Gi-5

Front 1

Does gastrin have direct acid secretion effect on parietal cells? If not, how does it affect acid secretion?

What are the two hormone that stop acid secretion from the parietal cell?

Back 1

1. No, it affect it through ECL cells that releases histamine.

2. Somatostatin and prostaglandins.

Front 2

1. What are vagus nerves effect on acid secretion? (2 things)

2. Does smoking increase PUD risk? How about EtOH?

Back 2

It directly affect pareital cell and incresae acid secretion.

It inhibit somatostatin releas from D cell.

2. smoking= no, etoh=yes

Front 3

1. What % of patient may be affected by symptomatic diverticulitis?

2. What is the pathophysiology of diverticulosis?

3. What is the down side of using CT for diagnosis?

Back 3

1. 20%

2. high luminal pressure cause mucosal protrusion through weak areas where the vasa recta penetrate the bowel wall resulting in tics

3. 20% false positive rate

Front 4

What is the classification of diverticulitis?

Back 4

Stage 1: small confined pericolonic abscess

Stage 2: larger confined pericolonic collection.

Stage 3: generalized suppurative peritonitis (perforated diverticulitis)

Stage 4: fecal peritonitis

Front 5

Patient with diverticulitis developed jaundice and hepatic abscess is suggestive of what as complication?

Back 5

pylephlebitis.

Front 6

1. What is the requirement for OUTPATIENT treatment for diverticulitis?

2. What is the recurrence rate for diverticulitis?

Back 6

tolerated po and mild first attack.

2. 5-10% have second attack in 2 years.

Front 7

What is the treatment of listeria

Back 7

ampicillin and gentamicin.

Front 8

1. What are the three most common GI endocrine tumors?

2. Which dermal layer does the GI endocrine tumor arises?

3. Why is it hard to differentiate histologically?

4. What is one imaging modality that can be utilize to localize a GI endocrine tumor?

Back 8

1. Carcinoid follow by gastrinoma follow by insulinoma.

2. Arise from the endodermal stem cell (amin precursor uptake and decarboxylation tumor or APUDomas)

3. They lack of mitotic figures and has uniform nuclei

4. Angiogram because it is highly vascularized

Front 9

1. What type of cells are the origin of carcinoids?

2. Where is carcinoid most commonly found?

3. Where are rectal carcinoid tumor most commonly found?

4. Where is the gastric carcinoid tumor come from (which cell)

5. Which type of carcinoid most commonly produce symptoms?

Back 9

1. Enterochromaffin cells

2. Appendix (>50%)

3. >90% are found 4-13cm above the anal verge

4. histamine secreting enterochromaffin like cells.

5. small intestinal carcinoid

Front 10

Where does the small intestinal carcinoid most commonly located at?

What are one thing to keep in mind for patient with ileal carcinoids?

Back 10

Within 2 feet of IC valve.

regional lymph node spread

Front 11

What are the two most common symptoms of carcinoid?

Usually with symptoms, what is one thing you want to make sure?

What is the test that should be done in patient iwth carcinoid syndrome?

Why should Echo be done?

Back 11

1. Diarrhea and flushing

2. rule out liver met.

3. 5-HIAA measurement.

4. It can locate within the valves

Front 12

What is the treatment for appendix carcinoid?

Back 12

<2cm = appendectomy
>2cm then right hemi-colectomy

Front 13

What is the treatment for rectal carcinoid?

Back 13

<1cm= local resection
>2cm=rectal ultrasound then consider radical resectioni.

Front 14

What do you use to treat carcinoid syndrome?

Is surgery effective? How about radation?

Back 14

1. Octreotide

2. Srugery has NOT increased survival but did improve symptoms. Radiation is only use for symptoms relieve in bone mets.

Front 15

When do you use chemo for carcinoid? (3 situations) What are the two regimen?

Back 15

patient with debilitating symptoms that can't be controlled with octreotide, imparied liver function or cardiac invovlement.

Uses streptozotocin + doxorubicin

Front 16

What is the 5 year survival for patient with local carcinoid? regional lymph node involvement and liver mets?

what is the median survival for patient with carcinoid syndrome?

Back 16

local=95%
regional lymph node invovlement=65%
liver met = 20%

2.5 years median survival rate.

Mayo clinic review

Front 17

What is rapid urease test? Is it invasive? Is it good for primary diagnosis? confirmation of cure? detect viable bacteria?

Back 17

A gel tablet containing urea and a pH indicator, when an infected biopsy is placed into the gel, urea is converted to ammonia and pH increas and changes color.

It is good for primary diagnosis, confirmation and detect viable organism

Front 18

Which H. Pylori test is NOT good to confirm cure? How about detect viable H. Pylori?

Back 18

Serology is NOT good to detect cure

Serology and stool antigen is NOT good for detect viable h. pylori

Front 19

1. Majority of patients treated by H. Pylori are undetectable using the stool antigen test by how many days after treatment?

2. What is consider the second line therapy for H. Pylori or patient with PCN allergy?

3. What NSAID gastropathy look like endoscopically?

4. Are H2 blockers good prophylaxis for NSAID induced ulcers?

Back 19

1. Day 5

2. 14 days of PPI, Bismuth (120mg QID), metronidazole (500 TID) and tetracycline (500 TID).

3. small erosion/ulcer in antrum

4. NO, maybe good for DU but NOT GU

Front 20

What is the down side of using misoprostol for prophylaxis of NSAID induced ulcer?

Are they good for DU? GU?

Back 20

Side effect of diarrhea and not effective in treating dyspepsia.

Good for both as compare to H2 whihc is only good for DU prophylaxis.

Front 21

1. What % of patient with ZES have MEN-I?

2. Why does ZES patient have enlarged gastric fold?

3. What is two major diagnosis criteria for ZES?

4. How do you do a secretin test?

Back 21

1. 25%

2. High gastric which has trophic hormone for the oxyntic gland poriton of the gastric lining, leading to hyperplasia of the mucosa.

3. High gastrin and NO achlorhydria.

4. Measure gastrin before secretin, then inject secretin 2U/kg and measure gastrin, if gastrin increase by 200pg/mL then it is +

Front 22

1. Can patients with chronic gastric outlet obstruction having high gastrin level? why?

Back 22

1. Yes, the chronic gastric distention lead to increases in gastrin and acid.

Front 23

What are the LA classifciation of esophagitis?

Back 23

A. mucosal breakage, <5mm long confined to the mucosal fold

B. Mucosal breakage, >5mm long confined to the mucosal fold but not continuous between the tops of 2 folds.

C. Mucosal break continuous between the tops of 2 or more folds involving <75 of the esophageal circumference

D. mucosal break involving >75% of esophagal circumfrence.

Front 24

1. In ZE, where is the gastrinoma most oftenly occur? How about the second most common area?

2. What are 3 common cause of hypergastinemia?

3. What are the two treatment for ZES?

4. When is surgery NOT recommended? (2 situation)

Back 24

1. 50% in duodenal wall and pancreas being second

2. Hypochlorhydria, s/p vagotomy and patient on PPI

3. Octreotide, surgery

4. MEN1 and liver mets.

Front 25

1. Where does the insulinoma usually originate?

2. Ususally insulinoma is solitary or multiple? If multiple then you should suspect?

3. How often are insulinoma malignant?

4. Female vs. male predominance? When do they usually present?

Back 25

1. beta cell in pancreas

2. Usually solitary and if multiple, should suspect MEN1

3. 5-10%

4. Female, present 20-75 years of age.

Front 26

1. How do you diagnose insulinoma?

2. How do you explain patient who has low glucose but low c-peptide?

3. How often are the octreotide receptors present in patient with insulinoma?

4. What are the treatment for insulinoma?

5. How do you treat metastatic insulinoma?

Back 26

1. low glucose, high insulin level. Can do 72 hour fasting test.

2. abusing insulin

3. 50%

4. Surgery which cure 70-95% of patient. Diazoxide inhibit insulin release

5. octreotide, diazoxide and chemotherapy (streptozocin + doxorubicin)

Front 27

1. According to Mayo review book, how much blood is needed for melena? How about hematochezia?

2. How much blood (units) of transfusion predict rebleeding and mortality?

Back 27

1. 100mL = melena, 1L = hematochezia

2. 4 units for re-bleeding, >6 units mortality.

Front 28

1. If you have a non-variceal bleed, when does rebleeding typically occur?

2. What is the purpose of PPI or acid suppression in GI bleed?

3. Stress gastritis leads to clinical bleed in ? ICU patients

4. Where does most of the mallory weiss tear occur in the gastric or esophageal side?

Back 28

1. 98% within first 96 hours.

2. Get pH>6 for coagulation

3. <3%

4. gastric

Front 29

1. Can you use beta blockers to prevent portal hypertensive gastropathy?

2. Where does aortoenteric fistula most commonly occur?

3. How does hemosuccus pancreaticus usually occur?

4. What is needed to diagnose hemosuccus pancreaticus?

Back 29

1. Yes

2. 75% of them occur within the duodenum, usually 3rd portion

3. peripancreatic blood vessels bleed into the pancreatic duct.

4. Angiogram.

Front 30

1. Where does solitary rectal ulcer usually present?

2. Which blood vessel does embolic disease usually take place? Why?

3. Which artery account for 50% of the primary mesenteric ischemia?

4. What is sitophobia? What is this a symptom of?

Back 30

1. 6-10cm on the anterior wall

2. SMA emboli, because it is usually the larger diameter and narrow angle of take off from the aorta

3. SMA emboli

4. fear of eating, usually suggest chronic mesenteric ischemia

Front 31

What is the Blue rubber bleb nevus syndrome?

