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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
What are the risk factors for canine gastric dilation-volvulus?
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
26
In canine gastric dilation-volvulus cases what does the stomach dilate with?
gas, fluid, or ingesta
27
Which way does the stomach typically roate when dilated in dogs?
clockwise
28
How does canine gastric dilation-volvulus lead to infarction?
obstruction of venous drainage causing congestion, then edema, and eventual infarction
29
What happens to the spleen in canine gastric dilation-volvulus?
it is typically bent into a V-shape which will become markedly congested and may undergo torsion, infarction, or rupture
30
How does a dilated stomach in dogs affect the vena cava?
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
31
What clinical signs are associated with canine gastric dilation?
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
32
What are common parasites that cause disease of the stomach and abomasum?
Bots, Haemonchus, Ostertagiasis
33
What lesions does bot larvae cause?
focal hemorrhage and ulceration, intestinal blockage if uncommonly large numbers are present
34
What species are infected with Haemonchus?
sheep and goats
35
What clinical signs does Haemonchus cause?
Ill thrift, anemia, and hypoproteinemia (decreased oncotic pressure causing edema)
36
What clinical signs are associated with Ostertagiasis?
loss of appetite, diarrhea, wasting, +/- edema
37
What is the pathogenesis of Ostertagia?
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
What are the consequences of Ostertagia?
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
What species typically get infectious gatric and abomasal ulceration?
ruminants
40
What species typically get non-infectious gastric and abomasal ulceration?
pigs, horses, and ruminants
41
What is non-infectious gastric and abomasal ulceration due to?
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
When should you consider viral abomasitis?
when there are multifocal abomasal ulcers with systemic signs
43
What population of ruminants typucally get non-infectious abomasal ulcers?
young calves, dairy cows, and feedlot animals
44
What is non-infectious gastric and abomasal ulceration associated with?
stress +/- nutritional deficiences
45
What can non-infectious abomasal ulcer perforation cause?
peritonitis
46
What clinical signs are associated with gastric ulcers in swine?
reduced growth rate and increased mortality
47
What gross necropsy findinds are found in swine with gastric ulcers?
the pig is pale, +/- consolidation of the anteroventral lung, melena in the intestine and spiral colon, and ulceration of the pars esophagea
48
What factors contribute to gastric ulcer development in swine?
feed, issues that lead to irregular feeding patterns, stress, and breed
49
What feed properties contribute to ulceration?
small feed particle size, pelleting feeds, diets with high levels of unsaturated fats, low fiber, high energy diets
50
True or False: There is no relationship between outbreaks of respiratory disease and gastric ulceration in swine.
FALSE
51
Why does respiratory disease contribute to gastric ulcer development in swine?
1. Pneumonia may lead to irregular feeding patterns 2. Stress of intercurrent disease 3. Histamine is released stimulating acid secretion
52
What clinical signs are associated with equine gastric ulcers?
colic, weight loss, teeth grinding, poor appetite
53
What are the causes of ulcers in horses?
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
What is the role of prostaglandins in protection of the gastric mucosa?
they augment the secretion of bicarbonate and mucus and augment mucosal blood flow
55
How do NSAIDs prevent the formation of prostaglandins?
they inhibit cyclooxygenase
56
What is the most common gastric/abomasal neoplasia in cattle?
lymphoma
57
What is the most common gastric/abomasal neoplasia in cats?
lymphoma
58
What is the most common gastric/abomasal neoplasia in dogs?
gastric carcinoma
59
What species is squamous cell carcinoma of the gastric/abomasal neoplasia only seen in?
pigs and horses
60
What is the biologic behavior of gastric carcinomas?
disease is usually advanced at presentation, highly invasive tumor, metastasis is expected
61
Where do gastric carcinomas typically metastasize?
regional lymph nodes, intraperitoneal, liver, and spleen
62
True or False: Primary gastric lymphomas are common.
FALSE
63
What changes to the stomach do primary gastric lymphomas cause?
diffuse to nodular thickening of the gastric mucosa
64
In cattle, where is coccidiosis found and at what age?
colon, less than 3 weeks
65
In cattle, where is E. coli infection found and at what age?
Intestine, less than 7 days
66
In cattle, where does Johne's disease isolate and at what age?
ileum, greater than 8months
67
What are the intestinal villi covered by?
mature enterocytes that live only for a few days, die and are sloughed
68
What is the role of mature villus enterocytes?
digestion and absorption
69
What are small intestinal crypts?
epithelial invaginations lined by younger epithelial cells which are involved in secretion
70
What are crypt base stem cells the source of?
all enterocytes
71
What happens to enterocytes as they mature?
they migrate to the villus tips, nature, and acquire digestive and absorptive capabilities
72
Where does much of the final breakdown of ingesta into absorbable nutrients occur at?
the brush border of villus epithelial cells
73
Where are the majority nutrients that need to be absorbed transmitted through?
villous epithelial cells
74
What does loss of fully functional mature superficial villous epithelial cells lead to?
malabsorptive/maldigestive diarrhea
75
What are the impacts of diarrhea?
systemic effects, weight loss +/- malnutrition, toxemia, and Bacteremia
76
What systemic effects occur as the result of diarrhea?
dehydration, potassium loss, and metabolic acidosis
77
How does diarrhea lead to toxemia?
increased mucosal permeability causing the absorption of toxins
78
How does diarrhea lead to bacteremia?
breakdown of the mucosal barrier allows bacteria to enter systemic circulation
79
What are the major mechanisms of diarrhea?
maldigestion, malabsorption, secretory, increased vascular permeability
80
What is maldigestive diarrhea caused by?
inadequate levels of enzymes needed to break down ingesta
81
What is the impact of maldigestive diarrhea?
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
What are some examples of causative agents of maldigestive diarrhea?
exocrine pancreatic insufficiency, congenital lactace deficiency, and atrophic rhinitis
83
What is malabsorptive diarrhea?
nutrients are not absorbed because cells responsible for absorption are decreased in number, injured, and/or defective
84
What is the impact of malabsorptive diarrhea?
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
What viruses cause malabsorptive diarrhea?
Rotavirus, Coronavirus, and Coccidiosis
86
What is atrophic enteritis?
when the intestinal villi are diminished
87
What mechanisms cause atrophic enteritis?
damage to mature villus enterocytes and damage to the proliferative compartment (crypts)
88
What is the pathogenesis of atrophic enteritis?
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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