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

Unit 3 - GI Lecture 3 Flashcards

1
Q

What leads to ruminal bloat?

A

interference with removal of excess gas

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2
Q

What are the respiratory consequences of bloat?

A

increased intra-abdominal pressure, causing pressure on the diaphragm, respiration is inhibited

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3
Q

What are the hemodynamic consequences of bloat?

A

bloated rumen compresses the posterior vena cava which causes the redirection of venous return to the heart

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4
Q

What are the two types of bloat?

A

primary and secondary

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5
Q

What is primary bloat also known as?

A

frothy bloat

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6
Q

What is primary bloat?

A

an acute bloat of cattle in feedlots or pastured on succulent legumes

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7
Q

What is the cause of primary bloat?

A

it is dietary and due to the formation of a stable foam in the rumen which fills the gas cap

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8
Q

How does foam cause bloat?

A

it prevents the clearance of material from the cardia which prevents normal eructation

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9
Q

What is secondary bloat also known as?

A

free gas bloat

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10
Q

Is secondary bloat acute or chronic?

A

chronic

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11
Q

What can cause seondary bloat?

A

internal or external obstructions of the esophagus, forestomach adhesions, abscesses, peritonitis, functional disturbances, or rumen atony

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12
Q

You found an animal dead in the field, what makes you suspect that its bloat?

A

the animal is found on its back in a sawhorse stance and the rumen is markedly distended

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13
Q

What is found on necropsy of an animal with bloat?

A
  1. edema, congestion, and hemorrhage of the lymph nodes and muscles of the head and neck
  2. The cervical esophagus is congested but the thoracic portion of the esophagus is pale and blanched
  3. An abundance of foam in the rumen
  4. The lungs are compressed, and intrabronchial hemorrhage may be present
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14
Q

What are the common diseases of the stomach/abomasum?

A

dilation/displacement, infectious, ulceration, hyperplastic/neoplastic

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15
Q

What species is gastric dilation and volvulus observed in?

A

horses, dogs, pigs, and cattle

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16
Q

What is a displaced abomasum?

A

the abomasum is above the rumen when it should be slighlty anterior to the rumen

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17
Q

What about the anatomy of a horse causes gastric dilation?

A

they can’t burp or vomit

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18
Q

When may gastric dilation occur in horses?

A

when excessive gas is produced and/or outflow from the stomach is inhibited

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19
Q

What causes gastric dilation in horses?

A

excessive gas production or decreased gastric emptying due to small intestinal disease

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20
Q

What causes excessive gas production in horses?

A

eating excess fermentable carbohydrates, sudden access to lush pasture, or excessive intake of water

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21
Q

What small intestinal diseases lead to decreased gastric emptying in horses?

A

inflammatory, obstruction, or ileus

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22
Q

What clinical sign is associated with gastric dilation in horses?

A

colic

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23
Q

What may gastric dilation lead to?

A

gastric rupture

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24
Q

What does gastric rupture lead to?

A

released gastric contents into the peritoneal cavity which causes peritonitis

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25
Q

What are the risk factors for canine gastric dilation-volvulus?

A

increasing age, primary relative affected by GDV, lean body conformation, rapid eating, eating from a raised bowl, eating one meal daily, exercise, stress after a meal, a fearful temperment

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26
Q

In canine gastric dilation-volvulus cases what does the stomach dilate with?

A

gas, fluid, or ingesta

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27
Q

Which way does the stomach typically roate when dilated in dogs?

A

clockwise

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28
Q

How does canine gastric dilation-volvulus lead to infarction?

A

obstruction of venous drainage causing congestion, then edema, and eventual infarction

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29
Q

What happens to the spleen in canine gastric dilation-volvulus?

A

it is typically bent into a V-shape which will become markedly congested and may undergo torsion, infarction, or rupture

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30
Q

How does a dilated stomach in dogs affect the vena cava?

A

it compresses it, results in sequestration of blood in dilated splanchnic, renal, and posterior muscular capillary beds leading to hypovolemic shock, metabolic acidosis, and cardiac arrhythmias

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31
Q

What clinical signs are associated with canine gastric dilation?

