the pars intermediate produces:
melanotrophes:
- POMC = precursor for the below
- alpha MSH
- CLIP
- beta endorphin
- beta MSH
- beta LPH
- ACTH
what hormones upregulate POMC activity and which downregulate
upregulate:
- coticotrophin RH
- arginine vasopressin
downregulate:
- dopamine
ACTH is a minor post translational product of POMC. why? whch one is most active under adenoma influence
ACTH is further cleaved into other products
- beta endorphin is the more active form
what is the difference between PPID and HAC in dogs
what is the mechanism behind PPID
less dopamine from hypothalamus to inhibit POMC cleavage
how is PPID treated
PPID is a ____ disease that results from the ________ of the pituitary _______
PPID is a central disease that results from the hypertrophy of the pituiatary pars intermedia
what are the clinical signs of PPID
Why do horses with PPID experience hypertrichosis
why do horses with PPID experience laminitis
why do horse with PPID experience lethargy/docility
beta endorphins have sedative effect (increase in circ)
Why do we see neurologic impairment in horses with PPID
what factors and tests help make a diagnosis of PPID
diagnosis only confirmed post mortem
describe the process of a resting ACTH test for diagnosis of PPID
describe the process of TRH stim testing to diagnose PPID
inaccruate in autumn months
what tests do we NOT do for PPID
how can we theoretically measure POMC to diagnose PPID
not avaible commercially
how can we use imaging to diagnose PPID and what are the pros/cons
why dont we perform ACTH stim tests on horses
useless in horses because unlike other species, equine cushings is central and not peripheral in origin