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HORSE MEDICINE Flashcards

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1
Q

fWhat are the top 3 differentials for weight loss in a horse

A

1) Nutrition (low quantity or quality)
2) Dental Disease
3) Parasite

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2
Q

What are your differentials for a horse with weight loss

A

1) Increased demand - illness, pregnancy/lactation, increased workload, environmental factors

2) Inadequate intake - low quantity, low quality, low uptake (dental disease or GI disease)

3) inappropriate utilization - liver disease, GI disease (malabsorption or maldigestion, parasites)

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3
Q

What should you do if a horse presents to you with weight loss?

A

-Measure quantity of feed
-Measure quality of feed consumed
-Check teeth
-Perform a fecal
-blood work, abdominal U/S, abdominocentesis, abdominal x-rays, absorption testing

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4
Q

How do you determine the caloric maintenance requirements for a horse

A

Maintenance: 0.033 x BWT (kg)
light work: x 1.2
moderate work: x 1.4
hardwork: up to x 1.9 DE for maintencane

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5
Q

Charlie is a 12yo QH gelding weighing 500kg (1100Ib) in excellent health and a couch potato. How many calories does Charlie need per day?

A

Maintenance: 0.033 x 500kg = 16.7 Mcal/day for weight maintenance
This can be divided to 0.8Mcal/Ib (Hay) or 1.3Mcal/Ib
100% forage diet = 20.8Ibs (2% body weight)
90% forage/10% grains = 18.8 Ib forage / 1.3Ib grain

about 4 flakes a day

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6
Q

T/F: grain is an essential part of the horse’s diet

A

False- grain is not an essential part of the equine diet

*Cornerstone of the diet is hay
Hay should meet as mich of the horse’s protein, energy and fiber needs are possible

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7
Q

T/F: all hay “flakes” are created equally

A

False
but a flake of small bale hay is about 5Ibs

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8
Q

A flake is about

A

5 pounds of hay- not all are created equally

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9
Q

The digestible energy and nutritive value (quality) of hay is dependent on the

A

plant maturity at the time of harvest

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10
Q

Hay analyses look for

A

Increased in Crude protein
Decreased in acid detergent fiber (ADF: lignin and cellulose (digestibility of nutritionist))
Decreases in neutral detergent (NDF: structural carbohydrates)

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11
Q

Alfalfa that is in early bloom has _________ calories/pound, ________ crude protein, and ______ Ca2+ than alfalfa in full bloom

A

Early bloom: more calories, more crude protein, more calcium

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12
Q

What hay has the highest Crude protein
a) alfalfa (early bloom)
b) alfalfa (full bloom)
c) orchard grass (early bloom)
d) timothy (early bloom)

A

alfalfa (early bloom)

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13
Q

What hay has the highest mcal/Ib
a) alfalfa (early bloom)
b) alfalfa (full bloom)
c) orchard grass (early bloom)
d) timothy (early bloom)

A

alfalfa (early bloom)

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14
Q

What hay has the highest Ca++ %
a) alfalfa (early bloom)
b) alfalfa (full bloom)
c) orchard grass (early bloom)
d) timothy (early bloom)

A

alfalfa (early bloom)

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15
Q

How often do you need a horse

A

If possible allow access to feed (hay) 24hrs/day
Preferable feed small meals frequently

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16
Q

Lily is a 4yo TBH mare weighing 450kg (1000Ibs) that is a race horse- hard to keep weight on her. How many calories does Lily need per day?

A

0.0363 x 450kg x 1.9 = 31Mcal/day for maintenance weight of heavy exercise animals.

Hay= 0.8Mcal/Ib
100% hay diet = 24.8 Ibs hay/day

Grain 1.3Mcal/day
70% hay diet = 17.36 Ib hay/day ; 30% ???

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17
Q

How many calories does hay typically have in it

A

0.8Mcal/Ib

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18
Q

How many calories does grain typically have in it

A

1.3Mcal/Ib

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19
Q

How can you add more high fat content into a horse’s diet, which is popular for equine athletes

A

-Vegetable oils
-Linseeds
-Ricebran

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20
Q

High fat diets in horses, like with vegetable oils, linseeds, and ricebran spares the use of _____________ and increases the use of ___________
this leads to less production of lactic acid and heat during exercise

A

spares use of glucose/glycogen and increases the use of body fat

*Requires an adaption period of 3 weeks

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21
Q

How long does it take for a horse to adapt to a high fat diet to spare the use of glucose and increase the use of body fat and reduce excitable behavior in horses

A

about 3 weeks

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22
Q

What effect does carbs (certain grains) have on a horse’s behavior

A

certain grains can make horses hot

Dietary fats (corn oil) reduce excitable behaviors in horses

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23
Q

Vegetable oils, such as corn oil, may offer natural protection against__________

A

gastric ulceration

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24
Q

What are the benefits and disadvantages of using a fat supplemented diet in horses

A

Pros: energy density, no mastication required, less risk of GI disturbance, behavioral benefits, GI protection (ulcers), glycogen sparing effect

Cons: weight gain, reduced palatability, cost, messiness, shelf life (unsaturated FA), insulin sensitivty?

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25
Q

Vegetable oils vary in terms of proportions of

A

1) Saturated vs unsaturated fatty acids
2) Omega 3 vs omega 6 fatty acids

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26
Q

Canola, corn, flaxseed, olive, soybean, and sunflower are all types of

A

vegatable oils
differ in their proportions of saturated vs unsaturated fatty acids and omega 3 vs omega 6 fatty acids

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27
Q

Why do we not just feed horses more grain

A

health problems associated with feeding large grain meals
Digestive disturbances: colic, colitis, diarrhea, gastric ulcers, laminitis (endotoxin)

Metabolic: laminitis (insulin resistance), tying up, obesity, hoint disease, hyperlipemia

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28
Q

How do oats differ from corn

A

Oats: palatable, best nutrient balanced, starch is foregit digested, “sugar high”

Corn: denser than oats (overfeeding), not nutrient balanced, starch mostly hindgut digested (hindgut acidosis and colic) unless processed

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29
Q

Are oats or corn more likely to cause a sugar high

A

oats

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30
Q

Are oats or corn more likely to cause hindgut acidosis

A

Corn- it is mostly hindgut digested (oat is foregut digested) corn needs to be processed

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31
Q

Forage based diets are typically deficient in

A

trace minerals (copper, zinc) and vitamins
provide vitamin/mineral supplements to the diet

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32
Q

YOu should limit concentrates to about

A

3Ibs/meal (if they are even needed at all)

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33
Q

To increase the energy content of a horse’s diet ________

A

supplement with fats, rather than carbohydrates

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34
Q

________ can be fed to a horse whole while ______ needs to be processed

A

oats ; corn

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35
Q

Asa general rule of thumb, you should aim for approximately _____ percent of a horse’s BW in hay/day

A

2%

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36
Q

What are good indicators of hay quality

A

Numerous factors affect the quality of hay and include the type of hay, maturity of the plant at harvest, season of harvest, handling of the crop during harvest and storage condition.

In general, the characteristics of good quality roughage include high leaf-to-stem ratio, fresh smell and appearance, cleanliness, and natural color. Despite the fact that these characteristics are good indicators of quality, hay should be analyzed to determine its actual nutrition content especially if it is being fed to horses suffering from endocrine/metabolic conditions.

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37
Q

The following statement is TRUE or FALSE?

Grain is not an essential part of the equine diet.

A

True

Despite the fact that many horse owners consider a normal equine diet to consist of hay and grain(s), grains are not an essential part of a horse’s diet. Forage (e.g. pasture, hay) should meet as much of the horse’s proteins, energy, and fiber needs as possible.

When additional energy is needed, it is safer to use fats and fermentable fibers before grains. Modern feeds with added fat and digestible fiber are recommended over high-starch feeds.

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38
Q

T/F The starch contained in whole corn is mostly hindgut digested, thus increasing the horse’s risk of developing hindgut acidosis.

A

True

Most of the starch (72%) from whole or cracked corn is not digested in the foregut and proceeds to the hindgut where it is rapidly fermented. That process results in the production of lactic acid, which lowers the large intestinal pH (=hindgut acidosis) which can result in bacterial death and endotoxin release. For these reasons, corn should be processed (e.g. ground, pelleted, extruded) for all horses, and pelleted feeds should not contain more than 25% of corn.

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39
Q

Please calculate the energy needs for a 1,200 lbs horse with a normal metabolism that performs a moderate amount of work.

How many flakes of grass hay would you need to feed to provide 100% of this horse’s energy needs?

A

The energy requirements for a 1,200 lbs horse (=545 kg) with a normal metabolism (0.0333 Mcal/kg) and a moderate workload (X 1.4) are the following:

1.4 X 545 kg X 0.0333 Mcal = ~ 25.4 Mcal/day

Additional information needed:

1 lbs of hay contains approximately = 0.8 Mcal/lbs
1 flake of hay weighs approximately = 5 lbs
The number of flakes of hay this horse needs to be fed to cover 100% of its energy needs is:

25.4 Mcal/day /0.8 Mcal = 31.76 lbs of hay
31.76 lbs / 5 lbs = 6.35 flakes ~ 6 flakes of hay

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40
Q

What are the clinical signs of equine esophageal disease

A

-Dysphagia
-Frequent swallowing
-Coughing
-Hyper-salivation (ptyalism)
-regurgitation of feed (mouth, nostrils)
-Anxiety, neck stretching
-Swilling, emphysema

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41
Q

T/F you should use barium if perforation is suspected

A

False- do not use barium if perforation is suspected. barium within the tissue can cause inflammation

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42
Q

What is nasogastric intubation in a horse used for

A

passage of nasogastric tube can help determine if there is an obstruction present. If esophageal obstruction (choke) is suspected, care should be taken not to damage the mucosa.

can sometimes be passed beyond the obstruction and enter the stomach, giving false impression that either an obstruction did not exist of had been relieved. Esophageal perforation at obstructed site may also allow passage of tube beyond the obstruction. If the perforation is cervically located, the tube may ass subcutaneously to the thoracic inlet

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43
Q

What should you be careful for when doing nasogastric intubation to check for choke

A

avoid causing more damage to the esophageal mucosa

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44
Q

What is the color of the normal esophageal mucosa

A

whitish-tan to slightly

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45
Q

The esophagus is normally _______ when coated with the barium solution, allowing visualization of the smooth, longitudinal folds

A

collpased

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46
Q

What should you give a horse for sedation when performing a good oral examination

A

-A2 agonists - Xylazine or Detomidine
-Acepromazine
-Buscopan-muscle relaxant
-Methocarbamol (Robaxin)
-Lidocaine (topical)

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47
Q

Why is the use of atropine for oral examination controversial

A

it will only relax the smooth muscle of the distal 1/3 esophagus, which is not where the chokes usually occur. also risk for colic (GI ileus)?

