Endocrine Flashcards
What are the parts of the anterior pituitary gland?
Pars distalis and pars tuberalis
Where is the pars intermedia located?
Between the anterior and posterior parts
Describe the physiology of the pituitary gland
Stress -> hypothalamus releases CRH and vasopressin -> pituitary secretes ACTH -> adrenals secrete cortisol
What type of feedback loop does cortisol have on the pituitary and hypothalamus?
Negative feedback loop
What is the main type of cell in the pars intermedia?
Melanotropes
What disorder in humans has similar lesions to PPID in horses?
Parkinson’s disease
How does dopamine normally influence pituitary hormones?
Interacts with melanotropes to inhibit ACTH and alpha-MSH which control cortisol release
How is dopamine different in PPID horses?
Oxidative neurodegeneration damages dopaminergic hypothalamic neurons. This leads to the loss of inhibitory tone in pars intermedia (increased ACTH production)
What are clinical signs of PPID?
Hypertrichosis, chronic or intermittent lameness, sole abscesses, PU/PD, sweating, muscle wasting, lethargy, recurrent infections, abnormal fat deposits, inappropriate lactation, blindness, seizures
What clinicopathologic changes are associated with PPID?
Hyperglycemia, hyperinsulinemia, hypertriglyceridemia, increased liver enzymes, increased ACTH (consistent but not always active). Sometimes anemia, neutrophilia, lymphopenia, high fecal egg count.
How is PPID diagnosed?
Clinical signs, age, endogenous ACTH concentration (consider seasonal RR- higher in the fall), response to therapy, necropsy
What is the gold standard for PPID diagnosis?
Stimulation test. Grain fasted then administer 1mg TRH IV, draw sample in EDTA tubes 10 min later, submit plasma for ACTH measurement. Recommended to do in the spring.
Would you expect ACTH to be high or low for a horse with PPID?
High
How is PPID treated?
Pergolide (dopaminergic agonist, can reduce appetite), cyproheptadine (serotonin agonist, can be added on), management (deworming, manage laminitis, hair-trims, adequate nutrition)
What are the 3 main components of equine metabolic syndrome?
Obesity, insulin dysregulation, and laminitis
What is the common signalment for equine metabolic syndrome?
Likely susceptible from birth, 5-10 years old at presentation, described as “easy keepers”
What clinical signs are associated with equine metabolic syndrome?
Laminitis, obesity, regional adiposity (cresty neck, around tail head, behind shoulder, prepuce or mammary gland), “easy keeper”
How is equine metabolic syndrome diagnosed?
Based on signalment, clinical signs, diagnosis of insulin resistance (IV glucose tolerance test or combined glucose insulin tolerance test)
Describe the combined glucose insulin test
Grain fast overnight, obtain baseline glucose and insulin, administer dextrose IV then insulin IV, then check BG at intervals. If insulin >100uU/mL at 45 min- resistant
What insulin concentration measurement is consistent with hyperinsulinemia?
> 50uU/mL
What result on an insulin tolerance test is consistent with insulin resistance?
<50% decrease in BG from baseline 30 mins after insulin administration
How is equine metabolic syndrome managed?
Restrict/eliminate grazing, don’t feed grain, provide mineral/vitamin/protein ration balancer, add daily exercise (unless laminitis present). Levothyroxine can be used to increase metabolic rate, activity level, and insulin sensitivity. Metformin hydrochloride can be used to increase insulin sensitivity.
How does adult hypothyroidism occur in horses?
VERY RARE- from exogenous compounds, pituitary disorders, iodine deficiency or excess, or neoplasia
What clinical signs are consistent with adult hypothyroidism?
Lethargy, poor performance, obesity, laminitis, cresty neck, EMS or PPID
