Hypocorticism
So, as with all hormonal imbalances, this can be primary, secondary or tertiary. Primary hypocorticism the result of adrenal insufficiency (Addison's disease), while secondary hypocortisolism pertains to cases of hypocorticism which are not caused by the adrenal gland. The most common cause is exogenous glucocorticoids which causes suppression of the hypothalamic-pituitary-adrenal axis, other causes include destructive CNS tumours and cerebral trauma.
First we will consider the general symptoms of hypocorticism, then go on to address addison's (primary hypocorticism) and secondary hypocorticism separately.
Symptoms of hypocorticism include:
- Nausea + vomiting
- Weakness + fatigue
- Fever
- Hypotension
- Hyperpigmentation of buccal mucosa (addisons only - caused by high ACTH)
- Addisonian crisis (see box)
- Weight loss
- Depression
In hypocortisolism we see a decrease in the production of cortisol (and possibly aldosterone) from the adrenal glands. In addison's disease, the most common cause is as an autoimmune disease, while in the developing world the most common cause is TB, although other causes can include sepsis, and bleeding into both adrenal glands (so called Waterhouse-Friderichsen syndrome). Adisons most commonly affects middle-aged females, and is less common than secondary adrenal insufficiency. Addison is associated with the development of other autoimmune diseases including T1DM, Hashimoto’s, celiac and vitiligo.
Image: “1818 The Adrenal Glands” by OpenStax College, CC BY 3.0, via Wikimedia Commons.
In addisons, we also see hyponatraemia and hyperkalaemia, this is due to the loss of production of aldosterone (as well as cortisol) meaning there is decreased diuresis (meaning an inability to excrete free water) along with a downregulation of potassium excretion for which aldosterone is required. Other laboratory findings include: low blood sugar (loss of glucocorticoid glucogenic effect), eosinophilia and lymphocytosis and metabolic acidosis (due to sodium reabsorption which is linked with H+ secretion in the renal distal tubule).
Investigations in suspected cases of addisons should include:
- Baseline electrolytes
- Measure early morning serum cortisol (<100nmol/L warrants further investigation
- Perform the short Synacthen test (Synacthen is an ACTH analog, measure cortisol before and after, adrenal insufficiency if cortisol levels do not rise, this also helps detect primary or secondary insufficiency).
- Perform plasma ACTH (high in addisons, low in secondary)
- Carry out thyroid function and look for other aetiologies
Management
- Ensure education
- Replace glucocorticoids and mineralocorticoids (hydrocortisone and fludrocortisone)