Cushing and glucocorticoid use are also associated with hypokalemia and leukocytosis (though increased susceptibility to infections because of diminished function).
Also: hyperglycemia, hyperlipidemia, osteoporosis, and metabolic alkalosis (caused by increased urinary loss of H+)
Basic Science Correlate
Mechanism of Metabolic Alkalosis
Cortisol has both mineralocorticoid or aldosterone effects on the kidney. Excess adrenal steroids increase hydrogen ion excretion at the alpha-intercalated cell of the late distal/early collecting duct. Hypokalemia results from potassium excretion through the principal cell.
Delayed wound healing, renal calculi from increased calcium levels, and glucoma may also be seen.
Myopathy in Cushing syndrome is characterized by progressive painless muscle weakness predominantly involving the proximal muscles. It is due to the direct catabolic effects of cortisol on skeletal muscle, leading to muscle atrophy.
Glucocorticoid-induced muscle atrophy is thought to be mediated by the inhibition of Akt-1, an intracellular signaling molecule with tyrosine kinase activity. Interference of IGF-1 signaling may also contribute. Furthermore, glucocorticoids may decrease muscle cell differentiation and protein synthesis.
Dx
best initial test is low-dose (1 mg) dexamethasone suppression test
It may be false positive in case of alcoholism, depression, stress, anorexia/ bulimia, obesity, etc. Also, enzyme inducers that increase the metabolic breakdown of dexamethasone can give abnormal (false negative) results (e.g, phenytoin, carbamazepine, rifampin, etc.)
24-hr free urinary cortisol is more specific and so confirmatory for hypercortisolism
The 3rd screening test available for Cushing is the midnight salivary cortisol.
Normal = lowest at midnight
Cushing = abnormally elevated at midnight
Early-morning cortisol
After hypercorticolism (Cushing) is confirmed,