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48
Q

What is the most common esophageal disorder in horses

A

esophageal obstruction- usually due to intraluminal impaction

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49
Q

The proximal 2/3 of the horse esophagus has no serosal layer, meaning it

A

takes longer to heal

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50
Q

What are vital structures adjacent to the esophagus that are at risk with choke

A

-Vagosympathetic trunk
-Recurrent laryngeal nerve
-Carotid artery

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51
Q

High choke means there is is an esophageal obstruction in the

A

cervical part of the esophagus- at risk for aspiration pneumonia

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52
Q

Low choke means there is an esophageal obstruction in the

A

thoracic inlet

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53
Q

Intrathoracic choke is rare but it means that there is an esophageal obstruction in the

A

lower esophageal sphincter

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54
Q

How do you treat esophageal obstructions in horses

A

1) Sedation/Muscle relaxation (Xylazine/ Detomidine or Acepromazine and then allow a nasal gastric tube to help pass the obstruction into the stomach. Avoid pressure if not removed do lavage

2) Lavage

3) Drugs : NSAIDs, antibiotics (broad spectrum if aspiration)

4) Support: treat dehydration and electrolytes, treat esophageal inflammation and aspiration pneumonia. Horses with excessive salivation will have hypochloremic metabolic alkalosis - give 0.9% NaCl

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55
Q

T/F you should use lubricating agents, such as mineral oil and softening agents (DSS) during lavage to relieve esophageal obstructions in horses

A

False- they are contraindicated - cause granulomatous pneumonia because they are non-degradable

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56
Q

What are the predisposing factors of esophageal obstructions in camelids

A

The bosses that are dominant
greed eaters
pelleted foods

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57
Q

How do you treat esophageal obstructions in camelids

A

needle trocar if bloated
sedation
antibiotics if aspiration occured
prolonged salivary salivary loss: metabolic derrangements
may need general anesthesia/intubation/gentle lavage

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58
Q

may follow choke
results in weight loss, regurgitation, recurrent choke, recurrent bloat
most are idiopathic but can result from organophosphates and myasthenia gravis

A

Megaesophagus

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59
Q

What solution should you use when doing lavage to dislodge an esophageal obstruction

A

warm water, preferably with 0.9% sodium chloride solution

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60
Q

Which of the following clinical signs is NOT found in a horse with esophageal disease?
Dysphagia
Ptyalism
Diarrhea
Stretching of neck
Coughing during swallowing

A

Diarrhea

The hallmark of esophageal disorders in the horse is dysphagia. Additional clinical signs, particularly for proximal esophageal disorders, include frequent, ineffectual attempts to initiate swallowing, coughing during swallowing, ptyalism (excessive salivation), and nasal regurgitation of feed mixed with saliva. Other clinical signs include anxiety, restlessness, and stretching of the neck.

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61
Q

The following statement in TRUE or FALSE?

An esophageal feed obstruction (choke) should be treated as a medical emergency.

A

True
Esophageal obstruction should be considered an emergency because prolonged pressure on the esophageal mucosa by the obstructing material can result in extensive tissue damage, with subsequent scar tissue formation and stricture.

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62
Q

Treatment of a horse with an esophageal obstruction (choke) typically consists of administration of heavy sedation, passage of a nasogastric tube, and gentle lavage with warm water.

What is/are the goals for administering sedation?

Relaxation of the esophageal musculature
Allowing safe handling of the horse
Reducing the risk of fluid aspiration when lavaging
All of the above

A

All of the above

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63
Q

the margo plicatus is a

A

distinct margin that separates the non-glandular and glandular portion of the stomach.

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64
Q

has stratified squamous epithelium and serves to contain the horse’s food without aiding in the chemical breakdown of the ingesta

A

non-glandular portion (squamous mucosa)

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65
Q

What are the 4 types of secretory epithelial cells that horses have on their glandular mucosa. What do they secrete?

A

Mucous cells: secrete an alkaline mucous
Parietal cells: secrete HCl
Chief cells: secrete pepsin
G cells: secrete gastrin

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66
Q

How might equine gastric rupture occur

A

abnormalities which interfere with the normal aboral movement of fluid through the small intestine may cause the accumulation of fluid in the stomach. Severe gastric dilation can occur and then rupture if not reated

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67
Q

What allows there to be a one-way valve in the equine stomach

A

the anatomic arrangement of the esophagus and cardia

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68
Q

What kind of horse is gastric ulceration more common in

A

race horses

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69
Q

What causes gastric ulceration in a horse

A

an imbalance betweeh the mucosal aggressive factors (HCl, pepsin, bile acids, and organic acids) and the mucosal protective factors (mucus, bicarbonate, and mucosal perfusion)

Mucosa is damaged by excessive exposure to HCl and pepsin. Non-glandular mucosa response to acid irritation by increasing thickness of its keratin layer- only providing minimal protection.

Causes: Anything that impairs mucosal lining, NSAIDs, Stress, Impaired gastric blood flow, reperfusion injury

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70
Q

What is the predominant stimulato to hydrochloric acid secretion

A

gastric, histamine, and acetylcholine via the vagus nerve.
Gastric- g cells within the gastric glands
histamine- mast cells and enterochromafin-like (ECL)

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71
Q

Ingestion of feed stimulates acid secretion in horses, what is also stimualted by eating to buffer the acid?

A

bicarbonate-rich salivary secretions

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72
Q

What are the protective factors of equine stomach, secreted by the glandular portion

A

Mucous cells: alkaline mucous coating mucosa like a gel
also increased PGE2 secretion

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73
Q

What portion of the equine stomach is most sensitive to acid induced injury?

A

The squamous epithelium (non-glandular) less mucosal protective properties (thick mucus and bicarb later like glandular mucosa has)

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74
Q

What are the 5 causes of gastric ulcerations in horses

A

1) Strenuous exercise - less blood flow and increased acid contact time
2) Stress/illness- decreased PGE2, blood flow, and mucous with increased HCl
3) NSAIDS- Decreased PGE2, blood flow and mucous with increased HCl
4) Feeding- Lenght of meal, type of feed (saliva production, gastrin release, calcium content)
5) infectious causes- H. pylori

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75
Q

What might be an infectious cause of gastric ulceration?

A

Helicobacter pylori (sporadically been found in horses with gastric ulceration)

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76
Q

What are the clinical signs associated with gastric ulceration in adult horses

A

colic, poor body condition, poor hair coat, poor performance, changing appetite, attitude changes, “girthiness”, back pain

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77
Q

What is the difference in clinical signs of gastric ulceration of foals vs adult horses

A

Foals get diarrhea, excessive salivation (1-4mo),
f*oals can perforate

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78
Q

What are the clinical signs of gastric ulceration in foals

A

colic, teeth grinding, DIARRHEA, excessive salivation, reduced appetite

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79
Q

What can be unreliable tests for gastric ulceration in adult horses

A

Fecal occult blood test and constrast radiography

*Testing for fecal occult blood is only of value in young foals isnce the colonic microflora throughly digest hemoglobin

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80
Q

How do you treat gastric ulceration in horses

A

Management- avoid stress, allow access to feed 24hours/day preferable feed small meals frequently, vegetable oils may offer natural protection against ulceration

Medical to decrease gastric acidity and improve mucosal protection
Antacids- Mallox,
Proton pump inhibitor- omeprazole
Anti-histamines (Cimetidine, Ranitidine, Famotidin)
Mucosal protectants- Sucralafate, bismuth subsalylate, misprostol
PGE2 analog- Misprostol

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81
Q

What are drugs that serve as mucosal protectants for gastric ulceration

A

Sucralfate (bandage to unprotected surface, immediate pain relief, does promote healing, does not alter gastric pH, does not prevent ulceration)
Bismuth subsalicylate
Misoprostol (Synthetic PGE2 analog

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82
Q

serves as a bandage to unprotected surface, immediate pain relief, does promote healing, does not alter gastric pH, does not prevent ulceration

A

Sucralfate

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83
Q

Misoprostol is a

A

synthetic PGE2 analogue used to help gastric ulceration

Misoprostol is a synthetic prostaglandin E analog and has been shown to be effective in the treatment of gastric ulcers in humans and horses. The proposed mechanism of action involves both inhibition of gastric acid secretion and mucosal cytoprotection. Reported adverse effects include colic and diarrhea.

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84
Q

What is omeprazole’s mechanism of action

A

inhibiting proton pump which is the final pathway in hydrochloric acid secretion used to help with gastric ulceration

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85
Q

What is the prognosis for gastric ulceration

A

Good: if only squamous mucosa and management changes

Fair: if glandular mucosa

Poor: if perforated

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86
Q

What is the only definitive diagnostic for gastric ulceration

A

Gastroscopy

While a presumptive diagnosis of gastric ulceration is often based on the presence of age-related clinical signs and response to therapy, gastroscopy is the only definitive diagnosis currently available. Diagnostic procedures aimed at the detection of fecal occult blood or plasma protein (e.g. albumin) are unreliable.

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87
Q

True or false: duodenal ulcers and strictures are more common in adult horses than foals.

A

False: they are more common in foals.

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88
Q

What is the primary H2 antagonist used in horses with gastric ulcers?

A

Ranitidine

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89
Q

80% of equine gastric ulcers occur in which part of the stomach?

A

Squamous

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90
Q

The parietal cells in the glandular mucosa of the stomach produce the gastric hydrochloric acid.

Which of the following does NOT stimulate cellular HCl production?
A) Histamine
B) Prostaglandin
C) Acetylcholine
D) Gastrin

A

Prostaglandin

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91
Q

Which of the following is considered to be (a) factor(s) in gastric ulcer formation in horses?

Choose all that apply
Decreased PG E2 production
Increased mucosal blood flow
Large grain meals
Feeding alfalfa
Decreased mucosal blood flow
Decreased mucous production

A

Decreased PG E2 production
Large grain meals
Decreased mucosal blood flow
Decreased mucous production

Factors that have been implicated in gastric ulcer formation in horses include inhibition of prostaglandin E2 synthesis (e.g. by NSAID administration and stress). PG E2 increases blood flow to the stomach mucosa, promotes secretion of bicarbonate-rich mucus (which creates a lumen-to-mucosa gradient in pH from 1.5 to 6.5), and decreases acid secretion. In addition to decreased synthesis of PG E2, other factors that impair gastric blood flow (e.g. intense exercise) may also contribute to ulcer formation. Mucosal capillary perfusion is an integral component of mucosal protection, since disruption of mucosal perfusion readily produces ulcerations. Cellular restitution refers to the regeneration of surface epithelial cells in response to an irritating substance.

Eating behavior has also been shown to have an effect on the risk of gastric ulcer formation. For example, restricting access to roughage and feeding a large amount of concentrate (which reduces the time spent eating and increases postprandial gastrin release) promotes increased gastric acidity. In contrast, high roughage diets tend to stimulate production of bicarbonate-rich saliva, which will help buffer gastric acid. Concentrates stimulate a greater postprandial serum gastrin response than roughage, thus increasing hydrochloric acid production. Moreover, the calcium contained in alfalfa can act as a natural antacid buffer for hydrochloric acid.

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92
Q

What is the best diet for managing horses with gastric ulcers

A

Alfalfa- high calcium content acting as a natural antacid buffer for HCl

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93
Q

What is the most common gastric neoplasia in the horse

A

Squamous cell carcinoma (actually originate from squamous epithelium of esophagus)

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94
Q

How do you diagnose gastric neoplasia like squamous cell carcinoma in a horse

A

pass nasograstric tube for resistance
neoplastic cells may be found in fluid recovered by gastric lavage
Endoscopy- positive diagnosis and biopsy
laparotomy or laparoscopy

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95
Q

What are the equine liver specific enzymes

A

SDH- hepatocellular
GGT- biliary

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96
Q

What are the equine liver associated enzymes

A

AST + LDH: Hepatocellular
AP: biliary

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97
Q

Gamma Glutamyl Transferase (GGT)

A

a biliary specific enzyme
technically not liver specific (Renal tubules-released into urine; Mammary- secreted into colostrum; and pancreas)

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98
Q

What can release GGT

A

Liver
Renal tubule cells - into urine
Mammary glands - secreted into colostrum
Pancreas

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99
Q

What enzyme is high in colostrum fed ruminant neonates

A

GGT

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100
Q

T/F ALT is not useful in large animals

A

True

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101
Q

How do you differentiate between liver disease and liver failure

A

liver failure: inability to perform its normal function
1) Nutrient metabolism (Carbs, lipids, proteins)
2) Biosynthesis (protein biosynthesis)
3) Detoxification/Excretion (Bilirubin, blood ammonia, BUN, phylloerythrin)
4) Immunity
5) Digestion

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102
Q

Hepatic encephalopathy is a clinical sign of

A

liver failure
early: agitation, wandering
late: somnolence, coma

due to increased ammonia and decreased BUN excretion through the urea cycle

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103
Q

May be the first clinical sign of pyrrolizidine alkaloid toxicity or biliary obstruction

A

photosensitization

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104
Q

photosensitization is most severe on

A

non-pigmented skin where reactive compounds are most directly exposed to the UV spectrum.

