Equine Endocrinopathies/Metabolic Disease Flashcards
how is equine polydipsia defined?
> 100ml/kg/day
what does PPID stand for?
pituitary pars intermedia dysfunction
equine cushing’s disease
which horses are more likely to develop PPID?
common in aged horses
60% of over 20s at post-mortem but not all will have clinical signs
which horses should be tested for PPID?
those displaying clinical signs
all horses with laminitis unless young
what is the pathophysiology of PPID?
not fully understood
decrease in production of dopamine from hypothalamus, causes decrease in inhibition of pituitary gland
leads to pituitary adenoma –> overproduction of hormones
results in a range of clinical signs
what are the clinical signs of PPID?
long curly coat (unknown cause)
laminitis (due to insulin resistance)
PUPD (poss due to decreased secretion of vasopressin)
weight loss
docility
neurological impairment (adenoma)
infertility, skin diseases, periodontal disease
why do horses with PPID lose weight?
could be due to:
cortisol production
associated other diseases
parasites - reduced immune function with PPID
how is PPID diagnosed?
clinical signs and signalment
gold-standard is post-mortem only
ACTH test and TRH stimulation test
why should the reference ranges for PPID testing be adjusted for autumn?
pars intermedia more active in autumn (august to december)
what is the first-line test for PPID?
ACTH test - tests resting plasma ACTH concentration
how is the ACTH test perfomed?
collect blood - cold, not frozen
plasma is sent off to lab for analysis
reference range adjusted for autumn
when is a TRH stimulation test carried out for PPID diagnosis?
if basal ACTH result is borderline
how is a TRH stimulation test performed?
take blood sample
inject TRH
blood sample again at 10 mins (+/- 30 mins)
how should dose rates for PPID be checked?
re-test in 4-6 weeks
repeat annually as disease progresses
what if there is a high clinical suspicion of PPID but a negative test result?
start treatment anyway and assess clinical response
consider routine checking of aged horses regardless
how can PPID be managed (non-medically)?
farriery clipping parasite control dental care feeding
how can PPID be medically managed/treated?
dopamine agonist - pergolide tablets
start with 1mg and monitor/adjust dose
reassess annually
what is a common sign that pergolide dose is too high?
may go off food - resolves on lower dose
what must you not do with an ACTH sample?
shake about - haemolysis
leave in a warm place
freeze before separating the plasma
send unseparated sample
what is the pathophysiology of equine metabolic syndrome (EMS)?
obesity/regional adiposity due to insulin dysregulation/resistance
leads to sublinical/clinical laminitis
what are the signs of compensated insulin dysregulation?
high insulin
normal glucose
may have at rest, or only as a response to feeding
could be EMS or PPID (or both)
what are the signs of uncompensated insulin dysregulation?
high insulin and high glucose
glucose in urine
type 2 DM
what is the direct cause of laminitis in EMS?
hyperinsulinaemia is the direct cause
what is the role of genetics in EMS?
genetic predisposition for ID in hardy breeds
ID facilitates breakdown of glucose & fat stores & stimulates hepatic gluconeogenesis
ability to mobilise energy stores and prioritise vital tissues is a survival benefit if poor diet
what is the link between IR and obesity in hardy breeds?
strong association
IR horses get overweight during summer
weight loss in winter associated with poorer diet restores insulin sensitivity by the spring
what is the body condition score for obesity in horses?
7/9-9/9
what are the body conditions signs of EMS?
cresty neck
fat tail head
preuputial swelling/mammary gland enlargement
what are the differential diagnoses for EMS?
insulin dysregulation can be EMS/PPID or both - can be hard to be sure
based on history and signalment
test for both
can horses be lean and insulin resistant?
yes
what is the first-line diagnostic test for EMS?
starve overnight and take blood sample for glucose/insulin
bolus glucose/corn syrup
blood sample again for insulin and glucose at 2-3 hours
usually IR = hyperinsulinaemia and normoglycaemia
how can we non-medically manage EMS?
diet - low carb, no concentrate, no grass/grass muzzle
exercise - major benefit but difficult if laminitic
weight loss - feed 1/3rd less than normal diet, 1.5kg forage per 100kg, soak hay >1 hour, haynet with small holes to make last longer
how can EMS be medically managed?
metformin
not bioavailable in horses but blocks SI carb absorption - decreases IR only by weight loss
what is the pathogenesis of hyperlipaemia?
fatty acid mobilisation triggered by negative energy balance and stress (catecholamine and glucocorticoid release)
disease of acute starvation
which horses are at an increased risk of hyperlipidaemia?
obesity
ponies
pregnancy
donkeys (more likely to be IR)
why are pregnant horses more likely to develop hyperlipaemia?
progesterone in pregnancy causes IR
which concurrent conditions worsens lyperlipaemia?
liver failure (hepatic lipidosis)
what other conditions can hyperlipaemia lead to?
kidney failure
pancreatitis
which hormone impedes development if hyperlipaemia?
insulin
IR horses are at risk of hyperlipaemia (EMS, glucocorticoids, catecholamines, progesterone)
what are the signs of hyperlipaemia?
depression
anorexia
ataxia
icterus
what are the main principles for hyperlipaemia management?
improvement of energy intake and balance
treatment of hepatic disease
elimination of stress/treatment of concurrent disease
inhibition of fat mobilisation from adipose tissue
increased triglyceride uptake by peripheral tissues
how can hyperlipaemia be medically treated?
glucose infusion (5% at 2ml/kg/hr)
partial parenteral nutrition
monitor blood glucose (hourly at first) - may need insulin
what is the prognosis for hyperlipaemia?
60-100% mortality
what is the best prevention for hyperlipaemia?
client education
identification of at-risks
glucose infusion and insulin if required, to avoid hyperlipaemia
