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
What is lymphangiectasia general caused by?
a process which puts back pressure on the lymph vessels leading them to dilate
26
What are the specific causes of intestinal lymphangiectasia?
lymphoma, a mesenteric lymphadenitis, peritonitis, inflammatory bowel disease (IBD)
27
What does intestinal lymphangiectasia result in?
malabsorption (especially of fats), rupture of lymphatics causing protein loss, chronic diarrhea, wasting, and hypoproteinemia
28
What can hypoproteinemia lead to?
edema, ascites, and hydrothorax
29
What lesions are associated with intestinal lymphangiectasia?
distension of villus lacteals often accompanied by distension of submucosal, serosal, and mesenteric lymphatics
30
What is inflammatory bowel disease characterized by?
an infiltrate of inflammatory cells in the intestinal lamina propria
31
What is IBD an idiopathic and common cause of?
diarrhea and vomiting in both dogs and cats
32
What clinical signs are associated with inflammatory bowel disease?
diarrhea (chronic or intermittent), +/- vomiting, and weight loss
33
What does IBD result from?
a complex interaction between host genetics, the intestinal microenvironment, and the immune system
34
How do immmunological mechanisms lead to IBD?
it is believed to result from an inappropriate immune response to dietary antigens and/or commensal microbial flora
35
What does ETEC stand for?
enterotoxigenic E. coli
36
What does AEEC stand for?
attaching-effacing E. coli
37
What species does ETEC commonly affect?
PIGS, calves, and lambs
38
What is the mechanism of ETEC?
1. Attach 2. Proliferate 3. Release toxins 4. Secretory diarrhea
39
Where does ETEC localize?
the small intestine
40
What species does AEEC commonly affect?
pigs, rabbits, lambs, dogs, calves, +/- cats
41
What is the mechanism of AEEC?
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
Where does AEEC localize?
intestine and colon
43
What supportive evidence is needed to diagnose an E. coli infection?
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
Clostridium perfringens causes enteric disease as a result of the _________ ___ _______.
elaboration of toxins
45
What conditions that may provide C. perfringens an opportunity to overgrow and cause disease?
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
Clostridium perfringens type C is an important cause of what?
hemorrhagic and necrotixing enteritis in several species
47
What are the commonly affected species by Clostridium perfringens type C?
pigs, calves, foals, sheep, and goats
48
What is the signalment for a Clostridium perfringens type C infection?
most typically observed in the first week of life or following a dramatic dietary change
49
What clinical signs are associated with a Clostridium perfringens type C infection?
hemorrhagic diarrhea and rapid death, animal may be found dead with no prior clinical signs
50
Where are lesions associated with a Clostridium perfringens type C infection typically located?
small intestine typically the jejunum
51
What type of lesion is associated with a Clostridium perfringens type C infection?
fibrinonecrotic and hemorrhagic enteritis +/- emphysema of the intestinal wall and segmental necrotic enteritis
52
What Clostridium perfringens type C toxin is in charge of the lesions associated with the infection?
beta toxin
53
What does histopath typically look like in animals with a Clostridium perfringens type C infection?
necrotic intestinal villi are covered by numerous, large, gram-positive bacilli
54
What should you use to diagnose a Clostridium perfringens type C infection?
gross lesions, histopath, gram-stained mucosal scraping, bacterial culture
55
What is the pathogenesis of necrotic enteritis due to coccidiosis?
1. Coccidiosis 2. malabsorption/maldigestion 3. C. perfringens proliferates on the unabsorbed ingesta 4. releases toxins 5. necrotic enteritis