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Equine Medicine > Unit 2 - Upper GI and Endotoxemia > Flashcards

Unit 2 - Upper GI and Endotoxemia Flashcards

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
Q

What is the treatment for post esophageal obstruction?

A

Endoscopy, radiographs, systemic antimicrobials, sucralfate, NSAIDs, diet modifications, dental exam

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26
Q

Where does esophageal perforation occur?

A

in the cervical region

27
Q

What can cause esophageal perforation?

A

external trauma, impaction necrosis, diverticulum rupture, or iatrogenic with an NG tube

28
Q

How is esophageal perforation diagnosed?

A

cellulitis, tissue necrosis, and endotoxemia

29
Q

How is esophageal perforation treated?

A

Debridement, supportive care, esophagostomy tube

30
Q

What is the prognosis for esophageal perforation?

A

poor

31
Q

What is the prevalence of Equine Gastric Ulcer Syndrome (EGUS) in foals? Adults?

A

25-50% in foals, 60-90% in adults

32
Q

What separates the non-glandular from the glandular part of the equine stomach?

A

the margo plicatus

33
Q

Where are gastric ulcers most commonly found in horses?

A

in the non-glandular region adjacent to the margo plicatus - NSAID ulcers may be in the glandular region

34
Q

What might lead to foal gastric ulcers?

A

They may have duodenal ulcers which leat do gastric ulcers from delayed gastric emptying

35
Q

What can cause stomach ulcers on a physiologic level?

A

Horses continuously secrete HCl - the result from a disequilibrium between aggressive factors and protective mechanisms

36
Q

What are squamous ulcers likely related to?

A

increased acid exposure

37
Q

What are glandular ulcers likely related to?

A

disruption in blood flow and prostaglandins

38
Q

If stomach ulcers are due to fasting, what can be done to mitigate this?

A

Provide high roughage diets - alfalfa may decrease acidity

39
Q

Why do performance horses have a higher incidence of gastric ulcers?

A

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
Q

What clinical signs are associated with gastric ulcers?

A

Poor appetite, not wanting to eat grain, weight loss, attitude changes, dullness, decreased performance, and low grade colic

41
Q

How are gastric ulcers diagnosed?

A

Gastroscopy

42
Q

What is a grade 0 ulcer?

A

Stomach lining is intact, and there is no appearance of reddening

43
Q

What is a grade 1 ulcer?

A

Stomach lining is intact, but there are areas of reddening

44
Q

What is a grade 2 ulcer?

A

Stomach has small single or multiple ulcers

45
Q

What is a grade 3 ulcer?

A

Stomach has large single or multiple ulcers

46
Q

What is a grade 4 ulcer?

A

Stomach has extensive ulcers; often merge to give areas of deep ulceration

47
Q

What is the treatment for stomach ulcers?

A

Alfalfa hay, gastric acid secretion (H2 antagonists, or omeprazole), and adherence to ulcers

48
Q

How are stomach ulcers prevented?

A

Management changes, alfalfa hay, and Ulcergard

49
Q

Aside from gastric ulcers, what other disease processes can affect the equine stomach?

A

Pyloric stenosis and delayed gastric emptying, gastric dilation and rupture, gastric impaction, gastritis, and neoplasia (SCC)

50
Q

What causes endotoxemia?

A

presence of endotoxin in the bloodstream

51
Q

What disease processes can endotoxemia result in?

A

Systemic inflammatory response syndrome (SIRS), sepsis, septic shock, and multiorgan dysfunction syndrome

52
Q

__________ equals endotoxin.

A

Lipopolysaccharide

53
Q

When gram-negative bacteria die, what to they release into the systemic circulation?

A

large aggregates of lipopolysaccharide

54
Q

What are the three components of the LPS?

A

O-region (in extracellular environment), lipid A region (in outer bacterial membrane), and core polysaccharide region (holds O and A together)

55
Q

What infections can cause endotoxemia?

A

any gram negative bacteria

56
Q

What is the pathogenesis of endotoxemia?

A

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
Q

What happens when the coagulation cascade is activated?

A

it causes hemostatic disorders such as DIC

58
Q

What happens when endotoxin activates the immune system?

A

It causes release of anaphylatoxins resulting in vasodilation and increased vascular permeability

59
Q

What are the clinical signs of endotoxemia?

A

Depression, weak arterial pulses, prolonged CRT, congested mucus membranes, tachycardia, fever, thrombosis or bleeding, renal failure, laminitis, respiratory distress and colic

60
Q

What clinical pathology abnormalities are associated with endotoxemia?

A

Neutropenia, hyperglycemia/hypoglycemia, and changes reflective of primary disease

61
Q

How is endotoxemia treated?

A

Supportive care, NSAIDs to counteract the effects of endotoxin, hyperimmunized plasma, polymyxin B, DMSO, Pentoxifylline, and heparin

62
Q

What NSAIDs can you use to treat endotoxemia?

A

Flunixin Meglumine, Phenylbutazone, and ketoprofen

63
Q

What is the prognosis for endotoxemia?

A

Guarded - early aggressive treatment can improve the outcome

Equine Medicine (27 decks)

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