Flashcards in COLON Deck (41)
Embryology of large bowel
Derives from midgut- up to 2/3 mid-transverse colon. Derives from hindgut up to proximal anus. Distal anus forms from ectoderm
What marks the part of anus that formed from hindgut vs. ectoderm?
Blood supply to large bowel
Follow embryologic origins: midgut (SMA), hindgut (IMA), distal anus (internal pudendal artery branches). Rectum: internal iliac artery via middle rectal and inferior rectal arteries
Why do L and R sided colon cancers present so differently?
Colon progressively narrows distally, so L sided more likely to present with change in bowel habits/obstruction/hematochezia; R sided more likely to present indolently with anemia/fatigue/melena.
Normal flora of colon
Sterile at birth. Once colonized 99% anaerobic (mostly B fragilis) and 1% aerobic (mostly E coli)
Difference between constipation and obstipation
Constipation you can pass flatus, obstipation you can't
What is the cause of postvagotomy diarrhea?
After a truncal vagotomy, denervation of extrahepatic biliary tree -> rapid transit of uncon bile salts into colon, impeding water absorption -> diarrhea. Tx: cholestyramine. If that fails, surgical reversal of small intestine to prolong transit time.
Treatment of C diff
Flagyl first line (PO, IV if can' take PO). Second line is PO vancomycin
Actinomycosis [Actinomyces Israelii)
Infection of the GI tract (usu the ileocecal region) with A. israelii, classically after appendectomy. Presents with weight loss, night sweats, draining fistulae, abdominal mass. Dx: "sunburst" pattern of sulfur granules of pathology, culture. Tx: drainage + abx (tetracycline or penicillin)
Diffuse mucosal ulceration, invasive infection with enteric organisms, can lead to sepsis; In patients with ANC
Radiation induced colitis
Dose dependent. Early (during course of XRT) = N/V, cramps, diarrhea, mucosal edema/ulceration. Late (weeks to up to 20 yrs later) = tenesmus, bleeding, abscess, fistula involving rectum, increased frequency of BMs.
How to treat late radiation induced colitis?
Stool softener, topical 5-ASA, steroid enema. Dilation for strictures, colostomy + fistula repair
What watershed part of bowel is most vulnerable to ischemic colitis?
What is the most common clinical setting for ischemic colitis?
Classically, after AAA repair (impaired blood flow through the IMA)
UC colon cancer risk
10% at 10 yrs, 2% per year thereafter
Pathophys of diverticulitis
Inflammation caused by (usu tiny) perforationi of the diverticulum secondary to increased pressure or osbtruction by inspissated feces -> feces extravasate onto serosal surface but infection usu well contained in immunocompetent patient
Imaging of choice for diverticulitis
CT scan (don't do colonoscopy or barium enema bc can cause perf, but do them in follow up)
What are the most common causes of lower GI bleed (LGIB)?
Diverticulosis (brisk bleed) and angiodysplasia (slow bleed)
What causes LGIB in angiodysplasia?
Chronic intermittent obstructiton of submucosal veins 2/2 repeated muscular contractions -> dilated venules and dilation of the venules and arteriolar capillary units feeding them -> AV communication
Why does angiodysplasia occur more commonly in cecum/right colon?
LaPlace law: greater diameter of right colon = more wall tension
Large bowel obstruction
Less common than SBO. Make sure it is a complete obstruction (not passing any gas or stool for 8-12 hrs), since partial obstruction does not require surgery, while complete large bowel obstruction is a surgical emergency (since NGT will not decompress in this case)
Most common place for volvulus
Sigmoid colon (70%), cecum (30%)
Management of cecal volvulus
Right hemicolectomy if vascular compromise. Cecopexy otherwise adequate
Management of sigmoid volvulus
Firs try to decompress with sigmoidoscopy. [Once resolved, will want to do elective resection to prevent high risk of recurrence]. If this fails, or if strangulation/perf present -> emergent laparotomy.
Histologic types of colonic polyps
Inflammatory (UC), lymphoid, hyperplastic (no malign potential), adenomatous (premalignant), hamartomatous (Peutz-Jeghers, juvenile polyps)
Familial adenomatous polyposis
Autosomal dominant. 100% chance of colon cancer w/o colectomy (get it once polyps present).
Autosomal dominant. Innumerable polyps + osteomas, epidermal cysts, fibromatosis. 100% chance of colon cancer w/o colectomy
Autosomal recessive. Adenomatous colonic polyps + CNS tumors, esp gliomas
Hereditary nonpolyposis colon cancer syndrome (HNPCC) aka Lynch syndrome
Autosomal dominant. Lynch syndrome I: pts w/o multiple polyps who devel R sided colon cancer. Lynch syndrome II: same as I plus risk of extracolonic adenocarcinomas of uterus, ovary, cervix, breast