Addison’s disease sometimes calledadrenal insufficiency occurs when the adrenal gland is not producing enoughhormones in the body. These hormones are made in the adrenal gland, which islocated above the two kidneys in our body. When this adrenal gland does notproduce enough hormones in order for the body to function properly, Addison’sdisease occurs. The three hormones that are secreted in the adrenal gland arealdosterone, glucocorticoids, and androgens.
These hormones play a key role inthe cause of Addison with cortisol and aldosterone being the important one. Eachhormone has different functions like regulating blood pressure, as well as thebody’s response to stress. There are two types of Addison’s disease, primaryand secondary, both of which have different causes and characteristics.
Thereis different ways that Addison’s disease can be diagnosed, as well as differenttypes of treatment for those who are diagnosed with the disease. Aldosteroneis accountable for the balance of sodium and potassium in the blood, as well ashelp with maintaining blood pressure. When the production of aldosterone islow, the body loses a lot of sodium and gains a lot of potassium. The sodiumreduction leads to a decreasing amount of fluid in the blood (blood volume) andblood pressure. This reduction of sodium can also cause hyponatremia, some ofthe symptoms of hyponatremia includes; feeling confused, fatigued, seizures andmuscle twitches. On the other hand, too much potassium in the body can causehyperkalemia.
Hyperkalemia is a very high level of potassium, even though highpotassium causes irregular pulse, heartbeat and nausea, it doesn’t necessarilymean it may have symptoms. Both hyperkalemia and hyponatremia arecharacteristics of Addison’s disease. Cortisolbelongs to the class of hormones called glucocorticoid. Which is produced inthe zona fasciculate of the adrenal cortex.
Glucocorticoids are known for theirability to increase plasma glucose concentration. Cortisol is regulated by thehypothalamus. The control pathway for cortisol is called thehypothalamic-pituitary-adrenal (HPA). The hypothalamus first releasecorticotrophin-releasing hormone (CRH) into the hypothalamic-hypophyseal portalsystem and it is gets transported to the anterior pituitary. From there, CRHstimulates the release of adrenocorticotropic hormone (ACTH) amino acid proteinhormone.
ACTH then stimulates the adrenal gland to produce cortisol. Cortisolthen acts as a negative feedback signal, inhibiting and controlling ACTH andCRH secretion. When Addison disease occurs, the negative feedback of thecortisol is cut, which means ACTH and CRH are not getting signal. Glucose willbe low because cortisol depends on ACTH to produce glucose, which causeshypoglycemia. Low testosterone alsooccurs because of the ACTH decreasing.
If there is not enough cortisol beingmade in the body, the body can’t cope with the long-term stress. Anotherhormone that is secreted by the adrenal cortex is androgen, the sex hormone thatis mostly dominant in men. Androgen is secreted in the zona retucalaris of the adrenalcortex. Androgen is also stimulated by ACTH and makes testosterone. If there wereless androgen in the body, the body would not be able to make testosterone.
Whenthe body cannot make enough cortisol or aldosterone, it is converted intoandrogens, in newborns that are girls; a lot of androgens translate into masculinizationof the external genitalia. This condition however occurs rarely. ThomasAddison first explained Addison’s disease in 1855; he described thecharacteristics of the disease and what the cause might be. It was only lateron that the functions of adrenal gland were recognized in the connection withAddison’s disease. In primary Addison’s disease, the adrenal cortex doesn’twork because there is an antibody attack on it, so it is destroyed. This couldhappen because of infectious causes, like TB, which is the most common cause ofadrenal deficiency in places that are still developing. In this case ACTH productionis high because there is no negative feedback from the adrenal cortex going tothe CRH, so the CRH makes a lot of ACTH from anterior pituitary so that theadrenal gland can work, however the adrenal gland is destroyed. CRH alsoreleases melanocytes stimulating hormone by the side of ACTH.
This means thatthere is higher production of ACTH and melanocyte stimulating hormone but nonegative feedback, this lead to hyperpigmentation in the skin because of theexcess melanocytes. Hyperpigmentation is the one thing that separates primaryfrom secondary adrenal insufficiency. Secondary Addison’s disease is when thepituitary is not secreting enough ACTH, which means that there is low ACTH. Thetwo hormones that are affected by this are cortisol and androgens because theyare both stimulated by ACTH.
Because ACTH is not high, hyper pigmentation doesnot occur in secondary Addison’s disease. Thesymptoms and characteristics of Addison’s disease include; agitation, confusion,fatigue, abdominal pain and fever also occur at times. In some cases, weighloss, joint and back pain also occurs. Another characteristics of Addison’sdisease are the darkening of the skin. Addison disease is diagnosed by abiochemical testing The plasma cortisol in the body should be about 479 nmol/L,if it is lower than that, that means the numbers show adrenal insufficiency.
Another way that Addison’s disease is diagnosed is by giving the patient aninjection of ACTH, and samples of blood and urine are taken before and afterthe injection. If the cortisol level does not increase or change only bylittle, then it means the patient has adrenal insuffiency. CRH stimulation testcan also be done if the ACTH injection does not work. In the CRH test, apatient is given injection of synthetic CRH and blood gets taken before andafter the injection. People who have the disease respond to this test byproducing a high amount of ACTH or delayed response but they do not producecortisol. Itis important to diagnose Addison’s disease as early as possible so that thepatient does not suffer from chronic illness.
The treatment of Addison’sinvolves replacing the hormone the body is missing or cannot make. This is thereplacement of the glucocorticoid and mineralocorticoid hormone. If cortisol islow, then a patient can take replacement hormone such as; corticosteroid,hysrocortisone, predistone and other cortisol replacing hormones by mouth morethan one time a day. However, if aldosterone is also deficient, then thepatient can take mineralocorticoid hormone once or twice a day.