How is it inherited?

Back 31

It is an autosomal dominant disorder consist of intestinal/cutaneous cavernous hemangioma with bluish rubbery consistency

Front 32

What is Dego's syndrome?

Back 32

A malignant atrophic papulosis consist of painless skin papules with cigarette paper like white center and telangiectatic peripheral and GI/CNS involvement. Due to a vasculopathy leading to thrombotic process of blood vessels

Front 33

What is epidermolysis bullosa?

Back 33

Trauma induced blisters in oral cavity, esophagus and anal area

Front 34

Where does pemphigus vulgaris usually involves?

Back 34

oral esophageal and lower GI tract

Front 35

Where does bullous pemphigoid involves?

Back 35

oral, esophagus and anal area.

Front 36

Where does Lichen planus affect and what symptoms can it be associated with?

Back 36

involves mouth and esophagus

associated with stricture, dysphagia which is also associated with hepatitis C

Front 37

What is Tylosis? How is it pass on?

Back 37

It is an autosomal dominat disease affecting the skin (palmoplantar keratoderma) and esophagus (SqCCa of esophagus)

Front 38

What is Burton's disease?
What is the pathophysiology?
How do you diagnose it?
How is it related to GI?

Back 38

It is hypogammaglobulinemia which is X-linked hereditary defect in B cell

Diagnosed by biopsy which shows no plasma cell

Causea GI infection, SBBO and perirectal abscess

Front 39

How often do you detect selective IgA deficiency?

What does it do?

Which population does it have a higher prevalence to this condition?

What 4 different GI condition can it be related to?

Back 39

Occurs 1:500, can be sporadic but can also be familial.

It is a lack of secretory IgA1 and 2

Patient with celiac disease have higher prevalence of this

Can be associated with pernicious anemia, SBBO, Crohn's and nodular lymphoid hyperplasia

Front 40

How is common variable hypogammaglobulinemia associated with GI? (10)

Back 40

Can lead to SBBO, malabsorption, pancreatic insufficency, sprue, gastric cancer, AIH, PSC, cancer/lymphoma of large/small bowel and pernicious anemia.

Front 41

How is hereditary angioedema gets pass on?

How do you diagnose it?

What are two common drug that can lead to this problem?

Back 41

Autosomal dominant (chromosome 11)

Quantitative or qualitative deficiency of C1 esterase inhibitor.

check level and function of C1 esterase and C4 level (it is reduced during attack)

ACEI and ARB

Front 42

1. Can polycystic kidney disease lead to cyst of liver and Caroli's disease?

2. Can Addison's disease cause anorexia, nasuea, vomiting, weight loss, malabsorption, abdominal pain?

3. Which kind of porphyria is the most common porphyria? How do you diagnsoe it and how is it pass on? Does it have skin findings?

Back 42

1. yes

2. Yes

3. Acute intermittent porphyria. It is diagnosed by increase ALA and porphobilinogen. It is autosomal dominant without skin findings.

Front 43

Which type of porphyria is characterized by increase urine coproporphyrin and stool protoporphyrin? How is it pass on? Does it have skin findings?

Back 43

Variegate porphyria

It can have skin disease with or without the abdominal attack.

Autosomal dominant

Front 44

Which porphyria has elevated stool and urine coproporphyrin level and skin disease only with abdominal attack? How does it pass on?

Back 44

Hereditary coproporphyria. Autosomal dominant.

Front 45

Which type of prophyria shows ALA elevation and no skin findings. Pain usually occurs with fasting, alcohol, menstruation, medications. How do you diagnose it?

Back 45

ALA dehydratase deficiency.

Diagnsed by urine ALA and porphobilinogen are increased during attack.

Front 46

Can erythropoietic protoporphyria have skin findings? Can it lead to liver problems? why or why not?

Back 46

Yes

Yes, can lead to cirrhosis due to deposition of protoporphyrin.

Front 47

Sjoren can be associated with which two GI manifestation?

What about Felty's syndrome?

Back 47

1. Esophagela web and pancreatic insufficiency

2. RA, splenomegaly, neutropenia, NRH and portal HTN

Front 48

Is empiric antibiotic treatment in setting of variceal bleed indicated? Referrence? Dosage?

Back 48

Yes

Norfloxicin 400mg PO BID x 5-7 days

AASLD guideline 2007

Front 49

31 year old man with history of bowel obstruction present with melena. On exam, he has melena and multiple cutaneous hemangiomas scattered along the trunk, lips and tongue.

What is the diagnosis? HOw do you explain the bowel obstruction. How does this disease/condition get pass around? How do you treat this?

Back 49

Blue rubber bleb nevus syndrome

Autosomal dominant

small bowel lesions can severe as lead point for intussusception.

Surgery is treatment. Endoscopic therapy has not being tried due to usually large lesions.

Front 50

31 year old man present with melena and was found to have multiple hemangiomas with evidence of bone overgrowth, varicose veins and soft tissue hyperplasia. What is the diagnosis?

Back 50

Klippel Trenaunay Weber syndrome

Front 51

46 year old Asian American man present with jaundice, fever and RUQ pain. He has had off and on symptoms for 3 years and no history of viral hepatitis and recent weight lost. Lab is suggestive of cholangitis. U/S showed diffuse intra and extrahepatic duct diltatin along with innumerable stone in both intra and extrahepatic ducts. ERCP showed diffuse dilated bile ducts with stricturing. No malignancy detect on imaging. What is the diagnosis?

Back 51

Recurrent pyogenic cholangiohepatitis.

Front 52

54 year old Caucasian lady after retruning from Napel developed progressively worsen high fever, no diarrhea, but abdominal pain. CT showed thickening of cecum/ileum and there were diffuse salmon colored macules on her trunks. Diagnosis is?

Back 52

Typhoid fever.

Front 53

If >100cm of ileum is resected, then diarrhea is most likely due to? How about <100cm?

Back 53

>100cm, steatorrhea

<100cm, bile salt diarrhea due to bile salt be a stimulant for colonic secretion.

Front 54

What is the gold standard of diagnosing small bowel bacterial overgrowth?

Back 54

<1000 colony forming in jejunal aspirate in norma patient. SBBO has >10^5 colony forming unit of colonic bacteria.

Front 55

How does hydrogen breath test work?

What is consider positive?

Which is better? Lactulose vs. glucose? why?

Back 55

Oral administration of carbohydrate such as lactose or glucose which is fermented upon exposure to colonic type bacteria leading to production of hydrogen gas which can be detected.

Health hydrogen productin does not rise before 90 minutes following carbohydrate ingestion.

If SBBO, there there is an early rise of hydrogen gas.

Also if there is a >20 ppm rise by 180minute also indicative of SBBO.

Lactose is consider better because lactulose is not absorbed and thus ferment in the bowel whereas glucose is absorbed therefore can miss SBBO.

Front 56

How do you calculate stool anion gap?

how do you interrept it?

Back 56

290- 2x (Na+K)

If >50 then osmotic. If <50, then secretory diarrhea.

Front 57

1. Why does fatty diarrhea or carbohydrate intolerance cause low pH stool?

2. What are some questions to ask patients for suspected carbohydrate intolerance?

Back 57

1. Because the fatty acid which is negatively charged.

2. chewing gum (sorbitol), ingestion of food additive or high sugar content, abuse of sugar containing osmotic laxative (sorbitol, lactulose)

Front 58

28 year old female with fear of eating and 30 pound weight lost due to fear of eating and severe post prandial epigastric pain. ON exam, there is bruit over the epigastrium. What is the diagnosis?

Back 58

Median arcuate ligament syndrome where the median arcuate ligament is compressing on the celiac artery trunk

Front 59

Patient with recurent infection now with recurrent chronic diarrhea. Small bowel biopsy showed giardia in the absence of plasma cells in the lamina propria along with numerous lymphoid nodules? Diagnosis

Back 59

Common variable immunodeficiency

Front 60

How do you differentiate common hemosiderosis vs. hemochromatosis?

Back 60

hemosiderosis is common in hepatitis C, iron is seen in the Kupfer cells. Hemochromoatosis, iron is in the hepatocytes.

Front 61

Elderly patient found to have mucosal based pearly nodules scattered throughout his esophagus. Biospy revealed enlarged mature squamous cell with glycogen rich cytoplasm. What is the diagnossi?

Back 61

Glycogenosis acanthosis.

Front 62

What are the 4 histologic features of non-erosive or erosive esophagitis

Back 62

1. lengthening of the vascular pegs (rete pegs)
2. Hyperplasia of the epithelial surface
3. wide interceullar space
4. inflammatory infiltrate including eosinophils but <10 per high power field.

Front 63

How do you differentiate CMV vs. HSV esophagitis?

1. appearance of ulcers
2. number of ulcers
3. ?odynophagia
4. microscopic appearance?
5. treatment?

Back 63

1. CMV has long, serpiginous, deep ulcer vs. HSV has round, small, superificial volcano like ulcer

2. CMV has few ulcer vs. HSV has a lot

3. CMV has severe odynophagia and HSV is usually less severe

4. Owl eye for CMV, ground glass and eosinophilic dowdry bodies with multi-nucleated giant cells for HSV

5. ganciclovir for CMV and foscarnet second line. HSV is acyclovir.