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105
Q

What is the photosensitizing compound created during liver failure

A

phylloerythrin (normally removed from the liver, after chlorophyll is broken, and then removed by the liver and excreted in bile

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106
Q

Primary photosensitization

A

associated with photodynamic compounds foind in certain plants (Bishops weed, buckwheat, spring parsley, St Johns wort which are absorbed from the digestive react, react with the nonpigmented skin upon IV light.
associated with defective porphyrin metabolism in liver

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107
Q

Can be seen in liver failure because the liver is responsible for the synthesis of numerous factors evolved in coagulation and fibrinolysis

A

Coagulopathy/ hemorrhagic diathesis

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108
Q

What are the clinical signs of liver failure in horses

A

1) Hepatic encephalopathy (early: agitation, wandering/ late: somnolence, coma)
2) Photosensitization
3) Coagulopathy
4) Icterus
5) Weight loss
6) Edema and ascites

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109
Q

What are the 3 causes of icterus in the horse

A

1) Prehepatic - hemolysis
2) Hepatic- hepatocellular dysfuction
3) Posthepatic- cholestasis

*anorexia

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110
Q

in food animals: icterus is more often due to

A

likely due to hemolytic disease rather than hepatic and biliary disease
icterus is rare in cows

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111
Q

in horses: icterus is most likely caused by

A

anorexia, followed by hepatic and biliary disease

exception is foals- do not have enough fat stores, likely neonatal isoerythrolysis or Tyzzer’s Disease

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112
Q

How does equine liver disease result in weight loss

A

decreased feed intake, anorexia, loss of normal hepatocellular metabolic activites

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113
Q

Why do you get ecchymotic hemorhage, epixstaxis, melena, hematuria, and hemotomas in horses with liver disease

A

failure to synthesize II, V, VII, IX X

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114
Q

What factor has the shortest half life

A

Factor VII T1/2= 4-5hours
Will see deficiencies in extrinsic pathway first

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115
Q

Why do you see edema and ascites in horses with liver failure

A

Hypoalbuminemia,
secondary to vascular thrombis (hyperlipidemia in ponies)

half life of albumin is relative long (19-20 days) edema is a rare clinical sign

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116
Q

Why is edema a rare clinical sign in horses with liver failure

A

half life of albumin is relative long (19-20 days) edema

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117
Q

Blood concentration of bile acids will be _________ with liver disease

A

increased.
Serum concentration is not impacted by short term fasting (<14 hours). but prolonged fasting (>3days) will increase serum bile acids of three times the baseline.

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118
Q

What are the most commonly used equine liver function tests?

A

1) Serum bile acid concentrations
2) BUN
3) Dye elimination test - Bromsulphalein
4) Ultrasound and liver biopsy

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119
Q

What is Bromsulphalein (BSP) used for

A

A test for equine liver function. A substance that when injected is metabolized in the liver. Heparin tubes are collected 3,6,9,12 minutes.

BSP half life is prolonged when greater than 50% of hepatic function is lost

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120
Q

Why is a bile acid elevation not specific to equine liver failure

A

They are also increased when there is cholestasis and portosytemic shunting

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121
Q

Are CNS signs typically seen in acute or chronic equine liver disease

A

Acute

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122
Q

Is weight loss typically seen in acute or chronic equine liver disease

A

Chronic

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123
Q

Is photosensitivity typically seen in acute or chronic equine liver disease

A

Chronic

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124
Q

T/F: Chronic equine liver disease will often only have mild elevation of liver enzymes

A

True: Mild

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125
Q

T/F: Acute equine liver disease will often only have mild elevation of liver enzymes

A

False: often severe elevation in the liver enzymes

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126
Q

Theiler’s Disease typically impacts

A

adult horses

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127
Q

Tyzzer’s disease typically impacts

A

foals

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128
Q

Acute hepatitis in adult horses, acute onset with acute hepatic necrosis, liver failure, caused by viral etiology

A

Theiler’s Disease

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129
Q

What is the etiology of Theiler’s disease

A

A mystery but has a viral etiology.
Flaviviridae family- Theiler’s disease associated virus
Equine Parvovirus (EqPV-H) associated with antitoxin?

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130
Q

What is the causative agent of Tyzzer’s disease

A

Clostridium piliforme

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131
Q

What is the prognosis for horses with Theiler’s disease

A

guarded

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132
Q

What causes acite hepatitis, 7-42 days, often peracute with no signs of disease, killing foals with fever, anorexia, icterus, seizures, and coma

A

Tyzzer’s disease caused by Clostridium piliforme

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133
Q

What is the prognisis of foals with Tyzzer’s disease

A

extremely poor
Use supportive care, fluids, NSAIDs, nutrition, tx for hepatic encephalopathy

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134
Q

Does pyrrolizidine alkaloid toxicity cause acute or chronic liver failure in horses

A

Chronic liver failure- weight loss, photosensitivation, icterus, hepatic encephalopathy

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135
Q

The most common cause of chronic liver failure in horses in certain parts of the US

A

chronic megalocytic hepatopathy from pyrrolizidine alkaloid toxicity

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136
Q

Pathogenesis of pyrolizidine alkaloids

A

pyrroles alkylate nucleic acids and proteins (cross links DNA) stopping mitosis and protein synthesis. Hepatocytes then enlarge, forming megalocytes. When megalocytes die- fibrosis (cirrhosis) occurs
Hepatocytes around portal triad (zone 1) are affected first.
bile duct hyperplasia
can cross the placenta and toxic to the fetus

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137
Q

What area of hepatocytes are impacted first from pyrrolizidine alkaloid toxicity

A

Zone 1 is affected first (hepatocytes surrounding the portal triads)

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138
Q

What results in megalocytes?

A

pyrroles alkylate nucleic acids and proteins (cross links DNA) stopping mitosis and protein synthesis. Hepatocytes then enlarge, forming megalocytes.

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139
Q

pyrrolizidine alkaloid toxicity is typically diagnosed by presumptive signs, exposure history and lab evidence of hepatic disease. How do you get a definitive diagnosis

A

Liver biopsy- look for
1) megalocytosis
2) biliary hyperplasia
3) fibrosis

can also be detected in feed by high-performance liquid chromatography

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140
Q

What species is relatively resistant to pyrrolizidine alkaloids?

A

Sheep
-pre-graze pastures laden with PA containing plants

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141
Q

What is the prognosis for pyrrolizidine alkaloid toxicity

A

If fibrosis is present-> prognosis is poor
No treatment available
Serum bile acid concentration greater than 50umol/L is suggestive of grave prognosis

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142
Q

How do you manage a field with tons of pyrrolizidine alkaloid containing plants

A

Sheep
-pre-graze pastures laden with PA containing plants

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143
Q

Is an icteric horse more likely to be experiencing cholastasis or liver disease

A

Cholestasis

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144
Q

What is the cause of cholelithiasis in horses?

A

unknown but
Ascending infection, decreased bile flow and salmonella

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145
Q

What is associated with cholelithiasis in horses?

A

salmonellosis - ascending infection because they lack and exit port sphincter to prevent backflow of intestinal contents into the biliary tract.

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146
Q

Horses do not have an exit port sphincter in their biliary tract. Why is this clinically significant

A

salmonellosis and other enteric pathogens - ascending infection because they lack and exit port sphincter to prevent backflow of intestinal contents into the biliary tract.

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147
Q

How do you treat cholangitis/cholangiohepatitis in horses

A

Supportive care, antimicrobials, NSAIDs, liver support
Surgical approach is better (cholelithotripsy or choledochotomy)

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148
Q

What are the 3 clinical signs of cholangitis/cholangiohepatitis in horses?

A

1) Cholestais- icterus
2) Colic (recurrent)
3) fever (cholangitis)

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149
Q

What is the prognosis of cholangitis/cholangiohepatitis in horses?

A

poor if hepatic fibrosis is present.

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150
Q

What are your differentials for chronic liver failure in horses

A

-Pyrrolizidin Alkaloid toxicity
-Cholangitis/Cholangiohepatitis
-+/- Cholelithiasis

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151
Q

what are possible complication with liver biopsy in horses

A

hemorrhage
pneumothorax
peritonitis
abscess

*keep in mind they might have prolonged coagulation times with liver failure

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152
Q

What would you see on ultrasound if the horse has hepatomegaly

A

rounded edge and swollen

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153
Q

What are the intermediate hosts for liver flukes (Fasciola hepatica)

A

Snails

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154
Q

What causes bacillary hemoglobinuria

A

toxins produced by Clostridium hemolyticum (Clostridium novyi type D)

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155
Q

What is another name for Clostridium hemolyticum, the causative agent of bacilary hemoglobinuria

A

Clostridium novyi type D

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156
Q

What are the exotoxins that cause bacillary hemoglobinuria

A

beta toxin: phospholipase C- necrosis and hemolysis
eta toxin: tropomyosinase
theta toxin: lipase

*Cause hepatic necrosis and intravascular hemolysis

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157
Q

What is the pathogenesis of bacillary hemoglobinuria

A

spores of Cl. hemolyticum are ingested and cross the intestinal mucosa. spores reach the liver by portal circulation and can persist in the liver tissuw for long periods of time within the Kupffer cells. Following a hepatic insult (liver fluke migration, hepatic inflammation or abscesses, liver biopsy)

Creates an anaerobic environment , spores become activated and germinate, Beta, eta, and theta toxins are produced. causing hepatic necrosis and hemolysis, icterus, hemoglobinuria

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158
Q

In most cases, the liver insult seen in Red water disease by Clostrium hemolyticum (novyi type D) is due to

A

migration of Fasciola hepatica

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159
Q

What are the clinical signs of bacillary hemoglobinuria?

A

Hemolysis: Red serum/plasma, hemoglobinuria, anemia (pale mm, tachycardia)
icterus (pre-hepatic)
DIC
blood tinged frother (mouth and nose)
Rectal bleeding, blood in feces
ischemic hepatic infarct

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160
Q

What is another differential you need to rule out when an animal has bacillary hemoglobinuria?

