COLON

Question 1

Embryology of large bowel

Answer 1

Derives from midgut- up to 2/3 mid-transverse colon. Derives from hindgut up to proximal anus. Distal anus forms from ectoderm

Question 2

What marks the part of anus that formed from hindgut vs. ectoderm?

Answer 2

Dentate line

Question 3

Blood supply to large bowel

Answer 3

Follow embryologic origins: midgut (SMA), hindgut (IMA), distal anus (internal pudendal artery branches). Rectum: internal iliac artery via middle rectal and inferior rectal arteries

Question 4

Why do L and R sided colon cancers present so differently?

Answer 4

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.

Question 5

Normal flora of colon

Answer 5

Sterile at birth. Once colonized 99% anaerobic (mostly B fragilis) and 1% aerobic (mostly E coli)

Question 6

Difference between constipation and obstipation

Answer 6

Constipation you can pass flatus, obstipation you can’t

Question 7

What is the cause of postvagotomy diarrhea?

Answer 7

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.

Question 8

Treatment of C diff

Answer 8

Flagyl first line (PO, IV if can’ take PO). Second line is PO vancomycin

Question 9

Actinomycosis [Actinomyces Israelii)

Answer 9

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)

Question 10

Neutropenic colitis

Answer 10

Diffuse mucosal ulceration, invasive infection with enteric organisms, can lead to sepsis; In patients with ANC

Question 11

Radiation induced colitis

Answer 11

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.

Question 12

How to treat late radiation induced colitis?

Answer 12

Stool softener, topical 5-ASA, steroid enema. Dilation for strictures, colostomy + fistula repair

Question 13

What watershed part of bowel is most vulnerable to ischemic colitis?

Answer 13

Splenic flexure

Question 14

What is the most common clinical setting for ischemic colitis?

Answer 14

Classically, after AAA repair (impaired blood flow through the IMA)

Question 15

UC colon cancer risk

Answer 15

10% at 10 yrs, 2% per year thereafter

Question 16

Pathophys of diverticulitis

Answer 16

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

Question 17

Imaging of choice for diverticulitis

Answer 17

CT scan (don’t do colonoscopy or barium enema bc can cause perf, but do them in follow up)

Question 18

What are the most common causes of lower GI bleed (LGIB)?

Answer 18

Diverticulosis (brisk bleed) and angiodysplasia (slow bleed)

Question 19

What causes LGIB in angiodysplasia?

Answer 19

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

Question 20

Why does angiodysplasia occur more commonly in cecum/right colon?

Answer 20

LaPlace law: greater diameter of right colon = more wall tension

Question 21

Large bowel obstruction

Answer 21

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)

Question 22

Most common place for volvulus

Answer 22

Sigmoid colon (70%), cecum (30%)

Question 23

Management of cecal volvulus

Answer 23

Right hemicolectomy if vascular compromise. Cecopexy otherwise adequate

Question 24

Management of sigmoid volvulus

Answer 24

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.

Question 25

Histologic types of colonic polyps

Answer 25

Inflammatory (UC), lymphoid, hyperplastic (no malign potential), adenomatous (premalignant), hamartomatous (Peutz-Jeghers, juvenile polyps)

Question 26

Familial adenomatous polyposis

Answer 26

Autosomal dominant. 100% chance of colon cancer w/o colectomy (get it once polyps present).

Question 27

Gardner’s syndrome

Answer 27

Autosomal dominant. Innumerable polyps + osteomas, epidermal cysts, fibromatosis. 100% chance of colon cancer w/o colectomy

Question 28

Turcot’s syndrome

Answer 28

Autosomal recessive. Adenomatous colonic polyps + CNS tumors, esp gliomas

Question 29

Hereditary nonpolyposis colon cancer syndrome (HNPCC) aka Lynch syndrome

Answer 29

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

Question 30

Peutz-Jeghers syndrome

Answer 30

Autosomal dominant. Hamartomatous polyps + melanotic pigmentation of face/lips/palms. Increased risk of pancreatic, breast, lung, ovarian, uterine cancer

Question 31

CEA (carcioembryonic antigen)

Answer 31

CEA mainly used as a tumor marker to monitor CRC tx, to identify recurrences after surgical resection, for staging or to localize cancer spread through measurement of biological fluids. CEA levels may also be raised in gastric carcinoma, pancreatic carcinoma, lung carcinoma, breast carcinoma, and medullary thyroid carcinoma, as well as some non-neoplastic conditions like ulcerative colitis, pancreatitis, cirrhosis, COPD, Crohn’s disease, hypothyroidism as well as in smokers.

Question 32

Apple core filling defect

Answer 32

XRay sign for colon cancer

Question 33

Treatment of hemorrhoids

Answer 33

Depends on severity (from protrusion into lumen with no prolapse to prolapse that cannot be reduced). Nonresectional (only for nonsensate areas, aka above dentate line): band ligation, coagulation, sclerotherapy. Excision required for severe.

Question 34

Anal fissure treatment

Answer 34

Sitz baths, fiber supplement, more fluids. If this fails, can do lateral internal sphincterotomy or forceful anal dilation

Question 35

What is a seton?

Answer 35

Heavy suture loop through anal tract to keep it patent for drainage and stimulate fibrosis

Question 36

Paget’s disease of perianal skin

Answer 36

Adenocarcinoma in situ

Question 37

Bowen’s disease of perianal skin

Answer 37

Squamous carcinoma in situ

Question 38

Anal canal tumor types

Answer 38

SCC or transitional cell/cloacogenic carcinoma, or malignant melanoma (worst prognosis)

Question 39

Anal cancer treatment

Answer 39

Primary treatment is combo of chemo and radiation

Question 40

Rectal cancer

Answer 40

Responds to radiation therapy, whereas colon cancers do not. High risk of local recurrence at site of resection for rectal cancer

Question 41

What improves survival in stage III colon cancer?

Answer 41

Adjuvant chemo after surgery