A
  1. Continuously paces
  2. Salivating, panting, whining
  3. Unproductive vomiting or retching
  4. Excessive drooling, usually accompanied by retching noises
  5. Swelling in abdominal area
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32
Q

What are common parasites that cause disease of the stomach and abomasum?

A

Bots, Haemonchus, Ostertagiasis

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33
Q

What lesions does bot larvae cause?

A

focal hemorrhage and ulceration, intestinal blockage if uncommonly large numbers are present

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34
Q

What species are infected with Haemonchus?

A

sheep and goats

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35
Q

What clinical signs does Haemonchus cause?

A

Ill thrift, anemia, and hypoproteinemia (decreased oncotic pressure causing edema)

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36
Q

What clinical signs are associated with Ostertagiasis?

A

loss of appetite, diarrhea, wasting, +/- edema

37
Q

What is the pathogenesis of Ostertagia?

A
  1. Ostertagia larvae live in the abomasal glands
  2. Larvae damage cells in the abomasum
  3. Replaced by immature cells that lack the ability to produce hydrochloric acid and pepsinogen
  4. Abomasal pH rises from 2-2.5 to 7
38
Q

What are the consequences of Ostertagia?

A

reduced pepsinogen secretion, reduced HCl production, proteins not denatured and digested due to lack of pepsin, increase in numbers of bacteria in the abomasum and GIT. Leakage of blood and blood-proteins into the gut

39
Q

What species typically get infectious gatric and abomasal ulceration?

A

ruminants

40
Q

What species typically get non-infectious gastric and abomasal ulceration?

A

pigs, horses, and ruminants

41
Q

What is non-infectious gastric and abomasal ulceration due to?

A

imbalance between necrotizing affects of gastric acid and pepsin and protective mechanisms (mucus coating stomach lining, bicarbonate neutralizing gastric acid, blood circulation aiding in cell renewal and repair)

42
Q

When should you consider viral abomasitis?

A

when there are multifocal abomasal ulcers with systemic signs

43
Q

What population of ruminants typucally get non-infectious abomasal ulcers?

A

young calves, dairy cows, and feedlot animals

44
Q

What is non-infectious gastric and abomasal ulceration associated with?

A

stress +/- nutritional deficiences

45
Q

What can non-infectious abomasal ulcer perforation cause?

A

peritonitis

46
Q

What clinical signs are associated with gastric ulcers in swine?

A

reduced growth rate and increased mortality

47
Q

What gross necropsy findinds are found in swine with gastric ulcers?

A

the pig is pale, +/- consolidation of the anteroventral lung, melena in the intestine and spiral colon, and ulceration of the pars esophagea

48
Q

What factors contribute to gastric ulcer development in swine?

A

feed, issues that lead to irregular feeding patterns, stress, and breed

49
Q

What feed properties contribute to ulceration?

A

small feed particle size, pelleting feeds, diets with high levels of unsaturated fats, low fiber, high energy diets

50
Q

True or False: There is no relationship between outbreaks of respiratory disease and gastric ulceration in swine.

A

FALSE

51
Q

Why does respiratory disease contribute to gastric ulcer development in swine?

A
  1. Pneumonia may lead to irregular feeding patterns
  2. Stress of intercurrent disease
  3. Histamine is released stimulating acid secretion
52
Q

What clinical signs are associated with equine gastric ulcers?

A

colic, weight loss, teeth grinding, poor appetite

53
Q

What are the causes of ulcers in horses?

A

infrequent, high carbohydrate meals, inadequate access to hay or pasture, heavy training schedules, high stress environments, excessive use of drugs, especially non-steroidal anti-inflammatories

54
Q

What is the role of prostaglandins in protection of the gastric mucosa?

A

they augment the secretion of bicarbonate and mucus and augment mucosal blood flow

55
Q

How do NSAIDs prevent the formation of prostaglandins?

A

they inhibit cyclooxygenase

56
Q

What is the most common gastric/abomasal neoplasia in cattle?

A

lymphoma

57
Q

What is the most common gastric/abomasal neoplasia in cats?

