Adrenal Cortex
• Adrenal gland
• hyperadrenocorticism and adrenal insufficiency.
• Hyperadrenocorticism
• pituitary-dependent (Cushing’s syndrome),
• adrenal-dependent
• iatrogenic
Hypoadrenocorticism
Hypoadrenocorticism usually results from adrenal gland failure (adrenal-dependent hypoadrenocorticism, Addison’s disease) The failure of ACTH secretion by the pituitary gland (pituitary-
dependent hypoadrenocorticism) rarely observed but the exact cause
should be determined.
• Chronic or high-dose glucocorticoid therapy may cause adrenal cortical atrophy which may result in when therapy is stopped suddenly.
• Iatrogenic hypoadrenocorticism caused by the sudden
discontinuation of glucorticoids after chronic or high dose therapy as the animal may have underlying adrenal cortical atrophy
• The signs of glucocorticoid deficiency can be seen but not the signs of
mineralocorticoid deficiency.
Basics
• Glucocorticoid secretion and function
1. The glucocorticoids (cortisol, corticosterone, and cortisone) are secreted by the zona fasciculata and zona reticularis of the adrenal cortex.
2. Glucocorticoid secretion is stimulated by adrenocorticotropic hormone (ACTH), which is released from the anterior pituitary under stimulation of corticotropin-releasing hormone (CRH) from the hypothalamus.
• Cortisol inhibits release of CRH
• suppressing ACTH secretion.
• glucocorticoid administration suppresses ACTH.
• Glucocorticoids antagonize the effects of insulin.
• They promote gluconeogenesis and glycogenesis while decreasing glucose uptake by insulin-sensitive tissues.
• Glucocorticoids increase lipolysis.
• Glucocorticoids suppress inflammation and immune response.
Mineralocorticoid secretion and function 1. Aldosterone
mineralocorticoid secreted by the zona glomerulosa 2. Aldosterone secretion is regulated involving
renin ACTH
rising serum potassium (K+) concentration stimulates 3. The kidney is the primary target organ of aldosterone.
a. reabsorption (Na+).
b. excretion of K+.
Hyperadrenocorticism
1. Pituitary-dependent hyperadrenocorticism
2. Adrenal-dependent hyperadrenocorticism results from functional adrenal cortical neoplasms that
3. Iatrogenic hyperadrenocorticism
Pituitary-dependent
hyperadrenocorticism
a. Hyperplasia or small neoplasms of the ACTH-secreting cells of the anterior pituitary.
b. High ACTH may also arise from the pars intermedia of the pituitary.
c. Chronic, excessive ACTH stimulation may result in bilateral adrenal
cortical hyperplasia.
Adrenal-dependent
hyperadrenocorticism
• Adrenal cortical neoplasms that autonomously secrete excessive
cortisol which are usually unilateral.
Iatrogenic hyperadrenocorticism
• Long-term glucocorticoid therapy.
• The clinical signs are indistinguishable from naturally occurring
hyperadrenocorticism.
LABORATORY EVALUATION OF THE ADRENAL CORTEX
• Plasma cortisol measurement
• 1. cortisol; dogs, cats,and horses.
• corticosterone In birds, is the principal glucocorticoid secreted by the adrenal gland.
• 2. there is minimal cross-reactivity with corticosterone and cortisone.
• 3. Prednisolone and other exogenous steroids will cross-react in commonly used cortisol immunoassays(except dexamethasone).
• 4. Resting or baseline cortisol values of animals with
hyperadrenocorticism may be within the reference interval.
ACTH Stimulation Test
• A baseline serum cortisol level > 2 mcg/dL can be used to rule out hypoadrenocorticism, while a cortisol level ≤ 2 mcg/dL necessitates an ACTH stimulation test.
• Cortisol is measured at baseline and then one hour following an IV or IM injection of synthetic ACTH (5 mcg/kg).
• Typical and atypical hypoadrenocorticism are defined by a pre- and
postcortisol concentration of ≤ 2 mcg/dL.
Dexamethasone Supression Test
• Low Dose
• High Dose
Low-dose dexamethasone suppression test
1. Screening the animals for the pituitary-dependent and adrenal-dependent hyperadrenocorticism.
2. Low-dose dexamethasone suppression test protocol
a. A blood sample is drawn for baseline plasma cortisol determination.
b. Dexamethasone is injected intraveneously at the following dosages:
(1) 0.01 mg/kg in the dog (2) 0.1 mg/kg in the cat
c. A second blood sample is drawn eight hours after administration of
dexamethasone for determination of plasma cortisol concentration.
High-dose dexamethasone suppression test
1. This test is used to distinguish dogs with pituitary-dependent
hyperadrenocorticism from dogs with adrenal-dependent hyperadrenocorticism.
2. High-dose dexamethasone suppression test protocol
a. A blood sample is drawn for baseline plasma cortisol determination.
b. Dexamethasone is injected intraveneously at the following dosages:
(1) 0.1 to 1.0 mg/kg in the dog (2) 1.0 mg/kg in the cat
c. A second blood sample is drawn eight hours after administration of dexamethasone for determination of plasma cortisol concentration.
