Digestive System III Pathology – Malabsorption, Dysentery & Inflammatory Bowel Disease

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A comprehensive set of question-and-answer flashcards covering diarrhea types, malabsorption syndromes, celiac disease, tropical sprue, dysenteries, and inflammatory bowel disease, including Crohn’s disease and ulcerative colitis.

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43 Terms

1
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What daily stool weight defines a diarrheal disease?

200 g of stool per day

2
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Which type of diarrhea produces isotonic stool that persists during fasting?

Secretory diarrhea

3
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Which diarrhea results from unabsorbed luminal solutes and stops with fasting?

Osmotic diarrhea

4
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Which diarrhea is associated with steatorrhea and is relieved by fasting?

Malabsorptive diarrhea

5
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Which diarrhea presents with purulent, bloody stools that continue during fasting?

Exudative diarrhea

6
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What is the hallmark clinical finding of malabsorption?

Steatorrhea—bulky, frothy, greasy, yellow or clay-colored stools rich in fat

7
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List three systemic manifestations of chronic malabsorption.

Weight loss, abdominal distention/borborygmi, and muscle wasting (also anorexia)

8
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Name four important causes of malabsorption mentioned in the lecture.

Celiac disease, tropical sprue, chronic pancreatitis, cystic fibrosis (many others acceptable)

9
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By what other names is celiac disease known?

Celiac sprue or gluten-sensitive enteropathy

10
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What dietary component triggers celiac disease?

Gluten (specifically gliadin peptides) in genetically susceptible individuals

11
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Which HLA haplotypes are most strongly linked to celiac disease?

HLA-DQ2 or HLA-DQ8

12
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Which three autoantibodies are characteristic of celiac disease?

Anti-tissue transglutaminase (tTG), anti-endomysial, and anti-gliadin antibodies

13
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What are the classic small-bowel histologic changes in celiac disease?

Villous atrophy, crypt hyperplasia, and increased intraepithelial lymphocytes

14
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Into what three clinical categories can celiac disease presentations be grouped?

Classical, non-classical, and subclinical

15
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Give two classical intestinal manifestations of celiac disease.

Chronic diarrhea and weight loss (also abdominal pain, bloating, poor appetite, distension)

16
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Give two non-classical extra-intestinal manifestations of celiac disease.

Iron-deficiency anemia, dermatitis herpetiformis, chronic fatigue, short stature, alopecia, etc.

17
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Which serologic test is the most sensitive for active celiac disease?

IgA anti-tissue transglutaminase (anti-TG2) antibody

18
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Which serologic test is nearly 100 % specific for celiac disease?

IgA anti-endomysial antibody (EMA)

19
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From which part of the intestine are biopsies typically taken to diagnose celiac disease?

Second portion of the duodenum or proximal jejunum

20
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When can biopsy be omitted in pediatric celiac diagnosis under European guidelines?

If IgA anti-TG2 exceeds 10× the upper normal limit and IgA-EMA is positive on a second sample

21
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What differentiates tropical sprue from celiac disease regarding gluten intake?

Tropical sprue does NOT improve on gluten withdrawal

22
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What organisms are implicated in tropical sprue pathogenesis?

Enteric bacteria such as Escherichia coli, Klebsiella, and Enterobacter species

23
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What is the standard treatment for tropical sprue?

Tetracycline with folate supplementation for ~6 months

24
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Which bacterium is the most common cause of bacillary dysentery?

Shigella sonnei

25
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Which Shigella species can produce necrosis resembling ulcerative colitis?

Shigella flexneri and Shigella dysenteriae

26
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Histologically, what infiltrate characterizes acute bacillary dysentery?

Neutrophilic infiltrate with cryptitis and crypt abscesses

27
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What protozoan causes amoebic dysentery?

Entamoeba histolytica

28
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Which two colonic regions are most often affected by amoebic dysentery?

Cecum and ascending colon

29
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What is the classic gross ulcer shape produced by E. histolytica invasion?

Flask-shaped ulcers

30
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Name two serious colonic complications of amoebic dysentery.

Fulminant/necrotizing colitis and toxic megacolon (others: ameboma, perforation, strictures)

31
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What serious extra-intestinal complication results from amoebic liver abscess rupture?

Intraperitoneal, intrathoracic, or intrapericardial rupture possibly leading to secondary infection

32
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Define ameboma.

An inflammatory (pseudotumor) mass of granulation tissue and fibrosis mimicking carcinoma, usually in cecum/ascending colon

33
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What fundamental mechanism underlies inflammatory bowel disease (IBD)?

Inappropriate mucosal immune activation toward intestinal microbiota in genetically predisposed hosts

34
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How does Crohn’s disease typically involve the GI tract?

Discontinuous, segmental, transmural lesions affecting any part from mouth to anus

35
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List two hallmark histologic features of Crohn’s disease.

Transmural inflammation with lymphoid aggregates and non-caseating granulomas (≈50 % of cases)

36
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Name three classic gross findings in Crohn’s disease.

Creeping fat, cobblestone mucosa with aphthous ulcers, and bowel wall thickening/strictures (also fistulas)

37
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What microscopic pattern distinguishes Crohn’s disease distribution?

Patchy, segmental ‘skip’ lesions with intervening normal mucosa

38
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Where does ulcerative colitis always begin, and how does it spread?

Begins in the rectum and extends proximally in a continuous pattern

39
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In ulcerative colitis, inflammation is limited to which layers?

Mucosa and submucosa (no transmural inflammation)

40
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Which histologic features of chronicity are seen in ulcerative colitis?

Crypt architectural distortion, basal lymphoplasmacytosis, and Paneth cell metaplasia

41
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What gross lesions are common in ulcerative colitis but absent in Crohn’s disease?

Continuous superficial ulceration and pseudopolyps without skip lesions or creeping fat

42
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How does the risk of colorectal carcinoma change in ulcerative colitis?

Risk increases with duration of disease and severity/extent of inflammation

43
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State one key pathologic difference between Crohn’s disease and ulcerative colitis.

Granulomas and transmural inflammation are common in Crohn’s but absent in ulcerative colitis