Gastro 4 Flashcards
(15 cards)
Small & Large Intestine: Crohn’s disease
Can involve both the large and small intestine in a segmental manner (skip lesions)
Thick intestinal wall due to transmural edema, inflammation & fibrosis
Involves mucosa & deeper layers of the intestinal wall (transmural)
Focal granulomatous inflammation is common of Crohn’s disease
Transmural inflammation with fibrosis; creeping fat; intestinal obstruction; malabsorption of nutrients; dysplasia
Ulcerative colitis
Typically involves the rectum ± large intestine
Contiguous involvement of the large intestine is referred to as pancolitis
The lack of skip areas in UC distinguishes UC from Crohn’s
Chronic inflammation predisposes to epithelial dysplasia and adenocarcinoma
Severe cases may present with toxic megacolon and require immediate colectomy
Small & Large Intestine Tumors: Polyps
- Most adenocarcinomas of the intestine arise from precursor polyps
- macroscopic tissue mass that bulges outward from normal surface
- morphological distinction between sessile and pedunculated polyps
Non-neoplastic Polyps: Inflammatory polyp
- Whitish appearance due to lymphocyte infiltration
- Usually occur as solitary rectal polyps
Arise from chronic abrasion
Non-neoplastic Polyps: Hyperplastic polyps
Thought to arise from ‘delayed shedding’ of old epithelial cells
No risk for malignant conversion
Non-neoplastic Polyps: Hamartomatous polyps
-Increased risk for cancer
Juvenile polyps
-Usually present
(Neoplastic) Adenomas of the Colon
Potential for adenoma polyps to develop into carcinoma
Histologic examination reveals characteristic epithelial dysplasia
Adenomatous polyps vary in architectural as tubular or villous polyps, but both contain epithelial dysplasia
Sessile serrated adenomas
Familial Adenomatous polyposis (FAP)
Patients with familial adenomatous polyposis have an autosomal dominant inherited abnormality of one copy of the APC gene
FAP develop thousands of polyps in the large intestine
Hereditary Nonpolyposis Colorectal Cancer (HNPCC)
aka Lynch syndrome
Familial cancer clusters of colon, ovary, endometrium, stomach, ureter, brain, skin, liver, skin
Arises from mutations in DNA mismatch repair genes (MSH2, MLH1)
Colorectal Carcinoma
2nd to lung cancer deaths
Peak age of onset 60-70 yrs, > males
Associated with high fat, high sugar, low fiber diet
Occur most frequently in colon/rectum compared with small intestine
Highly mucinous tumors with signet ring cells are more invasive & associated with a worse prognosis
Most important prognostic factors are depth of CA invasion & lymph node metastases
Right (ascending colon) colon carcinoma
Can present with occult bleeding, cramping, changed bowel habits
Tumors grow as exophytic, polypoid masses
Extend along the wall of the ascending colon
Rarely cause obstruction
Left (descending colon) colon carcinoma
Presents with fatigue & anemia
Tumors grow as constrictive rings along the distal colon
Can cause GI obstruction
Staging of GI Carcinomas by
TNM System
Obstruction results in bacterial overgrowth and acute inflammation of the mucosa, possibly progressing to
acute appendicitis
common in the tip of the appendix, rarely metastasize
Carcinoid tumors
