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103 Cards in this Set

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what is the main function of small bowel vs. large bowel?

small bowel: nutrients and water resorption


large bowel: water resorption

what part of duodenum is retroperitoneal? where is most the ulcer found

-90% ulcer found in bulb-> 1st portion


- 2nd and 3rd portion of duo are retroperitoneum. descending and transverse

what is the transition point of 3rd and 4th portion of duo

transition pt is at the acute angle between sma and aorta. SMA is anterior, aorta is posterior

how long is jejunum? ileum? where is maximum place for absorption? how to distinguish them by looking at them

-jejunum : 100 cm


- ielum : 150 cm


- maximum place for absorption is at jejunum except for B12, folate, conj bile acid at TI, non conj bile acid at ileum. iron: absorp in duo


- jejunum: long vasa recta, circular musle fold


- ileum: short vasa recta, flat

how much salt and water absorped in jejunum

- 95% NACL and 90% of water absorbed in jejunum

what enzymes are at the intestinal brush border

lactase, maltase, sucrase, limit dextrinase

what are the usual size of small bowel vs. transverse colon vs. cecum

3/6/9 cm

what is sma finally become

sma will become ileocolic artery

what are the cell types in small bowel? 5. its function

- absorption cells


- Goblet cells: secretes mucin


-Paneth cells: secretory granules, enzymes


- Enterochromaffi cells: APUD, 5 hydroxytryptamine release, carcinoid precursor


- M cells: antigen presenting cells in intestinal wall

what are the functions of brunners glands? peyers patch?where do you see increase in peyres patch?

-brunners gland- >make alkaline solution


-peyers patch= lymphoid tissue. increase in ileum

does small bowel has heme and Fe transporter

yes have both heme and Fe transporter

what are the phases of migrating motor complex

4 phase


- phase 1: rest


- phase 2: acceleration and gb contraction


-phase 3: peristalsis


- phase 4: deceleration

what phase does motilin act on

motilin acts on phase 3. peristalsis. most important hormine in migrating motor complex

how much bile salts are absorped? where are conj vs. non conj form absorp? why gallstones form after TI resect

- 95% bile salts absorped


- 50% active absorption: conj bile acids at TI via Na /K ATPase. conj bile acid only absorbed at TI.


- 50% passive absorption: non conj bile acids: 45% at ileum, 5% at colon


- after TI resect, decreased conj bile acids absorped-> increase cholesterol-> gallstones form.

how to diagnose short gut syndrome? diagnostic test? how much small bowel you need at least? treatment?

-diagnose of short gut syndrome is based on symptoms, not length of bowel.


- symptoms: steatorrhea, malnutrition, weight loss. lose fat, B12, electrolytes, water.


- diagnostic test: sudan red stain-> see fat + in stool, schilling test->check for B12 absorption (radiolabeled B12 in urine)


- needs at least 75 cm small bowel, or 50 cm small bowel with competent ileocecal valve


- treatment: PPI, restrict fat, lomotil

what are 4 causes of steatorrhea? what are the effects from steatorrhea

- short gut syndrome


-pancreatitis causing decreased pancreatic enzymes


- increase gastric secretions, decrease pH-> increase intestinal motility and interfere with fat absorption


- interfere with bile acid absorption from ileum resection-> cant absorb fat


-steatorrhea-> causing malabsorption especially fat soluble vitamin and essential fatty acids.

what are the causes of fistula? what portion of small bowel most likely have high output fistula?proximal fistula: more likelihood to close or less?

FRIENDSS


- foreign body, radiation, inflammatory bowel disease, epithelialization,, neoplastic, distal obstruction, sepsis/infection, steroids


-high ouput fistula most likely at proximal small bowel. -duodenum r proximal jejunum.


