Equine Metabolic/Endocrine Disease Flashcards

1
Q

What is equine polydipsia defined as?

A

> 100ml/kg/day water intake

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2
Q

What is the typical signalment for Pituitary Pars Intermedia Dysfunction (PPID)?

A

Common in old-aged horses
Clinical signs in 20-30% of over 15s
Can occur in younger horses
Test all horses with laminitis unless young

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3
Q

What is the mechanism of PPID?

A

Decrease in production of dopamine from hypothalamus
Decrease in inhibition of pituitary
Pituitary adenoma (micro/macro)
Overproduction of hormones

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4
Q

What are the clinical signs of PPID?

A
Variable! May be no clinical signs
Long curly coat
Laminitis
PUPD
Weight loss
Docile
Neurologic impairment
Hyperhidrosis
Change in fat distribution, bulging fat pads
Infertility
Skin disease
Periodontal disease
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5
Q

What is the first-line test for PPID?

A

ACTH test
Resting plasma ACTH collection - horse not stressed
Collect blood - cold, not frozen
Send plasma
Adjust reference range for autumn (when pars intermedia more active)

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6
Q

What is the second diagnostic test for PPID?

A

TRH stimulation test
Use if basal ACTH borderline, not conclusive
Basal blood sample, inject TRH, blood sample again at 10 mins +/- 30 mins post-injection

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7
Q

How can we manage PPID?

A
Farriery
Clipping
Parasite control
Dental care
Feeding
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8
Q

How can we medically treat PPID?

A
Dopamine agonist - Pergoglide tablets
Start with 1mg/horse SID or divided BID
Monitor, adjust dose, reassess annually
May go off food - resolves on lower doses
Usually very effective
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9
Q

What are the three main things seen with Equine Metabolic Syndrome (EMS)?

A

Obesity or regional adiposity
Insulin dysregulation/resistance
Subclinical and clinical laminitis

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10
Q

What kind of insulin dysregulation do we see in EMS and PPID and what does this mean for blood samples?

A

Compensated:
High insulin, normal glucose
May have this at rest or only as a response to feeding

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11
Q

Describe laminitis seen with EMS.

A

Clinical or subclinical

Hyperinsulinaemia is direct cause of laminitis

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12
Q

What is the role of genetics in EMS?

A

Genetic predisposition for insulin dysregulation in hardy breeds
Insulin dysregulation facilitates breakdown of glucose and fat stores and stimulates hepatic gluconeogenesis
Keeps a glucose supply for vital tissues e.g. CNS
Ability to mobilise energy stores and prioritise vital tissues = survival benefit if poor diet

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13
Q

How are obesity and insulin dysregulation linked?

A

Wild horses = get fat over summer (develop insulin dysregulation), lose weight in winter (restoring insulin sensitivity by spring)
Domestic horses no longer subject to seasonal weight loss, have a lack of exercise, chronic progressive obesity and laminitis ensue

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14
Q

What are the clinical signs of EMS?

A

Obesity - BCS 7/9 - 9/9
Regional adiposity - cresty neck, tail head, preputial swelling/mammary glands
Subclinical/clinical laminitis
Possible related disease e.g. hyperlipaemia, lipoma

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15
Q

How can we diagnose EMS?

A
Starve overnight
Blood sample glucose and insulin
Bolus glucose/corn syrup
Blood sample glucose and insulin at 2-3hrs
Hyperinsulinaemia and normoglycaemia
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16
Q

How can we manage EMS?

A

Diet - low carb, no concentrate, multivitamin/mineral supplement, no grass/grass muzzle
Exercise - major effect on insulin sensitivity, but if laminitic?
Weight loss - feed 1/3 less than before, min. 1.5kg forage per 100kg, soak hay > 1hr, haynet with small holes

17
Q

How can we medically manage EMS?

A

Metformin
Increases insulin sensitivity in humans
Horses no bioavailability but blocks small intestine carbohydrate absorption
Decreases insulin dysregulation only by weight loss

18
Q

Describe hyperlipaemia.

A

Fatty acid mobilisation triggered by negative energy balance/stress (catecholamine and glucocorticoid release)

19
Q

What are the risk factors for hyperlipaemia?

A

Obesity
Ponies
Pregnant
Donkeys

20
Q

What can hyperlipaemia cause?

A
Hepatic lipidosis
Liver failure
Lactescent blood
Fat embolism
Kidney failure
Pancreatitis
21
Q

What are the clinical signs of hyperlipaemia?

A

Depression
Anorexia
Ataxia
Icterus

22
Q

How can we treat hyperlipaemia?

A

Improve energy intake and balance
Treatment of hepatic disease
Elimination of stress, treatment of concurrent disease
Tempt to eat / enteral nutrition (by stomach tube)
Glucose infusion (5% at 2ml/kg/hr)
Partial parenteral nutrition - monitor blood glucose, hourly at first, may need insulin (SC or infusion)

23
Q

What is the prognosis for horses with hyperlipaemia?

A

60-100% mortality

24
Q

How can we prevent hyperlipaemia?

A

Client education

Identify ‘at risk’s - glucose infusion and insulin if required, to avoid hyperlipaemia