Hyperadrenocorticism Flashcards
What is Canine Cushing’s Syndrome?
The constellation of clinical sings/abnormalities resulting from chronic glucocorticoid exposure caused by a tumor in the pituitary (80-85%) or adrenal glands.
Etiology of pituitary dependent hyperadrenocorticism
Excess production of ACTH with loss of negative feedback control on the pituitary
Frequency and amplitude of ACTH secretion is increased
Results in bilateral hyperplasia of the adrenal glands
Etiology of adrenal dependent hyperadrenocorticism
Excessive production of cortisol
Causes negative feedback on the pituitary resulting in suppression of ACTH production
Tumors function independently of hypothalamic/pituitary control
Usually unilateral adrenal involvement - uninvolved adrenal gland develops cortical atrophy as it receives no ACTH stim as a result of negative feedback
Tumor cells in the adrenal gland retain ACTH receptors and therefore may respond to exogenous ACTH
Signalment for hyperadrenocorticism
Mainly dogs
Any breed usually middle aged
More females
PDH - more common in small/toy breeds
ADH - affects large breed dogs more frequently
Prognosis for hyperadrenocorticism
Degree of ALP elevations does not reflect severity of disease or response to treatment
Pituitary microadenomas - good long term prognosis
Pituitary macroadenomas - poor without treatment; fair with effective treatment
Adrenal tumors - good to poor depending on type and tx
Treatment options for adrenal dependent hyperadrenocorticism
Medical
- Trilostane or Mitotane
Surgical
- Adrenalectomy
- can still reoccur in other adrenal gland or can later develop PDH
Goals of treatment for hyperadrenocorticism
Improve quality of life
Eliminate clinical signs
Avoid adverse effects
Medical is treatment of choice for _________ dependent hyperadrenocorticism, and surgical is the the treatment of choice for ___________ dependent hyperadrenocorticism.
Medical - pituitary
Surgical - adrenal
This drug is a chemotherapeutic agent used to treat pituitary dependent hyperadrenocorticism.
Mitotane - adrenolytic; selective necrosis in the zona fasciulata and zona reticular is, often sparing the zona glomerulosa
Adverse effects of Mitotane
Hypoadrenocorticism
Drug induced CNS signs
Can be very severe
This drug used to treat pituitary dependent hyperadrenocorticism is a synthetic steroid analog; enzyme inhibitor that prevents formation of cortisol; competitively inhibits 3 beta hydroxy steroid dehydrogenase
Trilostane
Effects are reversible and dose dependent
Adverse effects of Trilostane
Hypoadrenocorticism
Idiosyncratic adrenal necrosis
GI upset
Mild electrolyte abnormalities due to partial inhibition of aldosterone
Risk of death due to Addisonian crisis
More user friendly but very expensive
Only use Vetoryl brand - compounded has poor efficacy
Protocol for administering Trilostane to treat hyperadrenocorticism
Begin Trilostane tx generally at 1 mg/kg BID or 2 mg/kg SID (increased absorption when given with food)
Recheck ACTH stim / electrolytes at 14 and 30 days and adjust dose as needed
Recheck ACTH stim 10-14 days after any dose adjustment
Are selegilene (MAO inhibitor) and ketoconazole (inhibits steroid production) considered effective treatments for pituitary dependent hyperadrenocorticism?
No
DFDX for an adrenal tumor
Functional adenoma - producing cortisol
Nonfunctional adenoma - doing nothing
Cortical adenocarcinoma - may be functional
Pheochromocytoma - medullary tumor producing catecholamines
Other - metastasis
What are the most common clinical signs of hyperadrenocorticism?
PU/PD
Polyphagia
Panting
(P)Alopecia
(P)Abdominal enlargement
Dermatologic problems seen with hyperadrenocorticism
Truncal alopecia
Thin skin, easily bruised
Difficulty healing - collagen inhibition
Recurrent pyodermas - immune suppression
Adult onset demodicosus - immune suppression
Calcinosis cutis - only in dogs
Cutaneous hyperpigmentation
Urinary signs of hyperadrenocorticism
PU/PD - most common presenting complaint; blocks action of ADH at collecting tubules
Recurrent UTIs - due to presence of dilute urine and poor immune response; recommend urine cultures
Muskuloskeletal signs of hyperadrenocorticism
Generalized weakness
Muscle wasting - protein catabolism, collagen breakdown
What causes abdominal distention in patients with hyperadrenocorticism?
Fat redistribution
Hepatomegaly - increased glycogen storage
Weak abdominal muscles
Respiratory signs of hyperadrenocorticism
Panting - muscle weakness, pressure on diaphragm bony enlarged liver a and abdominal fat accumulation, pulmonary mineralization
If severe dyspnea is seen, suspect pulmonary thromboembolism (PTE) - glucocorticoid induced hypercoagulability
Complications/infections associated with hyperadrenocorticism
Hypertension
Pyelonephritis / UTIs
Pancreatitis
Urinary calculi
Gallbladder mucocele
DM - push pre-diabetic animals into full diabetes by causing insulin resistance
Hypercoagulability - pulmonary thromboembolism
Neurologic signs caused by compression by pituitary mass - macroadenoma
Inappetance / anorexia - most common
Dullness - most common
Disorientation
Circling
Ataxia
Behavioral changes