-proximal fistula= more high output- >less likely to close with conservative management

colonic vs. small bowel fistula: what is most likely to close

-colonic fistula more likely to close.

what is the most common cause of small bowel vs. large bowel obstruction in pts with previous sx vs. no hx of sx

- LBO: mc cause is cancer in both hx sx or non sx pts


- SBO: hx of sx-> adhesions is mcc. no hx of sx: hernia is mcc.

what type of bowel obstruction that you might not see distension and can still have obstibpation?

in open loop proximal small bowel obstruction or close loop small bowel obstruction. often absent distention and may still have obstitation

why you see air level in sbo?

from swallow nitrogen

should you aggressively fluid resus pts with sbo>

can have third spacing into bowel lumen-> need aggressive fludi resus

how many % of psbo vs. c sbo will response to just conservative management

- 80% psbo will resolve vs. 40% c sbo will resolve.

what is the rule of 2 in Meckel diverticulum? what cause it? is it a true diverticulum? what is the most common type of tissue found it in? how to dx? what can it cause? what if find it incidental?when to resect vs. diverticulectomy

- Meckel: in 2 yo , 2inches long, 2 feet from ilealcecal valve, 2% of population, 2 types: gastric vs. pancreatic


- cause by failure of obliterate omphalomesenteric duct. it is a true diverticulum


- MC type of tissue is pancreatic tissue-> can cause diverticulitis. MC type of tissue in symptomatic pts is gastric type-> bleeding


-dx with Meckel scan


-can cause diverticulitis, bleeding. in adult cause obstruction


- if finding incidental, leave alone unless symptoms, or suspect have gastric tissue -> feel thickened diverticulum or has a narrow neck


- resect if has gastric tissue.


-diverticulectomy if small and not complicated diverticulitis, bleeding. Segmental resection if complicated diverticulitis such as perforation, neck >1/3 small bowel lumen, diverticulitis involve the base

in GI bleed of kids < 2yo, think

50% of painless lower GI bleeds in kids <2y is meckel divert.

what do you need to rule out when find duo diverticula? where in small bowel find diverticula frequent?treatment? what if diverticula is juxta-ampullary

- need to rule out gb -duo fistula in duo diverticula


- frequency of small bowel diverticulum : duodenum>jejunum>ileum


- treat: leaves alone if asymptomatic: pain, perf, bleeding, obstruction. if symptomatic resect


- if juxta ampullary: ercp with stent if pancreatitis, choledochoJejunostomy if cholangitis/biliary obstruction

what is the age of first presentation in Crohn? increased frequency in what population? what are the extraintestinal manifestation of Crohn? where can it occur in GI tract? what is the MC involved bowel part?

- First presentation of Crohn: 15-35 yo


- increased population in Ashkenazi Jews


- extraintestinal manifestation of Crohn: rheumatoid arthritis, arthralgias, pyoderma gangrenosum, ocular disease, growth failure, megaloblastic failure from folate and vit B12 malabsorption


- occur from mouth to anus, spare rectum


- MC involved bowel part is TI

what is the mc sites for initial presentation for Crohn? dx with? what does path shows?

at initial presentation


- TI and cecum only: 40%


- colon only 35%


- small bowel only 20%


- perianal/anal: 5%. MC findings are large skin tag-> do not resect


- dx with colonoscopy with bx


- path : transmural inflammation (vs UC: mucosal involvement only), skip lesions (segmental lesions), cobblestoning, creeping fat , narrow deep ulcers

what is the treatment for Crohn? is it a curable disease? how much % will need sx? recur rate after sx

- it is not a curable disease like UC. no agents affect the natural course of disease


- maintenance therapy: sulfalazine and loperamide , steroids for acute flair.


- infliximab = remicade: tnf alpha inhibitor: in steroid refractory, fistula.


-flagyl: for fistula/perianal disease


-cipro/flagyl in toxic megacolon/colitis


- 90% will eventually need surgery. 50% recur rate after sx

how to treat complications related to Crohns: obstruction? abscess? toxic megacolon/colitis? hemorrhage? blind loop obstruction? fissures? ec fistula? perineal fistula? anorectovagina fistula? when resect crohn disease, do you need margins?diffuse disease of colon in crohn?

