You guys already know that mineralocorticoids are hormones secreted by the outer layer of the adrenal

gland. The main effect of the mineralocorticoid hormones is to regulate the fluid balance of the body.

So here we have Aldostrone is the most important secreted mineralocorticoid. We can see the
aldosterone receptors in a number of organs such as the kidneys, colon, heart, and sweat glands but it
affects the kidney more than others.

So Aldosterone is hydrophobic so it need to bind globulin to transport until reach the target cell. Then it
enters the cell, interacts with mineralocorticoid receptors, and travels to the nucleus. Then Aldosterone
starts a complex process in the nucleus that results in the transcription of DNA into mRNA, which
produces cell-specific proteins. And these cell- specific protein will regulate sodium and potassium ione
and transport water accross the cell membranes.

In addition, during the process formation of urine in the renal nephrons, aldosterone increase reabsorb
sodium and water from urine which expands the blood volume and increases blood pressure, so to
maintain normal salt concentration in the body, potassium ions are transported into the urine, so that's
why normal sodium and water levels are maintained in the blood and other body tissues.

The two major regulators of aldosterone secretion are increases in extracellular potassium ion
concentration and angiotensin II. So with small increases in the potassium ion blood level can stimulate
aldosterone secretion. And the reduced renal blood flow because of f decreased blood volume begins a
process that results in the formation of angiotensin II. Angiotensin II is a potent peptide that constricts
blood vessels, raises blood pressure, and stimulates aldosterone secretion.

When there is a deficiency of mineralocorticoids, the replacement therapy is necessary because the
mineralocorticoids are essential for life.

So we can use Fludrocortisone which is synthetic adrenocorticosteroid with dual activity, used in
conjunction with a glucocorticoid to achieve total replacement therapy in primary and secondary
adrenocortical insufficiency. It is administered orally in doses of 0.1 mg three times per week to 0.2 mg
per day.

Excessive use of the mineralocorticoids results in sodium and water retention and the loss of potassium.
The main symptoms are edema, hypertension, arrhythmias, and muscle weakness due to potassium
deficiency. In some patients, edema can lead to congestive heart failure. If you experience dizziness,
headaches, or swelling in your lower extremities, call your doctor. Other side effects include excessive
sweating, bruising, and an allergic skin rash. . Adverse effects are usually reduce by adjusting the dose.

Steroids are administered for their anti-inflammatory activity in patients with normal adrenal function.
Steroids can cause changes in body weight, electrolyte balance, and cardiac function, which can lead to
elevated blood pressure, hypertension, and edema. Patients should be weighed daily to monitor changes
in overall body weight and don't misuse these drugs.

Patients should be asked if they are tired or if they have cramps or weakness in their extremities, becoz
these are symptoms of hypokalemia. Patients with Addison's disease are frequently sensitive to drug
effects, resulting in an exaggerated response to drug therapy. Patients on high-dose therapy, in
particular, should be monitored for changes in sleep patterns and mood, particularly depression or
psychotic episodes.

Steroids should be used cautiously in patients who have GI ulceration, renal disease, congestive heart
failure, ocular herpes simplex, diabetes mellitus, emotional instability, or psychotic tendencies. In all of
these conditions, steroids may cause increease the underlying disease.

Ophthalmic complications during prolonged corticosteroid therapy include posterior subcapsular

cataract, glaucoma, possible damage to optic nerves,and enhancement of secondary ocular infections
due to fungi or virus.