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Intestine 1 Flashcards

1
Q

Define Protein-Losing Enteropathy (PLE)

A

Loss of protein via the GI Tract as a result of intestinal Pathology—>Hypoproteinemia

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2
Q

Name 3 consequences for a Protein-Losing Enteropathy (PLE)

A

Weight Loss, Wasting, Edema

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3
Q

Name 3 Types of PLE

A
  1. With Ulceration
    • Loss of blood and plasma protein through intestinal Ulcers (chronic histiocytic colitis;boxer colitis, Salmonellosis (mucosal damage))
  2. W/O Ulceration
    • Increased mucosal permeability. Mucosa intact. (eg. IBD, Alimentary Lymphoma)
  3. Deceased lymphatic drainage Lymphatic
    • fluid lost to GI (eg. Lymphangectasia)
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4
Q

Small Intestinal Diarrhea is characterized by what?

A

LARGE volume; Small Increase in frequency Blood from small intestine will be partly digested–>BLACK, Tarry Feces Water absorption in the large intestine is normally very efficient; may compensate for small intestinal lesion (esp. Horse)

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5
Q

Large Intestinal Diarrhea is characterized by what?

A

SMALL volume; Large Increase in Frequency Tenesmus is a prominent sign May contain A LOT mucus and fresh blood

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6
Q

Water absorption by the Small intestine or Large intestine may be overwhelmed by what mechanisms?

A
  • Overwhelming quantity of ingesta
  • change in composition of ingesta
  • Decreased absorptive capacity
    • Infiltrative diseases or inflammation
  • Reduced fecal transit time
    • mechanical stimulation or inflammation–>strong propulsive contractions
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7
Q

Define Osmotic Diarrhea

A

Molecules accumulate w/in the intestinal lumen due to problems with digestion and/or absorption–> elevation in intraluminal osmotic pressure–>fluid drawn into lumen Temporary feed withholding often helps alleviate clinical signs

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8
Q

Name and Describe 2 mechanisms of osmotic diarrhea and give an example of each

A
  • Maldigestion- large molecules are not broken down–> Cannot be absorbed
    • Poorly digestible feed (poorly digestible milk replacer
    • Lactose intolerance
    • Deficiencies in digestive factors (EPI; complete biliary obstruction)
  • Malabsorption: DECREASE in absorptive capacity
    • loss of enterocytes
    • villous atrophy
    • shortened intestinal tract
    • barrier to absorption-infiltrative diseases
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9
Q

What are the 3 phases of intestinal digestion?

A

Intraluminal Phase, Mucosal Phase, Delivery Phase

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10
Q

What phases of digestion are disrupted during osmotic diarrhea?

A

MUCOSAL Peptidase (Amino acids absorbed) Oligo-& saccharidases: Monosaccharides (absorbed)

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11
Q

Which Phase(s) are disrupted during maldigestion?

A

Intraluminal Phase, Mucosal phase

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12
Q

List three consequences of loss of enterocytes

A

Absorptive surface area of the mucosa is reduced–>OSMOTIC diarrhea Diminished breakdown of some molecules (maldigestion)–>OSMOTIC diarrhea Damage to protecive mucosal barrier–>EXUDATIVE diarrhea

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13
Q

True or False Malabsorption is usually accompanied by some degree of maldigestion

A

TRUE Malabsorption results in a structural and/or functional mucosal abnormality that impairs absorptive capability–>loss of surface area or presence of barrier to absorption –>loss of digestive and absorptive functions

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14
Q

What are 3 things that will decrease absorptive surface area?

A

Villous Atrophy Enterocyte Loss Short intestinal tract

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15
Q

What is villous atrophy?

A

It is the shortening of the villi Usually follows enterocyte loss Can be chronic (IBD) or transient (rotavirus)

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16
Q

What diseases are associated with villous atrophy?

A

Rotavirus, Coronavirus–>Loss of mature enterocytes Parvovirus, BVDV–>Loss of proliferative enterocytes (Mature cells continue to extrude but are not replaced) IBD, Lymphoma–>Chronic mucosal infiltration by inflammatory or neoplastic cells

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17
Q

What cells does Coronavirus target?

A

MATURE enterocytes

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18
Q

What can Crypt hyperplasia lead too? What is it a result of?

A

It can lead too villous atrophy It can be a result of chronic mucosal infiltration–>crypt hyperplasia–>immature enterocytes shed prematurely–>villous atrophy

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19
Q

What is the general mechanism for Exudative Diarrhea?

A

Mucosal damage/infiltration–>increased mucosal Permeability–>passive transmucosal leakage of fluid, electrolytes, protein, and/or blood

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20
Q

What are three mechanisms for exudative diarrhea?