Front 64

patient with difficult colonoscopy with air insufflation showed white patches in teh ascending colon suggestive of leukoplakia. biopsy showed clear spaces in the mucosa and submucosa suggestive of fat cells but without nuclei. What is the suspected diagnosis? How do you explain the histologic finding?

Back 64

Pseudolipomatosis from insufflation artifiact. Air dissect into the submucosal plane.

The clear spaces are actually air itself, therefore no nuclei.

Front 65

What is the Bismuth classification of cholangiocarcinom?

Back 65

Type 1: involve the chd, but no involvement of bifurcation

2: involves the bifurcation

3A: Involves the right and CHD

3B. Involves the left and CHD

4. Involves the CHD, bifurcation and both L and R hepatic duct.

Front 66

1. What are the chances that UC patients relative have IBD? What about Crohns?

2. Which genes (2) are associated with Crohn's

Back 66

1. 10-15 for UC and 15% for CD

2. CARD15/NOD2 and MDR1

Front 67

1. What percentage of women with IBD in remission before pregnancy has flare? When does it usually happen?

2. Which IBD is associated with smoker?

3. IBD exists more freqeuently in what climate?

4. What is the % of patient with UC that have extraintestinal symptoms?

Back 67

1. 1/3, usually happen at first trimester and postpartum

2. UC = non-smoker, CD= smoker

3. cold climate

4. 36%

Front 68

1. How often is ASCA positive in patient with CD? UC?

2. What about pANCA?

Back 68

1. ASCA + in 2/3 of CD and 1/3 of UC

2. pANCA is + in 2/3 of UC and 1/3 of CD

Front 69

1. What is sulfasalazine make up of?

2. How does it work?

3. How do various mesalamine product work to release drug in TI or intestine?

4. In UC/CD what disease does abx work for?

Back 69

1. 5-aminosalicylate + sulfapyridine link by Azo bond

2. It gets cleaved by bacteria to relase both product

3. Asacol (dissolve in pH of 7) or covered with ethylcellulose (Pentasa)

4. Abx most useful in post ileal resection and fistulizing CD

Front 70

1. Is MTX effective in inducing remission and maintenance of remission in patient with CD or UC?

2. What is the PO conversion of 4mg/kg IV of CSA?

3. Is Tacrolimus useful in treating CD or UC?

4. Wha tis the cumulative frequency of acute pouchitis reach ?% by 5 year?

Back 70

1. Yes, 15-25mg IM/PO Qweek for CD

2. 12-16mg/kg PO daily

3. Yes, 0.2mg/kg daily for fistulizing CD

4. 50

Front 71

1. What is the prevalence of ankylosing spondylitis in IBD?
Which has higher CD or UC?

2. How often does HLA-B27 occur in IBD patients

3. What is the treatment?

4. Is it related to IBD disease severity?

Back 71

1. 1-6%, CD>UC

2. 50-75%

3. physical therapy, analgesic and anti-inflammatory agents

4. NO

Front 72

1. What is the type 1 peripheral arthritis associated with IBD?

2. Is it self-limiting?

3. What about type 2?

4. Is it associated with IBD disease process?

5. What are the treatment for this type of arthritis (type 1 and 2)?

Back 72

1. Type 1, more common, asymmetric oligoarticular arithritis, affecting larger joint

2. self-limiting

3. type 2 more chronic symmetric polyarthritis similar to RA but no RF.

4. NO

5. analgesic, sulfasalazine, steroid may be needed and occasionally IFX and MTX are used.

Front 73

1. What direction to cut for pancreatic sphincterotomy?

2. Use pure cut, blend cut vs coag mode for pancreatic sphincterotmy? why?

3. What is the complication rate in patient treated with pancreatic sphincterotomy? What is the post ERCP pancreatitis rate?

4. Why does post ERCP pancreatitis occurs more in patient with SOD then chronic pancreatitis?

Back 73

1. 1-2 'oclock

2. Pure cut to minimize pancreatitis and future stenosis/fibrosis

3. 10-15% complication rate with post ERCP pancreatitis occuring about 10-12%

4. More in SOD patient due to thought that fibrosis offer some protection from inflammation

Front 74

1. Which direction to cut for minor duct papillotomy?

2. What type of stent is recommended?

3. What is a saccular dilation of the termial dorsal duct?

4. What is the average basal sphincter pressure for the minor papilla?

5. What is the minor papilla restenosis rate? referrence?

Back 74

1. 10-12 o'clock

2. use small 3Fr x 6-8cm stent without internal flange

3. 15% have santorinicele

4. 40mmHg

5. 20% (Toth 2001 GIE)

Front 75

1. What is the average papilla to bifurcation length?

2. 1 Fr = ?mm?

3. What are some complication from the SEMS? and % (5)

Back 75

1. 9cm

2. 0.33

3. migration (6%), cholecystitis (3-12%), pancreatitis, cholangitis, tumor in growth.

Front 76

1. what are the Wall stents made out of?

2. What are the rest SEMS made out of?

3. What is the covered material for Wallstent? What about Viabil?

Back 76

1. Steel

2. Nitinol

3. Polyurethane, viabil non-porous polytetrafluoroethylene

Front 77

1. Occular complication of IBD occurs in what % of patients?

2. Which type of anterior uveitis mirror the IBD disease activity? Which is associate with HLAB-27?

3. How do you treat the uvieitis? (3)

Back 77

1. 1-13%

2. Acute form, associated with HLA-B27 does NOT mirror the disease activity. The chronic from which is NOT associated with HLAB-27 does mirror the IBD disease activity

3. sulfasalazine, topical steroid, cycloplegic agent.

Front 78

Which IBD associated eye problem causes ocular pain, redness, photophobia or blurred vision?

Back 78

Uveitis

Front 79

Which IBD associated with eye problme present with eye irritation and conjunctival erythema? Does it correlate with IBD disease activity? How do you treat it?

Back 79

Episcleritis and scleritis

mirror IBD disease acivity

tx with topical or oral steroid.

Front 80

How often does pyoderma gangrenosum occur in patient with IBD?

Does it mirror the IBD disease activity?

What do you treat it with?

Back 80

12%

independent of IBD disease

tx with steroid, then immunsuppressive therapy like CSA, tacroliums, AZA or MMF

Front 81

Erythema nodusum

More in CD or UC?
Which sex?
Does disease activity correlate with underlying IBD disease activity?

What is the treatment?

Back 81

More in CD (15%) vs UC (5%)
more in young women

activity correlate with IBD, therefore treatment is to treat underyling IBD.

Front 82

1. CD or UC is associated with AIH more?

2. How often does osteopenia occur in patient with IBD? What is the treatment?

3. Why does patient with IBD or other steatorrhea has problem with oxalate stone?

Back 82

1. more with UC

2. 50-70%, tx with 1200mg Ca + 800U of vitamin D

3. fatty acid bind to calcium which would normally bind colonic oxalate and leading to more oxalate to be absorbed by the colon and leading to oxalate stone formation.

Front 83

How does c. diff toxin work on damaging colonic mucosa?

Can you just test for one toxin for C. diff. why or why not?

Back 83

toxin A bind to mucosal receptor and cause cytotoxicity by disrupting cytoplasmic microfilament and lead to apoptosis, then toxin B can enter the damaged mucosa and cause further cytotoxicity resulting in hemorrhage, necrosis and inflammation.

NO, because some C.diff make only one strain of toxin.

Front 84

The order of examining the pancreas using EUS

Back 84

1. find the celiac artery and bifurcation of splenic/HA
2. advance and torque counter clock to exam the genu
3. Withdrawan from this region and rotate clockwise to exam body/tail
4. HOP: advance scope into the duodenal apex and locate the liver then put liver at upper left.

Front 85

What is the normal duct size at head, body and tail? Is there any changes as patient gets older?

Back 85

3,2,1 at tail. Allow 1mm for each when patient >60.

Front 86

1. What are the hyperechoic/thicken duct margin seen on EUS correlate to on histology?

2. What about the hypoechoic lobules?

Back 86

1. fibrosis

2. the edema seen surround by the fibrosis.

Front 87

1. What is the risk of developing pancreatic CA in 10-20 years in patient with chronic pancreatitis?

2. How good is FGD-PET scan for pancreatic cancer?

3. How do you perform contrast EUS?

Back 87

1. fair, one study report sensitivity of 88%

2. give optison IV to assess hyper vs. hypoperfusion. Usually take up to 10-15 seconds and last for 3 mint. Give 1:10, 10mL solution first injected then 5 min after the first. Look for hypoperfusion (malignancy) vs. hyperperfusion(benign)

Front 88

1. How sensitive is EUS for detecting pancreatic lesion?

2. What 3 factors can lead to poor detection of lesion using EUS?

Back 88

1. Sensitivity 96% (85-100%)

2. if there is changes consistent with chronic pancreatitis, diffusely infiltrative carcinoma, recent pancreatitis

Front 89

What are the 3 most comon criteria use to determine whether there is vascular invasion by pancreatic tumor?

What is the accuracy, sen and spec?

Back 89

1. irregular vascular wall
2. venous collateral
3. visible tumor in the vessel

accuracy is 40-100%
sen:40-90%
spec:90-100%

Front 90

How good is EUS in detecting venous invasion for pancreatic cancer

1. better then CT? or not?
2. Sensitivity for portal involvement?
3. Sen for SMV? SMA? CAX?
4. How about arterial invasion?

