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Cushing's Disease and Equine PPID (Pituitary Pars Intermedia…
Cushing's Disease and Equine PPID
Pituitary Pars Intermedia Dysfunction
(PPID)
over secretion of hormones from pars intermedia of pituitary gland
POMC secreted from melanotroph
physiologic role in horses is poorly characterized
pathophys
primary dysfunction of the hypothalamus
hypothalamic neurons that produce dopamine degenerate
gradual onset of clinical signs
incurable but manageable
signs
abnormal shedding
progressive haircoat retention
hypertrichosis (shaggy hair coat)
excessive hair growth
muscle wasting
due to excessive cortisol secretion
atrophy of topline and neck muscles
pot-bellied appearance
PU/PD
due to hyperglycemia and/or reduced production of ADH
immunosuppression
cortisol dysregulation: causes higher parasite load and increased risk of infection
acute and chronic laminitis (higher risk with PPID)
common in middle age and geriatric horses
diagnostics
diagnosis of early disease is difficult
endogenous ACTH conc
significant elevation suggests PPID
no risk of triggering laminitis
dexamethasone suppression test
impaired suppression suggests PPID
similar sensitivity and specificity as ACTH
requires multiple DVM visits
risk of causing/aggravating laminitis
neurodegenerative disorder
treatment
dopamine receptor agonist
peroglide mesylate (Prascent tablets)
lifelong treatment is required for regulation
Cushing's Disease
chronic exposure to excessive serum conc of glucocorticoids (cortisol)
common in
breeds <20 kg (pituitary dependent)
dogs >9 yo
females
breeds >20 kg (adrenal dependent)
spontaneous
pituitary dependent: 85% of cases
functional microadenoma on pituitary = secrete excessive ACTH
results in excessive stimulation of zona fasiculata and reticularis, excessive cortisol secretion, and bilateral hyperplasia
adrenal tumor: 15% of cases
functional adenoma/adenocarcinoma of adrenal cortex (typically unilateral)
results in excessive secretion of cortisol independent of ACTH
non-affected adrenal gland will atrophy
iatrogenic
inappropriate administration of glucocorticoids
signs
panting
due to fat accumulation, muscle wasting/weakness, compression of diaphragm from hepatomegaly, pulmonary interstitial mineralization
polyphagia
unique to Cushing's
excess glucocorticoids stimulate hunger
exercise intolerance
due to muscle wasting and weakness
polydipsia
due to excessive water loss from polyuria
lameness
rupture of ACL and patellar luxation common
polyuria
cortisol might interfere with ADH secretion =
form of central diabetes insipidus
results in lack of urine concentration
physical findings
muscle atrophy
dermatologic signs
non-inflammatory, non-itchy, symmetrical alopecia
very thin skin
blackheads
poor wound healing
predisposition to bacterial/fungal infections
hepatomegaly
due to glycogen accumulation
pendulous abdomen
due to weak abdominal muscles, fat accumulation, enlarged bladder, and enlarged liver
complications
hypertension (50% of cases)
diabetes mellitus (5-10% of cases)
UTIs