- obstruction: medical management usually will work


- abscess: drainage


- toxic megacolon/colitis: medical management, sx if refractory


- hemorrhage: unusual but can happen. sx if refractory


- blind loop obstruction: sx


-fissures: NO lateral internal sphincteroplasty.


-EC fistula: conservaive


-perineal fistula: r/o abscess, use seton, let heal on its own


-anorectovaginal fistuna: may need rectal advancement flap, possible colostomy


- dont need margin in resection of crohn, 2 cm gross negative


- diffuse disease of colon in crohn: proctocolectomy and ileostomy. no pouch or ilio anal anastomosis in crohn.

what if incidiental finding of crohn in ppl think acute appy

appendectomy if cecum healthy

when to do stricturoplasty in crohn and what type of stricturoplasty should you do ? contraindications for stricturoplasty? what is the complications % in stricturoplasty?

- if single segment-> prefer resection.


- contraindications for stricturoplasty: malnutrion, perforation, malignancy, fistula, inflammation.


-short stricture <10 cm: Heinke Mikulicz: longitudinal incision , close transversely


- medium stricture 10-20 cm: Fenney


- long >20 cm: Michelassi: side to side isoperistalsis stricturoplasty


- 10% leakage/abscess/fistula rate with stricturoplasty.

does crohn increase risk for colon cancer like UC?

crohn causing pancolitis, increase Colon CA risk same as UC

what are the complications of removing TI?

- folate, B12 deficiency-> megaloblastic anemia


- bile salts absorption failure-> gallstones, steatorrhea, deficiency in fat soluble vitamins, essential fatty acids.


-decrease oxalate bidnign to calcium secondary to increase intraluminal fat in intestine bc fat binds calcium-> increase oxalate absorption in colon-> secrets in urine-> increase Caoxalate stones in kidney

bowel carcinoid: secrete by what cells? test to dx?

-serotonin secretes by Kulchitsky cells (enterochromaffin cells/argentaffin cells).


- part of the amine precursor uptake decarboxylase system APUD


- see 5HIAA in urine- break down product of serotonin


chrombogranin A level is the highest sensitivity test to detect carcinoid tumor


-octerotide scan is best test to localize tumor

what is carcinoid syndrome? when will you see this? causes by what factor? where do you find most common



- carcinoid syndrome: when have bulky liver metastasis: intermittent flushing (caused by kallikrein), diarrhea (serotonin), asthma like symptoms - bradykinin, R heart valve lesions


- most common in appendix (50%), then ileum, then rectum

when have carcinoid syndrome with primary small bowel carcinoid tumor, what does this mean?

mean there is liver metastasis


- liver usually clear serotonin

if resect liver mets in bowel carcinoid, what else should you do?

also should get cholecystectomy in case will give octreotide post op for alleviate symptoms 2/2 mets and also for future embolization .

what is best test to localized carcinoid tumor? best test?

octreotide scan: best test to localize carcinoid tumor


- chromogranin A level: highest sensitivity for detecting a carcinoid tumor

what are pts with small bowel carcinoid at increase risk for?

pts with small bowel carcinoid tumor at increase risk for multiple primaries and second unrelated malignancies

what to do if find carcinoid tumor with appendectomy?

- appendectomy if carcinoid tumor <2cm -> appy is enough. If >2cm or involve base-> R hemi

what are the chemo for unresectable carcinoid tumor? meds to alleviate symptoms? treat bradykinin effect? kallikrein effect?

-streptozosin and 5FU are chemo for nonresectable disease


- give octreotide to alleviate carcinoid syndrome symptoms




- bradykinin-> bronchospasm-> give albuterol


-kallikrein effect-> flushing-> give alpha blockers: phenothiazine



what can cause falsely elevate 5HIAA

fruit

what are the type of benign small bowel tumors?

- adenoma


- hamartomas

what to do with small bowel adenomas? where mostly found

- need to resect if identify, can cause obstruct, bleed. can try resect with egd


-mostly found in duodenum

what genetic disorder related to GI hamartomas? is it dominant vs. recessive? what are other clinical findings related to this genetic disorder? this disorder have increase risk of what type of cancer?ppx sX?

