

1. T5-T10

2. Auerbach which locate between the longitudinal and circular muscular layers.

3. Meissner's plexus (submucosal)

Front 289

1. Which cranial nerve innervate the GI tract from stomach to the right colon?

2. What factor regulate the electrical activity of GI smooth muscle?

3. What form a non-neural pacemaker system and function as intermediate between the neurogenic and myogenic control system?

Back 289

1. Vagus

2. Myogenic factors

3. Interstitial cells of Cajal.

Front 290

1. What are 2 common excitatory substance for GI tract and 3 inhibitory substances?

2. What does interdigestive migrating motor complex do? How long does each cycle last?

Back 290

1. acetylcholine and substance P (excitatory). NO, somatostatin, VIP (inhibitory)


2. It moves stuff from ileum to colon. Each cycle last 60-90 minutes

Front 291

1. The duration of post prandial digestive complex is proportional to what?

2. What is the 1/2 emptying time for non-nutritional liquids?

3. Why is there initially a "lag" phase followed by linear expulsion interms of stomach motility?

Back 291

1. porportional to number of calories consumed. 1 hr every 200kcal.

2. <20 minutes

3. Because solids are retained in the stomach until they are <2mm in diameter before it is emptyied.

Front 292

How can you tell base on postprandial manometric profile the difference between neuropathic vs. myopathic patients suffering from motility problems?

Back 292

Uncoordinated contractility in neuropathic vs. weak contraction in myopathic patients.

Front 293

What is the dreaded complication from Reglan use? Is it reversible all the time?

Back 293

Tardive dyskinesia due to anti-dopaminergic activity and not always reversible.

Front 294

Dumping syndrome
1. In what 2 situation does it typically occur?

2. What is the pathology behind it?

3. How do you test for it?

4. How do you treat it?

Back 294

1. Occur after truncal vagotomy and gastric drainage procedure

2. Rapid gastric emptying leads to a high calory content of liquid phase of the meal evokes a rapid insulin response and secondary hypoglycemia.

3. Test for in dual phase gastric emptying study

4. Treat with dietary measures (low nutrient liquid) and/or octreotide (50-100mcg QAc)

Front 295

What 5 conditions can you see rapid transit of small bowel? How do you treat? (5 options)

Back 295

Postvagotomy diarrhea
short bowel syndrome
diabetic diarrhea
carcinoid diarrhea
IBS

Treat with loperamide, verapamil, clonidine, octreotide and >50g fat diet.

Front 296

1. How long does 6MP or AZA typically reach its full effect in treating IBD?

2. What is Infliximab?

Back 296

1. 12-16 weeks

2. Chimeric monoclonal IgG1 against TNF

Front 297

1. Which study showed that schedule dosing of infliximab is superior to episodic therapy in maintain response and remission both in luminal and fistulizing Crohn's disease?

2. In AZA treatment naive patients with luminal Crohn's what regimen is best in inducing steroid free remission and mucosal healing of the bowel?

Back 297

1. ACCENT I and ACCENTII

2. SONIC study showed that combination of IFX + AZA is > IFX alone in inducing remission up to 24 weeks. It is also better compare to AZA monotherapy.

Front 298

Is there synergism between MTX and IFX for the induction and maintenance of steroid free remission in luminal Crohn's disase?

Back 298

No, Fegan 2008, Gastroenterology.

Front 299

What is the suggested management in Crohn's patient who previously failed AZA now required IFX? Is IFX + AZA better compare to IFX alone?

Back 299

No data to support higher efficacy for combination beyond 6 months, therefore recommend stop AZA > 6 months.

Front 300

Which trial demonstrate IFX is effective in treating refractory moderate to severe ulcerative colitis?

Back 300

ACT

Front 301

1. What 3 types of problem does anti-IFX antibody cause?

2. How many % of patient each year have to stop therapy due to intolerance?

Back 301

1. acute infusion reaction, delayed serum sickness like reaction and lost of response.

2. 10%

Front 302

1. What is Adalimumab, how is it administered/used? What type of IBD is it approved to treat?

Back 302

1. Fully humanized IgG1 monoclonal antibody against TNF. It is given SQ every 2 week and treats luminal Crohn's

Front 303

How effective is Adalimumab in treating moderate/severe Crohn's compare to placebo?

What is the response rate compare to placebo? How was the study done?

Back 303

CHARM trial Sandborn 2007, Gastroenterology

Open label induction with 80mg at week 0, and 40mg at week 2 and then randomly to groups that were given Qwk and Q2wk 40mg injection.

Both exhibit improvement (CDAI <150) compare to placebo at week 26 (40-47% vs. 17%) and wk 56 (36-41% vs. 12%).

Front 304

Which study provided clue to whether adalimumb is able to rescue patient who lost response to IFX?

Back 304

GAIN study Sandborn et al. 2007 AIM

Double blind, placebo controlled randomized trial.

325 pt who had mod/severe Crohn's lost or intolerant to IFX.

At week 4, 21% of patient who had got adalimumab 160mg at week 0 followed by 80mg at week 2 achieved remission compare to placebo of 7%.

Front 305

What is Certolizumab pegol (Cimzia)

Back 305

A pegylated humanized fragment antigen binding (Fab) that binds TNF

Front 306

What syndrome produces pseudo-obstruction of the common bile duct?

Back 306

In Mirizzi's syndrome, a gallstone impacted in the cystic duct leads to compression and obstruction of the bile duct.

Front 307

What are the cresent-shaped folds of the cystic duct mucosa that may block passage of stones into the common bile duct?

Back 307

Spiral valves of Heister.

Front 308

What is the underlying cause of acrodermatitis enteropathica?

Back 308

Zinc deficiency

Front 309

What diagnoses should be considered when there are skin findings consistent with PCT in addition to acute episodes of abdominal pain, nausea, vomiting, paralysis and seizures?

Back 309

Variegate porphyria (VP) and hereditary coproporphyria (HCP).

Front 310

What skin signs may aid in the diagnosis of acute pancreatitis?

Back 310

Cullen's sign (periumbilical bruising) and/or Grey Turner's sign (flank bruising)

Front 311

On the basis of radiology and endoscopic findings, most patients with Crohn's disease can be subdivided into three anatomic groups. Name those groups and the approximate percentage of each.

Back 311

Colon alone: 15-25%
Small intestine and colon: 40-55%
Small intestine alone: 30-40%

Front 312

1. What is the median survival from time of diagnosis to OLT or death for patient with PSC?

2. Treatment for PSC?

3. Does PSC recur after OLT? At what rate? (base on what?)

Back 312

1. 9-18 years
2. Urso @ 22-25mg/kg
3. Yes, 20-25% after 5-10 years, AASLD 2010 recommendations