endocrinology (hyperadrenocorticism) Flashcards
what is the physiopathological mechanism explaining hyperadrenocorticism
most affected cats secrete excessive cortisol, however, hyperadrenocorticism may occur due to the secretion of other hormones with glucocorticoid activity (e.g., progesterone, estradiol, testosterone, …)
the vast majority of cats (approximately 80%) have pituitary-dependent HAC with the remaining having adrenal tumors
most pituitary-dependent cases seem to arise from ACTH secereting microadenomas in the pars distalis, or the pars intermedia, while adrenal tumors may be either benign or malignant and are usually unilateral
what is the epidemiology of hyperadrenocorticism
this is a rare disease in cats
average age of presentation is 10 years old
what are the clinical signs of hypoadrenocorticism
the most common clinical signs in cats with HAC are:
- PU/PD (90%)
- polyphagia (70%)
- wight loss (30%)
- lethargy
pot-bellied appearance with thinning of the skin, alopecia and poor hair coat
- skin fragility syndrome is a particular feature of feline HAC and can result in spontaneous skin tears
muscle atrophy, hepatomegaly and fragile skin are also common
some cats with HAC develop folded pinnae and/or curled whiskers
affected cats mau also have skin comedones on the ventral abdominal skin
bacterial or fungal infections are common in cats with HAC secondary to immunodepression
explain the machanism of PU/PD seen in HAC
in the vast majority of cases, the PU/PD is a result of concurrent (often insulin resistant) diabetes mellitus, but some cats with HAC without diabetes have also been reported to be PU/PD
what are the laboratory changes seen with HAC
routine blood work is often unremarkable but lymphopenia is the most common abnormality seen
cats can also have a mild to moderate anemia
elevated liver enzymes are seen in around 30% of cases
- IMPORTANT: cats do not possess the steroid-induced isoenzyme of alkaline phosphatase
how can you investigate hyperadrenocorticism
low-dose dexamethasone suppression test
urine cortisol to creatinine ratio
ACTH stimulation test
explain the low-dose dexamethasoone suppression test
his test is considered the best for initial screening for HAC (high sensitivity)
a 0.1 mg/kg dose of dexamethasone is given IV
serum cortisol is measured at 0, 4 and 8 hours
it has been suggested that up to 80 % of HAC fail to suppress at 8 hours
- thus, further testing may be needed
explain the urine cortisol to creatinine ratio
measurement of a home collected UCCR on two consecutive morning urine samples may be a useful screening test to rule out HAC
- normal result suggest HAC is very unlikely
- a positive test is relatively non-specific and may be elevated due to stress or other illness (especially hyperthyroidism)
explain the ACTH stimulation test
it is not considered a good screening test for HAC in cats
a 0.125 mg synthetic ACTH dose is administered IV
evaluate cortisol at 0, 1 and 2 or 3 hours
how can you differentiate PDH and ADH
if the 4 hours cortisol level from the LDDST is less than 40 nmol/l or the 4 or 8 hour cortisol is greater than 40 nmol/l but less than 50% of the 0 hour cortisol reading then PDH is more likely
a high dose dexamethasone suppression test can be done
- 1 mg/kg dexamethasone IV then serum cortisol measurements at 0, 4 and 8 hours
CT or MRI may be valuable in identifying a pituitary tumor and/or adrenomegaly
what is the treatment for HAC
trilostane
- it is an inhibitor of the 3-beta-hydroxysteroid dehydrogenase enzyme
- it reduces synthesis of cortisol, aldosterone and adrenal androgens
- it appears safe and effective in cats
- starting dose of 1-2 mg/kg/day which can be increased to every 12 hours and at higher doses if needed
- successful therapy will result in improved (but not completely normalised) clinical condition, improved routine blood tests and normalisation of the ACTH response test (measured 2-4 hours post medication)
cabergoline
- 10 µg/kg every 2 days
what could you say about sex steroid producing adrenal tumors
rarely, the cause of clinical HAC in some cats may be a sex steroid producing adrenal tumor rather than a cortisol-secreting tumor alonne
several cases are reported where more than one sex steroid was produced (e.g., progesterone, testosterone, estradiol)
- progesterone producing tumors can lead to diabetes mellitus development and clinical signs of HAC - other sex steroids (e.g., testosterone, ...) may lead to seaxualised behaviors and physical changes instead (e.g., urine spraying, penile spines, ....)
how a diagnosis of sex steroid producing adrenal tumor can be made
diagnosis is made with ACTH stimulation test and sexual setroids measurement
- affected cats usually have low serum cortisol levels despite clinical signs suggestive of hypercortisolism
what are the treatment options for a sex steroid producing adrenal tumor
treatment with trilostane can be tried but adrenalectomy is the treatment of choice with resolution of clinical signs and return of sex steroid hormone concentration to within reference intervals in weeks to months
what are phaeochromocytomas and what is their frequency in cats
phaeochromocytomas are tumors of the adrenal medulla which, if functional, result in autonomous secretion of catecholamines
they are extremely rare tumors in cats with major clinical signs due to persistent hypertension