A

Anthrax (Bacillus anthracis)

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161
Q

How do you diagnose bacillary hemoglobinuria

A

1) Fluorescent antibody test on impression smears taken from liver infarct for Cl. hemolyticum antigens

2) Necropsy- icterus, red urine, petechia, ecchymoses, red-tinged fluids, ischemic infarct

3) Clinically: anemia, increased plasma protein, DIC (fibrin degradation products, decreased platelet counts)

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162
Q

What does Clostridium novyi type D cause

A

Bacillary hemoglobinuria

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163
Q

What does Clostridium novyi type B cause

A

Blacks disease

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164
Q

What are the toxins of Clostridium novyi type B? What do they cause

A

alpha, beta, zeta (local and systemic effects)

Hepatic necrosis, endothelial damage*, resulting in passage of RBCs into tissue, neuronal damage

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165
Q

What are the clinical signs associated with Black’s disease

A

Animals usually found dead
Clinical signs are nonspecific
no red urine or external (nose/rectal) bleeding

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166
Q

What is seen upon the necropsy of an animal with Black’s disease

A

hemorrhage of suncutaneous tissues results in black discolaration of carcass - looks like diffuse bruising of all muscles
Diagnose with impression smear taken from the margin of the liver lesion - revealing numerous large gram + rods. Confirm diagnosis with fluorescent antibody testing to identify Cl. novyi type B should be performed

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167
Q

How do you diagnose Black’s disease

A

Diagnose with impression smear taken from the margin of the liver lesion - revealing numerous large gram + rods. Confirm diagnosis with fluorescent antibody testing to identify Cl. novyi type B should be performed

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168
Q

How do you prevent Blacks disease

A

vaccination - last 5 to 6 months
control flukes

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169
Q

How do you prevent Bacillary hemoglobinuria

A

vaccination - last 5 to 6 months
control flukes

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170
Q

Decreased production is a sign of acute or chronic liver failure in cattle

A

Chronic disease

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171
Q

________ are a common complication of ruminal acidosis

A

Liver abscesses

172
Q

What kind of ruminants are at risk for developing liver abscesses

A

ruminants that are fed excessive amounts of fermentable carbohydrates (grains/concentrations, finely ground silage) generally, starch and sugars

common among feedlot cattle (25-30%)

173
Q

What causes bovine liver abscesses

A

during ruminal acidosis (ruminitis), typically when fed excessive amounts of fermentable carbohydrates,, Fusobacterium necrophorum overgrows and invades the eroded wall and is carried by the portal circulation to the liver. Once lodged it produces toxins that destroy keukocytes and aids in pathogenic process

174
Q

What causes liver abscesses in neonatal calves

A

ascending infection of the umbilical vein.
Prevent with good hygiene and umbilical disinfection

175
Q

Symptoms of liver abscesses in cattle

A

-Subclinical: reduced gain, decreased productivity
Laminitis
Endotoxemia (Rumen acidosis)
Less common: acute hepatitis: fever, arched back, mild colic due to hepatic swelling
Caudal vena cava syndrome- abscess can erode into the caudal vena cava, producing caudal vena cava thrombosis

176
Q

What is caudal vena cava syndrome

A

a serious sequela following liver abscesses- erosion into the caudal vena cava
produces caudal vena cava thrombosis

177
Q

How do you diagnose liver abscesses in cattle

A

*Farm HX (production, liver abscesses, laminitis

Inflammatory leukogram with hyperfibrinogenmia in acute stage
Increased liver enzymes (SDH, AST, possibly GGT, and AP) in the acute stage

Subacute to chronic- hematology and chem may be normal, although TP may be evident from immunoglobulin production

178
Q

How do you treat liver abscesses in cattle?

A

Prognosis for complete recovery is poor

179
Q

How do you prevent liver abscesses in cattle?

A

gradual change of the amount of carbohydrates fed (3-4 week period)
feed ration in small amounts frequently
add antibiotics to reduce incidence of liver abscesses in high risk feeder cattle (commonly Tylosin)

Avoid slug feeding with refers to ingestion of large quantities of grain-rich ration.

180
Q

within the cell wall of all gram negative bacteria
released during replication and death
can cause shock if released into circulation

A

endotoxins

181
Q

T/F: endotoxins are within the cell wall of all gram negative bacteria

A

True

182
Q

Are endotoxins or exotoxins heat resistance

A

Endotoxins

183
Q

What are the components of endotoxins

A

1) Lipid A (hydrophobic)
2) O-specific polysaccharides (Hydrophilic)
3) Core region (Hydrophilic)

184
Q

What prevents the absorption of most of the endotoxins from being absorbed?

A

Mucosa barrier:
epithelial cells
antibodies
enzymes

185
Q

How does impaired liver function result in endotoxemia?

A

failure to filter out toxins, bacteria, etc.

186
Q

How might there be an impairment in the mucosa leading to endotoxemia

A

ischemia and inflammation allow endotoxins to enter into the circulation
-Inflammation changes the permeability of the mucosa when diseases
this causes massive portal bacterial and toxins overload the liver leading to endotoxemia and sepsis

187
Q

What happens once endotoxins enter the circulation

A

it interacts with circulating proteins (LPS binding protein) or it may be removed by macrophages in liver, spleen and pulmonary vasculture.
LPS binding protein interacts with lipid A portion of endotoxin.

Combination of LBP and and endotoxin interact with cell surface receptor, CD14- a patter recognition receptor on phagocytes

Soluble CD14 can also interact with LBP/endotoxin to activate cells without receptor (endothelial cells)

Signals are intracellularly transmitted to signal release of proinflammatory mediators (TNF-a + Tissue factor) and anti-inflammatory mediators (IL-10)

188
Q

What is released when LPS binding protein and endotoxin is bound to CD14

A

Proinf: TNF-a and tissue factor

Anti-inflammatory: IL-10

189
Q

TNF-a is a

A

proinflammatory mediator/cytokine released after the onset of endotoxemia. Initiates a cascade of responses:
-Hypotension
-Hemoconcentration
-Metabolic acidosis
-DIC
Stimulates synthesis of Interleukins, acute phase proteins, tissue factor

TNF-a concentration has been associated with prognosis for survival

190
Q

What is a result of TNF-a in endotoxemia

A

-Hypotension
-Hemoconcentration
-Metabolic acidosis
-DIC

Stimulates: interleukins, acute phase proteins and tissue factor

191
Q

The majority of the effect seen in endotoxemia are due to

A

overproduction and release of inflammatory mediators by the immune cells

192
Q

A glycoprotein synthesized by mononuclear phagocytes and mononuclear in response to endotoxin. Comes into contact with coagulation factor VII in plasma- activating the extrinsic arm of the coagulation cascade. Formation of microthrombi
Makes the vasculature sticky, leaky, and soggy

A

Tissue factor

193
Q

What does it mean when endotoxin makes the microvasculature “sticky, leaky, and soggy”

A

Results in
1) Leukopenia- leukocyte margination
2) Fluid leakage- hypovolemia and hypoproteinemia
3) Pooling of blood in microvasculature- injected blood vessels and hypotension

194
Q

How does endotoxin cause leukopenia and neutropenia

A

activated endothelium, margination, from sticking against the vascualar wall

195
Q

Endotoxemia causes (Hypotension/Hypertension)

A

Hypotension

196
Q

What are the clinical diseases associated with endotoxemia

A

1) Sepsis
2) Colic
3) Colitis

197
Q

What are the clinical signs of endotoxemia

A

1) Increased HR and RR
2) Ileus
3) Mild to moderate colic
4) Congested mucous membranes
5) Injected vessels
6) Increased CRT
7) Decreased peripheral pulses
8) DIC- thrombosis, petechiation, ecchymosis
9) Laminitis- may progress after systemic signs improve
10) Hemoconcentration

198
Q

How do you treat endotoxemia in the horse

A

1) Prevent uptake of endotoxin into the circulation: Remove source- umbilicus, colic surgery, effusions or bind endotoxin within the GI lumen using a Bio-sponge and activated charcoal

2) Neutralization of endotoxin already present in system: Antiendotoxin antiserum (core and lupud A, enhances opsonization- has some adverse reactions) or polymyxin B- antibiotic that forms complexes beneficial effect seen but has nephrotoxicity

3) Prevention of release of inflammatory mediators
NSAIDS- prevent endotoxin-induced synthesis of prostaglandins and thromboxane- give Flunixin Meglumine- low dose to decrease nephrotoxicity risk
Glucocorticoids- No beneficial effects- increase likelihood of laminitis

4) Prevention of endotoxin-induced cellular activation
Toxic oxygen metabolite scavengers- Allopurinol or DMSO- reduces mucosal injury and prevent receptor interaction and tissue injury

199
Q

How do you prevent the uptake of endotoxins in the horse

A

Remove source- umbilicus, colic surgery, effusions or bind endotoxin within the GI lumen using a Bio-sponge and activated charcoal

200
Q

How do you neutralize endotoxins in the circulation

A

1) Antiendotoxin antiserum: antibodies directed against the core and lipid A regions to enhance opsonization of intact bacteria, remove endotoxin from the blood- given 1.5ml/kg

2) Polymyxin B- broadspectrum antibiotics that forms a stable complex with lipid A for the treatment of endotoxemia in horses . Can cause respiratory paralysis and nephrotoxicity

201
Q

broadspectrum antibiotics that forms a stable complex with lipid A for the treatment of endotoxemia in horses . Can cause respiratory paralysis and nephrotoxicity

A

Polymyxin B

202
Q

antibodies directed against the core and lipid A regions to enhance opsonization of intact bacteria, remove endotoxin from the blood- given 1.5ml/kg

A

Antiendotoxin antiserum

203
Q

Why should you not use glucocorticoids in treating endotoxemia in horses

A

because it increases the risk of laminitis

204
Q

Do you want to use low or high dose of Flunixin Meglumine (Banamine) in treating endotoxemia in horses?

A

Low dose (0.25 mg/kg QID,TID
decreases risk of nephrotoxicity

205
Q

What NSAID should you use to present inflammatory mediator (prostaglandins and thromboxane) release in horses with endotoxemia?

A

Flunixin Meglumine (Banamine)
low dose to decrease risk of nephrotoxicity

206
Q

What is Allopurinol used for

A

it is a hydroxyl radical scavenger and inhibitor of xanthine oxidase activity, prevents toxic oxygen metabolities from causing damage during endotoxemia

207
Q

it is a hydroxyl radical scavenger and inhibitor of xanthine oxidase activity, prevents toxic oxygen metabolities from causing damage during endotoxemia

A

Allopurinol or DMSO

208
Q

The following statement is TRUE or FALSE?

The presence of photosensitization in horses and livestock species is always indicative of liver disease/failure?

True
False

A

The statement is false.

Photosensitization can be classified into two basic types; primary and secondary.

Primary photosensitization is associated with photodynamic compounds found in certain plants (e.g. Bishop’s weed, Buckwheat, Spring parsley, St. John’s wort), which once absorbed from the digestive tract, react in the nonpigmented skin with UV light.
Secondary or hepatogenous photosensitization, as the name implies, results when an animal’s liver is sufficiently diseased to be unable to remove plant by-products that can react with UV light. Phylloerythrin, a bacterial breakdown product of chlorophyll, is the photosensitizing compound. Normally, phylloerythrin is removed by the liver and is excreted in bile. Hepatic photosensitization can be further subdivided into that attributable to hepatocellular disease as opposed to that caused by biliary disease and cholestasis.

209
Q

Which of the following CBC abnormalities is commonly seen in the early stages of endotoxemia?

A

In the early stages of endotoxemia and sepsis, profound neutropenia with toxic neutrophil morphology with a left shift is often evident. Neutropenia is due to margination and transmigration of cells and occurs within an hour of onset of endotoxemia. Other abnormalities notes on the CBC and biochemistry panel reflect nonspecific secondary changes (e.g. hyperglycemia, polycytemia and metabolic acidosis due to hypovolemia, azotemia due to hypovolemia and hypotension).

210
Q

Which of the following drugs binds circulating endotoxin, thereby preventing its interacting with receptors and hastening its elimination?

A

Polymyxin B

Polymyxin B is a broad-spectrum antibiotic that forms a stable complex with lipid A, thus preventing its interaction with cellular receptors and hastening its elimination.

Flunixin meglumine (Banamine) is a NSAID and reduces the synthesis of inflammatory mediators.

Dimethyl sulphoxide (DMSO) is a potent scavenger of hydroxyl radicals.

