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RUSVM Nutrition Summer 2017 > Clinical Equine Nutrition > Flashcards

Clinical Equine Nutrition Flashcards

1
Q

What are some feeding management issues?

A

competition, vices, and dental problems.

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2
Q

What are some clinical signs seen with esophageal obstruction?

A

dysphagia, watery feed tinged nasal discharge*****, gagging, repeated attempts to swallow, stretching of the neck, and anxiety (some paw the ground)

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3
Q

What are the main culprits in causing esophageal obstruction?

A

pelleted feed (95%), hay cubes, beet pulp.

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4
Q

How do you treat esophageal obstructions?

A

sedation, naso-gastric tube, +/- tx for aspiration.

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5
Q

How do you manage/prevent esophageal obstruction?

A

slow down eating, separate the “bully”, soak the feed. These guys are commonly repeat offenders.

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6
Q

What are some abnormal oral behaviors that are associated with feed management?

A

cribbing, wind sucking, wood chewing.

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7
Q

T/F: weaving, stall walking, and head shaking are also issues associated with poor feed management.

A

False.

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8
Q

What are some concerns with cribbing?

A

poor performance, weight loss, incisor wear, flatulent colic, epiploic foramen entrapment, destruction of property.

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9
Q

How is cribbing treated?

A

Can place collars on them, masks, rings in between incisors, surgically cut the “strap” muscles, or can give anti-depressants or NMDA receptor blockers. This doesn’t address the reason for the cribbing

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10
Q

Is wind sucking different from cribbing?

A

Yes. It can lead to cribbing though.

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11
Q

What are some clinical signs of dental issues?

A

weight loss, dropping feed, difficulty eating, and quidding.

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12
Q

Enamel points are found where?

A

along the buccal surface.

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13
Q

Are enamel points and molar hooks different?

A

yes. Molar hooks are on the front end of the tooth.

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14
Q

What can enamel points or molar hooks lead to?

A

ulceration of the mouth.

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15
Q

T/F: alfalfa is the “gold standard” hay.

A

True.

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16
Q

Who can alfalfa cause a problem in?

A

foals. Increased Ca can interfere with other electrolyte absorption and the increased P can promote osteochondrosis.

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17
Q

What is another concern with alfalfa?

A

blister beetles. Can cause cantharidin toxicosis.

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18
Q

What are some clinical signs seen with cantharidin toxicosis?

A

colic, anorexia, depression, GIT erosions, frequent urination, colitis.

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19
Q

What is a problem that can be seen with fescue?

A

contamination with endophyte.

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20
Q

What are some clinical signs that indicate fescue toxicosis?

A

prolonged gestation, premature separation of the placenta, dystocia, retained placenta, agalactia.

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21
Q

T/F: you can safely feed fescue to gestating mares until their 3rd trimester.

A

True. Move them off of the fescue pasture in late gestation.

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22
Q

What are some ways to prevent fescue toxicosis?

A

cut the grass, domperidone, buy fungus free fescue, or re-seed.

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23
Q

T/F: red clover can cause major issues (like dehydration) for horses if infected with mold.

A

False. Can cause excessive drooling due to slaframine, but there are no significant issues that come along with this.

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24
Q

What should you do with a horse that is hypersalivating due to red clover?

A

remove from the clover.

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25
Q

What is the most common clinical sign seen with grain overload?

A

colic. Can also see colitis, laminitis, or gastric rupture.

26
Q

How can non-structural carbs cause colic?

A

they are highly digestible and rapidly ferment in the hind gut, leading to gas distention.

27
Q

How do you treat colic?

A

flunixin (NSAID), rectal exam to ID structures involved, and NG intubation.

28
Q

A horse that has laminitis should not get what in their diet?

A

carbs.

29
Q

How do you treat laminitis?

A

varies case by case, but very important to shoe the horse and provide sole support.

30
Q

Horses are ____ more sensitive to ionophores than poultry.