Back 90

1. superior or equivalent to CT
2. Sen >80%
3. SMV (17-83%), SMA (17%), Cax (50%)
4. 56% for sen and accuracy is 50%

Front 91

What is the accuracy for resectability for pancreatic CA?

Back 91

sen:69%, spec: 82% and accuracy is 77%

Front 92

1. What is the sen, spec and NPV? for EUS with FNA for pancreatic ca?

2. what increases yield and decrease yield of the FNA?

3. What is the rate of pancreatitis and peritoneal seeding?

Back 92

1. sen:85, spec:98 and NPV is 55%, so if negative FNA doesn't mean negative test.

2. yield increase with on site cytopathologist and 5-7 passes. Yield decrase when there is chronic pancreatitis

3. 2% pancreatitis, 2.2% peritoneal seeding.

Front 93

1. How many % of pancreatic tumors are neuroendocrine tumor?

2. What is the T staging and N staging accuracy for ampullary tumor using EUS?

Back 93

1. <10%

2. T:78%, N:62%

Front 94

1. Does serous cystadenoma has risk for malignancy?

2. What is the hallmark appearance for solid or pseudopapillary neoplasm?

Back 94

1. Yes, 3%

2. mostly found in young women and hallmark is central hemorrhagic cystic degeneration and a pseudocapsule that may calcifiy.

Front 95

What are the 10 things to note during an EUS exam of a pancreatic cyst.

Back 95

1. wall thickenss
2. distance from lumen
3. interposed vessels
4. focal irregularity
5. papillary projection
6. Mural nodules
7. associated mass/calcification
8. septation
9. debris/echogenic material in cyst
10.connected to PD

Front 96

1. Long term sequeale such as stenosis and non-obstructive cholangitis occur in what % of patients 6-13 years after sphincterotomy?

2. How many layers are the biliary ducts?

3. Is IDUS good to determine malignancy from PSC?

Back 96

1. 13%

2. first (mucosa), second (smooth muscle), third (connective tissue)

3. NO

Front 97

1. For ampullary tumors, is EUS with biopsy good for diagnosis?

2. What are the two limitation for endoscopic resection?

Back 97

1. No, was 19-30% of time it maybe underestimated

2. tumor with risk of lymph node met and intraductal invasion inside PD or CBD

Front 98

What is th TNM staging for ampullary CA?

Back 98

T1: (tumor not extending beyond the sphincter) T1d0 (no risk for lymphatic spread, T1d1:30% lymph spread

T2: tumor into the MP layer of duodenal wall

T3: tumor invadingthe adjacent pancreas <2cm

T4: invade the pancreas deeply or involved adjacent organs.

Front 99

1. What is the most reliable preoperative staging modality for ampullary tumor?

2. What is this modality's limitation?

Back 99

1. EUS

2. limited in showing infiltration of duodenal submucosa.

Front 100

1. What are 3 indication for surgical treatment for ampullary mass?

2. Why is rectal cancer need EUS?

3. Do you FNA peritumor lymph nodes? why or why not?

Back 100

1. >T1 lesion or intraductal infiltration, ulcers

2. Because if patient with T3, T4 or TxN1-2 (stage 2 or 3 disease) patient need neoadjuvant therapy.

3. No, perirectal nodes are not seen, therefore if they are seen, they are suspicious.

Front 101

What is the TNM staging for pancreatic CA?

Back 101

Tis:carcinoma in situ
T1: tumor in pancreas, <2cm
T2: tumor in pancreas, >2cm
T3: tumor extends beyond the pancras but without any involvement of the celiac axis or SMA
T4: tumor involves the CAX or SMA (unresectable tumor)

N0: No involved regional lymph node
N1: any involved regional lymph nod

Mx: can't be assessed
M0: No distant met
M1: distant met

Front 102

What is the staging for pancreatic CA?

Back 102

stage 0: Tis
stage 1a: T1N0M0
stage 1b: T2N0m0
stage 2a: T3N0M0
stage 2b: T1-3, N1M0
stage 3: T4 with any N, M0
stage 4: any T, any N, M1

Front 103

1. How much nutritient is supplied by portal vein vs. HA for liver?

2. Why patient with NAFLD tend to have fatty deposites in zone 3?

3. Which zone tend to be affected with patient who ingested direct hepatotoxin? how about those were metabolized into hepatotoxin?

Back 103

1. 2/3 portal and 1/3 HA.

2. Hepatocytes in Zone 3 are more associated with lipid synthesis and glycolysis.

3. Zone 3 = direct toxin, Zone 1-2 = metabolite

Front 104

What is the Rosemont classification of chronic pancreatitis?

Back 104

Parenchymal major A
1. hyperechoic foci with shadowing
2. well circumscribed lobularity
Ductal major A
1. Main duct calculi

Parenchyma major B
1. lobularity with honeycombing

Minor parenchymal criteria
1. cysts
2. Stranding
3. Non-shadowing hyperechoic foci
4. Lobularity with noncontiguous lobules

Minor ductal criteria
1. dilated duct
2. irregular main pancreatic duct controur
3. dilated side branches >=1mm
4. hyperechoic duct margin.

CP is consistent if
1. 1 major A feature + >3 minor
2. 1 major A + major B
3. 2 major A

Front 105

What are some influencing factors on panreatic imaging and impact on EUS?

Back 105

1. alcholism, advanced age, male, obesity and smoking can lead to "asymptomatic fibrosis"

Front 106

What are the manometrical 3 findings of achalasia?

Back 106

1. absence of peristalsis in the esophageal body
2. a hypertensive LES
3. poorly relaxing LES with a residual pressure >8mmHg

Front 107

1. What are the 3 subtype of achalasia seen by the high resolution manometery?

2. Which type has best prognosis?

Back 107

Type 1: classic achalasia has no distal esophageal pressurization >30mmHg

Type 2. (achalasia with esophageal compression) has >=2 test swallows associated with an esophageal pressurization >30mmHg

Type 3: (spastic achalasia) have >=2 spastic contraction with or without a period of compartmentalized pressurization.

2. Type 2 has best prognosis.

Front 108

What is the best endoscopic treatment for achalasia? What is the evidence?

Back 108

Leyden Cochrane review (6 RCT) 2006 showed that 30% had symptom recurrence at 12 months vs. 74% for botox injection.

Front 109

1. What is the esophageal perforatin rate for dilating achalasia?

2. What is the "down" side for patient who are undergoing botox injection into the LES for achalasia?

3. What is the surgical risk for esophagomyotomy?

4. What do you use to assess for the "completion" of post surgical myotomy?

Back 109

1. 2-6%

2. "increase difficulty of performing esophagomyotomy at later date"

3. complication in 6% and death in 0.1% for lap. myotomy

4. post surgery manometry showed <10mm Hg.

Front 110

1. How is Heller myotomy done?

2. What is the best predictor of patients who will need additional therapy after myotomy is?

3. What is the major draw back for myotomy? How do you fix it?

4. Which fundoplication is better for patient who had achalasia and had myotomy?

Back 110

1. A longitudinal incison is initiated on the gatric side approximately 2cm distal to the GEJ and extend proximally 7cm above the junciton.

2. esophageal dilation of >6cm before surgery.

3. 50% will have GERD and fixed by Nissen or Dor (ant. fundoplication)

4. Dor, less dysphagia than Nissen.

Front 111

Has there any data regarding surgical treatment vs. dilation in treatment of achalasia?

Back 111

Csendes et al (Gut 1989) RCT.
Esophagomyotomy vs. dilation
study showed equivalent result regarding effectiveness at relieving symptosm initially, but follow up favor surgery.

Front 112

What is the best treatment for achalasia? base on what evidence?

Back 112

Urbach (J gastro surgery 2001)
analysis model base on risk, need for repeat procedure, and overall cost determine lap Heller myotomy with fundoplication was preferred strategy UNLESS patient risk of operative surgery is >0.7%

Front 113

1. What are the 2 major PRIMARY bile salt components?

2. What are the two SECONDARY bile acid?

3. Which 4 clotting factors and 2 anticlotting factors are affected by vitamin K?

4. What are delta bilirubin?

Back 113

1. cholic acid (60%) and chendeoxycholic acid (25%).

2. Deoxycholic and lithocholic acid

3. 2, 7, 9, 10. Protein C and S

4. is bilirubin which is covalently bound to serum albumin. In pt with prolonged and marked jaundice, the delta bilirubin can increase

Front 114

What disease is a rare, autosomal recessive disorder which lead to unconjugated hyperbilirubinemia featured by lack of UDP-glucuronosyl transferase?

Back 114

Crigler Najjar syndrome type I

Front 115

1. What is the difference between Crigler Najjar type I and II?

2. What are some treatment of type II?

Back 115

1. Type I is complete absent of UDPG transferase activity. Type II is milder form which retained 50% of its activity

2. Can be treated by phenobarbital which induce UDP-G transferase enzyme activity.

Front 116

1. What are two congenital cause of indirect hyperbilirubinemia?

2. How do you distinguish Dubin Johnson vs. Rotor's on liver histology?

Back 116

1. Gilbert and Crigler-Najaar

2. Dubin Johnson has black liver

Front 117

1. Give 4 CYP inhibitors?

2. Give 8 inducer of CYPs?

3. What are the 3 highest relative liver toxicity for NSAIDs?

Back 117

1. Erythromycin, ketoconazole, cimetidine, quinidine.

2. cigarette, charcoal, omeprazole, ethanol, isoniazide, anti-sz meds, rifampin, glucocorticoids.