A

Loss of mucosal epithelium->loss of barrier function Mucosal inflammation->inflammatory mediators->increased vessel permeability–>lamina proprial edema–>leakage of fluid and plasma proteins into lumen increased mucosal hydrostatic pressure/decreased plasma oncotic pressure–>fluid pushed or pulled into lumen

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21
Q

What can cause decreased plasma oncotic pressure within the villus?

A

Hypoalbuminemia

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22
Q

T or F The large intestine is more resistant to leakage as a result of increased hydrostatic pressure

A

TRUE

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23
Q

What can cause intestinal hypermotility?

A

Stress, pharmaceuticals, hormonal dysfunction (hyperthroidism)

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24
Q

What can cause intestinal hypomotility?

A

decreased latitudinal peristalsis with normal longitudinal peristalsis may contribute to decreased transit time

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25
Q

Define Secretory Diarrhea

A

Excessive luminal secretions due to an imbalance between absorptive and secretory mechanisms Caused most commonly by bacterial toxins or inflammatory mediators

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26
Q

What is the MOST important cause of secretory diarrhea?

A

BACTERIAL EXOTOXINS they often affect absorption of Na+ and Cl- and therefore water

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27
Q

When do you normal see Cryptosporidium in Calves?

A

Between 1-3 Weeks

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28
Q

When do you normally see Coccidia in Calves?

A

Between 4-8 weeks

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29
Q

when do you normally see coronavirus in calves?

A

Between 0-3 weeks

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30
Q

When do you normally see rotavirus?

A

Between 0-2 Weeks

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31
Q

When do you normally see E.Coli in calves?

A

Between 0-1 Week

32
Q

When do you normally see salmonella in a calf?

A

This can infect at any age, but it is usually between 0-4 weeks

33
Q

What is a predisposing factor to ETEC in neonates?

A

FAILURE of passive transfer MOST common cause of diarrhea in neonatal calves

34
Q

What are four clinical signs of ETEC?

A

Diarrhea (yellow scours) Dehydration Acidosis Electrolyte imbalances

35
Q

How and where does ETEC cause infection?

A

They must adhere to the enterocytes through the use of PILI–>proliferation They produce EXOTOXINS (heat labile, heat stabile) that affect Na+ and Cl- (and water) absorption/secretion (CL- in cryptes) in villi in the small intestine via increased intracellular cAMP Disrupt luminal pressure

36
Q

What type of diarrhea does ETEC cause?

A

Secretory, SMALL intestinal Diarrhea

37
Q

What is a result of ETEC infection?

A

PROFUSE diarrhea, and SEVERE dehydration Dilated, fluid-filled intestine

38
Q

What histopathological features are there for ETEC?

A

Usually, NONE

39
Q

Salmonellosis causes SEVERE mucosal damage in what tissues?

A

SMALL and LARGE intestine

40
Q

T or F Salmonellosis causes severe ulceration and inflammation.

A

TRUE These two damages result in loss of mucosal barrier and increased mucosal permeability resulting in exudative diarrhea

41
Q

T or F Some strains of salmonellosis release exotoxins

A

True These exotoxins can result in HYPERSECRETION

42
Q

Salmonellosis is an important cause of colitis in what species?

A

HORSES (pigs, foals, calves, occasionally lambs)

43
Q

What is a predisposing factor to Salmonellosis?

A

STRESS

44
Q

T or F Salmonella infection can result in some animals to become carriers

A

TRUE, can shed bacteria in times of stress

45
Q

Clostridia perfringens (types B & C) are what on gram stain?

A

GRAM +

46
Q

T or F Clostridia perfringens do not produce exotoxins

A

FALSE They produce exotoxins that are highly cytotoxic–>SEVERE mucosal damage–>NECROHEMORRHAGIC diarrhea/sudden death

47
Q

Who are more susceptible to C. Perfringens infection?

A

Neonates

48
Q

What are your gross findings with C. Perfringens??

A

Segmental/diffuse, dark red Small intestine with dark red, liquid ingesta

49
Q

Upon histopathology what do you see with C. Perfringens?

A

Diffuse/ segmental mucosal necrosis and hemorrhage Enteroadhered, G+ bacilli

50
Q

What is a predisposing factor for salmonellosis?

