large intestina Flashcards
what is the tumor marker to measure response to treatment of colonic adenocarcinoma
CEA
acquired malformation of mucosal/submucosal capillary beds leading to increase risk of rupture and hematochezia.
angiodysplasia (most common at cecum and right colon due to high wall tension/stress)
(morphological: tortuous blood vessels)
what population is ischemic bowel disease common
women > 70 with heart/ vascular disease
what is necrotizing enterocolitis
acute disorder leading to transmural necrosis
- most common acquired GI emergency in neonates
- at risk if premature
characteristic inflammation and gross appearance of UC vs Crohns
UC: pseudopolyps, and loss of hausfrau = “lead pip sign”
-crypt abscesses with neutrophils
Crohns: cobblestone mucosa, creeping fat, strictures (“string sign”)
-noncaseasting granulomas *TH1
most common neoplastic polyps
colonic adenomas
adenomatous polyps
genes associated with Crohns
NOD2 (increased NFKB)
ATG16L1
IRGM
details of juvenile polyps
- age: <5 yo
- location: rectum
- sporadic= solitary; no dysplasia
- congenital = multiple; dysplastic; risk of GI adenocarcinoma
- characteriscically CYSTIC
- gene: SMAD4 (TGFb signaling)
- polyps can bleed
chronic colitis associated with dense collagenous layer, increased intraepithelial lymphocytes (assoc with celiac and AI dz) , and mixed inflammatory infiltrate seen in older women and sx of chronic watery diarrhea
micropscopic colitis (NL on radiograph and endoscopy)
non classic AR FAP (adenomatous polyp)
not APC mutation, it is MYH mutation and the onset is 30-50 yo not 10-15
details of Gardner syndrome (adenomatous polyp)
***classic FAP, osteomas, and fibromatosis
(OFF)
(osteomas, thyroid/desmoid tumors, skin cysts)
two types of hamartomous polyps (occur spontaneously via genetics or acquired)
juvenile and Peutz Jehgers syndrome
most common cause of ischemic colitis and other causes. include sx
MCC: SMA atherosclerosis leading to infarct at watershed areas (splenic flexure)
other: AAA, OC, heart emboli, decreases BP, hypercoagability, CMV, radiation
ischemia sx: post prandial pain, weight loss,
infarction sx: ab pain, blood diarrhea
2 phases: hypo injury and repurfusion injury (RI = most damage)
chronic colitis from surgical treatment and current stony use and associated hallmark NUMEROUS MUCOSAL LYMPH FOLLICLES
diversion colitis
-colitis forms in diverted segment; common in UC
outpouching of mucosa/submucosa though muscularis propria layer due to increased intraluminal pressure usually at weak points where vasa recta transverse the MP layer (Sigmoid colon)
diverticulosis
sx of UC vs Crohns
UC: LLQ pain, bloody diarrhea, *no malabsorption , and associated with p ANCA and primary sclerosing cholangitis and TOXIC MEGACOLON
crohns: RLQ pain, non bloody diarrhea, fat malabsorption and steatorheea, calcium oxalate kidney stones, and fistulas
associated with erythema nodosum, uveitis, sacroilitis, migratory polyarthitis,
dx of IBS
dx: ab pain 3day /mo for 3 months with improvement of pain on defection
colonic adenocarcinoma pts have increased risk of ____
strep bovis endocardiits
sx of diverticulosis
usually asx
sx: hematochezia, cramping, digestion, feel like can’t empty rectum completely, can lead to diverticulitis (which is LLQ appendicitis like pain)
does UC or crohns have high reoccurrence after surgery
Crohns
IBD + ____ = increased risk of cancer
IBD + primary sclerosing cholangitis
wall involvement of UC vs Crohns
UC: mucosal and submucosal inflammation only in a continuous pattern of the colon only
crohns: transmural inflammation with knife like fissures in a skip lesion pattern anywhere on GI but most common in terminal ileum
unqiue traits of sporadic type of colon adenocarcinoma
APC mutation related, adenoma carcinoma sequence, villious type
- left side: annular “napkin lesion”
- left side sx: LLQ pain, occult bleeding, changed bowel habits
details of “classic” FAP (adenomatous polyp)
- AD DO, age 10-15
- colorectal adenomas as a teen and high likely hood of malignant progression
- APC mutation
- extra GI sx: congenital hypertrophy of retinal pigment epithelium
what is the malignant potential of crohns vs UC
UC: always risk of malignancy (based on extent of colonic involved)
Crohns: only if colonic
what are the two pathway associated with development of colonic adenocarcinoma
- adenoma-carcinoma sequence (APC/ B catenin pathway)
* sporadic type - MSI pathway (defect DNA mismatch repair system)
* HNPCC type serrated sessile adenoma
Turcot syndrome (adenomatous polyp)
classic FAP and CNS tumors ( medulloblastoma and glioblastoma)
chronic relapsing ab pain, gas, bloating, bowel habit changes (diarrhea/constipation) most common in middle aged females (20-40)
*NO CHRONIC INFLAMMATION
IBS (irritable bowel syndrome)
dx: pain 3day /mo for 3 months with improvement of pain on defection
unqiue traits of HNPCC type of colon adenocarcinoma
MSH2/MLH1 gene AD DO MSI pathway serrated type right side: polyploid exophytic mass right side sx: iron def anemia, fatigue
details of Peutz Jeghers syndrome
- age: 5-10 yo
- AD DO
- gene: STK 11
- multiple polyps all over GI with hyperpigmentation on lips, oral mucosa, genitals (freckle like)
- *INCREASED RISK OF COLORECTAL, BREAST, and GYNECOLOGIC cancer
diagnostic staging factors of colonic adenocarcinoma
T: invasion depth
N: LN metastasis (liver is common site)
M: distant spread
describe the adenocarcinoma pathway
- APC mutation - polyp risk
- KRAS mutation - adenomatous poly form
- p53 mutation/increased COX2 - carcinoma on left side
* *ASPRIN CAN STOP THIS PATHWAY
details of GVHD colitis
- follows stem cell transplant
- histoL epithelial cell apoptosis (esp crypt cells)
- sx: watery diarrhea (maybe bloody sometimes)