3. Diclofenac, sulindac, phenylbutazone.

Front 118

What type of toxicity typically lead to hepatitis vs. cholestasis? intrinsic, idiosyncratic and hypersensitivity?

Back 118

Hepatitis: Intrinsic

Cholestasis: idiosyncratic, hypersensitivity.

Front 119

1. What are 3 drugs that can lead to microvesicular steatosis?

2. What is the common cause of VOD in tropical area? How about in US?

3. Is there benefit for NAC treatment even after 24 hours of known overdose?

4. What are the 5 risk factors for developing drug induced liver injury?

Back 119

1. Valproic acid, tetracycline, nucleoside analogs.

2. In tropical: herbal (alkaloid) tea. US: chemo/bone marrow transplant.

3. Yes

4. age >60, female, obesity, chronic EtOH use, hx of drug induced liver injury

Front 120

1. How does valproic acid lead to hepatotoxicity? What type of "steatosis" does it cause?

Back 120

1. It interfer mitochondrial oxidative phosphorulation, leads to microvesicular steatosis without inflammation.

Front 121

1. What is the accuracy for T staging for rectal tumor? How about N staging?

2. Are they better then CT/MRI?

3. What is the recurrence rate of rectal CA?

Back 121

1. Accuracy T:87%, N:75%

2. T staging is but not N staging.

3. 20-50%

Front 122

1. Where is ALKP located within? hepatocyte or bile duct cells?

2. What changes does bile duct make in respond to prolong cholestasis.

3. What are the 5 common "infiltrative" process in patient with cholestasis?

4. Which type of alcoholic hepatitis have very bad prognosis?

Back 122

1. The canalicular membrance of hepatocytes

2. They increase in length/tortousity but NOT in number

3. sarcoidosis, TB, amyloidosis, lymphoma and hepatic mets.

4. Those with high ALKP which is a type of alcohol hepatitis that has high perisinusoidal fibrosis which has very poor prognosis. Also stopping EtOH does NOT improve the chlestasis.

Front 123

1. Which HLA type is associated with PBC?

2. Can patients with cholestatic disease have high copper and urine excretion of copper?

3. What fraction of lipid are elevated in PBC usually?

4. Which enzyme is anti-mitochondrial antibody against?

5. What is the common renal dysfunction seen in patient with long standing PBC and Wilsons? What is the pathophysiology?

Back 123

1. HLA-DRW8

2. Yes

3. HDL and lipoprotein X

4. pyruvate dehydrogenase within the mitochondria

5. RTA due to excessive urinary copper excretion leads to copper toxicity in renal tubules.

Front 124

1. What is the average duration of PBC from diagnosis to death?

2. Which lab feature of PBC has higher risk for need of OLT?

3. Which stage of PBC patients has the highest benefit histologically from Urso treatment?

4. Does MTX work for PBC?

5. What is the 3 sequential treatment for pruritus in PBC patients?

6. What is the cause of pruritus in patient with PBC or other cholestasis disease?

7. How does Rifampin thought to work in treating pruritus for PBC?

Back 124

1. 24 years

2. bilirbuin >10

3. stage 1-2

4. RTC demonstrated NO benefit

5. antihistamine then Urso/cholestyramine then Rifampin then Naltrexone

6. The hydrophobic bile salt.

7. Reduce intestinal flora and therefore decrease the secondary hydrophobic bile salt.

Front 125

1. Which HLA are associated with PSC? ARe they exclusively associated with PSC?

2. Which two acute viral hepatitis is transmitted through oral-fecal route?

3. Can HEV be a chronic infection?

4. Are IgM for diagnosis of CMV sufficient? If not, what is?

5. How do you differenitate Mono from EBV vs. CMV?

6. When does fecal shedding of HAV start? Until how long?

Back 125

1. B8 and or DR3. NO

2. HAV and HEV

3. Yes with post OLT patient

4. NO, false + and false - commonly occur. Need documented seroconversion from negative to positive or a rising titer to formally diagnose acute CMV infection.

5. EBV mono has heterophile antibodies and CMV mono does not

6. Within 2-3 weeks of exposure last 1-3 months or even longer.

Front 126

1. Patient who has serological recovery from HAV started to have jaundice again. What is the likely diagnosis?

2. How long is the incubation period for HAV?

3. What is recommended to HAV patient's close contact?

4. How many genotype of HEV is there and which types are associated with sporadic and non-travel cases?

5. What population has high mortality rate from HEV?

6. What are some 3 risk factors for acquiring HEV?

Back 126

1. Recurrent HAV infection.

2. 30 days

3. Vaccination. 20-50% of close contact may acquire virus

4. 4. type 3 and 4

5. pregnant people

6. Visiting pig farm or farm, consumption of raw pork, shellfish or pets

Front 127

1. Which HBV genotype has been associated with more severe chronic hepatitis and acute liver failure in US?

2. How do you assess patient on HD when they need HBV vaccine?

3. Which HDV genotype has been associated with acute liver failure?

4. When should treatment be consider in patient with acute Hepatitis C? (2 situations)

5. What is the chances of clearing HCV in patient with acute hepatitis C with 3-6 month of IFN/RBV tx?

6. Which test do you use to test for PCT in HCV patients?

Back 127

1. C = severe chronic, D= liver failure in US

2. When their HepBsAB lvel drop below 10mIU/mL

3. I

4. If no clearance of HCV by 3-4 months in SYMPTOMATIC patients and immediately in ASYMPTOMATIC patient.

5. 90-95% clearance

6. Urine prophyrin

Front 128

1. Which race of patients usually have cirrhosis on presentation for their AIH?

2. How do you generally differentiate PBC and AIH histologically?

3. What is the main genetic susceptibility factor in white North American for AIH?

4. What is the significance of ANA and ASMA disappearance for AIH? Is it predicative of treatment outcome?

5. Presence of which antibody predicts more severe disease and high frequency of relapse on withdrawal?

6. Which anti-LKM subtype associate with hepatitis D?

Back 128

1. African American

2. lack of bile duct involvement in AIH

3. DR3 and DR4

4. associate with improve histology and ALT/AST NOT outcome

5. Anti-SLA/LP or antibody to soluble liver antigen/liver pancreas.

6. anti-LKM3

Front 129

1. What is polyendocrinopathy-candidiasis ectodermal dystrophy associated with?

2. What are 3 predictor of AIH relapse?

3. What is the recurrence rate in AIH patient post OLT?

4. What are 3 major problems facing pregnant AIH patients? What are the estimated percentage of each problem?

5. What is the estimate % of post deliver AIH flare?

Back 129

1. Anti-LKM AIH (type II AIH)

2. long time to remission, failure to maintain consistently normal ALT during remission, presence of high number of portal plasma cells

3. 15-20%

4. fetal lost 15-25%, preterm deliver and exacerbation lead to severe hepatitis <10%

5. 50%

Front 130

1. How do you define acute liver failure?

2. How do you define sub-acute liver failure?

Back 130

1. Acute: development of hepatic encephalopathy with severe hypoprothrombinemia INR>1.5 occurring after onset of jaundice in pt without pre-exisitng liver disease within 7-21 days after onset of jaundice

2. Subacute: Above but occured between 21 days to 26 weeks

Front 131

1. Can parvovirus B19 cause acute liver failure?

2. Do you often see high viral DNA in patient with fulminant hepatitis B?

3. Which hepatitis B genotype cause more acute liver failure?

4. What are 7 common drugs that cause ALF?

Back 131

1. Yes

2. No

3. Genotype D

4. INH, sulfonamide, valproate, phenytoin, disulfiram, diclofenac, ketoconazole

Front 132

1. According to acute liver failure study group, which sex has more ALF?

2. Can you see hyperamylasemia in patient with acute liver failure?

3. Which complication is believe to be the cause of 50% of mortality for patient with ALF?

Back 132

1. female

2. yes

3. cerebral edema.

Front 133

1. According to the acute liver failure study group, what % of patient survive, need OLT and what % died without OLT?

2. What is the treatment for Amanita poisoning?

3. What are two treatment for cerebral edema in patient with ALF?

Back 133

1. 45% recovery, 25% OLT, 30% die

2. Pen G and NAC

3. Mannitol and hypertonic saline (NA betwen 145-155)

Front 134

1. What is the annual probability of patient with CHB progress to cirrhosis>

Back 134

1. 2-6%

Front 135

1. In hepatitis B, what is the best predictor of response to interferon therapy?

2. Which HBV genotype appear to be less responsive to treatment with IFN?

3. Are IFN treatment side effect more or less common in HBV patient compare to HCV?

5. What are the 5 positive predictors of response to IFNin HBeAg- patients?

Back 135

1. High ALT level

2. C

3. they are less compare to HCV patients

4. High ALT level, low HGV DNA (above 20,000IU), active necroinflammatory lesion on biopsy, short duration of disease prior to tx, absence of immunosuppressive disease or therapy.

Front 136

1. Does presence of cirrhosis affect the response to interferon in patient with chronic HBV? how about HCV?

2. What class of anti-virals are lamivudine, telbivudine and entecavir belong to?

3. What about adefovir and tenofovir?

4. What is the resistant rate for entecavir in patient with resistance to lamivudine?

Back 136

1. No, does not affect HBV but does affect HCV.

2. Nucleoside analog

3. Nucleotide analogs

4. 10%

Front 137

ARP

Back 137

automotive repair parts= receive store issue parts for cese.