Allopurinol is a hydroxyl radical scavenger and inhibitor of xanthine oxidase activity

Dexamethasone is a glucocorticosteroid and is a potent inhibitor of inflammatory mediator synthesis. Despite this, no beneficial effects of steroid use was found in large, multicenter studies of humans with gram-negative sepsis. In addition, corticosteroids are also often implied to increase the likelihood of laminitis in endotoxic horses. Thus, corticosteroids are not recommended in the treatment of endotoxemia.

211
Q

Endotoxemia is unlikely to occur in which of the following disease processes?
Large colon impaction
Strangulating lipoma
Pleuropneumonia
E. coli mastitis
Colitis

A

In horses, most diseases characterized by endotoxemia/sepsis affect the gastrointestinal tract (e.g. intestinal inflammation or ischemia) or involve bacterial infections of the pleural or peritoneal cavities. In cattle, gram negative mastitis and metritis are common causes for endotoxemia. As large colon impactions typically do not result in an impairment of the intestinal barrier, they are usually not associated with endotoxemia.

212
Q

Which of the following clinical signs are commonly encountered in endotoxic horses?
Tachycardia
Injected scleral blood vessels
Coughing
Colic
Laminits
Urticaria

A

Tachycardia, injected scleral blood vessels, colic, and laminitis

Horses given endotoxin experimentally develop tachycardia, a fever, ileus, mild to moderate abdominal pain (e.g. pawing, looking at flank region, stretching out, lying down), congested mucous membranes (+/- a “toxic” line), prolonged the capillary refill time (CRT), as well as signs of dehydration, such as reduced skin turgor, tacky mucous membranes, hemoconcentration (↑ PCV), rapid and weak peripheral pulses, cold extremities, and sweating. Vascular damage and hemorrhagic diathesis may be seen as petechial and ecchymotic hemorrhages. A poor prognostic sign is the development of a hypercoagulative state, with thrombosis of vessels, and subsequent increased bleeding tendency (a consequence of platelet and coagulation factor consumption and uncontrolled activation of fibrinolyis). Signs of laminitis, a complication of endotoxemia, may also develop.

213
Q

What are the two types of infiltrative intestinal diseases?

A

1) Inflammatory (IBD) - granulomatous enteritis, lymphocytic-plasmacytic, idiopathic eosinophilic, multisystemic eosinophilic epitheliotrophic disease (MEED)
2) Lymphosarcoma

214
Q

What do horses with small intestine disease not get?

A

Diarrhea (diarrhea is apparent in large intestinal disease)

they only get weight loss

215
Q

What are the clinical signs of equine small intwstinal disease

A

1) Weight loss and lethargy- thickening of mucosa and blunting of the villi -> malabsorption

2) Edema- loss of tight junctions and ulcerations leading to protein loss and edema

3) Depending on type, severity and location- colic (granulomatous enteritis and eosinophilic enteritis) and skin lesions -eosinophilic enteritis and MEED

216
Q

How do you get edema with equine small intestinal diseases

A

loss of tight junctions and ulcerations leading to protein loss and edema

217
Q

How do you get weight loss with equine small intestinal diseases

A

Weight loss and lethargy- thickening of mucosa and blunting of the villi -> malabsorption

218
Q

agregates of macrophages and epitheloid cells, occasionally giant cell macrophages, usually diffuse across the small intestine

A

granulomatous enteritis

219
Q

infiltration of the mucosa and submucosa with eosinophils, lymphocytes, and macrophages- segmental/multifocal across small intestine, skin, oral cavity, esophagus, salivary glands, liver, lung, mesenteric lymph nodes, and pancreas

A

MEED- multisystemic eosinophilic epitheliotrophic disease

220
Q

How will small intestinal infiltrative disease look like on ultrasonography

A

thickened small intestine, several loops of moderately distended small intestine

221
Q

What test can you se to detect malabsorption in horses with granulmatous enterities and lymphocytic-plasmacytic enteritis

A

Carbohydrate absorption test.

Horse fasted for 18 hours
10% solution of glucose of D-xylose is goven through nasogastric tube
Blood for glucose/D-xylose is collected at 0,30,60,90,120,150,180,210,and 240 minutes
Plasma peak levels should occur between 60 and 120 minutes. Delayed or flattened peaks are consistent with malabsorption diagnosis

222
Q

when should the peak in the carbohydrate absorption test occur in order to rule out malabsorption

A

Peak should occur between 60-120 minutes after administering glucose/D-xylose

223
Q

How is a carbohydrate absorption test performed?

A

Carbohydrate absorption test.

Horse fasted for 18 hours
10% solution of glucose of D-xylose is goven through nasogastric tube
Blood for glucose/D-xylose is collected at 0,30,60,90,120,150,180,210,and 240 minutes
Plasma peak levels should occur between 60 and 120 minutes. Delayed or flattened peaks are consistent with malabsorption diagnosis

224
Q

How is infiltrative intestinal disease definitively diagnosed?

A

Biopsy and histopathology to see the predominant cell type present in the intestinal lesions
-exploratory celiotomy or flank laparotomy is required

225
Q

How do you treat infiltrative bowel disease

A

-Corticosteroids (limit timing)
-Metronidazole- anti-inflammatory and antimicrobial (no idea on efficacy
-Anthelmintics (eosinophilic enterocolitis)

226
Q

Adult horse diarrhea usually involved abnormality in the

A

large intestine (large colon +/- cecum)

227
Q

What are your differentials for diarrhea in a horse

A

1) Salmonellosis *
2) Intestinal clostridiosis (Cl. difficile and Cl. perfringens)*
3) Potomac Horse Fever*
4) Equine coronavirus*
5) antibiotic-associated colitis*
6) NSAID toxicity
7) intestinal parasites
8) nutritional causes
9) sand induced
10) toxin exposure
11) peritonitis *

*=usually acute

228
Q

Salmonella in a horse typically causes (acute/chronic) diarrhea

A

usually acute

229
Q

Intestinal clostridiosis (difficile and perfringens) in a horse typically causes (acute/chronic) diarrhea

A

usually acute

230
Q

Potomac horse fever in a horse typically causes (acute/chronic) diarrhea

A

usually acute

231
Q

Equine coronavirus in a horse typically causes (acute/chronic) diarrhea

A

usually acute

232
Q

Antibiotic-associated colitis in a horse typically causes (acute/chronic) diarrhea

A

usually acute

233
Q

What are some common diarrhea causing parasites in horses

A

Cynthostomiasis
Strongylus vulgaris
Parascaris equorum
Cryptosporidia

234
Q

What is the diagnostic approach to diarrhea in a horse

A

-CBC/Chem/VBG, UA

-Abdominal ultrasonography +/- abdominocentesis- assessment of bowel wall thickness (severity and prognosis)- rule out sand and peritonitis

-Fecal examination- PCR analysis (IDEXX diarrhea panel), fecal egg count (cyathostomiasis, ascarids), check for sand (sedimentation)

-Abdominal x-rays (sand and assess amount

-Other test (aerobic culture for salmonella, anaerobic culture for Clostridia spp, CLostridial toxin ELISAs, PHF serology

235
Q

A gram - facultative anaerobe that causes acute diarrhea in the horse

A

Salmonella
type species S. bongori and S. enterica

236
Q

what are the risk factors for salmonellosis in the horse

A

-Age
-Stress (shipping, surgery, feed changes, illness)
-Disruption of GI flora and motility (colic and ABCs)
-Environment- hot and humid, persistence, multiplication
-Insects (mechanical fectors)
-Birds- vector and resevoir
-Other horses: feco-oral, aergoenous, fomites, water, feeds
-Cattle- Vertical from S.dublin
-Rodents- vector and reservoir

237
Q

What are the clinical signs of Salmonellosis in horses

A

1) Asymptomatic: from lower infectious dose, varying prevalence

2) Colitis: fulminant disease- pipe stream diarrea- ileus, colic, and laminitis

3) Abortion- S. abortus equi not seen in US in decades

4) Febrile illness- delayed onset of signs, rapid fecal shedding, mild change in fecal consistency, often self-limiting

5) Sepsis - often fatal, isolation from liver, mesenteric lymph nodes, kidney, foals: joints

238
Q

How do you diagnose salmonellosis in horses

A

culture of fecal sample using enrichment techniques (enrichment broth of Selenite or tetrathionate) and selective media (XLD agar: xylose-lysine deso-oxycholate) keep samples chilled and place directly in enriched media
aerorbic culture
potentially PCR

239
Q

How do you treat Salmonellosis in horses

A

Early- replace lost fluids
not much that you can do
antibiotics is controversial unless they are neutropenic or patient has signs of septicemia then use a broad spectrum antibiotic

240
Q

How does intestinal hyperammonemia in horses occur

A

due to increased blood NH4+ concentration
1) increased absorption due to altered permeability of GI wall
2) Increased production, overgrowth of ammonia producing bacterial
3) Failure of liver to clear ammonia leading to hepatic encephopathy*** most likely

*Prognosis is guarded to poor if severe strcutural gastrointestinal lesions

241
Q

What is the most likely cause of intestinal hyperammonemia in the horse?

A

Failure of liver to clear ammonia leading to hepatic encephopathy

242
Q

What is the pathogenesis of Salmonellosis

A

1) most commonly oral infection
2) Attachement to mucosal cells- increased if GI stasis is present
3) Inflammation triggered - causes focal and diffuse PMN infiltrates, epithelial necrosis, edema formation
4) Tissue invasion and dissemination- gain entry via mononuclear phagocytes, M cells, and lymphatic system

243
Q

How does salmonella gain entry

A

via mononuclear phagocytes, M cells, and lymphatic system

244
Q

What are the post-mortem findings of a horse with Salmonellosis

A

Fibrinosuppurative and necrotizing typhlocolitis - inflammation in colon results in fresh blood in feces

245
Q

Is there increased Salmonella shedding at home or the hospital

A

at the hospital- stress
host susceptibility plays an important role in the pathogenicity

246
Q

What is the enrichment broth used to diagnose Salmonellosis

A

Selenite or tetrathionate

247
Q

What time of year does equine coronavirus infections typically occur

A

during the colder months (October to April)

248
Q

What are the risk factors to equine coronavirus

A

-Colder months (October to April)
-Midwest
-Draft horse
-Ranch/farm and breeding

249
Q

an enveloped RNA virus that causes acute diarrhea in horses

A

Equine Coronavirus

250
Q

Does Equine Coronavirus cause high morbidity or mortality

A

high morbidity (field outbreaks 10-83%)
fatalaties are rare

251
Q

What are the clinical signs of equine coronavirus

A

-Anorexia (97%)
-Lethargy (88%)
-Fever (83%)
-Diarrhea (23%)
-Colic (19%)
-Neurological signs (3%)

252
Q

When is equine coronavirus typically shed

A

incubates for 48-72 hours and then sheds 3-4 days post-infection and can shed up to 25 days

253
Q

How do you diagnose equine coronavirus in a horse

A

Detection of the virus in the feces by PCR

254
Q

How do you treat Equine Coronavirus?

