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Flashcards in lower GI pathology Deck (56):
1

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.

2

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

3

Celiac disease risk factors

Class II HLA-DQ2 or HLA-DQ8 allele, other autoimmune diseases

4

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

5

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

6

Celiac disease extra-intestinal manifestations

fatigue, iron deficiency anemia, puberty delay, dermatitis herpetiformis (blistering skin), enteropathy-associated T cell lymphoma, small intestinal adenocarcinoma

7

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

8

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

9

Whipple disease diagnosis

tissue biopsy shows organism- villi distended by swollen macrophage filled with whipple bacilli

10

Infectious causes of large bowel enterocolitis

bacterial, viral, parasitic, pseudomembraous colitis

11

Non infectious causes of colitis

ischemic colitis and microscopic colitis

12

Common bacteria causing bacterial colitis

Cholera, campylobacter, shigellosis, salmonellosis, E coli

13

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

14

Shigella source, symptoms, endoscopy findings

gram negative bacilli causing severe water or blood diarrhea and can mimic Crohns or UC. Endoscopy: Hemorrhage, exudates, pseudomembranes

15

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

16

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)

17

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

18

Pseudomembranous colitis clinical features

with fever, leukocytosis, abdominal pain, cramps, watery diarrhea

19

Pseudomembranous colitis histology

Pseudomembranes: adherent layer of inflammatory cells (neutrophils) and mucinous debris at site of colonic mucosal injury. Surface epithelium denuded, mucopurulent exudates

20

Regions of GI tract affected by CMV

from mouth to anus

21

regions of GI tract affected by herpes virus

esophagus and anorectum

22

List types of enteric viruses

rotavirus, adenovirus, norovirus

23

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

24

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

25

Norovirus- carriers, location

Contaminatd food or water, person to person, abnormalities in small intestine, self limited

26

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)

27

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)

28

transmission of nematodes

•Penetrates skin > enters venous system > travels to lungs > migrates up respiratory tract > down the esophagus > lodges in small intestine

29

Ischemic colitis predispositions

Older with cardiac or vascular dz, young long distance runners, women on oral contraceptives, hernias, volvulus.

30

Ischemic colitis clinical presentation

•severe abdominal pain, tenderness, nausea and vomiting, bloody diarrhea and blood in stool. Peristaltic sounds disappear, rigid abdomen, shock, sepsis

31

Ischemic colitis histology

•Varies from focal acute mucosal necrosis to full-thickness necrosis. Lamina propria fibrosis and atrophic crypts are seen with regeneration

32

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

33

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

34

Microscopic colitis associations

•celiac disease, lymphocytic gastritis and other autoimmune diseases such as thyroiditis

35

Microscopic colitis biopsy

•characteristic lymphocytic inflammation +/- a thickened subepithelial collagen layer

36

IBS clinical symptoms

Abdominal pain for at least 3 days/month over 3 months. Improvement with defecation. Change in stool frequency or form

37

IBD presentation

bimodal: teens-early 20s most common, second peak in 80s

38

IBD pathogenesis

NOT autoimmune: combo of host interactions with microbes, intestinal epithelial dysfunction, aberrant mucosal immune response

39

Describe mucosal immune response in IBD

T cell mediated: Th1 in Crohns and Th2 in ulcerative colitis. Dysregulation of cytokines

40

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)

41

Crohns genetics

NOD2, IBD5 and IL23R

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Ulcerative colitis genetics

HLA-A11, HLA-A7, HLA-DR2, HLA-DRB103 or DRB12

43

Crohns characteristics

skip lesions, ileal involvement, transmural chronic inflammation, strictures, ulcers, sinus tracts, fistulae.

44

Crohns clinical features

variable: mild diarrhea +/- blood, fever, abd pain, relapsing remitting. Extraintestinal: uveitis, polyarthritis, sacroiliitis, ankylosing spondylitis, erythema nodosum

45

Ulcerative colitis clinical features

bloody diarrhea with stringy, mucoid material, lower abd pain, symptoms relieved by defacation, extraintestinal: primary sclerosing cholangitis

46

Ulcerative colitis characteristics

rectal involvement, retrograde continous diffuse disease, no ileal involvement, disease worse distally, mucosal inflammation only, no fissures, sinuses, fistulas

47

Cancer and IBD

risk of adenocarcinoma is similar in CD and UC. Related to duration of disease, extent

48

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.

49

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

50

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

51

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

52

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

53

Pathogenesis of diverticular dz

•decreased dietary fiber > decreased stool bulk > elevated intraluminal pressure > mucosal herniation through focal defects in the bowel wall

54

Clinical features of diverticular disease

common in sigmoid colon and in older population. Asymptomatic or intermittent cramping, lower abdominal discomfort.

55

diverticulosis vs diverticulitis

Diverticulosis = presence of diverticula. Diverticulitis = inflammation of the diverticula, usually secondary to obstruction

56

Pathogenesis of appendicitis

Luminal obstruction by stone-like mass of stool “fecalith" > ischemic injury and stasis of luminal contents > inflammatory response