GI Pathology I Flashcards

1
Q

intestinal obstruction

A

*may occur at any level (small intestine most often)
*clinical manifestations - abdominal pain, distension, vomiting, constipation; surgical intervention usually required
*causes: hernias, intestinal adhesions, intussusception, volvulus

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2
Q

pathology of intestinal obstructions

A

*stasis and edema increase bulk of obstruction
*leads to arterial & venous compromise
*leads to tissue infarction

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3
Q

ischemic bowel disease

A

*acute compromise of major vessel
*most common > 70 years of age
*small bowel highly susceptible to ischemic injury

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4
Q

ischemic bowel disease - clinical manifestations

A

*sudden onset of cramping, LLQ abdominal pain
*decreased bowel sounds
*tenesmus
*bloody diarrhea
*severe cases may progress to shock/vascular collapse

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5
Q

causes of ischemic bowel disease

A

VASCULAR OCCLUSION:
1. arterial mesenteric thrombosis due to severe atherosclerosis
2. embolism: aortic atheromas, cardiac mural thrombi
3. mesenteric venous thrombosis (hypercoagulable states)

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6
Q

pathogenesis of ischemic bowel disease

A

2 phases:
1. initial hypoxic injury (at onset of vascular compromise)
2. reperfusion injury (at restoration of blood supply)
-leakage of gut lumen bacterial products into systemic circulation
-free radical production
-neutrophilic infiltration/inflammatory mediators

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7
Q

ischemic bowel disease - pathology

A

*damage can involve any or all bowel wall layers (mucosal layer is most susceptible)
*sharply defined demarcation: infarcted bowel intensely congested and dusky purple/red
*necrosis: early on, just the mucosa, but progresses to include more layers over time

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8
Q

malabsorption syndromes - overview

A

*defective absorption of fats, fat- and water-soluble vitamins, proteins, carbs, electrolytes and minerals, and water
*STEATORRHEA is hallmark
*examples:
-pancreatic insufficiency (cystic fibrosis)
-celiac disease
-Crohn disease

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9
Q

celiac disease - overview

A

*immune-mediated enteropathy caused by reaction to gluten
*worldwide growing incidence
*genetic susceptibility:
-HLA-DQ2
-HLA-DQ8

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10
Q

pathogenesis of celiac disease

A
  1. gluten (wheat storage protein) contains GLIADIN; gliadin resistant to further enzymatic digestion
  2. gliadin deaminated by tissue transglutaminase (tTG) and presented by APC to CD4+ T cells
  3. T cell cytokines damaging epithelium
  4. IgA antibody responses to tTG and gliadin (markers of disease activity; uncertain pathogenic significance)
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11
Q

celiac disease - clinical features

A

*pediatric celiac: irritability, abdominal distension, diarrhea, failure to thrive, anorexia, weight loss, muscle wasting
*adults: most commonly between 30-60 yrs; bulky steatorrhea, abdominal bloating
*SYMPTOMS ABATE WITH DIETARY GLUTEN EXCLUSION

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12
Q

celiac disease - diagnosis

A

*detection of antibodies to tTG and gliadin
*BIOPSY is beneficial for diagnosis
*symptoms abate with dietary gluten exclusion

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13
Q

complications of celiac disease

A

*dermatitis herpetiformis (an autoimmune blistering disease of the skin)
*increased incidence of enteropathy-associated T-cell lymphoma

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14
Q

celiac disease - gross morphology

A

*primarily affects distal duodenum and/or proximal jejunum
*rougher appearance
*more fissuring, large protrusions
*SCALLOPING ALONG THE FOLDS of the small bowel

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15
Q

celiac disease - microscopic morphology

A

*flat mucosa marked with villus atrophy (decreased surface area of the mucosal brush border, accounting for malabsorption
*intraepithelial T lymphocytosis
*crypt hyperplasia

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16
Q

pathogenesis of inflammatory bowel disease

A

*etiology unknown
1. mucosal immunity disruption (inadequate wound repair & epithelial barrier dysfunction; inadequate regulation of T cell responses)
2. host-microbial interactions (changes in gut microbiome contribute to inflammation)
3. defective autophagy contribute to dysregulated immune response

