Unit 2 - Upper GI and Endotoxemia Flashcards

(63 cards)

1
Q

How many deciduous teeth do horses have?

A

24

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2
Q

How many permanent teeth do horses have?

A

40 or 42

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3
Q

Is the maxilla or the mandible wider?

A

maxilla

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4
Q

What are some dental diseases that horses get?

A

Eruption disorders, oral trauma, dental decay, peridontal disease, dentigerous cyst (ear tooth), malalignment

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5
Q

What is monkey mouth?

A

prognathism, underbite

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6
Q

What is parrot mouth?

A

brachygnathism, over bite

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7
Q

What is dysphagia?

A

difficulty or inability to swallow

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8
Q

What are the classifications of dysphagia?

A

Prepharyngeal, pharyngeal, and postpharyngeal

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9
Q

What are the clinical sings of prepharyngeal dysphagia?

A

Dropping food, hypersalivation, and prehension difficulty

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10
Q

What are the clinical signs of pharyngeal dysphagia?

A

coughing, nasal discharge, gagging, and neck extension

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11
Q

What are the clinical signs of postpharyngeal dysphagia?

A

same signs as pharyngeal

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12
Q

How is dysphagia diagnosed?

A

Based on clinical signs, endoscopy, radiography, and ultrasonography

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13
Q

What are the differential diagnoses for dysphagia?

A

There are a lot, we are going to go general here: pain, muscular, obstructive, and neurologic

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14
Q

How is dysphagia treated?

A

resolve underlying disorder, dietary modifications, and esophagostomy tubes

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15
Q

What disease processes can affect the oral cavity?

A

foregin bodies, neoplasia, salivary gland conditions, infectious disease, congenital/developmental disorders, and salivation

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16
Q

What agent can cause excessive salivation?

A

Slaframine toxicosis (red clover)

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17
Q

What disease processes can affect the esophagus in horses?

A

Esophageal obstruction, esophagitis, motility disorders, stricture, diverticula, congenital, and perforation

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18
Q

What is the most common cause of esophageal obstruction?

A

Primary impaction

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19
Q

What can cause primary esophageal impaction?

A

roughage, bedding, grain, apples, and beet pulp

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20
Q

What is esophageal obstruction associated with?

A

poor dentition, wolfing, or gulping food

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21
Q

Is esophageal obstruction an emergency?

A

yes

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22
Q

Where are the common locations that esophageal obstruction occurs?

A

cervical, thoracic inlet, heart base, and caudal thorax

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23
Q

How is esophageal obstruction treated?

A

Relieve obstruction - heavy sedation, pass nasograstric tube, lavage with water, and protect the airway

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24
Q

If you cannot resolve esophageal obstruction, what is the treatment?

A

Wait and try again later - general anesthesia, muzzle, oxytocin, and maintain hydration

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25
What is the treatment for post esophageal obstruction?
Endoscopy, radiographs, systemic antimicrobials, sucralfate, NSAIDs, diet modifications, dental exam
26
Where does esophageal perforation occur?
in the cervical region
27
What can cause esophageal perforation?
external trauma, impaction necrosis, diverticulum rupture, or iatrogenic with an NG tube
28
How is esophageal perforation diagnosed?
cellulitis, tissue necrosis, and endotoxemia
29
How is esophageal perforation treated?
Debridement, supportive care, esophagostomy tube
30
What is the prognosis for esophageal perforation?
poor
31
What is the prevalence of Equine Gastric Ulcer Syndrome (EGUS) in foals? Adults?
25-50% in foals, 60-90% in adults
32
What separates the non-glandular from the glandular part of the equine stomach?
the margo plicatus
33
Where are gastric ulcers most commonly found in horses?
in the non-glandular region adjacent to the margo plicatus - NSAID ulcers may be in the glandular region
34
What might lead to foal gastric ulcers?
They may have duodenal ulcers which leat do gastric ulcers from delayed gastric emptying
35
What can cause stomach ulcers on a physiologic level?
Horses continuously secrete HCl - the result from a disequilibrium between aggressive factors and protective mechanisms
36
What are squamous ulcers likely related to?
increased acid exposure
37
What are glandular ulcers likely related to?
disruption in blood flow and prostaglandins
38
If stomach ulcers are due to fasting, what can be done to mitigate this?
Provide high roughage diets - alfalfa may decrease acidity
39
Why do performance horses have a higher incidence of gastric ulcers?
There is a lot of abdominal pressure which allows for splashing of the HCl around in the abdomen. Their high carbohydrate diets also produce a lot of volatile fatty acids which could lead to ulcers
40
What clinical signs are associated with gastric ulcers?
Poor appetite, not wanting to eat grain, weight loss, attitude changes, dullness, decreased performance, and low grade colic
41
How are gastric ulcers diagnosed?
Gastroscopy
42
What is a grade 0 ulcer?
Stomach lining is intact, and there is no appearance of reddening
43
What is a grade 1 ulcer?
Stomach lining is intact, but there are areas of reddening
44
What is a grade 2 ulcer?
Stomach has small single or multiple ulcers
45
What is a grade 3 ulcer?
Stomach has large single or multiple ulcers
46
What is a grade 4 ulcer?
Stomach has extensive ulcers; often merge to give areas of deep ulceration
47
What is the treatment for stomach ulcers?
Alfalfa hay, gastric acid secretion (H2 antagonists, or omeprazole), and adherence to ulcers
48
How are stomach ulcers prevented?
Management changes, alfalfa hay, and Ulcergard
49
Aside from gastric ulcers, what other disease processes can affect the equine stomach?
Pyloric stenosis and delayed gastric emptying, gastric dilation and rupture, gastric impaction, gastritis, and neoplasia (SCC)
50
What causes endotoxemia?
presence of endotoxin in the bloodstream
51
What disease processes can endotoxemia result in?
Systemic inflammatory response syndrome (SIRS), sepsis, septic shock, and multiorgan dysfunction syndrome
52
__________ equals endotoxin.
Lipopolysaccharide
53
When gram-negative bacteria die, what to they release into the systemic circulation?
large aggregates of lipopolysaccharide
54
What are the three components of the LPS?
O-region (in extracellular environment), lipid A region (in outer bacterial membrane), and core polysaccharide region (holds O and A together)
55
What infections can cause endotoxemia?
any gram negative bacteria
56
What is the pathogenesis of endotoxemia?
LPS binds to macrophages. The macrophages then activate and produce multiple cytokines (TNF, IL1, IL6, and IL8). The activation of these cytokines causes activation and propagation of inlammation (neutrophil activation). The coagulation cascade is activated and the immune system is activated.
57
What happens when the coagulation cascade is activated?
it causes hemostatic disorders such as DIC
58
What happens when endotoxin activates the immune system?
It causes release of anaphylatoxins resulting in vasodilation and increased vascular permeability
59
What are the clinical signs of endotoxemia?
Depression, weak arterial pulses, prolonged CRT, congested mucus membranes, tachycardia, fever, thrombosis or bleeding, renal failure, laminitis, respiratory distress and colic
60
What clinical pathology abnormalities are associated with endotoxemia?
Neutropenia, hyperglycemia/hypoglycemia, and changes reflective of primary disease
61
How is endotoxemia treated?
Supportive care, NSAIDs to counteract the effects of endotoxin, hyperimmunized plasma, polymyxin B, DMSO, Pentoxifylline, and heparin
62
What NSAIDs can you use to treat endotoxemia?
Flunixin Meglumine, Phenylbutazone, and ketoprofen
63
What is the prognosis for endotoxemia?
Guarded - early aggressive treatment can improve the outcome