lower GI pathology Flashcards
Types of intestinal obstruction
Herniation: protrusion of intestines into inguinal or femoral canal, ubilicus. Can lead to arterial/venous compromise, strangulation, infarction. Volvulus: twisting of loop of bowel about mesenteric base. Adhesions: fibrous bridges btw loops of bowel secondary to surgery, infection, inflammation. Intussusception: constricted intestine telescopes into immediately distal segment.
Pathogenesis of celiac disease
alpha gliadin peptide from gluten complexes with tissue transglutaminase > autoantibodies forms > inflammation and increased T cells > villous atrophy > tissue damage > loss of mucosal and brush border surface area > malabsorption in small intestine
Celiac disease risk factors
Class II HLA-DQ2 or HLA-DQ8 allele, other autoimmune diseases
compare celiac disease in pediatric vs adults
6-24 months: irritability, abd distension, anorexia, failure to thrive, weight loss. Older children: abd pain, nausea, vomiting, bloating, constipation. Adult: abd pain, diarrhea, weight loss, fatigue
Diagnosis of celiac disease
endoscopy: loss of surface villi. Serology: IgA Abs to tissue transglutaminase. Biopsy: villous blunting, increased intraepithelial lymphocytes, lymphoplasmacytosis of lamina propria
Celiac disease extra-intestinal manifestations
fatigue, iron deficiency anemia, puberty delay, dermatitis herpetiformis (blistering skin), enteropathy-associated T cell lymphoma, small intestinal adenocarcinoma
Whipple disease pathogenesis
Caused by gram-positive bacilli Tropheryma whippelii
Bacilli absorbed by lamina propria macrophages. Organism-laden macrophages accumulate within the small intestinal lamina propria and mesenteric lymph nodes → lymphatic obstruction. Impaired lymphatic transport causes malabsorptive diarrheaCaused by gram-positive bacilli Tropheryma whippelii
Bacilli absorbed by lamina propria macrophages. Organism-laden macrophages accumulate within the small intestinal lamina propria and mesenteric lymph nodes → lymphatic obstruction. Impaired lymphatic transport causes malabsorptive diarrheaCaused by gram-positive bacilli Tropheryma whippelii
Bacilli absorbed by lamina propria macrophages. Organism-laden macrophages accumulate within the small intestinal lamina propria and mesenteric lymph nodes → lymphatic obstruction. Impaired lymphatic transport causes malabsorptive diarrheaCaused by gram-positive bacilli Tropheryma whippelii
Bacilli absorbed by lamina propria macrophages. Organism-laden macrophages accumulate within the small intestinal lamina propria and mesenteric lymph nodes → lymphatic obstruction. Impaired lymphatic transport causes malabsorptive diarrhea
Whipple disease clinical features
Triad of diarrhea, weight loss, malabsorption. Other common symptoms: arthritis, lymphadenopathy, neurologic disease. Typically presents in middle-aged or elderly white males
Whipple disease diagnosis
tissue biopsy shows organism- villi distended by swollen macrophage filled with whipple bacilli
Infectious causes of large bowel enterocolitis
bacterial, viral, parasitic, pseudomembraous colitis
Non infectious causes of colitis
ischemic colitis and microscopic colitis
Common bacteria causing bacterial colitis
Cholera, campylobacter, shigellosis, salmonellosis, E coli
Campylobacter colitis source, symptoms, endoscopy findings
gram negative bacteria. Found in contaminated meat, water and unpasteurized dairy. Produces watery diarrhea +/- blood. C. Jejuni associated with food borne gastroenteritis, C. fetus seen in immunosuppressed. Endoscopy: friable colonic mucosa with erythema and hemorrhage
Shigella source, symptoms, endoscopy findings
gram negative bacilli causing severe water or blood diarrhea and can mimic Crohns or UC. Endoscopy: Hemorrhage, exudates, pseudomembranes
Salmonella source, types, findings
gram negative bacilli transmitted through food and water. Typhoid causes fever, abd pain and rash, diarrhea at 2nd week intially watery then bloody, perforation and toxic megacolon possible. Non-typhoid: mild self limited gastroenteritis with mucosal redness, ulceration and exudates
Types of E coli
enterotoxigenic and enteropathogenic (non invasive, travelers diarrhea), enteroinvasive (non bloody diarrhea, dysentery-like), enterohemorrhagic (non invasive, toxin producing, bloody diarrhea, cramps, edema, erosions, hemorrhage) and enteroadherent (non invasive, non bloody diarrnea, forms coat of adherent bacteria on surface)
Pathogenesis of pseudomembranous colitis
•Disruption of normal colonic flora by antibiotic allows C. difficile overgrowth → toxins released cause disruption of epithelial cytoskeleton, tight junction barrier loss, cytokine release and apoptosis
Pseudomembranous colitis clinical features
with fever, leukocytosis, abdominal pain, cramps, watery diarrhea
Pseudomembranous colitis histology
Pseudomembranes: adherent layer of inflammatory cells (neutrophils) and mucinous debris at site of colonic mucosal injury. Surface epithelium denuded, mucopurulent exudates
Regions of GI tract affected by CMV
from mouth to anus
regions of GI tract affected by herpes virus
esophagus and anorectum
List types of enteric viruses
rotavirus, adenovirus, norovirus
Rotavirus- population, pathophys
Children 6-24 months, most common cause of childhood severe diarrhea. Selectively infects and destroys mature enterocytes > villus surface repopulated by immature secretory cells > loss of absorptive function > net secretion of water and electolytes > osmotic diarrhea > dehydration
Adenovirus- population, biopsy, time course
Affects immunocompromised, AIDS and second most common form of pediatric diarrhea. Villous atrophy on biopsy, diarrhea resolves in 10 days
Norovirus- carriers, location
Contaminatd food or water, person to person, abnormalities in small intestine, self limited
List protozoam parasitic infections of lower GI and characteristic features
entamoeba histolytica (flask shaped ulcers), giardia lamblia (looks like schools of fish in duodenum), cryptosporidium parvum (basophilic spherical bodies on surface of enterocytes in small bowel)
List Helminthic parasitic infections of lower GI and characteristic features
Ascaris lumbricoides (roundworm- comes from fecal contaminated soil, giant worms), Strongyloides stercoralis (nematode- rash, eosinophilic and neutrophilic inflammation), Schistosomiasis (trematode- from contaminated water and skin penetration, calcified eggs in tissues and worms in veins)
transmission of nematodes
•Penetrates skin > enters venous system > travels to lungs > migrates up respiratory tract > down the esophagus > lodges in small intestine
Ischemic colitis predispositions
Older with cardiac or vascular dz, young long distance runners, women on oral contraceptives, hernias, volvulus.
