Pathology of Large Intestine

acquired malformation of submucosal and mucosal blood vessels

often present with bright red bloos in stool

angiodysplasia

where does angiodysplasia most often occur

cecum or right colon usually after 6th decade of life

nonocclusive transient hypoperfusion, usually due to atherosclerosis in SMA or IMA

ischemic colitis

left sided abdominal pain, may result in fibrosis that can lead to stricture and obstruction

ischemic colitis

congential toxic megacolon

hirschsprung disease

congenital absence of parasympathetic ganglion cells in rectum ALWAYS and sigmoid colon often → impaired colorectal relaxation and peristalsis → obstruction

hirschsprung disease

usually sporadic but 10% have downs syndrime

familial cases with RET mutaitons

hirschsprung disease

blind pi=ouch leading of alimentary tract lined by mucosa that communicates with gut lumen

NOT a true diverticulum, aka tics

colonic diverticulum

most in sigmoid colon

lack muscularis propria, outpouching due to focal weakness and increased pressure

assoc with western diet

rare before 30

colonic diverticulitis

most common cause of lower GI bleeding

colonic diverticulosis

outpouchings in diverticulosis

can lead to infections and can also trap stool

no muscle to push it out

acute colitis with adherent inflammatory exudate overlying sites of mucosal injury

usually after what

pseudomembranous colitis

usually after BROAD SPEC ANTIBIOTICS

broad spec antibiotics favor what in gut

c diff overgrowth

yellow white or yellow green mucosal plaques or pseudomembranes

pseudomembranous colitis

tx for pseudomembranous colitis

metronidazole, vancomycin, fidamoxicin, fecal transplant

linear configurations of karyorrhectic debris and neutrophils that adheers to mucosal surface

micro of pseudomembranous colitis

two most common inflammatory bowel diseases

crohns disease and ulcerative colitis

abdominal pain and diarrhea which may be bloody, need to rule out infection and ischemia

IBD

more likely to be bloody in UC

smoking has been seen to double the risk of this

crohn disease

granulomatous colitis, GRANULOMAS KEY MICROSCOPIC FINDING

crohn disease

assoc with ankylosing spondylitis (HLA B27), migratory polyarthritis, erythema nodosum, anti saccharoymces cervisiae antibodies (ASCA)

crohn disease

most common site for crohn disease

terminal ileum

patchy transmural granulomatous inflammation affecting entire thickness of bowel wall

crohn disease

skip lesions - intervening normal areas between areas

crohn disease

right lower quadrant pain and non bloody diarrhea

malabsorption due to small bowel damage

calcium oxalate stones

increased risk of carcinoma

crohn disease

cobblestone of mucosa

strictures (String sign)

focal ulcers fissues and fistulas

thickened wall with loss of mucosal folds

creeping fat, related to fibrosis of wall

NONcaseating GRANULOMA with lymphocytes

crohn disease

multinucleated giant cell in crohn disease, granuloma

assoc with sclerosing cholangitis, positive p-ANCA

smoking protects, milk may exacerbate

ulcerative colitis

starts in rectum, doesn’t skip grows continually

left lower quadrant pain, bloody diarrhea

UC

pseuodpolyps- edematous intact mucosa next to areas of ulceration

UC

loss of haustra looks like what on imaging

lead pipe sign

UC

inflammation is not transmural, limited to mucosa and submucosa

muscularis and seroa normal

UC

toxic damage in UC may lead to what

toxic megacolon, dilation stasis and gangrene

increased risk of what in UC

carcinoma (depends on extent adn duration of disease)

what has a negative assoc with UC

appendectomies

raised red islands of inflamed mucosa. between them is only remaining muscularis

UC, pseudopolyps

micro of UC vs CD

crypt abcesses

UC

CD vs UC

CD: small bowel (terminal ileum) and right colon

patchy

transmural, fistulas, strictures, seositis

non caseating granuloma

poor resp to surg

increased risk for cancer

UC: colon only, begin at rectum

continous, not transmural

superficial inflammation

no granulomas

good resp to surg

increased risk for cancer

lead pipe sign, UC

string sign, CD

if there are fistulas in IBD then it is

crohn disease

if it involves the small intestin in IBD then it is

NOT UC

does not move oast ileocecal valve

chronic recurring and relapsing abdominal pain associated with defecation and changes in bowel habits

can be diarrhea dominant constipation dominant or mixed

rome IV diagnostic

IBS

mass that protrudes into gut lumen

polyps

pedunculated with stalk or sessile without stalk

non neoplastic not precancerous serrated (sawtooth) or star shaped appearance of crypt epithelim

hyperplastic polyps

neoplastic may become cancerous often have tubular (rounded) glands or villous (papillary projections) or serrated (sawtooth)

adenomatous polyps/adenomas

greatest risk for developing cancer (polyps)

sessile and villous

inhertied mutation in APC gene on chromosome 5.q21

atusomal dominant

thousands of polyps

100% risk for developing colon cancer by age 50

prophylactic colectomy

FAP familial polyposis syndrome, familial adeomatous polyposis

most common form of colonic polyp

hyperplastic polypf

delayed shedding of surface epithelial cells with gland hyperplasia

assoc with cigarette smoking

hyperplastic polyp

small, sessile, on top of mucosal folds, same color as surrounding

well formed elongated glands and crypts with saw tooth or star appearance

hyperplastic polyps

msot common form of neoplastic colonic polyp

adenoma

premalignant with areas of dysplasia

not all are polypoid

adenoma

which adenomas have highest rate of malignant transformation (histology)

villous histology

adneoma

benign hamartomatous polyp generally solitary and not premalignant

juvenile polyp

many juvenile polyps and increased risk of progression to adenomas and carcinomas

SMAD4 or BMPR1A mutations

most common childhood polyp

juvenile polyp

granulation tissue and ulcer covering abundant custically dilated flands filled with mucus with an edematous and inflamed stroma

juvenile polyp

STK11 mutation, median age 11

rare autosomal dominant syndrome

peutz jeghers syndrome

multiple GI hamartomatous polyps and mucocutaneous hyperpigmentation

throughout GI tract

dark blue to brown macules on lips nostrils buccal mucosa palmar surfaces of the hands genitalia and perianal region

similar to freckles but distinguished by presence in buccal mucosa

peutz jeghers syndrome

how ar peutz jeghers spots distinguished frmo freckles

presence in buccal mucosa, non sunexposed areas

peutz jeghers syndrome has marked increase risk for what

seveal malignanices

arises in colon or rectum

most commonly arises from adenomatous polyp

colorectal adenocarcinoma

autosomal dominatn inheritance, microsatellite instability

mutation of DNA mismatch repair genes leading to incorrect copying of microsatellites during cell division

HNPCC aka lynch syndrome

loss of what might enhance survival of genetically abnormal clones

BAX proapoptotic protein

lynch syndrome increased risk for

colorectal ovarian and endometrial cancer

most in RIGHT colon

more in left colon vs more in right colon

adenoma carcinoma sequence left

lynch syndrome right

asymptomatic,

right sided tumors

classically grow as raised lesion

fatigue, weakness, variable abdominal pain, occult blood in stool (melena), iron deficiency anemia

colonic adenocarcinoma

FAP or lynch plus brain tumors

turcot syndrome

napkin ring/apple core type lesions in ____ sided tumors

colonic adenocarcinoma left sided

change in stool habits, bloody stool, crampy pain, obstruction

where does colonic adenocarcinoma spread to the most

lymph nodes, liver

lungs bone

serum tumor marker for colonic adenocarcinoma

CEA carcinoembryonic antigen