Front 138

1. What is the management for patient with PAN from hepatitis B?

2. When do you discontinue prophylactic anti-virals in patient receving chemotherpay with HBV?

Back 138

1. plasmapheresis, steroid + cyclophosphamide

2. start 1-2 weeks before starting chemo agents, then stop 6-12 months after stopping the chemo

Front 139

1. What is the rate of cirrhosis and HCC in patient with chronic HDV?

2. What do you do to treat HDV?

Back 139

1. 3% annually HCC, 4% annual rate for cirrhosis

2. IFN

Front 140

1. What is the current use "stop" rule for treating HCV?

2. What can you do in pt with HCV EVR (12 week with drop of >2 log reduction of RNA) and subsequently became RNA negative at week 24?

3. What is the management for those patient with genotype 2 and 3 who relapsed after 24 weeks of therapy? What is their chance of clearance with new therapy?

4. What is one experimental therapy for patient with HCV related cyroglobulinemia, vasculitis and nephritis?

Back 140

1. failure to induce a 2 log reduction in HCV RNA after 12 weeks of therapy

2. extend therapy to 72 week

3. retreat with PEG-IFN _ RBV for 48 weeks have a 60% clearance rate.

4. Rituximab

Front 141

1. Are telangiectasias and palmer erythema normal in pregnant people? why?

2. Is GGT increased or decreased in pregnancy?

3. Is cholesterol and triglycerides increased or decrease in pregnancy?

4. How about bile salt?

5. Coagulation factors?

Back 141

1. yes, because increase estrogen production

2. GGT is decreased

3. cholesterol/triglyceride is increased due to increase production.

4. Bile salt is increased due to decrease transport and secretion

5. Increased due to increase synthesis

Front 142

1. Are HCV antibody useful in diagnose infant HCV? How about RNA? How do you diagnose rule out HCV infection in newborn?

2. Can you treat children <2 with IFN?

Back 142

1. RNA and antibody can be falsely positive in infant (passive transfer of maternal antibody and RNA level) Diagnosis is usually made at 2 years of age.

2. contraindicated

Front 143

1. How will schistosomiasis react to pregnant patient?

2. How are lesions such as hepatic adenomas, FNH and hemangiomas managed during pregnancy?

Back 143

1. Increase progesterone may increase risk for abscess formation and worsen underlying disease.

2. They should be monitor during pregnancy with imaging due to potential increase in size.

Front 144

1. What ethnic group has high incidence of ICP?

2. What are two treatment for ICP?

3. When do patient with ICP usually complain of itching? AM? or PM?

4. Is GGT increase in patient with ICP?

Back 144

1. Araucanian Indians from Chile

2. Urso 15mg/kg/day + vitamin K

3. In the evening/afternoon

4. Normal GGT with elevated ALKP

Front 145

1. what are the hallmark findings of eclampsia?

2. What are 5 associated findings for HELLP syndrome?

Back 145

1. HTN, proteinuria and edema

2. pre-eclampsia, DIC, pulmonary edema, placental abruption and retinal detachement

Front 146

1. Which lobe of the liver is usually involved in rupture/infarct associated with pre-eclampsia and HELLP?

2. Is acute fatty liver of pregnancy associated with macro or microvesicular disease?

Back 146

1. Right lobe

2. Microvesicular

Front 147

1. In an adult with new onset portal vein thrombosis without cirrhosis, need to rule out what 2 conditions?

2. What about infant?

3. What is a dreaded complication from portal vein thrombosis that require surgical treatment?

Back 147

1. diverticulitis or appendicitis leads to pylephlebitis

2. umbilical vein
instrumentation/infection

3. SMV thrombosis

Front 148

1. Patient with low wedge hepatic venous pressure and free hepatic venous pressure usually means which level of resistance?

2. What about if both are high?

3. What about High wedge pressure but normal free pressure?

Back 148

1. Pre-sinusoidal. the HVPG is normal.

2. Post sinusoidal, normal HVPG

3. Sinusoidal, HVPG is high

Front 149

1. At what level of HVPG is consider portal HTN?

2. At what level of HVPG would you worry about ascites and risk of variceal bleed?

Back 149

1. 5-10

2. >=12

Front 150

1. What is the mortality rate of each variceal bleed?

2. When do you bring patient back for repeat EGD after banding?

3. What should be rule out if you see an isolated gastric varix? IGV1?

4. Is there role for primary prophylaxis for gastric varices using non-selective beta blocker?

5. Tx of isolated gastric varices from splenic vein thrombosis?

Back 150

1. 20-30%

2. 2-3 weeks

3. splenic vein thrombosis.

4. No

5. splenectomy/IR guided embolization of splenic artery.

Front 151

1. What is the treatment for IGV2?

2. Is there proven benefit using non-selective beta blocker for secondary prophylaxis for GV bleed?

3. Is non-selective beta blockers effective for preventing chronic bleed from portal hypertensive gastropathy?

4. Do all patient with GAVE have cirrhosis?

Back 151

1. TIPS, not effective as GOV1,2

2. No being shown to decrease risk of re-bleed.

3. Yes

4. No, only 50%

Front 152

1. How does amiloride work?

2. Most hepatohydrothorax occurs at which side?

3. Primary prophylaxis for SBP (pt with low peritoneal albumin) improves which two end points?

4. What is the most common cause of Budd-Chiari syndrome in adult?

5. What can be use as "prophyaxis" for VOD?

Back 152

1. It block sodium reabsorption from the distal tubules

2. right

3. improved mortality and lower rate of SBP

4. Myeloproliferative disorder like polycythemia vera.

5. Urso before chemo agent

Front 153

1. At what stage of encephalopathy does asterixis occur?

2. What are two mechanism in which the altered neurotransmission cause PSE?

Back 153

1. Stage 2

2. decreased glutamatergic neurotransmission due to glutamate sequestration within astrocytes as glutamine that is used to detoxify ammonia. (which is a excitatory neurotransmittor) It also increase GABA-ergic neurotransmission due to gut bacteria derived benzodiazepine escape hepatic metabolism. (GABA is a inhibitory neurotransmitter)

Front 154

1. How is PSE differ in patient with acute liver failure vs. cirrhosis?

2. Three mechanism of action of how lactulose work

3. What mean PAP is consider contraindication for OLT?

Back 154

1. ALF have more cerebral edema.

2. it is a catharsis (rid gut of bacteria, and stuff that makes ammonia), it acidify the gut lumen and trapping NH3 and NH4, and it inhibit ammonia producing bacteria due to acidification of gut.

3. >35mmHg.

Front 155

1. EtOH absorption rate higher in obese person or lower? why?

2. How much EtOH consumption/day lead to steatosis?

3. What is the dosage for methylprednisolone for EtOH hepatitis?

Back 155

1. Higher because etoh doesn't get absorbed in fat

2. 60g/day

3. 32mg/day for 4wks follow by 2 wk taper.

Front 156

What are 3 histologic findings of NASH?

Back 156

1. Macrovesicular steatosis, 2. hepatocellular ballooning degeneration and necrosis in zone 3 with or without Mallory's hyaline.
3. pericellular perivenular or perisinusoidal fibrosis.

Front 157

What are the 4 risk factors associated with more advanced NAFLD?

Back 157

1. Age >45
2. BMI>35
3. DMII
4. AST/ALT ratio <1

Front 158

1. What is the estimated progression to fibrosis and cirrhosis during the first 10 years of follow up after biopsy proven NASH?

2. What is the recommended weight lost for patient with NASH? How many g/wk?

3. How do you calculate an estimated Kcal required for a patient?

Back 158

1. 40%

2. 1600g/wk.

3. Current weight in lbs x 10

Front 159

1. How does TZD class drug improves NASH?

2. What is its side effect?

Back 159

1. It exert its effect via expression of several genes that regulate adipocytes which leads to mobilization of central fat, reduction of fat in liver and myocytes.

2. Weight gain

Front 160

1. Which joint does hemochromatosis affect?

2, Which area is hemochromatosis most prevalent?

3. Typically, the ferritin are elevated in hemochromatosis to what level in men and women?

Back 160

1. MCP joint

2. North european

3. 200 in women and 300 in men.

Front 161

What is the pathophysiology for hemochromatosis?

Back 161

Hfe gene product normally bind transferrin and help transport it intracellularly, however, if Hfe gene defect, this is NOT done, leading to body thinking it is a overall iron deficient state, therefore increase iron absorption. IT increases the DMT1 (mucosal iron transporter) and ferroportin (protein that transport iron from mucosal side to basolateral side) expression

Front 162

1. How much elemental iron is in 500mL of blood?

2. Do phlebotomy improves patient with arthritis? How about ESLD?

3. Do patient with hemochromatosis have normal life expectancy before ESLD set in?

4. How do you estimate serum free copper?

5. How much serum copper and serum free copper makes you suspicious for Wilson's

Back 162

1. 250mg

2. Doesn't improve arthritis, but improves quality of life for patient with ESLD.

3. yes

4. serum free = total serum copper - 3.15 (ceruloplasmin)

5. 80microgram serum copper and 200 microgram/dL for serum free copper

Front 163

1. what is the most common cause of OLT in USA?