-Peutz-Jegher syndrome: AD: see hamartoma throughout GI tract including small and large bowel, mucocutaneous melanotic skin pigmentation, pts with increase risk of extraintestinal malignancies- most common is breast cancer, and small risk of GI cancer


- dont need ppx colectomy

is malignant small bowel tumor common vs. rare? what are the types? location of small bowel most common with these cancer?


what is the most common type of small bowel malginant tumor

-rare


- adenocarcinoma: MC at duodenum


-leiomyosarcoma: MC jejunum and ielum


-lymphoma : MC at ileum




-MC SB malignant tumor is adenocarcinoma.

small bowel adenocarcinoma: where to find mostly? symptoms? RF? treatment?

- mostly in duo


- symptoms: bleed, obstruction. if at ampulla: jaundice


-RF: FAP, gardner, polyps, adneoma, von reckinhausen


- treat: resection + lymphadenectomy, whipple if duo 2nd portion

small bowel leiomyosarcoma: where to find mostly? what do you need to r/o ? treat?

- mc at jejunum, ileum


-need to ro gist-> ckit test


- treat: resect, no need lymphadenectomy

sb lymphoma: mc location? mc type? what population with sb lymphoma that at higher risk of bleed/perf? treat? prognosis

-most common at ileum


-mc type is NHL B type


- in pts with post transplantation: increase risk perf/bleed


- treat: wide en block resect inclduing nodes with lymphadenectomy. unless if 2nd portion duo-> chemo=xrt, no whipple


- prognosis 5 yr: 40% survival rate

do you usually repair parastoma hernia? risk increase with colostomy vs. ileostomy

- usually dont need to repair parastoma hernia. generally well tolerated


-higher risks with colostomy

what is the most common pathogen cause stoma infection? what is the most common cause of pouchitis (hartman pouch)? what is the mc cause of stoma stenosis-treatment?

- mc pathogen causing stoma infection is candida


- mcc pouchitis is bc lack of short chain fatty acids-> treat with short chain fatty acid enema


- mcc stoma stenosis is from ischemia. can treat with dilatation first.

what is the most common cause of fistula near stoma site?

- cause of fistula near stoma site-> worry about crohn

what is the most common cause of abscess underneath stoma site?

due to irrigation

what kind of stones that pts with ileostomy at risk for ?

gallstones from decreased bile acid absorption


and uric acid kidney stone due to loss of HCO3-

what is the first vs. second vs. third symptoms in appendicitis? what are the common symptoms in kids? elder?

-first symptoms is anorexia


-2nd: periumbilical pain


3-> vomitting


- in kids: most common symptoms are high fever, diarrhea, vomitting


-elder: minimal symptoms

appendicitis: if give rectal contrast, do you see contrast in lumen vs. lack of contrast if + inflammation

wont see contrast in appendiceal lumen if + appendicitis

what is most common point of perforation in appendicitis? why old pts and kids usually present with perforations? do infants have appendicitis?

- mc site of perforation of appendicitis is midpoint, antimesenteric border


- old pts have minimal symptoms, in kids usually have high fever/diarrhea/vomit-> delay in diagnosis


-infants rarely get appendicitis

what is the mc cause of appendicitis in adults vs. children? what is the process of developing appendicitis?

-adult: appendicolith


- children: viral illness causing lymphoid hyperplasia


-start with luminal obstruction- distension of appendix-> venous congestion-> thrombosis-> ischemia-> gangreneous necrosis-> rupture

what trimester usually have appendicitis? what is the most common cause of abdominal pain in pregnant pt in 1st trimester?when most likely to perforate in pregnant? what is fetal mortality rate with rupture

- abd pain in 1st trimester: mcc is appendicitis


- appendicitis: usually occur in 2nd trimester


-more likely to perforate in 3rd trimester- > bc confused with contractions


-fetal mortality rate 35% with rupture

if women child bearing age with suspected appendicitis, what other w/u need to be done

beta hcg and pelvic us

is appendix mucocele benign or malignant? treatment? what if rupture? mc of death in malignant appendix mucocele

-can be benign or malignant (signet ring cells)


- need to do open appendectomy to prevent spillage


- rupture-> can cause pseudomyxoma peritonei


- mc of death is sbo from peritoneal tumor spread

presumed appendicitis but find ruptured ovarian cyst, throbosed ovarian vein or regional enteritis not involve cecum, proceed with appendectomy?

proceed with appendectomy

what cause typhoid enteritis? seen in what population?symptoms? treat?

