Adrenal Gland Disorders

Adrenal Gland Disorders

• Adrenal gland disorders are conditions that interfere with the normal functioning of the adrenal glands.
• These glands produce hormones that affect growth, development, stress, and regulate kidney function.
• The adrenal glands are composed of two parts: the cortex and the medulla.
• The adrenal cortex produces mineralocorticoids, glucocorticoids (including cortisol), and androgens.
• The adrenal medulla produces epinephrine (adrenaline) and norepinephrine (noradrenaline).

Normal Adrenal Function

• Adrenocortical steroids affect all body tissues and organs.
• They help to keep the body's internal environment constant (homeostasis).
• The body provides a minimum amount of cortisol (20 mg in non-stressed adults).
• Adrenocorticotropic hormone (ACTH) is released by the anterior pituitary gland.
• In stressful situations, the pituitary gland rapidly increases the release of ACTH, and the adrenal cortex responds within minutes by synthesizing and secreting increased amounts of corticosteroids.
• The metabolic rate increases, sodium and water are retained, and small blood vessels become increasingly responsive to the actions of norepinephrine.

Hypothalamic-Pituitary-Adrenal (HPA) Axis

• Stress stimulates the hypothalamus to secrete corticotrophin-releasing hormone (CRH).
• CRH stimulates the anterior pituitary to release ACTH into circulation.
• ACTH promotes the rapid secretion of cortisol (within minutes) by the adrenal cortex.

Role of ACTH in Corticosteroid Secretion

• ACTH levels in the blood control the secretion of corticosteroids by the adrenal cortex.
• In non-stressful situations, the level of cortisol in the blood controls the secretion of ACTH.
• High plasma cortisol levels suppress ACTH release.
• Low plasma cortisol levels enhance the release of ACTH.
• The individual sleep cycle (circadian rhythm) controls ACTH secretion.

Cushing’s Syndrome

• A clinical condition resulting from cortisol hypersecretion.
• Associated with adrenal adenoma (tumor of the adrenal cortex).
• Does not usually result in an acute life-threatening situation.
• Hypercortisolism contributes to the early development of systemic diseases.
• Complications include obesity, hypertension, diabetes mellitus, hypercoagulability, dyslipidemia, atherosclerosis, depression, muscle weakness, impaired quality of life, and vertebral fractures.
• Treatment is by surgically removing all or part of the adrenal glands.

Primary Adrenocortical Insufficiency (Addison’s Disease)

• A life-threatening condition caused by cortisol deficiency.
• Autoimmune adrenalitis is a common cause (80% of cases).
• Clinical presentation in acute adrenal insufficiency includes hypotension, hypoglycemia, hyperpigmentation, and loss of consciousness, circulatory shock, hyponatremia, hyperkalemia, muscle cramps, nausea, vomiting, diarrhea, and unexplained fever.
• Impaired fasting glucose is often observed.
• Treatment involves administering physiologic doses of exogenous corticosteroids (cortisol).

Secondary Adrenocortical Insufficiency

• Most dangerous form of adrenal insufficiency.
• Can develop in stressful situations after the abrupt cessation or gradual withdrawal of exogenous corticosteroid therapy.
• The adrenal cortex returns to normal after 2 to 4 weeks of cessation.
• It is 2 to 3 times more common than primary adrenal insufficiency (Addison's disease).
• A greater potential threat than primary adrenal insufficiency in the development of acute adrenal crisis.
• Patients developing acute adrenal insufficiency are in immediate danger due to cortisol deficiency.
• Vascular collapse (shock) and cardiac arrest are the usual cause of death.
• Mechanisms for development of glucocorticosteroid deficiency include:
  • Sudden withdrawal of steroid hormone in a patient with primary adrenal insufficiency (Addison's disease).
  • Sudden withdrawal of steroid in a patient with a normal adrenal cortex who is receiving prolonged exogenous steroid treatment (secondary insufficiency).
  • After stress (physiological or psychological).
  • After bilateral adrenalectomy, or removal of a functional adrenal tumor.
  • After sudden destruction of the pituitary gland.
  • After both adrenal glands are injured through trauma, hemorrhage, infection, thrombosis, or tumor.

Management of Adrenal Insufficiency

• Replacement therapy with exogenous glucocorticoids.
• Can be given orally or parenterally.

Management of Adrenal Insufficiency in Dentistry

• Conscious Patients:
  • Termination of dental treatment if signs of adrenal insufficiency appear such as mental confusion, nausea, vomiting, or abdominal pain in patients on steroid therapy or those who have recently ceased long-term steroid therapy.
  • Positioning of the patient in the supine position with legs elevated slightly if signs of hypotension (mental confusion, profuse sweating) occur.
  • C-A-B (circulation-airway-breathing) basic life support as needed.
  • Monitoring of vital signs every 5 minutes.
  • Summoning of emergency medical assistance.
  • Administration of O2 at a flow rate of 5 to 10 L per minute.
  • Administration of glucocorticosteroids from the emergency kit.
  • In patients with chronic adrenal insufficiency, 50 to 100 mg hydrocortisone is administered every 6 to 8 hours.
• Unconscious Patients:
  • Recognition of unconsciousness (lack of response).
  • Positioning of the patient in the supine position with legs elevated slightly.
  • C-A-B (circulation-airway-breathing) basic life support immediately (CPR).
  • Obtain the emergency drug kit containing aromatic ammonia and administer O2.
  • Summoning of emergency medical assistance.
  • Evaluation of patient medical history for clues of possible cause.
  • Administration of glucocorticosteroids (100 mg hydrocortisone administered I/V or I/M) over 30 seconds, and I/V infusion together with 100 mg hydrocortisone over 2 hours.
  • I/V infusion of 1 L normal saline to combat hypotension, or 5% dextrose solution over 1 hour while waiting for emergency assistance.
  • Transfer to the hospital.

Diagnosis of Adrenal Insufficiency

• Diagnosis is confirmed by the laboratory test (ACTH stimulation test) before diagnosing any adrenal diseases.
• 4 mg of dexamethasone should be administered by I/V route every 6 to 8 hours while waiting for the result of the ACTH stimulation test.
• Dexamethasone is approximately 100 times more potent than cortisol.
• Administer IV fluids (normal saline) to counteract depletion of body fluid (hypovolemia).
• Administer 5% dextrose solution to combat hypoglycemia.