A

No specific treatment but most adult horses recover within a few days.
Supprotive treatment may include fluids, NSAIDs, electrolytesm and GI protectants

255
Q

What causes Potomac Horse fever

A

Neorickettsia risticii (intracellular bacteria)

256
Q

What does Neorickettsia risticii cause

A

Potomac horse fever

257
Q

What is another name for equine monocytic erlichiosis

A

Potomac horse fever

258
Q

What time of the year does Potomac horse fever typically occur during

A

Summer (June through September)

259
Q

DNA of Neorickettsia risticii has been found in

A

Aquatic snails
Aquatic larval insects

260
Q

What cell type does Neorickettsia risticii infect

A

blood monocytes, it is an intracellular bacteria

has a predilection for intestinal wall, especially the large colon

impaes absorption of Na and Cl from lumen causing a watery diarrhea

261
Q

How is Neorickettsia risticii transmitted to the horse

A

Life cycle involving snails (1st intermediate host), cercariae, larva aquatic insect (2nd intermediate horse), adult aquatic insect, and insectivores

262
Q

How do you diagnose potomac horse fever

A

serological testing using indirect fluorescent antibody (IFA)
-does not confirm if they are currently infected or if the antibodies were produced during a previous exposure or vaccination

263
Q

How do you treat Potomac Horse Fever

A

Tetracycline IV
Vaccination is available

*protection is incomplete as there are different strains- lessens the impact of the disease though

264
Q

What are the pros and cons of when to use antimicrobial therapy in horses

A

Pros: Neutropenic patient, risk of sepsis, Clostridial species, Potomac horse fever

Cons: may not alter the course of the disease, may interfere with competing GI flora, toxicity issues

265
Q

What time of year is Salmonellosis in horses more common

A

Late Summer months and fall- shedding and occur continuously or intermittently

266
Q

Which of the following clinical signs is NOT encountered in horses with small intestinal infiltrative disease unless disease?
Colic
Diarrhea
Weight loss
Edema
Lethargy

A

Diarrhea
The most prominent clinical sign of small intestinal infiltrative disease is weight-loss secondary to malabsorption. Diarrhea is not apparent unless the large intestine is also involved. Additional clinical signs of infiltrative intestinal disease include dependent edema (due to protein loss) and lethargy (due to malabsorption of nutrients). Occasionally, affected horses may be presented with colic.

267
Q

T/F: Horses with a Salmonella positive fecal culture result always have clinical signs such as diarrhea.

A

The statement is FALSE. Depending on the population surveilled, approximately 1 to 7% of horses are subclinically infected with salmonella and actively shed the organism without outward signs of clinical disease.

268
Q

The prevalence of diarrhea caused by which of the following agents is higher in the winter than the summer?
Equine Coronavirus
Potomac Horse Fever
Salmonellosis

A

Equine coronavirus infections are more commonly seen during the cold weather months (between October through April). In contrast, the incidence of Potomac Horse Fever is highest during the summer months (June through September). The peak incidence of salmonellosis in horses occurs in late summer and fall.

269
Q

The following statement is TRUE or FALSE?

The use of antibiotics is always indicated in horses with acute colitis.

A

The statement is FALSE.
The use of antimicrobials in the treatment of diarrhea is controversial. In cases of colitis caused by N. risticii, the efficacy of tetracycline intravenously has been documented clinically and experimentally. In contrast, the effect of antimicrobials in diarrhea caused by other microorganisms (e.g. Salmonella spp.) is not well documented and is associated with potential risks (e.g. interference with competing GI flora). In severely neutropenic patients the use of broad-spectrum antibiotics is justified to provide systemic protection from bacteremia.

270
Q

Do equine endocrine disorders have an increasing incidence?

A

-Aging horse population (more common with age)
-Improved diagnostics
-Awareness and education about endocrine disorders

271
Q

What are the two most common equine endocrine disorders

A

Equine Cushings Disease ( PPID)
Equine Metabolic Syndrome (EMS)

*also pheochromocytoma, thyroid disease in foals, diabetes insipidus

272
Q

In horses: Cushing’s disease is always caused by

A

abnormal function of the pituitary gland

*not necessarily high levels of cortisol in the blood like seen in dog and human (pars distalis)

273
Q

What part of the pituitary has increased secretion in Equine Cushing’s

A

Pars intermedia

274
Q

The pars intermedia of the anterior pituitary is composed of a homogenous population of

A

Melanotrophs - contain propiomelanocortin (POMC)produces a-MSH, b-END, and corticotropin-like intermediate lobe peptide (CLIP)

275
Q

The pars distalis of the anterior pituitary is composed of these 5 cell types

A

1) Somatotrophs- Growth hormone
2) Lactotrophs- Prolactin
3) Corticotrophs- POMC- ACTH, a-LIP, b-END
4) Thyrotrophs- TSH
5) Gonadotrophs- FSH and LH

276
Q

Within the anterior lobe of the pituitary, How are signals from the hypothalmus arrived to the pars distalis vs the pars intermedia

A

-Pars distalis- hormones released from hypothalmus, reach pituitary by portal system

-Pars intermedia- poorly vascularized- secretion is controleld by neurotransmitters that are released from axons (hypothalmus)

277
Q

How does POMC in the melanotrophs (pars intermedia) and the corticotrophs (pars distalis) differ

A

POMC (pars distalis) : ACTH (high), LPH, MSH, b-END)
ACTH acts on the adrenal gland to make cortisol

POMC (pars intermedia): MSH, b-end, ClP, ACTH (small) - POMC peptides serve various functions

278
Q

What inhibits the secretion from the melanotrophs of the pars intermedia

A

Dopamine

279
Q

What modulates secretion from the melanotrophs of the pars intermedia?

A

-Serotonin
-Epinephrine, Norepinephrin
-y-aminobutyric acid (GABA)

280
Q

T/F Melanotrophs respond to negative feedback

A

False: they do not

In the horse- increased secretion of pars intermedia (always) - POMC; a-MSH, bEND, etc (ACTH only a small amount)

281
Q

Why is Equine Cushing’s called PPID

A

because the pars intermedia is dysfunctioning to always secrete POMC: a-MSH, bEND, etc
No negative feedback

282
Q

How does PPID occur?

A

abnormal function of the pars intermedia because of a loss of hypothalamic control

Dopamine inhibits hormone secretion of the pars intermedia and dopamine’s inhibition decreases over time as nerve cells die off

Without inhibition of secretion, pituitary cells enlarge and may even undergo neoplastic change

283
Q

What is the signalment of horses with PPID

A

older horses (typically >15 years old)
Average 19-21 years old
All breeds affected
Increased in ponies? - pituitary adenomas

Youngest: 6 years

284
Q

What are the clinical signs of PPID?

A

1) Hypertrichosis/hirsutism (long shaggy hair coat, usually associated with abnormal shedding patter - late shedding or no shedding in spring)
2) Hyperhidrosis- excessive sweating
3) PU/PD (maybe)
4) Muscle loss

others in association with above and hoof abscess
1) Chronic/recurrent laminitis
2) lethargy
3) Chronic infections* (respiratory and sinus, GI parasites- ascarids) and delayed wound healing
4) Bulging of supraobrital fat
5) Blindness (rare)

285
Q

T/F: laminitis is common in horses with PPiD

A

True but not every horse with laminitis has PPID

286
Q

T/F you get clinical signs of hypertrichosis and hyperhirsutism in early PPID

A

False, not all signs have to be present. These typically arent common in early disease

287
Q

ACTH and cortisol may not be elevated in _______

A

early disease

288
Q

ACTH and cortisol levels are typically higher in what time of year?

A

fall time- CSU doesnt offer fall reference ranges

289
Q

Why might there be a false positive in testing for PPiD

A

1) ACTH and cortisol levels are typically higher in the fall
2) Stress (pain and trailering) can falsely elevated ACTH and cortisol

290
Q

What is the best test to run if you suspect early PPID in a horse

A

THR stimulation test (Thyroid Releasing Hormone Stim test)
When given TRH, Cushings horses will release the expected triiodothyronine (T3) and thyroxin (T4) but will also increase plasma ATCH concentration for 15 minutes. Useful for borderline cases (horses with clinical signs but normal resting endogenous ACTH levels) Collect 10-30 min following administration TRH IV. 30 minute sample is more reliable. Cutt offs are 100pg/mL at 10min post TRH and 35pg/mL at 30min post TRH

Positive: Initiate treatment
Negative: re-assess in 3-6 months

291
Q

Thyroid Releasing Hormone Stim Test

A

When given TRH, Cushings horses will release the expected triiodothyronine (T3) and thyroxin (T4) but will also increase plasma ATCH concentration for 15 minutes. Useful for borderline cases (horses with clinical signs but normal resting endogenous ACTH levels) Collect 10-30 min following administration TRH IV. 30 minute sample is more reliable. Cutt offs are 100pg/mL at 10min post TRH and 35pg/mL at 30min post TRH

Positive: Initiate treatment
Negative: re-assess in 3-6 months

292
Q

What is the best test to run if you have a horse with history and clinical signs consistent with PPID and you suspect moderate to advanced PPID

A

Baseline ACTH

Measuring the endogenous plasma ACTH

Positive: Initiate treatment
Negative: Do a TRH stim test (Positive initiate treatment, if not re-assess in 3-6 months)

293
Q

Of all the diagnosis methods of PPID, which are not affected by stress/pain

A

-Domperidone response test and a-MSH
-CT and MRI

294
Q

What are the methods used to diagnose PPID in a horse?

A

1) Dexamethasone suppression test (DST)
2) Resting plasma (endogenous) ACTH level
3) Resting plasma cortisol level
4) Thyroid-releasing hormone (TRH) response test
5)Domperidone response test and a-MSH **
6) Urinary cortisol:cretinine ration
7) CT and MRI **

*****= stress/pain do not impact these

295
Q

Used to be the golden standard for diagnosing PPID but has since fallen out.
Administration of dexamethasone in late afternoone should depress cortisol production to less than 10ng/ml in the morning
Horses with Cushings typically show a small degree of suppression which will not persist for the 17 to 19 hours in which the overnight protocol is performed

A

Dexamethasone Suppression Test

296
Q

May be a promising new test for diagnosis of PPID. Horses with PPID react to domperidone admin with exagerrated icnrease in endogenous ACTH concentration 2-4 hours after administration.

A

Domperidone Response test- not impacted by stress and pain

297
Q

How do you treat PPID in horses?

A

1) Dopamine agonists: Pergolide and Bromocriptine
2) Antiserotonergic actions: Cyproheptadine

298
Q

What is probably the most effective drug at treating PPID

A

Pergolide - a long-acting oral dopaminergic agonist

299
Q

What are the two dopaminergic agonists used for treating PPID

A

1) Pergolide (better)
2) Bromocriptine

300
Q

Bromocriptine

A

a dopaminergic agonist used to treat PPID
expensive and Pergolide works better

301
Q

Pergolide is used to treat

A

PPID in horses

302
Q

Cyprohepatadine

A

an antiserotonergic agent that has been used with limited success in treating parsintermedia dysfunction in horses.
Wide safety margin

303
Q

T/F: Mitotane/Op-DDD (Lysodren) can be used to treat PPID in horses

A

False- not effective- causes selective necrosis of zona fasiculata and reticularis)
commonly used to treat pituitary Cushings in dogs though

304
Q

Trilostane

A

a competitive inhibitor of 3-b-hydroxysteroid dehydrogenase to attempt to block endogenous cortisol production by the adrenal gland

not potent enough to block cortisol synthesis in patients with hypercortisolism

Pergolide seems to be better

305
Q

Is the prognosis for PPID good?

A

good if endocrinological control has been achieved and laminitis is well managed

306
Q

How should you monitor response to PPID therapy

A

-Clinical signs
-Endogenous ACTH
-Dexamethasone suppression test

Adjust therapy as needed

307
Q

What are the clinical signs of equine metabolic syndrome (EMS)

A

-Obesity (crest of neck, gluteal region, sheath, omental fat)
-“easy keepers”
-Laminitis
-Difficult to breed
-PU/PD (rare)

308
Q

What are the breed predilection for equine metabolic syndrome?

