Aldosterone and Hormone Replacement Therapy and Renal Dialysis

The patient in “The Red Hat Hikers” scenario is suffering from hyponatremia. Hyponatremia is defined as a serum sodium level of less than 136mEq/L. Sodium is an electrolyte that is found predominately in the extracellular fluid, and it is the chief regulator of water in the body. Sodium is also important for muscle contraction, nerve impulses, acid-base balance and chemical reactions that occur inside the cell (McCance & Huether, 2014). Normal sodium levels in the body are maintained by the kidneys and the hormone aldosterone. Aldosterone is secreted by the adrenal cortex at the completion of the renin-angiotensin-aldosterone system, and it helps stimulate the proximal tubules of the kidneys to reabsorb sodium and water. The anti-diuretic hormone (ADH) also indirectly affects sodium levels because it regulates water balance in the body (McCance & Huether, 2014).

The mineralocorticoid (aldosterone) is normally released by the adrenal cortex in response to decreased sodium and increased pottasium levels; the hormonally acts to promote the retention of Na and the excretion of K. It isn't working; hence the abnormal serum levels.

Alongside with organs, bones, and tissues, the human body also functions through hormones. Some of these hormones are produced by the adrenal glands which are located right above the kidneys. Adrenal glands produce hormones that give vital instructions to almost every organ and every tissue in your body. When someone’s adrenal glands do not produce enough amounts of certain hormones such as cortisol and aldosterone, this often leads to Addison’s Disease.

After having their first child, many women experience hormone imbalance and struggle to get that normal feeling again. Let 's start with what a hormone is. Hormones are a chemical substance that voyage through your bloodstream stimulating cells and tissues into action. Hormones are produced by the endocrine glands and are our body 's dispatchers. It only takes a minuscule amount of hormones to make enormous changes in the body. Hormone imbalance can cause symptoms like depression, acne, fatigue, endometriosis, and insomnia. These are just some of the symptoms I experienced after having my son. After talking to my doctor, I had two options; I could take artificial hormones or I could try to change my diet and take vitamins to get my body to regulate its own hormones. After researching both treatments, I found out that each had their benefits. Artificial Hormones perform quicker than diet and vitamins. Artificial hormones can induce a dependency on prescription drugs and have serious side effects. Diet and vitamins can benefit other divisions of your body. It was a tough choice because I wanted to feel better immediately, but I also wanted to make the healthiest choice for my body.

Addison disease that is severe or total deficiency of the hormones made in the adrenal cortex, caused by the destruction of the adrenal cortex. It is basically a hormonal disorder that occurs in all age groups and afflicts men and women equally.

A decrease of water in the blood is perceived by the Hypothalamus. The Hypothalamus nerve cells produce a kind of water pill hormone called (ADH). ADH hormones enters the anterior lobe of the pituitary gland and exist through the rear lobe of the pituitary gland. ADH starts an increase in the absorption of water to the distal consulate tubes and collecting ducts of the nephron. Water is transported from being filtered back into the blood, causing an increase collection of water in the blood leading to more blood volume. Therefore, increasing the blood pressure and decreasing the urine output amounts.

There are both risks and benefits associated with hormone therapy. Risks of Hormone Therapy include DVT, coronary heart disease, myocardial

The prevalence of Addison disease in the United States is 40-60 cases per 1 million population. Addison disease seldom occurs. In countries where data are available reported prevalence is 39 cases per 1 million population in Great Britain and 60 cases per 1 million population in Denmark. The prevalence and number of death relating to Addison disease are as a result of to a failure or delay in diagnosing or a failure to institute adequate mineralocorticoid replacement, glucocorticoid.

Joseph Sciabbarrasi, M.D. stresses, "In my clinical practice—over 15 years of experience in the use of Bioidentical hormone replacement therapy—I regularly see that we not only halt, but we reverse osteoporosis." And studies back that up.

Even with the references that they provided, they did not extract the information and present it in a way that made it comparable, detail-by-detail, to estrogen and progesterone. They were able to list why synthetic progestin was a risk, but not as to why it was a benefit, or why synthetic progestin was being administered in the first place for hormonal treatment. Even on line 6, on page 3, the researchers stated “despite the significant distinctions between progesterone and synthetic progestins…”, but failed to identify the significant distinctions between them. On page 2, line 15, they stated that “progesterone is likely to be more beneficial and carry fewer risks than its synthetic counterpart”, but did not include an analysis of the difference, or why cognitively they are important.

I agree and also put that Mr. Smith could have primary aldosteronism as his diagnosis. His potassium levels should be checked right away since this electrolyte has a profound effect on the heart when it is not within normal limits. Some patients may or may not have low potassium with this disease. According to Galati, Hopkins, Cheesman, Zhuk, & Levine (2013) “indications for screening have been expanded with recognition that many patients with primary aldosteronism do not have hypokalemia and that the disease may be familial” (421). Mr. Smith does complain of muscle weakness however and because of this would lead me to believe that in his case he probably does have low potassium. Depending on what Mr. Smith’s blood results show I would then

Addison’s disease was first detected by Thomas Addison in 1855, it is a disorder caused by insufficient levels of hormones produced by the adrenal glands such as adrenocortical. It is caused by damage or dysfunction of the whole adrenal cortex and can be referred to as adrenal insufficiency. This failure to produce adequate hormone levels results in the body attacking itself known as an autoimmune disorder. It occurs in both men and women at any age and has no racial preference. Addison’s is predominantly seen more in Western countries than developing ones. Although it is not known if it is less common in these areas or if people are dying undiagnosed. This concern was the topic of the journal review, Diagnosis and Management of Addison’s Disease. This article focused on Addison’s in South Africa.

Before I explain what we are going to see in people that have Addison’s disease, I would like to elaborate on what causes it. The number one cause or most common cause is “Idiopathic autoimmune adrenocortical insufficiency”. This results from autoimmune atrophy, fibrosis, and lymphocytic infiltration of the adrenal cortex. This usually spares the adrenal medulla. Of the reported cases, this accounts for 80%. The kidneys or the adrenal glands are another reason for the lack of production of the hormones. With the autoimmune disorder, the body mistakenly attacks the adrenal glands, destroying the outer layer of the glands. Long lasting diseases, or infections, such as TB, HIV, and some fungal infections can cause Addison’s disease. If a patient has cancer somewhere in their body and it spreads to the adrenal glands, it could also cause Addison’s. Prolonged or improper use of steroid hormones, such as prednisone, can cause secondary adrenal insufficiency. Less common causes can be caused by pituitary tumors or damage to the pituitary gland during surgery or radiation. In some cases, hereditary predisposition has been found to be the cause. Wrapping up the causes, the main causes are, adrenal dysgenesis (the glad has not

What is the effect of low and high salt on blood pressure and kidney function in normal mice (C57)?

A total of 811 patients with Addison's disease were identified, with 147 patients who were deceased. Overall the SMR was 1.15 (95% confidence intervals (CI) 0.96-1.35), similar in females (1.18 (0.92-1.44)) and males (1.10 (0.80-1.39)). Patients who were diagnosed before the age of 40 had significantly elevated SMR at 1.50 (95% CI 1.09-2.01), most pronounced in males (2.03 (1.19-2.86)). Acute adrenal failure was considered a major cause of death while infection and sudden death were more common than in the general population. The mean ages at death for females