Small Intestines and Appendix Flashcards
True Diverticulum vs. False Diverticulum
An outpouching of the intestine
TRUE diverticula are CONGENITAL and contain ALL LAYERS OF GASTRIC WALL (mucosa, submucosa, muscularis, serosa)
Usually occur in the SMALL BOWEL
False - ACQUIRED –> only have a partial/or no muscular layer; most commonly arise from the left side of the colon
Meckel Diverticulum
Most common type
Outpouching of all layers of the bowel wall (from failure of vittiline duct to develop)
RULE OF 2’s –> 2% population, 2 inches long, 2 feet proximally from the ileocecal valve, 2 years of age
Can involve pancreatic and gastric mucosa as well (not just intestinal) –> if this does occur, it could cause abnormal secretion of gastric acid in the small intestine, leading to ulcer/perforation!!! This is called HETEROTROPIA (normal tissue, wrong location – ectopic!?) –> small fraction of Meckel’s
APPENDICITIS LIKE PRESENTATION –> but can occur on left side too!!!
What are the 4 types of mechanical lesions of the small intestine?
Hernia
Adhesion
Volvulus
Intussusception
Two possible outcomes –> intestinal lumen obstruction, vascular supply obstruction
Herniation
Due to weakness/defects in the abdominal wall
Can result in vascular and intestinal lumen obstruction
TYPES –> inguinal, umbilical, incisional
Fibrous adhesions
Often after SURGERY
Occur between loops, which get stuck together/twisted and prevent movement during peristalsis
Can affect vascular supply in the mesentery
Volvulus
Twisting that catches the intestinal lumen as well as the mesentery and causes a fibrous adhesion between loops
Intusussception
When one part of the intestine TELESCOPES into another part of the intestine
Often there is a “lead point”/origin such as a polyp or tumor that causes part of the intestine to be pulled down into another part
Intestinal Lumen Obstruction
Outcomes usually less severe
External kinks/compressions can result from any of these lesions as well as tumors
Loss of muscular propulsion after surgery can also cause obstruction
Vascular Obstruction - ISCHEMIC INSULT
Ischemic injury can be caused by STRANGULATION of the vascular supply
ISCHEMIC BOWEL DISEASE –> arises from two main causes –> VASCULAR OBSTRUCTION (thrombus, tumor, mechanical lesion) or from LOW FLOW (hypotension, CVD, shock)
Acute - can result in Hemorrhage, perforation, progression to infection and sepsis –> can present with ACUTE ABDOMEN (severe abdominal pain of unknown etiology)
Chronic - also possible, vascular flow blocked in a slower fashion
More common in OLDER PATIENTS
Occurs via REPERFUSION rather than the insult to the vascular supply itself –> cytokines flood the area, and hemorrhage from the re-perfusion causes the actual damage!
More on ISCHEMIC BOWEL DISEASE
Grossly Dark black/brown bowel –> “dusky bowel”
Severity determined by the DURATION OF HYPOXIA
Severity determined by the presence of CHOLESTEROL PLATES - flat plates that dissolve during processing, causing vascular occlusion which can injusre the tissue
Intestinal segments at the end of their arterial supplies are particularly susceptible to ischemia –> WATERSHED ZONES –> SPLENIC FLEXURE (where SMA and IMA terminate) and SIGMOID COLON/RECTUM (where IMA, pudendal and ilial arterial supply end)
As severity increases, damage can progress to a SEPARATION OF THE EPITHELIUM eventually causing necrosis and an inflammatory response –> if the injury is isolated to one layer of the wall, then we wall can regenerate, but if it is through the FULL THICKNESS, then surgery is absolutely necessary and perforation is a concern
C Diff Infection
More a problem for the colon, but also small intestine
Identified by the presence of its TOXIN, not the pathogen itself
Toxin damages mucosal crypts and necrosis results on the mucosal surface –> bacteria proliferate in the LUMEN only
Results from USE OF OTHER ANTIBIOTICS that wipe out the intestinal flora
Layering of the mucosa with inflammatory exudative membrane consisting of neutrophils, cellular debris, mucous –> Pseudomembranous colitis
Whipple Disease
Intestinal lipodystrophy
Caused by TROPHERYMA WHIPPELII (actinomycete)
Infection of the LAMINA PROPRIA – becomes infiltrated with MACROPHAGES and LIPID VACUOLES
When diseased, macrophages get filled with bacteria and are visible on EM
Macrophages clog the lamina propria of the small bowel, so the disease causes FAT MALABSORPTION and STEATORRHEA (fat in feces) –> lymphatic drainage clogged
Can occur anywhere, but small intestine far more common
CMV Infection
Viral
Infects endothelial cells within the vascular supply, causing SMALL VESSEL OCCLUSION
Can infect STROMAL CELLS as well
Opportunistic infection that arises with HIV/AIDS
Mycobacteria infection
Associated with GRANULOMATOUS LESIONS of the wall
Need to stain to distinguish (TB can look like Yersinia)
Histology similar to Crohn’s
CELIAC DISEASE
Immune mediated enteropathy due to GLUTEN SENSITIVITY, resulting in the SMALL BOWEL VILLI
Aka SPRUE
Genetic susceptibility related to HLA-DQ2, HLA-DQ8
GLIADIN is the product of gluten breakdown –> as it is deamidated by TTG, an AUTOIMMUNE REACTION activates interleukins and T cells within the epithelium
Increased lymphocytes is the pathological landmark of the disease
Produce INTERFERON, DAMAGING SURFACE ENTEROCYTES –> also activates B cells which produces 3 antibodies –> Anti-Gliadin, Anti-endomysium (most important marker), Anti-tTG
As enterocytes are damaged, there is an attempt to replace them from the crypts –> VILLI (normally tall) FLATTEN –> not atrophy, but active PROLIFERATION!