17
Q

Crohn disease - definition

A

*chronic inflammatory disease of the terminal ileum/proximal colon associated with transmural inflammation and skip lesions

18
Q

clinical features of Crohn disease

A

*diagnosis of exclusion
*relapsing diarrhea, RLQ pain, fever
*asymptomatic remission lasts weeks/months
*extra-intestinal involvement: uveitis, migratory polyarthritis, sacro-ileitis, ankylosing spondylitis, erythema nodosum, cutaneous granulomas

19
Q

complications of Crohn disease

A

*increased risk of colonic adenocarcinoma in long-standing colonic disease
*fibrosing strictures and fistulas may develop, requiring surgical treatment

20
Q

Crohn disease - gross pathology

A

*involves terminal ileum, ileocecal valve, cecum
*gross features:
-skip lesions (sharply delineated diseased areas separated by uninvolved gut)
*thickened intestinal wall: COBBLESTONE MUCOSA, strictures, CREEPING FAT
*fissures & fistulas

21
Q

Crohn disease - microscopic pathology

A

*transmural edema, inflammation, fibrosis
*mucosal architecture distortion with branched glands
*lymphoid aggregates
*noncaseating GRANULOMAS

22
Q

ulcerative colitis - definition

A

*chronic inflammatory disease diffusely involving the mucosa of the colon and rectum

note - colectomy is curative

23
Q

clinical features of ulcerative colitis

A

*diagnosis of exclusion
*relapsing BLOODY diarrhea, LLQ pain, fever
*asymptomatic remission lasts weeks/months
*extra-intestinal involvement: primary sclerosing cholangitis, migratory polyarthritis, sacro-ileitis, ankylosing spondylitis, uveitis

24
Q

complications of ulcerative colitis

A

increased risk of colonic adenocarcinoma in long-standing colonic disease

25
ulcerative colitis - gross pathology
*always involves rectum with CONTIGUOUS spread (small bowel not affected) *gross features: -granular mucosal surface with ulcerations -pseudopolyps (protruding islands of regenerative epithelium) -no transmural thickening
26
ulcerative colitis - microscopic pathology
*contiguous inflammation without skips *limited to mucosa/submucosa *CRYPT ABSCESSES (neutrophils within glands) *mucosal architectural distortion *possible glandular dysplasia
27
pathogenesis of colorectal carcinoma
1. classic adenoma to carcinoma sequence: -APC/beta-catenin pathways -80% carcinomas -familial adenomatous polyposis 2. hereditary non-polyposis colorectal carcinoma -microsatellite instability (MSI) - DNA mismatch repair deficiency -mutations accumulate in microsatellite repeats -Lynch Syndrome
28
colorectal carcinoma of cecum/ascending colon - gross pathology
-raised, exophytic polyps -extend along one wall (rarely cause obstruction) -MSI -iron deficiency anemia
29
colorectal carcinoma of rectosigmoid/left side - gross pathology
-annular "napkin ring" -constrictive with luminal narrowing, causing obstruction -APC pathway
30
colorectal carcinoma - microscopic pathology
*epithelial dysplasia *invasive glands (differentiation depends on glands +/- mucin formation) *stromal desmoplasia/fibrosis
31
colon polyps
*epithelial cell proliferation with protuberance into lumen *very common -growth pattern: pedunculated = stalk; or sessile = without stalk -nonneoplastic = hyperplastic, inflammatory, hamartomatous -neoplastic = adenoma
32
hyperplastic colon polyps
*non-neoplastic = no malignant potential (difficult to distinguish from sessile serrated adenomas, thus frequently biopsied) -common in elderly, discovered during routine colonoscopy *increased goblet cells with IRREGULAR GLANDS (hyperplasia of goblet cells)
33
colon polyps - adenomas
*neoplastic = POTENTIAL for malignant transformation *present in 50% of adults > 50 years *may be pedunculated or sessile *epithelial dysplasia = nuclear atypia, stratification -loss of goblet cells -may be tubular, villous, serrated