- cause by samonella


- seen in children


-symptoms: RLQ, diarrhea, fever, headache, maculopapular rash, leukopenia, rare bleeding/perforation


- will see large mesenteric lymph nodes


-treat with bactrim.

what is the lugano staging for NHL of GI tract

there is no stage 3


-stage 1E1: mucosa or submucosa


1E2: muscularis propria or serosa


2e1: local nodes, paragastric, para intestinal nodes


2e2: distant nodes, para-aortic nodes, mesenteric nodes


4: disseminated extranodal involvement of cocomitant supra diaphragmatic nodal involvement


Ex: ileum NHL s/p resect now with mediastinal node + -> stage 4

what cells make CCK

I cells of duo and jejunum makes CCK

is complete sbo considered a simple sbo

yes. simple sbo can be partial or complete as long as there is no compromising intestinal blood flow.

is small bowel lymphoma associate with celiac disease? what is the most common type- B cell or T cell? most common location in small bowel

- small bowel lymphoma associate with celiac disease


- most are B cell


most common lymphoma at ileum

Lymphoma associate with H pylori: is it B cell or T cell

B cell mucosa associated lymphoid tissue lymphoma associate with H pylori

what is the mst common benign tumor of small intestine

adenomas.

what is the most common cause of intussusception in a 2 yo child: meckel diverticulum vs. lymphod hyperplasia? treatment?

lymphoid hyperplasia--> viral--> thats why you can reduce with hydrostatic or pneumatic enema multiple times and dont need to resect.


PREFER PNEUMATIC (AIR) reduction first. easier and quicker, less radiation and less perforation rate.

where in small bowel does most absorption of protein occur


a> mostly duo


b> duo + jejunum


c> mostly jejunum


d> jejunum + ileum


e> mostly ileum

mostly jejunum - 90% done here


duodenum and stomach is where protein breakdown but absorption mostly at jejunum

when should you do diverticulectomy when found meckel in a lap appy case

if narrow base: <2cm base


if broad base >2cm-> do segmental resection

what is the most appropriate test to differentiate sbo from post op ileus: xr or ct?

CT is the most sensitive test.

pts with mtp abd sx in past with 200 cm small bowel left, has a small 5 cm stricture: should you do limited resection or stricturoplasty Heineke Mikulics

do heineke mikilicz in pts with a single short area of stricture in jejunum or ileum with prior small bowel resection to preserve length.


-if have acute inflammation/phlegmon-> then resect. or if pts with no prior sx-> then can do resect.

what is the most common indication for ercp: choledocho or ascending cholangitis

choledocho

what cause blind loop syndrome? symptoms

-bacterial overgrowth


-symptoms causing steattorhea, fatigue, weakness, b12 deficiency, anemia

what is the most common cause of idiopathic (no pathological lead point) intussusception in kids? a> rotavirus vaccines b> soy milk based formua c>hypertrophied peyer patches d> adenovirus infection e> rotavirus infection

hypertrophied peyer patch

treatment of small bowel lymphma

B cell : usually Non hodkin b cell-> resect including nodes, if 1st/2nd duo-> chemoxrd.