Crypts elongate, Villi Flatten
Since this is technically an “adaptation ti injury,” the removal of the offending agent (GLUTEN) will allow for repair over the course of a few weeks!
Two types of INFLAMMATORY BOWEL DISEASE?
CROHN’S DISEASE
ULCERATIVE COLITIS
Crohn’s Disease
Affects the DISTAL SMALL INTESTINE (ileum)
Chronic, progressive, relapsing, non-infectious inflammatory disease of the intestinal wall
Typically transmural (full thickness)
Gross - easy to distinguish from normal colon –> THICK WALL, RIGID –> can be continuous or SKIP lesions with alternative healthy/crappy bowel
Histo –> inflammatory changes for ALL WALL LAYERS
lymphoid hyperplasia –> STRING OF PEARLS lymphoid aggregates
Ulcerated mucosa, inflammatory cells/fibrosis in the submucosa, fibrosis/inflammation/edema in the muscularis layer
Fissures within the wall from the mucosa to subserosa, which can lead to FISTULAS involving other organs
Can also see GRANULOMAS ~30%
Small apthous ulcers in a bearclaw type, cobblestone pattern
Characterized by pain and diarrhea in episode attacks with periods of quiescence; relapse is common
CAN DEVELOP INTO DYSPLASIA/CARCINOMA
Ulcerative Colitis
Mainly restricted to the COLON
CONFINED to mucosal and submucosal layers
ONLY see ulcerations, no thickening/transmural inflammation
CONTINUOUS disease that starts distal and INVADES proximal
Can also lead to dysplasia/carcinoma
Neoplasia of the Small Intestine
NEUROENDOCRINE (Carcinoid) TUMORS
–> most commonly found in the small intestine and appendix
Can range from hyperplasia to carcinomas
Can arise in the foregut, midgut, hind gut
In the MIDGUT they are MOST AGRESSIVE and can secrete serotonin or gastrin, depending on where they are
Commonly in multiples – dozens to hundreds!
LYMPHOMA –> 2nd most common place for lymphomas to arise, after the stomach
Zollinger-Ellison Syndrome
Hypersecretion of GASTRIN from a carcinoid (gastrinoma) causing SEVERE PEPTIC ULCERATION
Serum gastrin increased
Gastrinoma can be in pancreas, duodenum, stomach
What is the appendix?
A diverticulum of the CECUM that is located at McBurney’s Point in the RLQ –> only matters when it becomes inflamed, infected, or invaded
Acute Appendicitis
Teens/adolescents
Occurs following OBSTRUCTION of the appendiceal lumen by hyperplastic mucosal lymphoid tissue, stones, fecal debris, tumor
Blockage leads to MUCOUS COLLECTION, FECAL STAGNATION, BACTERIAL PROLIFERATION –> INFLAMMATION!
If untreated, can lead to abscess formation –> worst case can lead to NECROSIS and PERFORATION
Most accurate diagnostic tool for diagnosis? SPIRAL CT
Excise that shit
Mucocele
Mucous filled appendix
Can be due to a benign process (obstruction, scar tissue) or by a MUCINOUS TUMOR
MUST assume cancer –> remove before it ruptures so it cannot seed through the abdomen (if it does, pseudomyxoma peritoneii)
Other appendix tumors
CARCINOID = most frequent; often in the deep mucosa or submucosa; rarely metastasize; appendectomy usually sufficient
Mucinous Cystadenoma –> mucous-producing epithelium lines the appendix (unlike the flat, atrophic epitheium of the mucocele)
This can transition to CYSTADENOMA or a ruptured appendix