A

200x

31
Q

What is the most common ionophore used?

A

monensin

32
Q

What are some CS of ionophore toxicity?

A

trembling, sweating, cardiac arrhythmias, and death.

33
Q

Moldy corn poisoning causes what?

A

leukoencephalomalacia aka blind staggers. Will lead to liquefaction of the cerebral white matter.

34
Q

When do you see this mycotoxin grown in corn?

A

when the moisture content is greater than 15%

35
Q

What are some CS of moldy corn poisoning?

A

incoordination, depression, blindness, sweating, head pressing, seizures, coma, and death.

36
Q

How much of feed wt. should be good quality roughage?

A

35-40%

37
Q

___ cups of oil replace ____ cups of concentrate.

A

1 cup; 3-4 cups.

38
Q

What is the weaning on schedule for adding a fat supplement to a horse diet?

A

start at 30mL bid and increase over 2 weeks.

39
Q

How long can it take a horse to adapt to using fat as an energy source?

A

2-3 months.

40
Q

performance horses should have what kind of diets and how frequently?

A

high grain:low roughage diets, 3-4 meals/day.

41
Q

The digestion and absorption of what decreases with age?

A

protein, fiber, and phosphorous.

42
Q

If you’ve got an emaciated horse, how should you reintroduce food? Why?

A

Slowly*** if too fast, you can cause a fatal increase in blood insulin and cardiac and respiratory failure.

43
Q

What do you initially introduce to a starved horse?

A

roughage. Want to start on a low glycemic index diet.

44
Q

With starved horses, you want to introduce feed at ______ percent of maintenance based on current body weight.

A

50-75%

45
Q

How long should you wait before increasing the food by 125% in starved horses?

A

10 days.

46
Q

What is equine metabolic syndrome?

A

leads to obesity in horses. Frequently seen with intermittent laminitis. These horses have persistent hyperinsulinemia and are PPID negative.

47
Q

How do you treat equine metabolic syndrome?

A

low glycemic index diet (no grass, late cut hay), exercise, and levothyroxine sodium.

48
Q

What is hyperlipemia and who does it affect?

A

sudden and severe breakdown of body fat stores, seen in ponies, donkeys, and mini horses.

49
Q

What are some predisposing factors to hyperlipemia?

A

obesity, insulin resistance, and a pregnant or lactating female.

50
Q

What are some precipitating factors for hyperlipemia?

A

inadequate feed intake, stress, pain, and disease.

51
Q

What is the main clinical sign of hyperlipemia?

A

rapid weight loss. Will see it within a few days.

52
Q

How do you treat hyperlipemia?

A

tx identifiable precipitating factors and secondary problems, reduce LDLs (offer fresh, palatable feed or tube feed).

53
Q

What is the most common developmental orthopedic disease in thoroughbreds?

A

physitis/epiphysitis.

54
Q

T/F: physitis can lead to angular limb deformities.

A

True.

55
Q

How do you treat physitis?

A

decrease nutritional plane to roughage only, rest, give NSAIDs if necessary.

56
Q

What is osteochondrosis?

A

disturbances in endochondral differentiation, proliferation, maturation, and ossification of fast growing animals.

57
Q

Who is osteochondrosis most commonly seen in?

A

standardbred and warmblood breeds.

58
Q

What are some clinical signs of osteochondrosis?

A

joint effusion and potentially lameness.

59
Q

What are some common sites where oseochondrosis is seen?

A

distal intermediate ridge of the tibia, lateral trochlear ridge of the femur, and the medial femoral condyle.

60
Q

If you’ve got an orphan foal and don’t have a nurse mare available, what milk can you use instead?

A

Goat milk (can lead to constipation), cow’s milk (less fat, more sugar), or you can use mare’s milk replacement.

61
Q

When do you discontinue the milk replacement in an orphan foal?

A

at 3 months.

RUSVM Nutrition Summer 2017 (15 decks)

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