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Biology of Disease II > Exam 3: Intestines > Flashcards

Exam 3: Intestines Flashcards

1
Q
A
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2
Q

What are the innate mechanisms of GI protection?

A

IgA
Mucus
MAMPs
M cells
Peyer’s patches

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3
Q

Differentiate between small and large bowel diarrhea

A
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4
Q

Maldigestion/Malabsorption Diarrhea

A

Defective digestion/absorption = stools with increased osmolarity

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5
Q

Osmotic Diarrhea

A

Exerted by luminal solutes (undigested carbohydrates and proteins)

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6
Q

Hypersecretion Diarrhea

A

Excessive intestinal fluid secretion induced by enterotoxins

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7
Q

Exudative Diarrhea

A

Increased capillary or epithelial permeability

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8
Q

Deranged Motility Diarrhea

A

Intestinal hypermotility –> decreased intestinal transit time –> malabsorption
Decreased motility –> increased intestinal transit time –> bacterial overgrowth –> malabsorption

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9
Q

What are the notable congenital abnormalities of the intestines?

A

Stenosis = partial occlusion
Atresia = complete occlusion
Persistent Meckel’s Diverticulum
White lethal foal syndrome = aganglionosis

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10
Q

What are the major causes of intestinal obstruction?

A

Obturation of occlusion (luminal) - plication
Compression (outside)
Stenosis (stricture or scarring)
Displacement
Functional (ileus or absence of peristalsis)

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11
Q

What are the parts of intusseption?

A

Telescoping
Intussusceptum = entrapped segment
Intussuscipiens = enveloping segment

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12
Q

What causes intussusception?

A

Irritability
Hypermotility

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13
Q

What sequelae result from intestinal vascular compromise and intestinal displacements?

A

torsion, volvulus
Increased intestinal permeability
Endotoxemia
Sepsis
Rupture
Peritonitis

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14
Q

What are the common types of intestinal neoplasia?

A

Lymphoma (most common in cats, ruminants)
Adenoma/adenocarcinoma (most common in dogs, sheep)
Sarcomas
Carcinoids
Polyps

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15
Q

What are the sequelae of inflammatory bowel disease?

A

Malabsorption
Protein losing enteropathy

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16
Q

What is the pathogenesis of histiocytic ulcerative colitis?

A

Infiltration of histiocytes that contain PAS positive material

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17
Q

E. coli heat labile toxin causes diarrhea by what mechanism?

A

Induce intestinal secretion

18
Q

What are the lesions of clostridium perfringes enteritis?

A

Enterotoxemia
Sudden death in well-nourished animals
Necrotizing/hemorrhagic enterocolitis

19
Q

What are the toxigenic types of C. perfringes and what diseases do they cause?

A

A = necrohemorrhagic enteritis and abomasitis, hemorrhagic bowel syndrome, antibiotic enteritis, colitis X in horses
B = lamb dysentery
C = bloody diarrhea in neonates (esp piglets)
D= pulpy kidney disease and encephalomalacia in lambs
E = enteritis in lagomorphs, enterotoxemia in ruminants

20
Q

What are lesions of type D C. perfringens in sheep?

A

Pulpy Kidney (Overeating) Disease

21
Q

C. difficile is associated with what previous treatment?

A

Oral antibiotic use

22
Q

Lesions of Mycobacterium avium sp. Paratuberculosis

A

Diffuse granulomatous enteritis with prominent mucosal folds due to expansion of the lamina propria by macrophages - often distal ileum
Granulomatous lymphangitis and lymphadenitis
Mineralization

23
Q

Pathogenesis of Mycobacterium avium sp. Paratuberculosis

A

Inflammatory, malabsorptive diarrea

24
Q

Lesions of proliferative iletis in pigs

A

Marked thickening of intestinal wall (cobblestone or cerebriform appearance)
Mucosa covered by fibronecrotic pseudomembrane cast

25
Q

Pathogenesis of proliferative iletis in pigs

A

Proliferative hemorrhagiv enteropathy caused by Lawsonia intracellularis

26
Q

How would porcine proliferative ileitis and swine dysentery look different grossly?

A

Swine dysentery = luminal spirochetes with silver stain (not intracellular!!)
Proliferative enteritis = intracellular organisms

27
Q

What diseases are caused by E. coli?

A

Edema disease (pigs)

28
Q

Differentiate between peracute, acute, and chronic Salmonellosis

A

Peracute = young animals, acute necrosis of blood vessels
Acute = catarrhal enteritis with fibronecrotic ileotyphlocolitis, mesenteric lymphadenopathy, fibrinous cholecystitis
Chronic = button ulcers, rectal strictures

29
Q

Tropism: Parvovirus

A

Crypts
Peyer’s patches

30
Q

Tropism: Coronavirus

A

Tips and middle of villi
Crypt epithelium
Small and large intestines

31
Q

Tropism: Rotavirus

A

Upper 2/3 of intestinal villi
Only small intestine
Vacuolation of enterocytes

32
Q

Pathogenesis: Rotavirus

A

Fecal-oral route
Viral replication in mature enterocytes
Necrosis and sloughing of absorptive cells
Villus atrophy
Maldigested/malabsorptive diarrhea

33
Q

Lesions: Rotavirus

A

Grossly: diarrhea, hemorrhage, necrosis, serosal “ground glass appearance”
Histo: villus blunting

34
Q

Pathogenesis: Enteric Coronavirus

A

Ingestion
1-4 day incubation
2 DPI = virus enters and colonizes enterocytes of the upper duodenume
Spreads caudally through the small intestine and colon

35
Q

Lesions: Enteric Coronavirus

A

Villus blunting, crypt hyperplasia

36
Q

Pathogenesis: Parvovirus

A

Virus infects mitotically active cells (intestines = crypts)

37
Q

Lesions: Parvovirus

A

Myocardial necrosis
BM and lymphoid depletion (immune suppression)
Serosal hemorrhage, mucosal hemorrhage, crypt necrosis

38
Q

Death due to parascaris equorum infection is often due to what?

A

Infection and perforation

39
Q

Zoonotic risk of nematodes

A

Ocular toxocariasis
Neural larval migrans

40
Q

Sequela: Strongylus vulgarus

A

Eosinophilic endarteritis with aneurism

41
Q

Sequela: Anoplocephala peroliate

A

Intusussception, impaction, rupture

42
Q

Is cryptosporidium zoonotic?

A

Yes

Biology of Disease II (29 decks)

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