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Anatomic Pathology 2 > Unit 3 - GI Lecture 4 > Flashcards

Unit 3 - GI Lecture 4 Flashcards

1
Q

What are the consequences of atrophic enteritis?

A
  1. Markedly reduced surface area for digestion and absorption
  2. Villi are covered by immature cells with less digestive and absorptive capabilities
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2
Q

What does mechanism A of atrophic enteritis target?

A

superficial villus epithelial cells

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3
Q

What does mechanism B of atrophic enteritis target?

A

dividing crypt epithelial cells

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4
Q

What viruses use mechanism A of atrophic enteritis?

A

Rotavirus, Coronavirus (dogs, pigs), Coccidia (swine), Enteroinvasive bacteria (Salmonells, SEEC, E. Coli)

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5
Q

What agents use mechanism B of atrophic enteritis?

A

Parvovirus (cats, dogs), radiation, chemotheraputic agents

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6
Q

What agents use a combination of mechanisms A and B of atrophic enteritis?

A

Coccidia (bovine, Coronavirus (bovine), BVD (bovine)

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7
Q

What necropsy findings are associated with atrophic enteritis?

A

maldigestion, malabsorption, thin-walled intestine, watery diarrhea, mesenteric lymph nodes not typically enlarged

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8
Q

In the case of canine parvovirus, near complete loss of villus epithelial cells results in what?

A

an inability to digest and absorb, loss of mucosal integrity, and prolonged recovery

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9
Q

What is secretory diarrhea?

A

when pathogens produce toxins which result in increased active secretion

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10
Q

What is the pathogenesis of secretory diarrhea?

A
  1. Pathogenic strain attaches to villus epithelial cells by pili
  2. Pathogenic strain proliferates
  3. Release enterotoxins which increase intestinal secretion by altering electrolyte and water movement across the plasma membrane
  4. Secretory diarrhea
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11
Q

What necropsy/clinical findings are associated with secretory diarrhea?

A

watery diarrhea, rapid dehydration and death, mesenteric lymph nodes not typically enlarged, will have chyle in the lacteals

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12
Q

When does increased vascular permeability occur?

A

with inflammation of the intestinal mucosa

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13
Q

What is the pathogenesis of increased vascular permeability?

A
  1. Inflammation
  2. Release of inflammatory mediators
  3. vessel dilation
  4. Leakage of fluid and plasma proteins from vessels
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14
Q

In chronic cases if increased vascular permeability what can happen?

A
  1. Exudate continually seeps from the mucosal surface into the gut lumen
  2. Significant amount of plasma protein can be lost
  3. Panhypoproteinemia (protein losing enteropathy)
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15
Q

What is one function of the colon?

A

to reduce the volume of water and electrolytes lost in feces

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16
Q

What disorders in the colon causes diarrhea?

A

resorptive capacity surpassed due to increased fluid from the small intestine or resorptive functional capacity reduced

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17
Q

If there is a mild increase in fluid from the small intestine how does the colon respond and what is the clinical outcome?

A

the colon compensates by removing fluid from the colon and there is normal feces but decreased weight gain

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18
Q

If there is a marked increase in fluid volume from the small intestine how does the colon respond and what is the clinical outcome?

A

incomplete or colon compensation to remove fluid causing small bowel diarrhea

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19
Q

If thee is normal fluid volume in the small intestine and decreased fluid volume removed by the colon what is the clinical outcome?

A

large bowel diarrhea

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20
Q

If there is a marked increase in fluid volume from the small intestine and a decrease in fluid removal by the colon what is the clinical outcome?

A

explosive diarrhea

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21
Q

What is large bowel diarrhea due to?

A

the reduced capacity to absorb fluid and electrolytes presented from the small intestine

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22
Q

Describe the appearance of large bowel diarrhea.

A

frequent passage of small amounts of fluid feces occasionally with fresh mucus and undigested blood

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23
Q

What are the major diarrheal diseases of domestic species?

A

lymphangiectasia, immune mediated, or infectious

24
Q

What is lymphangiectasia?

A

a pathologic dilation of lymph vessels

25
Q

What is lymphangiectasia general caused by?

A

a process which puts back pressure on the lymph vessels leading them to dilate

26
Q

What are the specific causes of intestinal lymphangiectasia?

