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CVNT2 > Equine Endocrinopathies/Metabolic Disease > Flashcards

Equine Endocrinopathies/Metabolic Disease Flashcards

1
Q

how is equine polydipsia defined?

A

> 100ml/kg/day

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2
Q

what does PPID stand for?

A

pituitary pars intermedia dysfunction

equine cushing’s disease

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3
Q

which horses are more likely to develop PPID?

A

common in aged horses

60% of over 20s at post-mortem but not all will have clinical signs

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4
Q

which horses should be tested for PPID?

A

those displaying clinical signs

all horses with laminitis unless young

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5
Q

what is the pathophysiology of PPID?

A

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

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6
Q

what are the clinical signs of PPID?

A

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

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7
Q

why do horses with PPID lose weight?

A

could be due to:
cortisol production
associated other diseases
parasites - reduced immune function with PPID

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8
Q

how is PPID diagnosed?

A

clinical signs and signalment
gold-standard is post-mortem only
ACTH test and TRH stimulation test

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9
Q

why should the reference ranges for PPID testing be adjusted for autumn?

A

pars intermedia more active in autumn (august to december)

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10
Q

what is the first-line test for PPID?

A

ACTH test - tests resting plasma ACTH concentration

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11
Q

how is the ACTH test perfomed?

A

collect blood - cold, not frozen
plasma is sent off to lab for analysis

reference range adjusted for autumn

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12
Q

when is a TRH stimulation test carried out for PPID diagnosis?

A

if basal ACTH result is borderline

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13
Q

how is a TRH stimulation test performed?

A

take blood sample
inject TRH
blood sample again at 10 mins (+/- 30 mins)

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14
Q

how should dose rates for PPID be checked?

A

re-test in 4-6 weeks

repeat annually as disease progresses

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15
Q

what if there is a high clinical suspicion of PPID but a negative test result?

A

start treatment anyway and assess clinical response

consider routine checking of aged horses regardless

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16
Q

how can PPID be managed (non-medically)?

A 
farriery 
clipping 
parasite control 
dental care 
feeding
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17
Q

how can PPID be medically managed/treated?

A

dopamine agonist - pergolide tablets

start with 1mg and monitor/adjust dose
reassess annually

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18
Q

what is a common sign that pergolide dose is too high?

A

may go off food - resolves on lower dose

19
Q

what must you not do with an ACTH sample?

A

shake about - haemolysis

leave in a warm place

freeze before separating the plasma

send unseparated sample

20
Q

what is the pathophysiology of equine metabolic syndrome (EMS)?

A

obesity/regional adiposity due to insulin dysregulation/resistance

leads to sublinical/clinical laminitis

21
Q

what are the signs of compensated insulin dysregulation?

A

high insulin
normal glucose

may have at rest, or only as a response to feeding
could be EMS or PPID (or both)

22
Q

what are the signs of uncompensated insulin dysregulation?

A

high insulin and high glucose
glucose in urine
type 2 DM

23
Q

what is the direct cause of laminitis in EMS?

A

hyperinsulinaemia is the direct cause

24
Q

what is the role of genetics in EMS?

A

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

25
Q

what is the link between IR and obesity in hardy breeds?

A

strong association

IR horses get overweight during summer

weight loss in winter associated with poorer diet restores insulin sensitivity by the spring

26
Q

what is the body condition score for obesity in horses?

A

7/9-9/9

27
Q

what are the body conditions signs of EMS?

A

cresty neck

fat tail head

preuputial swelling/mammary gland enlargement

28
Q

what are the differential diagnoses for EMS?

A

insulin dysregulation can be EMS/PPID or both - can be hard to be sure

based on history and signalment
test for both

29
Q

can horses be lean and insulin resistant?

A

yes

30
Q

what is the first-line diagnostic test for EMS?

A

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

31
Q

how can we non-medically manage EMS?

A

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

32
Q

how can EMS be medically managed?

A

metformin

not bioavailable in horses but blocks SI carb absorption - decreases IR only by weight loss

33
Q

what is the pathogenesis of hyperlipaemia?

A

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

disease of acute starvation

34
Q

which horses are at an increased risk of hyperlipidaemia?

A

obesity
ponies
pregnancy
donkeys (more likely to be IR)

35
Q

why are pregnant horses more likely to develop hyperlipaemia?

A

progesterone in pregnancy causes IR

36
Q

which concurrent conditions worsens lyperlipaemia?

A

liver failure (hepatic lipidosis)

37
Q

what other conditions can hyperlipaemia lead to?

A

kidney failure

pancreatitis

38
Q

which hormone impedes development if hyperlipaemia?

A

insulin

IR horses are at risk of hyperlipaemia (EMS, glucocorticoids, catecholamines, progesterone)

39
Q

what are the signs of hyperlipaemia?

A

depression
anorexia
ataxia
icterus

40
Q

what are the main principles for hyperlipaemia management?

A

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

41
Q

how can hyperlipaemia be medically treated?

A

glucose infusion (5% at 2ml/kg/hr)

partial parenteral nutrition

monitor blood glucose (hourly at first) - may need insulin

42
Q

what is the prognosis for hyperlipaemia?

A

60-100% mortality

43
Q

what is the best prevention for hyperlipaemia?

A

client education
identification of at-risks

glucose infusion and insulin if required, to avoid hyperlipaemia

CVNT2 (47 decks)

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