I



February 1, 2001

ICM – 8AM

Dr. Trowers

Fathy/Robb

I020109.doc

Scribe for hire, James Morgan

COLONIC DISEASE

I. Anatomy

A. Begin with rectum ( sigmoid colon ( descending colon (left) ( splenic flexure (~60cm from anal verge) ( transverse colon ( hepatic flexure ( ascending colon (right)

B. Blood Supply

1. Inferior Mesenteric Artery (IMA) = supplies left colon ( mid transverse

2. Superior Mesenteric Artery (SMA) = supplies mid transverse ( right colon

3. Important when pt. has an embolus that has ischemic bowel disease w/bleeding to localize area needed for surgical removal

a. perform angiogram & see region of block

-if on the left side, then look for IMA blocking at its origination

C. Haustra

1. not actually permanent anatomic markings

a. represent sacculations of the transverse colon (not fixed)

b. help in production of segmental contraction

-retards flow of liquid stool (chyme)

-to and fro movement in Haustra enhance absorption of fluids/other substances

2. Diarrhea = essentially when Haustra are knocked out

a. so can’t absorb the needed liquid

b. has to come out somewhere

D. Anal/rectal sagittal section

1. Above pectinate line (dentate line)

a. has visceral innervation, blood supply, lymphatic drainage

1) get internal hemorrhoids here (not painful)

-can treat with banding (strangulate with a rubber band)

2) adenocarcinoma occurs here

2. Below pectinate line

a. has somatic innervation, blood supply, lymphatic drainage

1) so external hemorrhoids (very painful)

-cannot treat with banding b/c of the extreme pain it would cause

2) squamous cell carcinoma

3. Valves of Houston (semilunar, transverse folds in the rectum that support the weight of the feces)

a. if undergoing a flex-sig (flexible sigmoidoscopy) and perforate…

1) higher than middle rectal valve, then enter into the peritoneal area

-may get peritonitis

2) lower than middle valve, then much less chance of infection

b. so important to watch for if they had a perforation. (when on inpatient service)

4. Anal fissure (when pt. complains of a rectal discharge)

a. look for signs of a peri-rectal abscess

b. if left untreated can lead to more serious complications

-gave example that when he was in residency, one of the house officers treated her own peri-rectal abscess for about 1 month. She ended up in the hospital for 2 months and underwent extensive surgery b/c of septic complications

II. Physiology

A. After food consumption:

1. normally ~ 2hrs for meal to get to terminal ileum

2. chyme may take up to 3 days to go through colon (so 1-2 BM’s {bowel movement} every 1-3 days is normal)

-if 200gm (ml) of stool / 24 hrs

1. don’t usually have time to make this measurement

2. so ask if it wakes them up at night and how many times they go in one day

B. Fecal WBC count to determine if they have

1. enteroinvasive organism causing an ulcer

2. ulceration (other cause)

3. infection

C. Ova and parasite test

-very limited

-Hx of exposure / ( index of exposure

VI. Polyps

|Polyps |

|Neoplastic |Non-Neoplastic |

|Tubular Adenoma |Villous Adenoma |Tubulovilluous Adenoma|Hyperplastic |Inflammatory / |

| | | | |Hamartomatous |

| |(’st potential for |Most common polyp |Most common non-neoplastic | |

| |malignancy | | | |

| | | |< 0.05cm | |

|Polyps >1-2cm diameter + adenomatous component may develop into | | |

|carcinoma – important to remove them | | |

A. Pathology

1. pedunculated = has stalk and easy to remove

2. sessile = like gumdrop stuck to wall

B. Familial Hereditary Polyposis

1. >100 polyps (adenomatous)

2. will develop colon CA by age of 42 (often younger)

3. only proven Tx = total colectomy

4. NSAIDS may result in resorption/prevention of adenomas (but not enough info yet)

C. Other polyp info

1. pt. w/single polyp (adenomatous) has 20% chance of having 2nd polyp (synchronous)

2. pt. also have 7% chance of developing one in future (metachronous polyp)

VII. Colon Cancer

A. General Facts

1. 2nd most common cause of death secondary to malignancy (lung is 1st)

2. ~160,000 new cases/year

3. ~60,000 deaths

4. rare in people < 45 y/o (but he has seen it in 26 y/o female)

B. Speculated causes

1. Stasis and prolonged transit times by low residue diets

2. (fat/beef diets

3. bacterial toxins that can cause injury

4. carcinogens (ingested or from metabolic breakdown of bile acids and other stuff)

C. Clinical Presentation

1. R. sided lesion

a. Pres. Reagan during routine flex-sig found small polyps on L. colon (removed) – neglected to come for total colonoscopy

