Unit 2 - Upper GI and Endotoxemia Flashcards
How many deciduous teeth do horses have?
24
How many permanent teeth do horses have?
40 or 42
Is the maxilla or the mandible wider?
maxilla
What are some dental diseases that horses get?
Eruption disorders, oral trauma, dental decay, peridontal disease, dentigerous cyst (ear tooth), malalignment
What is monkey mouth?
prognathism, underbite
What is parrot mouth?
brachygnathism, over bite
What is dysphagia?
difficulty or inability to swallow
What are the classifications of dysphagia?
Prepharyngeal, pharyngeal, and postpharyngeal
What are the clinical sings of prepharyngeal dysphagia?
Dropping food, hypersalivation, and prehension difficulty
What are the clinical signs of pharyngeal dysphagia?
coughing, nasal discharge, gagging, and neck extension
What are the clinical signs of postpharyngeal dysphagia?
same signs as pharyngeal
How is dysphagia diagnosed?
Based on clinical signs, endoscopy, radiography, and ultrasonography
What are the differential diagnoses for dysphagia?
There are a lot, we are going to go general here: pain, muscular, obstructive, and neurologic
How is dysphagia treated?
resolve underlying disorder, dietary modifications, and esophagostomy tubes
What disease processes can affect the oral cavity?
foregin bodies, neoplasia, salivary gland conditions, infectious disease, congenital/developmental disorders, and salivation
What agent can cause excessive salivation?
Slaframine toxicosis (red clover)
What disease processes can affect the esophagus in horses?
Esophageal obstruction, esophagitis, motility disorders, stricture, diverticula, congenital, and perforation
What is the most common cause of esophageal obstruction?
Primary impaction
What can cause primary esophageal impaction?
roughage, bedding, grain, apples, and beet pulp
What is esophageal obstruction associated with?
poor dentition, wolfing, or gulping food
Is esophageal obstruction an emergency?
yes
Where are the common locations that esophageal obstruction occurs?
cervical, thoracic inlet, heart base, and caudal thorax
How is esophageal obstruction treated?
Relieve obstruction - heavy sedation, pass nasograstric tube, lavage with water, and protect the airway
If you cannot resolve esophageal obstruction, what is the treatment?
Wait and try again later - general anesthesia, muzzle, oxytocin, and maintain hydration
What is the treatment for post esophageal obstruction?
Endoscopy, radiographs, systemic antimicrobials, sucralfate, NSAIDs, diet modifications, dental exam
Where does esophageal perforation occur?
in the cervical region
What can cause esophageal perforation?
external trauma, impaction necrosis, diverticulum rupture, or iatrogenic with an NG tube
How is esophageal perforation diagnosed?
cellulitis, tissue necrosis, and endotoxemia
How is esophageal perforation treated?
Debridement, supportive care, esophagostomy tube
What is the prognosis for esophageal perforation?
poor
What is the prevalence of Equine Gastric Ulcer Syndrome (EGUS) in foals? Adults?
25-50% in foals, 60-90% in adults
What separates the non-glandular from the glandular part of the equine stomach?
the margo plicatus
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
What might lead to foal gastric ulcers?
They may have duodenal ulcers which leat do gastric ulcers from delayed gastric emptying
What can cause stomach ulcers on a physiologic level?
Horses continuously secrete HCl - the result from a disequilibrium between aggressive factors and protective mechanisms
What are squamous ulcers likely related to?
increased acid exposure
What are glandular ulcers likely related to?
disruption in blood flow and prostaglandins
If stomach ulcers are due to fasting, what can be done to mitigate this?
Provide high roughage diets - alfalfa may decrease acidity
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
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
How are gastric ulcers diagnosed?
Gastroscopy
What is a grade 0 ulcer?
Stomach lining is intact, and there is no appearance of reddening
What is a grade 1 ulcer?
Stomach lining is intact, but there are areas of reddening
What is a grade 2 ulcer?
Stomach has small single or multiple ulcers
What is a grade 3 ulcer?
Stomach has large single or multiple ulcers
What is a grade 4 ulcer?
Stomach has extensive ulcers; often merge to give areas of deep ulceration
What is the treatment for stomach ulcers?
Alfalfa hay, gastric acid secretion (H2 antagonists, or omeprazole), and adherence to ulcers
How are stomach ulcers prevented?
Management changes, alfalfa hay, and Ulcergard
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)
What causes endotoxemia?
presence of endotoxin in the bloodstream
What disease processes can endotoxemia result in?
Systemic inflammatory response syndrome (SIRS), sepsis, septic shock, and multiorgan dysfunction syndrome
__________ equals endotoxin.
Lipopolysaccharide
When gram-negative bacteria die, what to they release into the systemic circulation?
large aggregates of lipopolysaccharide
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)
What infections can cause endotoxemia?
any gram negative bacteria
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.
What happens when the coagulation cascade is activated?
it causes hemostatic disorders such as DIC
What happens when endotoxin activates the immune system?
It causes release of anaphylatoxins resulting in vasodilation and increased vascular permeability
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
What clinical pathology abnormalities are associated with endotoxemia?
Neutropenia, hyperglycemia/hypoglycemia, and changes reflective of primary disease
How is endotoxemia treated?
Supportive care, NSAIDs to counteract the effects of endotoxin, hyperimmunized plasma, polymyxin B, DMSO, Pentoxifylline, and heparin
What NSAIDs can you use to treat endotoxemia?
Flunixin Meglumine, Phenylbutazone, and ketoprofen
What is the prognosis for endotoxemia?
Guarded - early aggressive treatment can improve the outcome
