Equine Endocrine (PPID & EMS) Flashcards

1
Q

What is equine cushings disease?

A

TRICK QUESTION! don’t call it cushings, call it PPID

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2
Q

What are the three divisions of the Anterior pituitary?

A

Pars intermedia Pars distalis Pars tuberalis

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3
Q

What part of the anterior pituitary is affected in PPID?

A

Pars intermedia

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4
Q

What is produced by the posterior pituitary gland (aka pars nervosa)?

A

Oxytocin and ADH

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5
Q

What are the cells in the pars intermedia called?

A

Melanotropes

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6
Q

What’s POMC?

A

pro-opiomelanocortin

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7
Q

What is made from POMC?

A

B-endorphin

a-MSH (melanocyte stimulating hormone)

CLIP (cortisol like intermediate peptide)

<2% ACTH

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8
Q

Is the pars intermedia affected by glucocorticoids in the circulation?

A

Nope, no negative feedback from circulting gluco corts

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9
Q

What is the pars intermedia regulated by?

A

Dopamine inhibits

Serotonin (5HT3) stimulates

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10
Q

What happens when you get loss of dopaminergic inhibition?

A

PPID! & therefore over production of the hormones made by the pars intermedia

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11
Q

What causes the loss of dopaminergic inhibition?

A

We don’t know, does seem to have oxidative damage on post mortem but don’t know why.

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12
Q

What happens to the melanotropes in PPID?

A

Initially they just hypertrophy and produce more hormone, eventually adenomatous change

Slowly progressive

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13
Q

Why do we see such a rise in ACTH signs?

A

The ACTH produced is up to 6x more potent

Actual number of cortisol doesn’t increase very dramatically but is more active

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14
Q

What other parts of the pituitary might be compressed and thererfore malfunctional?

A

Posterior pituitary - less ADH prodcued

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15
Q

Why might you see blindness/seizures in PPID horses?

A

Compression of the brain due to massive pituitary adenoma (rare)

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16
Q

What age group does PPID affect?

A

Older horses. Average 19, very rare under 10

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17
Q

mares or geldings more common? (PPID)

A

no sex predilection

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18
Q

Ponies or horses more likely? (PPID)

A

Ponies!

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19
Q

What percentage or horses are affected by hypertrichosis?

A

55-80%

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20
Q

Why do you get hypertrichosis?

A

Reason unclear, pressure on thermoregulatory centre in brain?

We don’t actually know why..

21
Q

What proportion of PPID horses get laminitis? (roughly)

A

About 20%

Often ends up in demise of animal as recurrent/chronic

22
Q

Why do you get laminits with PPID?

A

Due to cortisol/insulin

23
Q

What proportion of PPID horses get weight loss?

A

88%

24
Q

Why do we get increased sweating in PPID?

A

Possibly due to increased catecholamines circulating and stimulating B-adrenergic controlled sweat glands

Or maybe just due to long hair coat?

25
Q

With PU/PD horses with PPID, can they concentrate their urine if water deprived?

A

Yes

26
Q

What are the theories for PUPD in PPID?

A

Cortisol antagonising actions of ADH on collecting ducts

Cortisol causing hyperglycaemia and osmotic diuresis

Destruction of other areas of pituitary gland with reduced ADH

Combination of the above?

No evidence as yet

27
Q

Where do you get a typical fat pad?

A

Supraorbital fat pad as opposed to normal dipped in fossa in older horses

28
Q

What two infections do they most often seem to get with PPID?

A

Sinusitis

Skin infections

29
Q

Why are PPID animals more susceptible to infections?

A

Impaired Neutrophil function (due to altered hormone concentrations)

30
Q

What test should you do if you have subtle signs of early PPID?

A

TRH stim test or resting ACTH test

31
Q

What test should you do if you have more advanced signs of PPID?

A

Resting ACTH sufficient, don’t need TRH stim

32
Q

Why might you do an oral sugar test in a possibly PPID horse?

A

Insulin status assesment

33
Q

When is the seasonal rise in hormone production in horses?

A

Autumn. Animals with PPID do an even greater seasonal rise so best time to test

34
Q

When is the best time to do a basal ACTH assay in a suspect PPID horse?

A

Autumn (as long as lab has seasonally adjusted ref range)

35
Q

Why do you give TRH?

A

TRH (for some reason) is a physiologic release factor for the pituitary

36
Q

What do you measure in a TRH stim test?

A

ACTH (not cortisol) at 0 and 30 minutes

37
Q

What result do you need on a TRH stim to call it positive at a) 10 minutes or b) 30 minutes

A

a) ACTH >100pg/ml
b) >36pg/ml

High sens and spes but does have effect by feeding and by season

38
Q

Why do you have insulin dysregulation in some PPID animals?

A

Answer not known, ideas are:

Cortisol antagonises insulin, body responds by producing more insulin

CLIP may stimulate insulin secretion

39
Q

Why does insulin dysregulation have a worse prognosis in PPID?

A

More likely to get laminitis

40
Q

Which treatment must you start with if you shoose to medically manage PPID?

A

Pergolide (trade name prescend)

41
Q

What does pergolide do?

A

It is a dopamine agonist and so replaces inhibition of the pituitary

42
Q

What are the possible side effects of pergolide?

A

Diarrhoea, Depression, Anorexia, Colic

43
Q

What is the dose rate of pergolide?

A

2mg/kg SID

44
Q

What is cyproheptadine?

A

It is a serotonin antagonist, so inhibits the stimulation of the gland.

Less effective than pergolide

45
Q

Why don’t we use Trilostane in horses?

A

Doens’t work at the level of the pituitary, works at the level of the adrenal so only really useful in signs related to the adrenal (cortisol and ACTH)

46
Q

How long does it take to imrpove on PPID medication?

A

Up to one year!

47
Q

What should you do if the horse tests negative for PPID on your treatment

A

Stay on same dose and repeat test in 6 months

48
Q

What should you do if you test for cushings when the horse is being managed and the clinical signs have improved but the test is still positive?

A

Stay on same dose or increase

49
Q

What should you do if the test is still positive after management and no clinical response?

A

Incresae dose by 1-2mg/kg/day

can add in cyproheptadine