A

Peruvian Pasos, Ponies, Saddlebreds, Morgan Horses, Warmbloods, and “hardy” breeds

309
Q

What age of horses does EMS typically affect?

A

Adult to middle aged horses (6 to 20 years of age)

310
Q

Dogs with hypothyroidism have similar clinical signs as horses with __________

A

Equine Metabolic Syndrome (Normal thyroid gland)
-Hypoactive
-Weight gain
-Obesity
-Dry hair coat
-Reproductive dysfunction
-Increased cholesterol

if low resting T3 and T4 are detected: consequences of EMS rather than the problem

311
Q

Hypothyroidism in foals

A

-Goiter
-Prognathism
-Ruptured common digital extensor tendons
-Forelimb contracture
-Retarded ossification
-Crushing of cuboidal bones

312
Q

-Goiter
-Prognathism
-Ruptured common digital extensor tendons
-Forelimb contracture
-Retarded ossification
-Crushing of cuboidal bones

A

hypothyroidism in foals

313
Q

What is the hallmark of equine metabolic syndrome

A

insulin resistance (glucose intolerance)

similar to type 2 diabetes mellitus

314
Q

Horses with EmS have glucose intolerance, what does that mean

A

following glucose administration, resolution of hyperglycemia is delayed

315
Q

Normal response to glucose vs those with insulin resistance

A

Normal: Horse eats grain, blood glucose increases, insulin is secreted (b-cells), insulin binds to cellular receptor, cells take up glucose and utilize it, blood glucose normalized)

Insulin resistance: Horse eats grain, insulin is secreted, cells do not respond to insulin, blood glucose does not normalize appropriately, b-cells continue to secrete insulin (hyperinsulinemia)

316
Q

What would the blood sample show of a horse with insulin resistance

A

Elevated insulin and low G:I ratio

317
Q

What is the role of adipocytes in insulin resistance

A

adipocytes are active participants in energy regulation
metabolically active products are released and interfere with insulin action
-Leptin, adiponectin, resistin, TNF-a, and IL-6

318
Q

How do you diagnose EMS

A

Fasting hyperinsulinemia

Dynamic glucose (+/- insulin tolerance test) - oral glucose tolerance test and CGIT
Oral sugar test: use when baseline insulin is WNL. at least 8 hours of fasting overnight. Administer 0.15mL/kg Karo Light Corn Syrup PO and administer insulin and glucose: baseline and 60 and 90 minutes- spin and separate serum and chilled/freeze for shipping

Abnormal predictive proxies (G:I rato)

319
Q

When should you do an Oral sugar test

A

when you suspect EMS and baseline insulin is within normal limits
at least 8 hours of fasting overnight. Administer 0.15mL/kg Karo Light Corn Syrup PO and administer insulin and glucose: baseline and 60 and 90 minutes- spin and separate serum and chilled/freeze for shipping

320
Q

when you suspect EMS and baseline insulin is within normal limits
at least 8 hours of fasting overnight. Administer 0.15mL/kg Karo Light Corn Syrup PO and administer insulin and glucose: baseline and 60 and 90 minutes- spin and separate serum and chilled/freeze for shipping

A

Oral sugar test

321
Q

How do you differentiate between PPID and EMS

A

EMS- testing of hypothalamic/pituitary/adrenal axis should be WNL in horses

caution-laminitic horse*

322
Q

How do you improve insulin sensitivity in horses with EMS

A

weight reduction
-reduce caloric intake and provide adequate exercise

this might be problematic in horses with active laminitis

323
Q

When you are trying to reduce the weight of a horse. What precautions should you take

A

Do not feed less than 1% of their body weight
Hyperlipidemia, hepatic lipidosis worsening IR, stereotypical behaviors
Feed 1.5% of the desired body weight

Avoid feed with a high glycemic index (GI) such as grain and molasses (ex: sweet feed is high, alfalfa is low)

Choose the right hay and restrict grazing (sugars in pasture grass)

324
Q

What are the medical therapy and supplements for EMS?

A

-Levothyroxine- start at high dose and gradually reduce dose over 3-6 months

-Sodium-glucose co-transporter 2 inhibitors (ertuglflozin) - inhibit the reuptake of glucose in the kidney, decreases insulin required for euglycemia
complication: hypertriglyceridemia *expensive

-Metformin- only effective in small number of horses, may lose efficacy over time

-Magnesium?
-Chromium?
-Resveratrol?

325
Q

Levothyroxine

A

used as therapy for EMS.
start at high dose and gradually reduce dose over 3-6 months and take them off

326
Q

inhibit the reuptake of glucose in the kidney, decreases insulin required for euglycemia
complication: hypertriglyceridemia *expensive

A

Sodium-glucose co-transporter 2 inhibitors (ertuglflozin)

327
Q

Combined glucose-insulin test (CGIT)

A

used to diagnose EMS in horses
Administer 150mg/kg dextrose and 0.1 U/kg regular insulin is given. Blood samples are collected at 1,5,15,25,35,45,60,75,90,105,120,135, 150 minutes after.
Insulin resistance is diagnosed when blood glucose concentration is higher than baseline at 45 min or insulin concentration is greater than 100uU/mL at 45 min

328
Q

Metformin

A

Antidiabetic- suppresses hepatic glucose production by activating AMP-activated protein kinase, which inhibits gluconeogenesis and lipogenesis while increasing fatty acid oxidation and lipolysis. Only small number of studies have been done in horses
some shown it decreases insulin concentration but failed to improve

329
Q

Does EMS have a good prognosis?

A

Good prognosis if laminitis is controlled, husbandry is good, and nutrition is appropriate

330
Q

Which of the following clinical signs can be observed in both horses suffering from Pituitary Pars Intermedia Dysfunction (PPID) AND in horses with Equine Metabolic Syndrome (EMS)?

Choose all that apply.
Laminitis
Pu/Pd
Hypertrichosis
Cresty neck
Hyperhidrosis

A

Laminitis
Pu/Pd

The clinical signs associated with PPID include:
Hypertrichosis/hirsutism
Hyperhidrosis (excessive sweating)
Pu/Pd
Muscle loss
Chronic/recurrent laminitis
Lethargy
Chronic infections and delayed wound healing
Bulging of the supraorbital fat
Blindness (rare)

The clinical signs associated with EMS include:
Obesity with regional adiposity in specific locations including the crest of the neck (“cresty neck”), over the gluteal region/close to the tail head and in the prepuce (“swollen sheath”) or mammary gland region.
“Easy keepers”
Difficult to breed successfully due to abnormal ovarian cycling activity
Laminitis
Pu/Pd (rare, with overt diabetes mellitus)

331
Q

Which of the following can assist you in differentiating horses suffering from PPID from horses with EMS?

Choose all that apply.
Age at onset of disease
Abnormal glucose tolerance test
Radiographic evidence of laminitis
Abnormal dexamethasone suppression test

A

Age at onset of disease
Abnormal dexamethasone suppression test

As laminitis and insulin resistance can be clinical signs of PPID as well as EMS, it is important to differentiate these two conditions from each other. EMS may be differentiated from PPID by:
1. Age of onset. The EMS phenotype is generally first recognized in younger horses, whereas PPID is more common in older horses (note: these conditions may coexist in some cases).
2. Clinical signs. Clinical signs suggestive of PPID but not EMS include delayed or failed shedding of the winter haircoat, hirsutism/hypertichosis, excessive sweating, and skeletal muscle atrophy.
3. Positive diagnostic test for PPID. For example, detection of an increased plasma adrenocorticotropin hormone concentration in the absence of cofounding factors such as pain and stress.

332
Q

The following statement is TRUE or FALSE?

The most effective treatment of PPID involves the administration of a dopamine agonist.

A

True. Hormone secretion of the pars intermedia is controlled by neurotransmitters released from axons that extend directly from the hypothalamus to the pars intermedia. Secretory control is primarily through inhibition by dopamine (with additional modulation by serotonin, b-adrenergic and g-aminobutyric acid (GABA)-ergic inputs). Therefore, the most effective way to reduce pars intermedia secretion is by administering a dopamine agonist. Probably the most effective drug currently available is pergolide, a long-acting oral type 2 dopaminergic agonist.

333
Q

You diagnose a severely obese horse (BCS 9/9, 670 kg = 1,471 lbs) with Equine Metabolic Syndrome (EMS) As part of your management plan you recommend to put the horse on a diet to induce weight loss. Your estimation of the horse’s ideal body weight is 520 kg (1,144 lbs).
How many kilograms of a low NSC grass hay should the horse be fed/day to achieve the desired weight loss without the risk of adverse health or behavioral consequences?

A

Weight loss should be induced in obese horses by restricting the total number of calories consumed and by increasing the horse’s level of physical activity. An obese horse should be placed on a diet consisting of hay fed in an amount equivalent to 1.5% of the ideal body weight (1.5 lbs of hay per 100 lbs bwt). If the horse fails to lose weight after a horse has been fed at an amount equivalent to 1.5% of ideal body weight for 30 days, this amount can be lowered to 1%. However, amounts fed should not fall below 1%, as severe calorie restriction may lead to hyperlipemia, worsening of IR, and stereotypical behaviors.
For the horse in this example:
Desired weight = 520 kg
1.5% of body weight = 7.8 kg

334
Q

Horses are hypsodont and anelodont, what does that mean

A

Hysodont- very long crown and short root

Naelodont- no new tooth length can be added

335
Q

occlusal surface

A

has sharp enamel points. what occludes with other teeth

336
Q

What does coronal mean

A

towards the crown of the tooth

337
Q

Crown located occlusal to the attaced gingiva and visible within the oral cavity

A
338
Q

What ate the portions of the horse teeth

A

1) Occlusal- occlusal surface
2) Coronal: toward the crown- clinical and reserve crown
3) Apical: toward the root tip
4) Radicular root

339
Q

Toward the cheek, premolars and molars

A

buccal

340
Q

towards the lips,
canine and incisors

A

labial

341
Q

toward the tongue

A

lingual

342
Q

toward the palate

A

palatal

343
Q

the space between adjacent teeth

A

interproximal space

344
Q

surface adjacent to tooth in front

A

mesial surface

345
Q

surface adjacent to tooth behind

A

distal surface

346
Q

What is the eruption rate of horse’s teeth

A

3mm per year on average

347
Q

What is the dental formula of the horse

A

3-1-3(4)-3
3-1-3-3

348
Q

Why is it important that the pulp horn is located on the labial aspect of the clinical crown

A

if the incisor is fractured and the labial peripheral enamel has been broken off the tooth it is very common to have pulp exposure

349
Q

Where are the pulp horns on the horse incisor

A

on the labial aspect

350
Q

What is the bright white structure that surrounds the tooth

A

peripheral enamel

351
Q

What lays over the pulp horn on the incisor

A

dentin

352
Q

what surrounds the infundibular cementum

A

infundibular enamel

353
Q

T/F: horse’s teeth continually erupt

A

False

354
Q

What kind of horses have canines

A

ALL MALE HORSES
Rudimentary in 7-28% of females

355
Q

How many root canals and pulp horns do equine incisors have

A

1root canal
1 pulp horn

356
Q

How many root canals and pulp horns do equine canines have

A

1 root canal and 1 pulp horn

357
Q

What is another name for the first premolar tooth

A

Wolf teeth
25% females
15% males
erupts at 6 months of age and +/- shed by 2.5 years
less common on mandibular

358
Q

What tooth is the Wolf tooth

A

1st premolar
25% females
15% males
erupts at 6 months of age and +/- shed by 2.5 years
less common on mandibular

359
Q

1st premolar
25% females
15% males
erupts at 6 months of age and +/- shed by 2.5 years
less common on mandibular

A

Wolf tooth

360
Q

The majority of horses with exfoliate the Wolf tooth when________

A

the permanent maxillary secondary premolar tooth erupts around age 2-3 years

as long as not in abnormal place and causing periodontal disease do not need to remove

361
Q

How many mandibular cheek teeth are there in the horse

A

6 (3 premolars and 3 molars)
two roots each

362
Q

What are the characteristics of mandibular cheek teeth

A

3 premolars
3 molars
-Two rooths
-5-6 pulp horns (extra PM2 and M3)
-No infundibulum

363
Q

Where is the extra pulp horn on mandibular premolar 2 and 3 located (6 pulp horns total)

A

on the mesial aspect of premolar 2 and the distal aspect of molar three

**This is where the large hooks form

When dealing with pulp horns, ensure that there isnt over reduction of else the pulp horn will be exposed

364
Q

In horses, peripheral enamel encircles the

A

pulp horns

365
Q

What mandibular cheek teeth have 5 pulp horns?