2. How many MELD points do patient with HPS get?

3. What are 4 factors that need to be evaluated for donor liver matching?

4. What is the problem with steatosis in donor liver for the recepient?

Back 163

1. HCV related ESLD

2. 20

3. blood type, steatosis of graft, size of liver, age of the donor liver

4. high fat lead to ischemia reperfusion injury and early graft dysfunction.

Front 164

1. What is the number one problem with living donor transplant for the recepient which is less of a problem for the cadaveric donor?

2. What is the most important predictor for spontaneous recovery from acute liver failure is?

3. Which two types of acute liver failure has best recovery prognosis?

4. Why does hemochromatosis recurr after transplant?

Back 164

1. bile leak

2. Etiology of the liver failure

3. HAV and tylenol toxicity.

4. Because the "error" of hemochromatosis is in the intestine (too much iron uptake), not in the liver

Front 165

1. When can OLT anastomosis stricture occur? When is the most common?

2. When is the highest risk for acute rejection?

3. What are the 3 hallmark of ACR?

Back 165

1. Anytime, but most common in 6 months.

2. Highest risk is within 6 month of post OLT

3. dense lymphocyte predominant inflammation centered in portal area, bile duct injury and destruction of the endothelial lining of portal/hepatic venules.

Front 166

1. What are 4 possible side effects of sirolimus?

2. Which immunosuppressant is consider more "renal friendly?"

3. What are 3 major cancers that needs to be kept in mind for patient post OLT?

4. What % of the post OLT patient for HCV can develop ESLD in 5 years?

5. What is the estimated SVR in HCV pt post OLT?

Back 166

1. hypertriglyceridemia, bone marrow suppression, bronchiolitis obliterans and HA thrombosis.

2. Sirolimus

3. lymphoma (PTLD), CRC and skin cancer.

4. 20-30%

5. 20-30%.

Front 167

1. What are 2 high risk factor for graft infection for HBV?

2. Can post HBV OLT patient develop resistance to HBIG? How do they get around that?

3. What kind of biliary anastomosis for patient with PSC ESLD during OLT?

4. What is the most common complication from chronic immunosuppressant use for OLT?

Back 167

1. Hep e antigen positive and DNA >100,000

2. yes, get around it by give neucleoside analog.

3. They do roux-en-Y choledochojejunostomy due to removal of entire recepient CBD.

4. HTN

Front 168

1. What is the % of patient who develop squamous cell esophageal cancer after having a lye injury?

2. What is the % of life time risk for developing squamous cell esophageal cancer in patient with Plummer Vinson syndrome?

3. Esophageal cancer patient with tumor located within 5cm of the cricopharyngeus should be consider for what type of therapy?

4. How far should the tumor be away from the cricopharyngeus to be resectable?

5. What is the treatment for patient with resectable esophageal T1 cancer?

Back 168

1. 3% after 20-40 years

2. 10%

3. chemoradiation

4. >5cm away from the cricopharyngeus.

5. Resection follow by adjuvant therapy.

Front 169

1. What is the estimated survival for esophageal cancer that is localized disease vs. all other stage disease?

2. What are 7 risk factors for gastric ca?

3. What treatment should be offered for patient with T1N0 or T2N0 gastric cancer?

4. What type of chemotherapy do they use for gastric CA

5. What is the difference in survival rate in localized proximal gastric vs. distal gastric cancer?

Back 169

1. 34% localized and 17% all disease stage.

2. smoker, blood type A, subtotal gastrectomy, pernicious anemia, gastric adenoma, hx of chronic gastric atrophy and diet high in perservative (smokign, pickling or salting).

3. Surgery but no adjuvant therpay.

4. Epirubicin/cisplatin/5FU (ECF) or docetaxel/cisplaatin/5FU (DCF)

5. Proximal 10-15% vs. distal (50%)

Front 170

1. What is the most common cancer of the biliary tract?

2. Gallbladder cancer is common in which two ethnicities?

3. What is the perferred surgical treatment for gallbladder cancer?

4. What is the treatment for local advanced gallbladder cancer?

5. Worldwide, what is the most common risk factor for cholangiocarcinoma?

Back 170

1. Gallbladder cancer

2. Native american and hispanics

3. hepatic resection and lymphadenectomy along with cholecystectomy.

4. 5FU based chemotherapy with radiation.

5. infection by liver flukes (clonorchis and Opisthorchis)

Front 171

What are 8 risk factors for gallbladder cancer?

Back 171

1. porcelain gallbladder
2. typhoid carrier
3. GB polyp >1cm
4. obesity
5. anomalous pancreaticobiliary duct junction
6. choledochal cyst
7. carcinogen such as nitrosamine/azotoluene
8. gallstone >3cm

Front 172

1. What is the major risk factor of small bowel cacrinoma?

2. What stage of colon cancer without metastatic disease is surgeyr the only therapy?

3. What is the treatment for stage III cancer with met?

4. When is stage II colon cancer given adjuvant therapy? (7 risk factors)

Back 172

1. Crohn's disease.

2. Stage I-III

3. surgery + adjuvant chemotherapy.

4. patien twith poor prognostic factors such as: T4 tumor, poor histologic grade, bowel obstruction, +margin, peritumoral lymphovascular invovlement, localized perofration or inadequate lymph node sampling.

Front 173

1. What virus is a risk factor for anal cancer?

2. What should be order to rule out met. anal cancer?

3. What is the treatment for anal cancer?

Back 173

1. HPV-16

2. CXR or CT of chest due to high rate of lung met.

3. Chemoradiation (Mitomycin/5FU)

Front 174

What is the T staging for esophageal CA?

Back 174

Tis=carcinoma in situ
T1= invasion of LP or submucosa
T1a=within mucosa

T2=invasion of MP

T3=invasion of adventitia

T4=invasion of adjacent structures.

Front 175

What is the T staging for gallbladder cancer?

What is the N staging for gallbladder ca?

Back 175

T1a=invade LP
T1b=invade MP
T2=invade perimuscular connective tissue without involving the liver
T3=perforate the serosa/visceral peritoneum directly invade liver or adjacent organgs.
T4=tumor invade main PV or HA

N1=regional lymph node

Front 176

What is the T staging for extrahepatic biliary cancer?

Back 176

T1=confined in bile duct
T2=invades beyond the wall of duct
T3=invade liver/GB/pancreas and or ipsilateral branches of the PV/HA
T4=tumor invades main PV or bilateral branches of PV, HA, adjacent organs.

Front 177

1. What is the treatment strategy of choice for adenocarcinoma of the esophagus? what about squamous cell CA of esophagus?

Back 177

1. Trimodality (chemoradiation + surgery) for adenocarcinoma. For SQCA, chemoradiation is probably just as good as surgery.

Front 178

What is the T stage for colon cancer

What is the N stage for colon cancer?

Back 178

T1=invade submucosa
T2=invade into MP
T3=invade through MP into subserosa
T4=invade other organ

N1=met in 1-3 regional node
N2=met to >4 regional node

Front 179

What is the current recommendation for colorectal screening with various test?

Back 179

1. FOBT or DNA Q year
2. Flex Q 5 year
3. DCBE Q5 years
4. CT colonography Q5 years
5. Colonoscopy 10 years

Front 180

1. How should patients who carries the FAP gene or indetermine with family hx of FAP be screened?

2. How about patient with family suspect of HNPCC

3. What is the chemoregimen for stage III colon cancer?

4. What are the 2 highest lifetime risk of extra-colonic cancer in HNPCC patients

Back 180

1. Q12 month flex. sig beginning at puberty

2. colonoscopy every 1-2 year starting age 20-25 or 10 years earlier than the youngest age of CRC

3.FOLFOX (5FU, leucovorin, oxaliplatin) or FOLFIRI (5FU, leucovorin and irinotecan)

4. Endometrial and ovarian

Front 181

1. 40-year-old man with a 3-month history of fatigue and pallor is found to be anemic and referred for colonoscopy. His procedure is significant for a cecal mass, and biopsies confirm adenocarcinoma. He reports no family history of colorectal cancer (CRC). He undergoes a right hemicolectomy and microsatellite testing is performed. His tumor is found to have microsatellite instabililty (MSI-H). This raises concern for Lynch syndrome (Hereditary Nonpolyposis Colorectal Cancer, HNPCC). The next step should be?

2. Once diagnosed with Lynch syndrome, how do you manage the patient's family?

3. What is the affected female's chance of developing endometrial CA? What about ovarian CA?

Back 181

1. Check for mis-match repair gene

2. Affected siblings should undergo a baseline colonoscopy in their 20s and then repeat colonoscopy every 1-2 years thereafter.

3. Women in these families have a 40-60% lifetime risk of developing endometrial cancer and a 10-12% lifetime risk of ovarian cancer.

Front 182

How does 5-ASA thought to be chemopreventive in UC?

Back 182

5-ASA is known to
1. inactivate reactive oxygen species,
2. increase apoptosis of epithelial cells,
3. activate PPAR-gamma ligand (thereby decreasing proliferation of epithelial cells),
4. interfere with COX activity,
5. decrease IL-2 production. IL-2 is known to stimulate clonal proliferation of T-cells and epithelial cells and may lead to carcinogenesi

Front 183

A first time screening colonoscopy in average risk asymptomatic men and women will result in polyp detection in what %? What % will have adenoma and advance adenoma?

