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DEMS I > lower GI pathology > Flashcards

lower GI pathology Flashcards

1
Q

Types of intestinal obstruction

A

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.

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2
Q

Pathogenesis of celiac disease

A

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

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3
Q

Celiac disease risk factors

A

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

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4
Q

compare celiac disease in pediatric vs adults

A

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

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5
Q

Diagnosis of celiac disease

A

endoscopy: loss of surface villi. Serology: IgA Abs to tissue transglutaminase. Biopsy: villous blunting, increased intraepithelial lymphocytes, lymphoplasmacytosis of lamina propria

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6
Q

Celiac disease extra-intestinal manifestations

A

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

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7
Q

Whipple disease pathogenesis

A

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

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8
Q

Whipple disease clinical features

A

Triad of diarrhea, weight loss, malabsorption. Other common symptoms: arthritis, lymphadenopathy, neurologic disease. Typically presents in middle-aged or elderly white males

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9
Q

Whipple disease diagnosis

A

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

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10
Q

Infectious causes of large bowel enterocolitis

A

bacterial, viral, parasitic, pseudomembraous colitis

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11
Q

Non infectious causes of colitis

A

ischemic colitis and microscopic colitis

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12
Q

Common bacteria causing bacterial colitis

A

Cholera, campylobacter, shigellosis, salmonellosis, E coli

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13
Q

Campylobacter colitis source, symptoms, endoscopy findings

A

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

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14
Q

Shigella source, symptoms, endoscopy findings

A

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

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15
Q

Salmonella source, types, findings

A

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

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16
Q

Types of E coli

A

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)

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17
Q

Pathogenesis of pseudomembranous colitis

A

•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

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18
Q

Pseudomembranous colitis clinical features

A

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

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19
Q

Pseudomembranous colitis histology

A

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

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20
Q

Regions of GI tract affected by CMV

A

from mouth to anus

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21
Q

regions of GI tract affected by herpes virus

A

esophagus and anorectum

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22
Q

List types of enteric viruses

A

rotavirus, adenovirus, norovirus

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23
Q

Rotavirus- population, pathophys

A

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
Q

Adenovirus- population, biopsy, time course

A

Affects immunocompromised, AIDS and second most common form of pediatric diarrhea. Villous atrophy on biopsy, diarrhea resolves in 10 days

25
Q

Norovirus- carriers, location

A

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

26
Q

List protozoam parasitic infections of lower GI and characteristic features

A

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
Q

List Helminthic parasitic infections of lower GI and characteristic features

A

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
Q

transmission of nematodes

A

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

29
Q

Ischemic colitis predispositions

A

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

30
Q

Ischemic colitis clinical presentation

A

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

31
Q

Ischemic colitis histology

A

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

32
Q

Where are the watershed areas

A

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
Q

What is microscopic colitis and types

A

Chronic non-bloody watery diarrhea without weight loss. Endoscopically normal. Mucosal inflammation on biopsy. Types: collagenous colitis and lymphocytic colitis

34
Q

Microscopic colitis associations

A

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

35
Q

Microscopic colitis biopsy

A

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

36
Q

IBS clinical symptoms

A

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

37
Q

IBD presentation

A

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

38
Q

IBD pathogenesis

A

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

39
Q

Describe mucosal immune response in IBD

A

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

40
Q

Describe epithelial defects in IBD

A

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
Q

Crohns genetics

A

NOD2, IBD5 and IL23R

42
Q

Ulcerative colitis genetics

A

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

43
Q

Crohns characteristics

A

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

44
Q

Crohns clinical features

A

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

45
Q

Ulcerative colitis clinical features

A

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

46
Q

Ulcerative colitis characteristics

A

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

47
Q

Cancer and IBD

A

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

48
Q

compare distribution of disease, bowel involved, strictures and wall appearance in crohns and UC

A

Crohns: skip lesions, ileum +/- colon, strictures yes, thickened wall appearance. UC: diffuse, colon only, strictures rare, thinned wall appearance.

49
Q

For Crohns: describe inflammation, pseudopolyps, ulcers, lymphoid reaction, fibrosis, serositis, granulomas, and fistula

A

Transmural inflammation, moderate pseudopolyps, deep knife like ulcers, marked lymphoid reaction,marked fibrosis, marked serositis, granulomas present in 35%, and fistula present

50
Q

For ulcerative colitis: describe inflammation, pseudopolyps, ulcers, lymphoid reaction, fibrosis, serositis, granulomas, and fistula

A

Mucosal inflammation only, marked pseudopolyps, superficial ulcers,moderate lymphoid reaction,mild/no fibrosis, mild/no serositis, no granulomas, and no fistulas

51
Q

For Crohns: describe perianal fistulas, fat/vit malaborption, malignant potential, recurrence after surgery, toxic megacolon?

A

perianal fistulas in colonic dz, fat/vit malaborption yes, malignant potential if colonic, recurrence after surgery common, NO toxic megacolon

52
Q

For ulcerative colitis: describe perianal fistulas, fat/vit malaborption, malignant potential, recurrence after surgery, toxic megacolon?

A

No perianal fistulas, No fat/vit malaborption, yes malignant potential, no recurrence after surgery, toxic megacolon possible

53
Q

Pathogenesis of diverticular dz

A

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

54
Q

Clinical features of diverticular disease

A

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

55
Q

diverticulosis vs diverticulitis

A

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

56
Q

Pathogenesis of appendicitis

A

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

DEMS I (28 decks)

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