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Cortisol

Cortisol, the adrenal steroid hormone is required for normal endocrine function. 

 

 

Cortisol production begins in the second month of fetal life. 

 

 

Normal daily production 15-20 mg/day.

Production controlled by closed feedback loop as the anterior pituitary secretes adrenocorticotropic hormone (ACTH) that stimulates adrenal cortisol production.

Inhibits ACTH release and completes the closed feedback loop system.

The major endogenous glucocorticoid in humans.
Overstimulation of the glucocorticoid receptor in target tissue is physiologically prevented by the enzyme l11beta hydroxysteroid dehydrogenase-2, which converts cortisol to the inactive steroid Cortisone.

In acute illness like sepsis, trauma, and burns cortisol production by the adrenal gland is increased by as many as six fold.

Normally bound to corticosteroid-binding globulin with less than 10% free cortisol bioavailable form.

Unbound cortisol is physiologically active, but laboratory levels only measure total cortisol levels.

Cortisol levels rise rapidly after wakening, a peaking within 30–45 minutes. 

 

 

Cortisol levels then gradually fall over the day, rising again in late afternoon. 

 

 

Cortisol levels fall in late evening, reaching a trough during the middle of the night, corresponding to the rest-activity cycle.

 

 

A flat circadian cortisol cycle has been linked with chronic fatigue syndrome, insomnia and burnout.

The hypothalamic-pituitary-adrenal axis (HPA) causes release of the corticotropin releasing hormone from the hypothalamus.

The HPA has a diurnal variation which is lost during acute stress.

 

Patients on chronic corticosteroids do not need to receive stress doses of such drugs after undergoing a surgical procedure as long as they receive their usual daily doses of medication. (Marik). 

Patients on chronic corticosteroids do not need to undergo adrenal function testing since such testing is overly sensitive and not predictive of adrenal crisis.

Patients receiving replacement doses of corticosteroids for primary HPA disease do require supplemental doses of corticosteroids in the perioperative period.

Chronic elevation of cortisol is associated with increased inflammatory proteins such as interleukin6 which can lead to fibrosis and scarring of blood vessel walls of the arterial circulation, and result in increased intima-media thickness.

Increased production of cortisol occurs during stress which increases glucose levels and availability.

 

 

Cortisol suppresses the highly demanding metabolic processes of the immune system, resulting in further availability of glucose.

 

Poor cortisol production is a hallmark of most forms of congenital adrenal hyperplasia.

Inefficient cortisol production results in rising levels of ACTH.

 

 

This increased ACTH stimulation induces hyperplasia and overactivity of the steroid-producing cells of the adrenal cortex. 

 

 

The defects causing adrenal hyperplasia are congenital.

 

Compounds that can induce apparent mineralocorticoid excess-cortisol, digitalis, and abiraterone.

 

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