Ischemic colitis clinical presentation
•severe abdominal pain, tenderness, nausea and vomiting, bloody diarrhea and blood in stool. Peristaltic sounds disappear, rigid abdomen, shock, sepsis
Ischemic colitis histology
•Varies from focal acute mucosal necrosis to full-thickness necrosis. Lamina propria fibrosis and atrophic crypts are seen with regeneration
Where are the watershed areas
Left/splenic flexure: supplied by superior and inferior mesenteric artery. Recto-sigmoid junction: supplied by inferior mesenteric and hypogastric arteries. These areas receive innervation from distal ends of arteries and are prone to ischemic colitis
What is microscopic colitis and types
Chronic non-bloody watery diarrhea without weight loss. Endoscopically normal. Mucosal inflammation on biopsy. Types: collagenous colitis and lymphocytic colitis
Microscopic colitis associations
•celiac disease, lymphocytic gastritis and other autoimmune diseases such as thyroiditis
Microscopic colitis biopsy
•characteristic lymphocytic inflammation +/- a thickened subepithelial collagen layer
IBS clinical symptoms
Abdominal pain for at least 3 days/month over 3 months. Improvement with defecation. Change in stool frequency or form
IBD presentation
bimodal: teens-early 20s most common, second peak in 80s
IBD pathogenesis
NOT autoimmune: combo of host interactions with microbes, intestinal epithelial dysfunction, aberrant mucosal immune response
Describe mucosal immune response in IBD
T cell mediated: Th1 in Crohns and Th2 in ulcerative colitis. Dysregulation of cytokines
Describe epithelial defects in IBD
Defects in epithelial tight junction barrier functions. Due to NoD2 polymorphism in Crohns (intracellular receptor for microbes) and ECM2 polymorphisms in UC (extracellular matrix protein)
Crohns genetics
NOD2, IBD5 and IL23R
Ulcerative colitis genetics
HLA-A11, HLA-A7, HLA-DR2, HLA-DRB103 or DRB12
Crohns characteristics
skip lesions, ileal involvement, transmural chronic inflammation, strictures, ulcers, sinus tracts, fistulae.
Crohns clinical features
variable: mild diarrhea +/- blood, fever, abd pain, relapsing remitting. Extraintestinal: uveitis, polyarthritis, sacroiliitis, ankylosing spondylitis, erythema nodosum
Ulcerative colitis clinical features
bloody diarrhea with stringy, mucoid material, lower abd pain, symptoms relieved by defacation, extraintestinal: primary sclerosing cholangitis
Ulcerative colitis characteristics
rectal involvement, retrograde continous diffuse disease, no ileal involvement, disease worse distally, mucosal inflammation only, no fissures, sinuses, fistulas
Cancer and IBD
risk of adenocarcinoma is similar in CD and UC. Related to duration of disease, extent
compare distribution of disease, bowel involved, strictures and wall appearance in crohns and UC
Crohns: skip lesions, ileum +/- colon, strictures yes, thickened wall appearance. UC: diffuse, colon only, strictures rare, thinned wall appearance.
For Crohns: describe inflammation, pseudopolyps, ulcers, lymphoid reaction, fibrosis, serositis, granulomas, and fistula
Transmural inflammation, moderate pseudopolyps, deep knife like ulcers, marked lymphoid reaction,marked fibrosis, marked serositis, granulomas present in 35%, and fistula present
For ulcerative colitis: describe inflammation, pseudopolyps, ulcers, lymphoid reaction, fibrosis, serositis, granulomas, and fistula
Mucosal inflammation only, marked pseudopolyps, superficial ulcers,moderate lymphoid reaction,mild/no fibrosis, mild/no serositis, no granulomas, and no fistulas
For Crohns: describe perianal fistulas, fat/vit malaborption, malignant potential, recurrence after surgery, toxic megacolon?
perianal fistulas in colonic dz, fat/vit malaborption yes, malignant potential if colonic, recurrence after surgery common, NO toxic megacolon
For ulcerative colitis: describe perianal fistulas, fat/vit malaborption, malignant potential, recurrence after surgery, toxic megacolon?
No perianal fistulas, No fat/vit malaborption, yes malignant potential, no recurrence after surgery, toxic megacolon possible
Pathogenesis of diverticular dz
•decreased dietary fiber > decreased stool bulk > elevated intraluminal pressure > mucosal herniation through focal defects in the bowel wall
Clinical features of diverticular disease
common in sigmoid colon and in older population. Asymptomatic or intermittent cramping, lower abdominal discomfort.
diverticulosis vs diverticulitis
Diverticulosis = presence of diverticula. Diverticulitis = inflammation of the diverticula, usually secondary to obstruction
Pathogenesis of appendicitis
Luminal obstruction by stone-like mass of stool “fecalith” > ischemic injury and stasis of luminal contents > inflammatory response