-came back 11 months later and found a grapefruit-sized mass in R. colon

b. not much Sx b/c stool that enters is mostly liquid still so could get by w/out problems

c. may have some pain, but not too bad

d. probably present with anemia

2. L. sided lesion

a. w/stenosis get obstructive Sx’s and pain

b. only thing that might get around it is liquid stool

-called Post-Obstructive Diarrhea secondary to L. sided obstructive colonic lesion

D. Diagnosis

1. DRE (the GI’s official handshake)

-again, can test fecal occult blood (if positive then should be really blue)

-but limited to length of your finger (ET would be a good GI guy)

2. Flex-sig or colonoscopy

a. main advantage is that if you find a polyp that seems like it could go to cancer, you can remove it immediately

b. studies on effects of flex-sig/polypectomy combination and chances of cancer

-25 year period in 18,000+ pt’s

-showed significant reduction in the adenoma-carcinoma sequence

E. (’d risk

1. adenomatous polyp > 1-2.5 cm

2. adenoma with villous component

F. Screening

1. 40 y/o = at least yearly DRE

2. 50 y/o = yearly DRE + fecal occult + flex-sig (every 3-5yrs)

3. some will say a BE, but colonoscopy is now more favored b/c can remove at that time

-esp. if beyond splenic flexure

G. Staging of Tumors and FYS (5-year survival rate)

1. Stage I = invasion up to and including muscularis propria (not beyond) = 80-90% FYS

2. Stage II = invasion through muscularis propria = 75% FYS

3. Stage III = invasion into deeper muscle + regional lymph node involvement = 30-50% FYS

4. Once Dx’d, take a CXR (chest x-ray) to check for metastases

-may also do a CT and check other organs (liver, spleen…)

H. More help on staging colorectal tumors

1. Endoscopic ultrasound

a. examine the gut wall and look at 5 levels

medial ( lateral = superficial mucosal layer ( deep mucosal layer ( submucosa ( muscularis propria (circular and longitudinal) ( pericolorectal fat

b. in males can see if prostate is involved

I. Treatment

1. If at least 5cm from anal ring to tumor, then can do resection without colostomy (85% time)

-if closer, then radical resection (only 15%) but will have total colostomy

2. Local disease = radiation therapy

3. Wide spread = chemotherapy

4. Treatment of choice = surgery coupled with the previous two as needed

5. Follow up (to check for recurrence)

-H&P to check for weight loss

-repeat colonoscopy and/or proximal flex-sig

-may see development outside of wall with ultrasound (lymph nodes)

VIII. Appendicitis

A. General

1. Most common cause of acute abdominal pain requiring surgery in U.S.

2. ~1/600 people will get appendicitis

3. initial pain in epigastric and periumbilical region is due to derivation of the appendix from midgut

IX. Ulcerative Colitis (Idiopathic Inflammatory Bowel Disease)

-most common chronic Inflammatory Bowel Disease (IBD) in the U.S.

A. UC characteristics (vs. Crohn’s)

1. primarily a mucosal disease (vs. Crohn’s = transmural)

2. not involved in small bowel (vs. Crohn’s = mouth ( anus)

3. crypt abscesses are fairly characteristic (but can be found in both)

B. Presentation

1. w/abdominal pain

2. cramping/diarrhea (may be bloody)

3. weight loss

C. Treatment

1. Sulfasalazine (initially)

2. may move to steroids

|Ulcerative Colitis (UC) |Crohn’s |

|Begins in rectum and extends proximally (only colon) |Inflammation anywhere along GI tract (mostly in the terminal ileum, and cecum) |

|Continuous involvement |Skip lesions (segmental involvement) |

|Mucosa / submucosa |Transmural involvement (leads to gross thickening of wall of gut) |

|Loose Bloody stools (almost always) |Not much any blood (if any) |

|Loss of Haustra b/c of scarring of mucosa |Cobblestone mucosa |

|Microabscesses and sometimes granulomas |Lymphoid infiltrates |

|Pyoderma gangrenosum |Non-caseating granulomas |

|Sclerosing cholangitis |Linear ulcers, fissures, fistulas |

|Greatly (’d risk of Colon Cancer (40x’s more than Crohn’s) |Migratory arthritis, erythema nodosum |

|Marked flare-ups of disease |Fairly constant |

X. Antibiotic Associated Colitis

A. ABX induced alteration of colonic bacteria

1. can lead to C. difficile overgrowth, cytopathic toxin formation and then pseudomembrane formation

a. 1st, stop the antibiotic

b. treat with Flagyl (metronidazole)

-non-nephrotoxic and cheap

c. if Flagyl doesn’t work, then Vancomycin

-but it is nephrotoxic and expensive

B. Vs. Antibiotic Induced Diarrhea

1. when take ABX for 1-2days

-causes shift in R. colon microflora

-( in production of SCFA (short chain fatty acids) – which enhance water transport in the gut

-has to go somewhere so ( diarrhea

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