A

STRESS

51
Q

Give the Pathogenesis of Salmonellosis

A

Salmonella adheres to enterocytes/M cells–> Transcellular pasage into lamina propria/peyer’s patches–>Phagocytosed by macrophages–>toxin production–> Neutrophil chemotaxis & Enterocyte apoptosis–>enterocyte loss, vascular damage Some strains release exotoxins that cause CL- channel closure–>hypersecretion also can cause a vascular thrombosis

52
Q

Describe the pathogenesis for Samonellosis

A

Salmonella adheres to enterocytes/M cells–> transcellular passage into lamina propria/peyer’s patches–> phagocytosed by macrophages–>toxin production–> neutrophil chemotaxis and enterocyte apoptosis–> enterocyte loss and vascular damage Some strains can cause Cl- channel closures resulting in hypersecretion Also can cause vascular thrombosis

53
Q

Write a Morphologic diagnosis for the following photo:

A

Enterocolitis (fibrinonecrotic), Acute, Multifocal to coalescing, severe

(Acute salmonellosis)

54
Q

When would you see salmonella in a calf?

A

0-4 Weeks

Salmonella can present at any age and is also a very common cause of colitis in horses

55
Q

What type of diarrhea do you see with salmonellosis?

A

Large & Small intestinal Diarrhea

Exudative: mucosal damage and vascular damage

Osmotic: Loss of surface area

Secretory (some exotoxin producing strains): Closure of Cl- channels

56
Q

What can you see as a result of Clostridia perfringens, types A-E?

A

They produce POTENT exotoxins (enterotoxemia)–>severe mucosal damage–>NECROHEMORRHAGIC diarrhea/SUDDEN death

57
Q

T or F

Clostria Perfringen types are Gram Negative bacteria

A

FALSE: They are Gram Positive RODS

58
Q

Where can you find Clostridium perfringens?

A

They are normal GI Flora and are found in the soil as well, but can proliferate and produce BAD toxins under certain conditions

59
Q

What will be your gross findings with Clostridia perfringens types B & C?

A

segmental/diffuse, dark red (transmural: existing or occuring across the entire wall of an organ or blood vessel) SMALL intestine

-DARK red, liquid ingesta

60
Q

What will you see microscopically with clostridia perfringens B and C?

A

segmental/ diffuse mucosal necrosis and hemorrhage with ENTEROADHERENT Gram+ bacilli

61
Q

What type of diarrhea will you see with clostridial enteritis? (C. Perfringens B and C)

A

Acute, Small intestinal, exudative diarrhea (mucosal damage)

62
Q

What is the difference between C. Difficile and C. perfringens?

A

C. Perfringens results in NECROHEMORRHAGIC diarrhea/sudden death, while C. Difficile results in Acute, necrotizing enterocolitis due to cytopathic bacterial exotoxins

63
Q

What species is especially important with C. Difficile infection?

A

HORSES

64
Q

What can cause an overgrowth of C. Difficile?

A

Stress, antibiotic therapy, surgery, GI stasis

(these all result in a disruption in normal GI flora)

65
Q

What is the causitive agent for Johne’s Disease?

A

Mycobacterium avium subsp. paratuberculosis

66
Q

When would you see infection of Johne’s Disease or Mycobacterium avium supsp. paratuberculosis?

A

Animals are infected at onset of disease is delayed, affecting adult ruminants >19 months

THIS IS NOT A DISEASE OF YOUNG ANIMALS!!!!!!

67
Q

What are clinical signs of Johne’s Disease or Mycobacterium avium supsp. paratuberculosis?

A
  • emactiaion
  • hypoproteinemia
  • intractable diarrhea (cattle only)
  • normal/increased appetite
68
Q

What cell does mycobacterium avium supsp. paratuberulosis infect?

A

MACROPHAGES

69
Q

Mycobacterium avium subsp. paratuberculosis attacks macrophages. How does this cause diarrhea?

A

SEVERE granulomatous inflammation of the ileum, cecum, proximal colon–>mucosal thickening–>malabsorption (infiltrative)

70
Q

What is the morphologic Dx for this photo?

What disease does this photo represent?

Possible etiologic agent?

A

Diffuse, Severe, Chronic, Granulomatous enteritis (ileitis)

Johne’s disease

Mycobacterium avium subsp. paratuberculosis

71
Q

Johne’s disease is characterized by thickening of the lamina propria and submucosa of the ileum, cecum, and proximal colon by macrophages. What 3 things are a result of this infiltrative bacteria?

A
  • Barrier to absorption (inflammatory cell infiltration-macrophages): osmotic diarrhea
  • increased mucosal permeability
  • villous atrophy: osmotic diarrhea
72
Q

Johne’s disease causes diarrhea of where?

A

SMALL and Large intestine

Mainly ileum

73
Q

What are you gross findings with johne’s disease?

A

moderately to severely thickened ileum, (cecum, proximal colon_

Mucosa has corrugated appearance

74
Q

What will you see for histopathology of johne’s disease?

A

granulamatous inflammmation of the lamina propria and submucosa of affected segments

-multinucleate GIANT cells

Acid-Fast, intracellular bacteria

75
Q
A

Sys Path (17 decks)

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