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Flashcards in Gastro 4 Deck (15)
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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