Colon & Anus Flashcards
Most common site of diverticular, polyploidy, and neoplastic growth?
SIGMOID COLON
Main symptoms of colon problems?
Diarrhea
Blood (gross and occult)
Low abdominal pain
Hirschprung’s Disease
Major CONGENITAL malformations of the colon –> aka congenital aganglionic megacolon
Massive enlargement of the colon proximal to a segment of aganglionic tissue in the LOWER RECTUM
Meissner’s Plexus and Auerbach’s Plexus never form (failure of neural crest cell migration) –> lack of innervation PREVENTS SMOOTH MUSCLE IN THE REGION from relaxing –> NO PERISTALSIS –> can’t pass fecal matter
Accumulation of feces causes the innervated areas of the rest of the colon to DILATE MASSIVELY
M > F
ULCERATIVE COLITIS
Idiopathic inflammatory bowel disease; chronic, non-infectious problem affecting the RECTUM and COLON
ALWAYS STARTS IN RECTUM –> spreads up the colon, and in the most severe cases reaches the CECUM, but is always limited to the COLON
3 Stages –> ACUTE (hyperemic, friable, ulcerated, distal more affected)
CHRONIC (polyps, pseudo polyps, toxic megacolon (dilates, becomes thin walled, transmural inflammation) –> HIGH perforation risk
Histology of UC
Edema and inflammation can be seen in the MUCOSA and SUBMUCOSA –> MUSCULARIS NEVER AFFECTED**
Abscesses can invade crypts, form ulcerated lesions
PMNs visualized invading crypts during an acute episode of UC (Hallmark)
NO GRANULOMA FORMATION
After 8-10 years, DYSPLASIA often seen
Chronic increases risk for carcinoma
Some key differences between Crohn’s and UC
UC = COLON only Crohn's = ILEUM +/- colon, GI
UC = CONTINUOUS; Crohn’s = SKIP
UC = Wall normal or thin; Crohn’s = THICK, RIGID
UC = Superficial, mucosal ulcers Crohn's = MUCOSAL ULCERS DEEP
UC = no fissures or fistulas; Crohn’s = Fissures, fistulas, sinuses
UC = Intensely vascular; Crohn’s = Edematous
UC = mucosa and maybe submucosa inflamed; Crohn’s = TRANSMURAL
UC = no granulomas; Crohn’s = granulomas possible
Microscopic Colitis
Two types: Collagenous and Lymphocytic
Collagenous – submucosal layer of COLLAGEN present
Lymphocytic – mucosa looks normal in both cases; only microscopic changes present; lymphocytic invasion
MIDDLE AGED WOMEN
Watery Diarrhea
Infections in the colon
MUCH MORE COMMON HERE THAN IN THE SMALL INTESTINE
Shigella, Salmonella, Campylobacter
Syphillis, gonorrhea in the anal/rectal region
C DIFF –> white plaques found covering the ulcerations; easily removed; plaques contain PMN exudates with mucin and necrotic debris; microscopically described as vulcaniform
Diverticular Disease
Linked to a FIBER DEFICIENCY in the diet
Formations of small outpouchings of the distal (sigmoid) colon with thickening of the muscularis propria between the diverticula
LOW fiber diets reduce bulk of feces and INCREASE intraluminal pressure within the colon
Diverticuli can take long time to form –> 50% of those over 60 are affected
Not harmful on their own – obstruction can lead to stool entrapment and associated inflammation/perforation
Peritonitis can occur
Fistulas to the bladder can occur –> pneumouria (peeing air) can occur; colovesicular fistula
Can also form STENOSIS of the colon
Non-neoplastic polyps
Projections above the mucosa
JUVENILE - non-neoplastic growths that mirror NORMAL colon tissue; largely composed of EXCESSIVE LAMINA PROPRIA covered with normal epithelium
PEUTZ-JEGHER - normal tissue growths that can occur in the large/small intestine; tend to have complex GLANDULAR structures and muscle dispersed throughout the polyps; abnormal mixture of normal tissues
HYPERPLASTIC - serrated due to the super-papillomatous epithelial surfaces found in the upper portions of affected crypts; lengtheneing of epithelial tubules; most often in the descending colon
Neoplastic Polyps
Serrated Polyps – physically similar to the HYPERPLASTIC polyps; more common in the RIGHT colon –> demonstrate “serrations” (saw tooth) of the epithelium along the entire length of the crypt; so, if epithelium is serrated at the bottom of the crypt, it is this; serrated polyps demonstrate ARCHITECTURAL dysplasia
Adenomatous Polyps –> benign, pre-cancerous polyps of the glandular epithelium that demonstrate dysplasia and cellular atypia –> TUBULAR –> ALL adenomatous polyps demonstrate dysplasia
Polyposis Syndromes
Peutz-Jeghers Syndrome –> Onset before age 15, results in SKIN MACULES as well as BREAST, LUNG, THYROID, PANCREAS, GONADAL, and BLADDER CANCER
Juvenile Polyposis –> Linked to PULMONARY AVM, and onset under 5 y.o.
Cowden Syndrome –> Harmartomatous polyps (normal tissue) and benign skin, breast and thyroid tumors in people < 15 y.o.
ALL polyposis syndromes are associated with genetic mutations and early age of onset, EXCEPT Cronkite-Canada Syndrome - no mutations, > 50 y.o.
EACH CARRIES INCREASED RISK OF COLON CARCINOMA AND ADENOCARCINOMA
Familial Adenomatous Polyposis
Presents with 4 types of syndromes –> CLASSIC (retinal pigmented epithelium hypertrophy); ATTENUATED (4th decade); GARDNER (adenomatosis + skin cysts and fibrous desmoids); TURCOT (adenomatosis + CNS tumor)
Each has MULTIPLE (over 100) adenomatous polyps in the colon and is associated with alterations in the APC regulatory genes
ALL present in childhood (except attenuated) and have a UNIQUE SYSTEMIC SIGN (each described above)
Cancers of the Colon
Two types of polyps –> PEDUNCULATED and SESSILE –> irrelevant to staging, invasion of the submucosa or deeper matters more
3 main ways carcinomas arise in the colon –> Familial Adenomatous Polyposis; Hereditary nonpolyposis colorectal cancer (Lynch syndrome); Sporadic/de novo (MOST COMMON)
80% involve problems with the APC genes on chromosome 5
Over 75% of colon cancer metastasis ENDS UP IN LIVER; 15% ends up in the LUNG
Anal Carcinoma
Anus is composed of 3 different types of epithelial lining –> COLUMNAR epithelium (like the rectum) in the upper 3rd; Transitional epithelium in the middle 3rd, squamous epithelium in the lower third (continuous with skin)
Tumors arising from each region REFLECT THE EPITHELIAL LINING OF THAT REGION