- if T cell-> chemotherapy. sx only reserve for palliation/obstruction. poor prognosis.

pt with crohn at risk for cancer of


a> adenocarcinoma of duo


b> adenocarcinoma of ileum


c> leiomyosarcoma of jejunum


d lymphoma of duo


e> lymphoma of ileum

--> adenocarcinoma of ileum. 10 fold higher risk of small bwel adenocarcinoma in crohn, majority arise in ileum.

what is most common presented symptoms of small intestinal carcinoid tumor?


ulceration


bleeding


abd pain


ischemia


intussusception

abdominal pain


ulceration is rare in carcinoid-> bleeding is rare

whats the difference in attenuated familal adenomatous polyposis syndrome

a variant of FAP


present later in life with fewer polyps, 10-100 usually at R colon

is reglan helps with ileus? does ng helps ileus

no


- early ambulation/ng dont improve ileus

what is prognosis for small bowel lymphoma?

40% at 5 yrs. if T cell even worse

baby with gastrochisis s/p bowel resection has 75 cm bowel left with competent ileal cecal valve. should you start tpn post op right away or keep npo wait for robf?

give tpn right away while waiting for bowel function returns. babies will take a long way to have bowel function return. can just wean off tpn later when start advancing more po

features suggestive of crohn more than UC


a> submucosa firbosis


b> transmural sparing


c> cryptitis


d> mucosal edema


e> neutrophilic infiltration of crypts of lieberkuhn

-> submucosa fibrosis. UC only affect mucosa, crohn is transmural.


-cryptitis/neutrophilic infiltration of cyrpt lieberkuhn-> UC



what are the most common 3 place of gist?

stomach-> small intestine-> rectum

NHL: where most common 3 locations in gi tract

stomach-> small bowel-> colon

carcinoid : where most common 3 locations in gi tract

appendix-> small bowel-> rectum

obliterative arteritis from radiation colitis happen when

part of chronic radiation injury. mostly 6-12 mths following radiation.

sma emboli: what pattern bowel ischemia you see

stomach and duo sparing and distal colon sparing

pts with sma emboli on ct, or exlap with patchy segmental small bowel ischemia along the jejunum and distal ielum with dusky coloration of ascending colon to mid transverse colon. whats best next step


a>resect the compromised bowel


b> palpate sma


c> doppler celiac artery


d> prepare the ilac artery for retrograde bypass

- B. palpate first. then can do fogarty . if not work and do bypass. then can reassess bowel after revascularize to see what needs to resect

what can cause ileus in this medications: beta blockers, alpha adrenergic agonist? histamine?

alpha agonist can cause ileus


antihistamine->ileus

treatment of small bowel hemangioma

rare, treat with egd or angioembo. if fail then resection

ercp: which scope use side view or one view? pt position? where is ampula vater? cbd orifice? pancreatic duct orifice?

-initial l lateral decub then after scope is in place in second portion of duo-> rotate patient to prone


- use a side viewing endoscope.


- ampulla of vater should be 12-1 o clock


- cbd orifice usually found at 11 o clock in ampulla


pancreatic duct orifice usually at 1 o clock of the ampulla.

ec fistula : when should you npo/tpn vs. keep regular diet

if low output <200 -> regular diet


if >200-> TPN

mc rf for gastric adenocarcinoma: smoking? processed meat? h pylori

h pylori

gist: should you resect with 2 cm margin or just grossly negative margin

can just resect with grossly negative margin

after bilroth 1, becomes diaphorectic, weak, light headed and tachy 30 min after ingestion of meals. is this early or late dumping syndrome

this is early dumping


-late dumping: see hypoglycemia!! 2-3 hrs after meal.

how does chronic afferent limb obstruction in bilroth 2 can cause megaloblastic anemia

- stsis-> bacterial overgrowht-> bind to deconjugated bile acid and vit bwe-> megalobastic anemia, fat absorption deficiency.

pain 2-3 hrs after eating: is it duo ulcer or gastric ulcer?

duo lulcer!. mc cause by H pylori

proximal tumor in gastric cardia: can you do subtotal or total gastrectomy? when to do neoadj chemo

need total gastrectomy. need 5 cm margins. at least 15 nodes


- neoadh chemo for T2 and above

what is mc cause of esopha perf when undergo egd for achalasia

at distal esophagus!!!!