Back 183

B. Polyps 30-50%; Adenomas 15-30%; Advanced Adenomas 5-10%

Front 184

1. What is the likelihood of met. for carcinoid of 1.5cm? What about >2cm?

2. What % of patient will have symptoms relief from carcinoid syndrome using octreotide?

3. What size is associated with post EMR stricture?

Back 184

1. 25% and if >2cm then 100%

2. 80-85%

3. >3cm and >3/4 of the esophageal lumen

Front 185

1. Which is at higher risk of stent occlusion without ASA + Plavix? bare metal or drug treated stent?

2. Which is better proprofol alone vs. proprofol + sedation?

3. Is bispectral index (BIS) useful in monitoring sedation?

4. Do patient with eosinophilic esophagitis have symptoms recurrence after stop of tx? How soon?

Back 185

1. bare metal

2. proprofol + sedation

3. No, study has been conflicting.

4. yes, 50% have recuurence of symptoms in 6-12 months

Front 186

What is the SONIC study? What did it show?

Back 186

n the SONIC study, moderate to severely active Crohn’s disease patients naïve to immune suppression were randomized to

azathioprine 2.5 mg/kg PO daily
infliximab 5 mg/kg IV loading (0, 2 and 6 weeks) and maintenance dosing (every 8 weeks)

azathioprine 2.5 mg/kg PO daily AND infliximab 5 mg/kg IV loading and maintenance infusions.

In this study, steroid free remission at 26 weeks was 30.6% with azathioprine alone, 44.4% with infliximab alone, and 56.8% with combination infliximab and azathioprine (p<0.001 compared to azathioprine and p=0.022 compared to infliximab). The adverse events were similar across both arms of this trial.

Front 187

Which surgical option will less affect fertility in female with UC?

Back 187

Subtotal colectomy with ileostomy and Hartman pouc

Front 188

Which 5 vaccines can't be given to patient on immunomodulators or anti-TNF?

Back 188

1. Measles, Mumps and Rubella (MMR),
2. Varicella,
3. Zoster,
4. BCG, and
5. Yellow fever

Front 189

1. Is Urso effective in preventing CRC in patient with cholestatic disease?

2. What is first line tx for pouchitits?

3. what % of patient will have reaction to 5-ASA product?

Back 189

1. Yes

2. Cipro not flagyl

3.Less than 10% of patients who start an aminosalicylate will develop problems with fever or increased diarrhea.

Front 190

1. Does IFX cross the placenta?

2. What is the treatment of choic in patient with diarrhea predominant IBS?

3. For patient with dyssynergic defecation as cause of idiopathic constipation. What is the treatment and how effective is it?

Back 190

1. Infliximab is an IgG1 antibody, which does not cross the placenta in the first trimester but does cross the placenta in the third trimester.

2. Aloestron

3. biofeedback 50-70% effective.

Front 191

What is the pathophysiology of hemochromoatosis?

Back 191

C282Y mutation have ineffective hepatic production of hepcidin. In turn, the decrease in hepcidin results in increased ferroportin-mediated transfer of iron at the basolateral surface of the enterocyte.

Front 192

1. What is Turcot syndrome?

2. What is the colorectal cancer risk for I1307K APC gene mutation?

3. What serological marker correlate with development of pouchitis in patient with UC?

4. What serological marker is associated with favorable respond to IFX in Crohn's patient.

Back 192

1. HNPCC + brain tumors (glioblastoma or astrocytoma) and adenomatous oligopolyposis

2. 20%

3. pANCA (high titer of pANCA is correlate with patient with pouchitis)

4. Negative pANCA is associated with favorable response to IFX in Crohns patient.

Front 193

1. Which marker correlate with more fibrostenotic Crohns disease?

2. Is there a decrease in fertility directly related to UC or CD?

3. How often is IBD diagnosed in the first degree relative of index patient?

4. How about the child of a patient with IBD?

5. Is "backwash" ileitis carry any prognostic factor?

Back 193

1. High level of ASCA but pANCA negative reflect more severe small bowel Crohn's

2. Not UC unless had surgery but

3. 10-25%

4. 3-7%

5. Yes, higher risk for dysplasia and ca

Front 194

1. What is the rate of closing fistula for CD patients using AZA/6MP?

2. What is the mean time to response of IFX? What is the % of clinical response and remission after 1 dose of IFX?

3. What is the fistulous healing rate for IFX?

4. What is the approximate risk for CA in patient with UC and found to have low grade dysplasia?

5. What is the clinical post operative recurrence rate in patient with small bowel Crohns?

Back 194

1. Non-cross over data showed 30% vs. 1%(placebo)

2. mean time to response is 7-9 days. 76% clinical response and 30% remission

3. 50%

4. 20%

5. 60% in 15 years.

Front 195

1. How to manage patient with hx of ICP during pregnancy?

2. Is NASH associated with higher cardiovascular risk?

3. Most important factor for perinatal transmission of HCV is?

Back 195

1. D. Monitor her laboratory tests and symptoms. When pruritus and/or abnormal liver tests occur, start urosodiol at 15 mg/kg body weight per day and plan delivery of the baby at 37 weeks if she does not develop jaundice.

2. yes

3. HIV

Front 196

Several medications are used in the treatment of obesity. Of the drugs approved by the FDA for treating obesity (orlistat, sibutramine, diethylpropion, phentermine, phendimetrazine, benzphetamine), which medication is not an anorexiant?

A. Sibutramine
B. Orlistat
C. Phentermine
D. Diethylpropion

Back 196

Orlistat

Front 197

What is the classification for obesity?

Back 197

Underweight – BMI < 18.5 kg/m2

Normal weight – BMI ≥ 18.5 – 24.9 kg/m2

Overweight – BMI ≥ 25.0 – 29.9 kg/m2

Class I Obesity – BMI = 30.0 – 34.9 kg/m2

Class II Obesity – BMI = 35.0 – 39.9 kg/m2

Class III Obesity – BMI ≥ 40.0 kg/m2

Front 198

1. Which two vitamin/trace element absorption is affected by achlorhydria?

2. How much % of pt with H. Pylori develop PUD vs. gastric CA/lymphoma?

Back 198

1. B12 and iron (can't convert ingested ferric to ferrous iron)

2. 15% PUD and 0.05% lymphoma/gastric CA

Front 199

1. Is colonoscopy indicated if gastric polyp is found?

2. What is the surviellence schedule for a gastric adenoma removed?

Back 199

1. Yes, as it often have colonic lesions.

2. 1 year, then Q3-5 years.

Front 200

1. Studies has shown that PPI improves which 3 clinical outcome?

2. Sucralfate is approve for use of what type of ulcer?

3. What is first line for stress ulcer prevention?

4. What is the resistance rate for flagyl, clarithromycin and amoxicillin in tx for H. Pylori?

Back 200

1. rebleeding, need for surgery and mortality

2. DU

3. H2 blocker.

4. Flagyl=37%, clarithromycin = 10% and amoxicillin = 2%

Front 201

1. Does NSAID affect ulcer healing and does it need to be stopped during treatment?

2. What are two demographic risk factor for NSAID gastritis/ulcer?

3. What is the toxic component of gluten that causes Celiac?

4. Which 4 region is Celiac prevalent?

Back 201

1. Yes, it does affect rapid healing but NO does not need to be stopped.

2. Older, female

3. Gliadin

4. Northern Europe, Northern Africa and India and Iran

Front 202

1. Which type of "worm" infection affects the pancreaticobiliary system?

2. What is the treatment ofr Strongyloides?

3. What are 4 most common primary cancer that can have small bowel mets?

Back 202

1. Ascaris.

2. Ivermectin or thiabendazole.

3. Melanoma>breast>lung>ovarian.

Front 203

1. IBS is estimated to affect what % of general population?

2. What are two dreaded complication from alosteron?

3. How do you give neostigamine for Ogilvies?

4. What are 3 Contraindication for neostigamine

Back 203

1. 15%

2. ischemic colitis and death

3. 2mg over 3 minutes.

4. Bradycardia, hx of asthma and renal failure.

Front 204

What is the histologic feature of solitary rectal ulcer syndrome? What other condition share similar pathology?

Back 204

thickened mucosal layer with distortion of the crypt architecture. The lamina propria is replaced with smooth muscle and collagen leading to hypertrophy and disorganization of the muscularis mucosa, an appearance that has been referred to as "fibromuscular obliteration"

Similary histology is seen in colitis cystica profunda.

Front 205

1. Having what surgery done at younger age appears to have protective effect for developing UC?

2. CRP is thought to be more useful in assessing CD vs. UC activity? Why?

3. What are 3 infectious cause of caseating granulomas other then CD?

4. What if you find non-caseating granulmoa?

5. What is the cummulative dose for MTX to avoid liver fibrosis?

Back 205

1. Appendectomy

2. CRP is more useful in assessment of CD activity as compared to UC. Thought to be transmural inflammation is needed to activate CRP.

3. Seen in Yersinia, chlamydia and fungal infection

4. TB

5. <3 grams.

Front 206

1. Has growth hormone being use to treat CD? is it effective?

2. How much % of patient does NOT respond to steroids?

3. How much % become steroid dependent?

4. Is budesonide recommended for maintenance of remission?

5. What is the increase risk of lymphoma using AZA/6MP? Source?

Back 206

1. yes, it is, but study is limited.

2. 20%

3. 1/3

4. No, due to high relapse rate.

5. Meta analysis (Kandiel 2005) showed 4 fold increase risk.