A

Premolar 3 and 4
Molar 1 and 2

366
Q

What mandibular cheek teeth have 6 pulp horns

A

Premolar 2 (mesial)
Molar 3 (distal)

367
Q

What do the mandibular premolars and molars do not have

A

an infundibulum

368
Q

Why do horses have peripheral cementum

A

due to their teeth continually erupting throughout their life
as the periodontal ligament must always be able to connect to alveolar bone and cementum

369
Q

the largest pulp horn of mandibular cheek teeth are always located

A

BUCALLY
-PH 1 and 2 are always located bucally

370
Q

What are the largest pulp horn of mandibular teeth

A

-PH 1 and 2
always located bucally

371
Q

How many maxillary cheek teeth are there in the horse

A

3 premolar and 3 molar teeth
-all of which have 3 roots

372
Q

How many roots do the maxillary cheek teeth have

A

all have 3 roots (2 lateral and 1 palatal)

373
Q

What maxillary cheek teeth have 5 pulp horns

A

Premolar 3 and 4
Molar 1 and 2

374
Q

What maxillary cheek teeth have extra pulp horns (6-7)

A

Premolar 2 and Molar 3
(1-2 extra)
*Located on the mesial aspect of premolar 2 and the distal aspect of molar 3 - where do the hooks form

375
Q

Where do the hooks form in the maxillary mandibular teeth

A

pulp horns located on the mesial aspect of premolar 2 and the distal aspect of molar 3 - where do the hooks form

376
Q

What teeth are located in the caudal maxillary sinus

A

2nd and 3rd molar teeth

377
Q

What sinus are the 2nd and 3rd molar teeth located in

A

the caudal maxillary sinus

378
Q

What sinus is the 1st molar located in

A

the rostral maxillary sinuses

379
Q

What teeth are located in the rostral maxillary sinus

A

-1st molar
-Distal aspect of 4th premolar tooth can be located in the rostral maxillary sinus, especialy when a horse is young and teeth are young. As horse ages, the tooth may erupt away from the sinus and no longer maintains the relationship

380
Q

What sinus is the distal aspect of the 4th premolar located within

A

Distal aspect of 4th premolar tooth can be located in the rostral maxillary sinus, especiialy when a horse is young and teeth are young. As horse ages, the tooth may erupt away from the sinus and no longer maintains the relationship

381
Q

T/F: maxillary teeth do not have infundibulum

A

false- they have 2 infundibulum (5-7 cm depth) length of reserve of crown

382
Q

Dental disease of ______________ can result in secondary sinusitis

A

Premolar 4 and all molars
-PM4 and M1- Rostral maxillary sinus
-M2 and M3- Caudal maxillary sinus

383
Q

What color do pulp horns appear

A

brown

384
Q

When do the wolf teeth erupt

A

around 6 months of age
will be gone by 2.5 years

385
Q

What is the last equine tooth to completely erupt

A

canine tooth (about 4-5 years)

386
Q

When do deciduous incisors erupt

A

I1-3 (6 days, 6 weeks, 6 months)

387
Q

When do permanent incisors erupt

A

I1-3 (2.5 y, 3.5y, 4.5y)

388
Q

When do the incisors erupt

A

Deciduous 6d, 6week, 6 month

Permanent: 2.5y, 3.5y,4.5y

389
Q

When do the deciduous premolars erupt

A

2 weeks

390
Q

When do cheek teeth erupt

A

M1: 1 year
M2: 2 year
PM2: 2.5y
PM3: 3 y
M3: 3.5y
PM4: 4 y

391
Q

How do you discern what a deciduous tooth is

A

in a young horse, they will look very worn down “caps”? idk

392
Q

Horses with PPID can cause ______ dental disease

A

periodontal disease - can get really nasty oral-nasal fistulas

393
Q

What are historical indicators for dental pathology

A

-Weight loss
-Abnormal mastication
-Excessive salivation
-Quidding
-Headshaking
-Response to bit
-Choke or colic

*Most common to have no signs

394
Q

used for when horses drop feed from their mouths while they are chewing, or leave balls of partially chewed hay or other food behind in their feed buckets
sign of dental pathology

A

quidding

395
Q

What can you see stall side observation for dental pathology

A

-Body condition score
-observe mastication
-symmetry of face (temporal muscles can atrophy)
-fiber in feces about 1 inch of length- mastication is adequate

396
Q

What is the significance of the point of the facial crest

A

it marks the line between the maxillary premolars and molars

397
Q

What equipment is used to perform an equine dental exam

A

-Adequate sedation
-Flush mouth thoroughly
-Full mouth speculums
-Head support
-Quality light source

*look for impacted feed- tells you where problem is

398
Q

What is the normal gingival sulcus depth in horse

A

0-1mm

399
Q

What do you palpate for an extraoral facial exam in a horse

A

-Point of facial crest
-Region of sinuses
-Periorbital region
-Retropulse the eye- push lightly on the eye
-Zygomatic arch
-Temporomandibular joint
-Muscles of mastication

-Ears (temporal teratoma- ear tooth)
-Parotid salivary gland
-Mandibular lymph nodes
-Intermandibular region
-Mandible (lingual and buccal)
-Rostral mandibular
-Incisive one region
-Nares
-Rostral maxilla

400
Q

What do you examine in an equine intraoral exam

A

-Mucocutaneous junction
-All regional soft tissue structures
-labial and alveolar mucosa
-Gingival attachment
-Dentral structures
-Interproximal spaces

401
Q

abnormal placement of individual teeth in any plane
resulting in pain (soft tissue laceration), abnormal attrition, and reduced masticatory function

A

Malocclusion

402
Q

What is a result of malocclusions in horses

A

pain (soft tissue laceration), abnormal attrition, and reduced masticatory function

403
Q

The average horse spends ______ hours eating forage

A

16 hours (12.5kg forage)

When taken off pasture- decreases to 11.5 hours (8kg forage and 4 kg concentrates)
3kg forage and 7 kg concentration- 6.1 hours eating
leads to malocclusion

404
Q

What is a class 1 malocclusion (MAL 1)

A

arcades appropriately aligned but individual tooth malpositioned in any plane
-Tooth overgrowth:
Sharp enamel points
Steps
Wave
Hooks (in conjunction with MAL2/3

-Rotation or tipped

405
Q

Sharp enamel points

A

a type of MAL 1 where anisognathic jaws lead to portions of the teeth that arent in contact with one another when at rest

Lead to ulceration or laceration- buccal or lingual mucosa

Maxilla-Buccal
Mandibular- Lingual

406
Q

horses have anisognathic jaws meaning

A

the mandible is skinnier than the maxilla

407
Q

Sharp enamel points happen on the _________ aspect of the maxilla and the ________ aspect of the mandible

A

Buccal aspect of maxilla
Lingual aspect of the mandible

408
Q

Sharp enamel points can lead to

A

ulceration and laceration of the buccal and lingual mucosa

409
Q

Step/Wave mouth

A

A type of MAL 1 where there is overgrowth in the middle of the arcade
Step-one tooth
Wave- multiple teeth
Nidus: missing teeth, expiring teeth, fractured teeth
occluding tooth problem

410
Q

Hook

A

when a portion of the mesial 2 PM or distal 3M tooth overlong
causes: Mal 2 or 3, bit seats, offset cheek teeth arcades, missing teeth and collapse of arcade

411
Q

Where do hooks typically form in

A

PM 2 (mesial)
M3 (distal)

*do not get them in the middle of the arcade

412
Q

When missing tooth on the mandible, what would result

A

overgrowth of the maxillary tooth that touch it

413
Q

What causes the formation of hooks

A

1) Mal 2 or 3 malocclusions
2) Bit seats: practice to increase performance, rounding mesial aspect of tooth. if only doing it on max/mand then it will overgrwo
3) offset cheek teeth: nx jaw lengths but one of the arcades si shifted
4) Missing teeth and collapse of arcade

414
Q

What is the oldest tooth and typically wears out first, could potentially lead to wave

A

The first molar tooth on the maxilla

415
Q

What type of malocclusion is mandibular brachygnathism “Parrot mouth”

A

Class 2 Malocclusion (MAL 2)

Hooks 106/206 and 311/411

416
Q

mandibular brachygnathism “Parrot mouth” leads to

A

Hooks on the maxilla 106/206 and 311/411

*Class two malocclusion

417
Q

Maxillary malocclusion “undershot/underbite/monkey-mouth/ sow mouth” is a Class ______ Malocclusion

A

Class 3

Hooks form on mandible 306/406 and 111/211

418
Q

Maxillary brachygnathism leads to

A

Hooks on mandible 306/406 and 111/211

419
Q

Mandibular brachygnathism (Class 2 MAL) results in ________ on _________ while mandibular brachygnathism (Class 3 MAL) results in _________ on _______

A

Mandibular Class 2: Hooks on 106/206 and 311/411

Maxillary Class 3: Hooks on 306/406 and 111/211

420
Q

Forms hooks on 306/406 and 111/211

A

Maxillary brachygnathism (Class 3) Underbite

(Maxillary M3 have hooks when maxilla is short)

421
Q

Forms hooks on 106/206 and 311/411

A

Mandibular brachygnathism “Parrot mouth” (Class 2)

(Mandibular M3 have hooks when mandible is short)

422
Q

Class 4 Malocclusion

A

one quadrant asymmetrical growth “Wry mouth or wind swept)
Maxilla shifts to one side in comparison to mandible

causes: post-trauma and congenital conformation

Mild maxillary is very common- require continual maintenance

Severe= respiratory distress because nose is curved

423
Q

What are the causes of Class 4 Malocclusion

A

post-trauma and congenital conformation

*Maxilla shifts to one side in comparison to mandible

424
Q

What is Wry mouth or wind swept

A

Class 4 Malocclusion one quadrant asymmetrical growth - slant or diagonal *eat and masticate normally typically
Maxilla shifts to one side in comparison to mandible

causes: post-trauma and congenital conformation

Mild maxillary is very common- require continual maintenance

Severe= respiratory distress because nose is curved

425
Q

reduction of overgrown dental material
Most common-reduction in enamel points- rounded to level of cementum and dentin
manages malocclisions

A

Odontoplasty “Float”

426
Q

What are the precautions of odontoplasty

A

remove no more than 3-4 mm every 3 months if more than just enamel is involved

just take of sharp enamel points

do not flatten completely- can expose pulp
just need to be comfortable for eating

427
Q

How do you manage older horses with expired teeth

A

shift from hay/pasture to older/senior maintenance feed because they do not have much dental structure

Clinical Science (5 decks)

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