equine pituitary dysfunction Flashcards

1
Q

the pars intermediate produces:

A

melanotrophes:
- POMC = precursor for the below
- alpha MSH
- CLIP
- beta endorphin
- beta MSH
- beta LPH
- ACTH

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2
Q

what hormones upregulate POMC activity and which downregulate

A

upregulate:
- coticotrophin RH
- arginine vasopressin

downregulate:
- dopamine

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3
Q

ACTH is a minor post translational product of POMC. why? whch one is most active under adenoma influence

A

ACTH is further cleaved into other products
- beta endorphin is the more active form

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4
Q

what is the difference between PPID and HAC in dogs

A
  • adenoma is in the pars intermedia rather than adenohypophysis
  • leading to excessive productio of POMCs derived from peptides
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5
Q

what is the mechanism behind PPID

A

less dopamine from hypothalamus to inhibit POMC cleavage

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6
Q

how is PPID treated

A
  • aim is to inhibit expression of POMC mRNA expression and POMC hormone release
  • give D2 agonist (decreases ACTH concentration in most cases)
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7
Q

PPID is a ____ disease that results from the ________ of the pituitary _______

A

PPID is a central disease that results from the hypertrophy of the pituiatary pars intermedia

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8
Q

what are the clinical signs of PPID

A
  • generalised hypertrichosis
  • weight loss/wastage
  • PU/PD
  • laminitis
  • recurring infections
  • poor performance
  • regional adiposity/potbelly
  • docility/lethargy
  • neurologic signs
  • infertiltiy
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9
Q

Why do horses with PPID experience hypertrichosis

A
  • do not shed, even in warm seasons
  • chronic elevation of MSH?
  • pituitary conpression on the hypothalamic thermoregulation centre
  • increased production androgens
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10
Q

why do horses with PPID experience laminitis

A
  • persistent hyperinsulinaemia triggered by CLIP release
  • possibly high glucocorticoid concentration
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11
Q

why do horse with PPID experience lethargy/docility

A

beta endorphins have sedative effect (increase in circ)

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12
Q

Why do we see neurologic impairment in horses with PPID

A
  • blindness due to compression of optic chiasm
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13
Q

what factors and tests help make a diagnosis of PPID

A
  • hx: age (over 15 years, but at least 7), pony?, persistent laminitis episodes, recurrent infections etc.
  • physical exam: muscle wasting, coat chanes, fat depsoits
  • biochemistry: variable (sometimes hyperglycemia/hyperinsulinaemia, rarely neutrophilia/lymphopenia/hypertriglyceridemia
  • testing: resting ACTH or TRH stim

diagnosis only confirmed post mortem

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14
Q

describe the process of a resting ACTH test for diagnosis of PPID

A
  • collect blood in EDTA tubes and separate plasma within 4 hours of collection (careful of high temps in car)
  • submit chilled
  • positive horses should hace high ACTH levels
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15
Q

describe the process of TRH stim testing to diagnose PPID

A
  • take baseline blood sample
  • administer 1 mg TRH iv
  • blood sample 10 minutes later
  • measure ACTH concentration
  • positiv if ACTH is >110pg/ml at 10 mins

inaccruate in autumn months

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16
Q

what tests do we NOT do for PPID

A
  • basal cortisol
  • dexamethasone suppression test
  • TRH stim test measuring cortisol levels
  • combined dex suppression and TRH
17
Q

how can we theoretically measure POMC to diagnose PPID

not avaible commercially

A
  • beta endorphin, alpha MSH and CLIP will be disproportionally higher than ACTH in horses with PPID
  • not availible commercially
  • not validated in horses
18
Q

how can we use imaging to diagnose PPID and what are the pros/cons

A
  • CT, MRI might identify pituitary enlargement
  • CT possible but requires contrast
  • MRI might be useful but hardly availible
  • both require GA or heavy sedation
  • costly
  • poor sensitivity
19
Q

why dont we perform ACTH stim tests on horses

A

useless in horses because unlike other species, equine cushings is central and not peripheral in origin