A

lymphoma, a mesenteric lymphadenitis, peritonitis, inflammatory bowel disease (IBD)

27
Q

What does intestinal lymphangiectasia result in?

A

malabsorption (especially of fats), rupture of lymphatics causing protein loss, chronic diarrhea, wasting, and hypoproteinemia

28
Q

What can hypoproteinemia lead to?

A

edema, ascites, and hydrothorax

29
Q

What lesions are associated with intestinal lymphangiectasia?

A

distension of villus lacteals often accompanied by distension of submucosal, serosal, and mesenteric lymphatics

30
Q

What is inflammatory bowel disease characterized by?

A

an infiltrate of inflammatory cells in the intestinal lamina propria

31
Q

What is IBD an idiopathic and common cause of?

A

diarrhea and vomiting in both dogs and cats

32
Q

What clinical signs are associated with inflammatory bowel disease?

A

diarrhea (chronic or intermittent), +/- vomiting, and weight loss

33
Q

What does IBD result from?

A

a complex interaction between host genetics, the intestinal microenvironment, and the immune system

34
Q

How do immmunological mechanisms lead to IBD?

A

it is believed to result from an inappropriate immune response to dietary antigens and/or commensal microbial flora

35
Q

What does ETEC stand for?

A

enterotoxigenic E. coli

36
Q

What does AEEC stand for?

A

attaching-effacing E. coli

37
Q

What species does ETEC commonly affect?

A

PIGS, calves, and lambs

38
Q

What is the mechanism of ETEC?

A
  1. Attach
  2. Proliferate
  3. Release toxins
  4. Secretory diarrhea
39
Q

Where does ETEC localize?

A

the small intestine

40
Q

What species does AEEC commonly affect?

A

pigs, rabbits, lambs, dogs, calves, +/- cats

41
Q

What is the mechanism of AEEC?

A
  1. Bacteria attach to enterocytes by a non-pillus adhesion factor
  2. Efface epithelial brush border and cause detachment and destruction of absorptive cells
  3. villus atrophy
  4. Malabsorption/maldigestion
42
Q

Where does AEEC localize?

A

intestine and colon

43
Q

What supportive evidence is needed to diagnose an E. coli infection?

A

culture of a heavy and relative pure population of a pathogenic colonoy type, histiologic evidence of villus colonization or attaching/effacing lesions, pathogenic genotype

44
Q

Clostridium perfringens causes enteric disease as a result of the _________ ___ _______.

A

elaboration of toxins

45
Q

What conditions that may provide C. perfringens an opportunity to overgrow and cause disease?

A
  1. A diet with excess protein and carbohydrate
  2. Abrupt feed changes that disturb the normal intestinal flora
  3. An insult oF the small intestinal mucosa leading to maldigestion/malabsorption
46
Q

Clostridium perfringens type C is an important cause of what?

A

hemorrhagic and necrotixing enteritis in several species

47
Q

What are the commonly affected species by Clostridium perfringens type C?

A

pigs, calves, foals, sheep, and goats

48
Q

What is the signalment for a Clostridium perfringens type C infection?

A

most typically observed in the first week of life or following a dramatic dietary change

49
Q

What clinical signs are associated with a Clostridium perfringens type C infection?

A

hemorrhagic diarrhea and rapid death, animal may be found dead with no prior clinical signs

50
Q

Where are lesions associated with a Clostridium perfringens type C infection typically located?

A

small intestine typically the jejunum

51
Q

What type of lesion is associated with a Clostridium perfringens type C infection?

A

fibrinonecrotic and hemorrhagic enteritis +/- emphysema of the intestinal wall and segmental necrotic enteritis

52
Q

What Clostridium perfringens type C toxin is in charge of the lesions associated with the infection?

A

beta toxin

53
Q

What does histopath typically look like in animals with a Clostridium perfringens type C infection?

A

necrotic intestinal villi are covered by numerous, large, gram-positive bacilli

54
Q

What should you use to diagnose a Clostridium perfringens type C infection?

A

gross lesions, histopath, gram-stained mucosal scraping, bacterial culture

55
Q

What is the pathogenesis of necrotic enteritis due to coccidiosis?

A
  1. Coccidiosis
  2. malabsorption/maldigestion
  3. C. perfringens proliferates on the unabsorbed ingesta
  4. releases toxins
  5. necrotic enteritis

Anatomic Pathology 2 (48 decks)

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