A

lymphoma

58
Q

What is the most common gastric/abomasal neoplasia in dogs?

A

gastric carcinoma

59
Q

What species is squamous cell carcinoma of the gastric/abomasal neoplasia only seen in?

A

pigs and horses

60
Q

What is the biologic behavior of gastric carcinomas?

A

disease is usually advanced at presentation, highly invasive tumor, metastasis is expected

61
Q

Where do gastric carcinomas typically metastasize?

A

regional lymph nodes, intraperitoneal, liver, and spleen

62
Q

True or False: Primary gastric lymphomas are common.

A

FALSE

63
Q

What changes to the stomach do primary gastric lymphomas cause?

A

diffuse to nodular thickening of the gastric mucosa

64
Q

In cattle, where is coccidiosis found and at what age?

A

colon, less than 3 weeks

65
Q

In cattle, where is E. coli infection found and at what age?

A

Intestine, less than 7 days

66
Q

In cattle, where does Johne’s disease isolate and at what age?

A

ileum, greater than 8months

67
Q

What are the intestinal villi covered by?

A

mature enterocytes that live only for a few days, die and are sloughed

68
Q

What is the role of mature villus enterocytes?

A

digestion and absorption

69
Q

What are small intestinal crypts?

A

epithelial invaginations lined by younger epithelial cells which are involved in secretion

70
Q

What are crypt base stem cells the source of?

A

all enterocytes

71
Q

What happens to enterocytes as they mature?

A

they migrate to the villus tips, nature, and acquire digestive and absorptive capabilities

72
Q

Where does much of the final breakdown of ingesta into absorbable nutrients occur at?

A

the brush border of villus epithelial cells

73
Q

Where are the majority nutrients that need to be absorbed transmitted through?

A

villous epithelial cells

74
Q

What does loss of fully functional mature superficial villous epithelial cells lead to?

A

malabsorptive/maldigestive diarrhea

75
Q

What are the impacts of diarrhea?

A

systemic effects, weight loss +/- malnutrition, toxemia, and Bacteremia

76
Q

What systemic effects occur as the result of diarrhea?

A

dehydration, potassium loss, and metabolic acidosis

77
Q

How does diarrhea lead to toxemia?

A

increased mucosal permeability causing the absorption of toxins

78
Q

How does diarrhea lead to bacteremia?

A

breakdown of the mucosal barrier allows bacteria to enter systemic circulation

79
Q

What are the major mechanisms of diarrhea?

A

maldigestion, malabsorption, secretory, increased vascular permeability

80
Q

What is maldigestive diarrhea caused by?

A

inadequate levels of enzymes needed to break down ingesta

81
Q

What is the impact of maldigestive diarrhea?

A

it exerts an osmotic pull and holds fluid in the gut lumen and undigested food is a substrate for intestinal bacteria, their proliferation, and production of waste products exacerbates the diarrhea

82
Q

What are some examples of causative agents of maldigestive diarrhea?

A

exocrine pancreatic insufficiency, congenital lactace deficiency, and atrophic rhinitis

83
Q

What is malabsorptive diarrhea?

A

nutrients are not absorbed because cells responsible for absorption are decreased in number, injured, and/or defective

84
Q

What is the impact of malabsorptive diarrhea?

A

it exerts an osmotic pull and holds fluid in the gut lumen and undigested food is a substrate for intestinal bacteria, their proliferation, and production of waste products exacerbates the diarrhea

85
Q

What viruses cause malabsorptive diarrhea?

A

Rotavirus, Coronavirus, and Coccidiosis

86
Q

What is atrophic enteritis?

A

when the intestinal villi are diminished

87
Q

What mechanisms cause atrophic enteritis?

A

damage to mature villus enterocytes and damage to the proliferative compartment (crypts)

88
Q

What is the pathogenesis of atrophic enteritis?

A
  1. Enterocyte loss exceeds crypt regenerative capacity
  2. Villus core conracts, minimizing the area of denuded basement membrane
  3. The remaining epithelial cells flattened to cover the exposed basement membrane
  4. End result is villus atrophy, blunting, and fusion

Anatomic Pathology 2 (48 decks)

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