Equine Metabolic/Endocrine Disease Flashcards
What is equine polydipsia defined as?
> 100ml/kg/day water intake
What is the typical signalment for Pituitary Pars Intermedia Dysfunction (PPID)?
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
What is the mechanism of PPID?
Decrease in production of dopamine from hypothalamus
Decrease in inhibition of pituitary
Pituitary adenoma (micro/macro)
Overproduction of hormones
What are the clinical signs of PPID?
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
What is the first-line test for PPID?
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)
What is the second diagnostic test for PPID?
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
How can we manage PPID?
Farriery Clipping Parasite control Dental care Feeding
How can we medically treat PPID?
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
What are the three main things seen with Equine Metabolic Syndrome (EMS)?
Obesity or regional adiposity
Insulin dysregulation/resistance
Subclinical and clinical laminitis
What kind of insulin dysregulation do we see in EMS and PPID and what does this mean for blood samples?
Compensated:
High insulin, normal glucose
May have this at rest or only as a response to feeding
Describe laminitis seen with EMS.
Clinical or subclinical
Hyperinsulinaemia is direct cause of laminitis
What is the role of genetics in EMS?
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
How are obesity and insulin dysregulation linked?
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
What are the clinical signs of EMS?
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
How can we diagnose EMS?
Starve overnight Blood sample glucose and insulin Bolus glucose/corn syrup Blood sample glucose and insulin at 2-3hrs Hyperinsulinaemia and normoglycaemia
How can we manage EMS?
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
How can we medically manage EMS?
Metformin
Increases insulin sensitivity in humans
Horses no bioavailability but blocks small intestine carbohydrate absorption
Decreases insulin dysregulation only by weight loss
Describe hyperlipaemia.
Fatty acid mobilisation triggered by negative energy balance/stress (catecholamine and glucocorticoid release)
What are the risk factors for hyperlipaemia?
Obesity
Ponies
Pregnant
Donkeys
What can hyperlipaemia cause?
Hepatic lipidosis Liver failure Lactescent blood Fat embolism Kidney failure Pancreatitis
What are the clinical signs of hyperlipaemia?
Depression
Anorexia
Ataxia
Icterus
How can we treat hyperlipaemia?
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)
What is the prognosis for horses with hyperlipaemia?
60-100% mortality
How can we prevent hyperlipaemia?
Client education
Identify ‘at risk’s - glucose infusion and insulin if required, to avoid hyperlipaemia
