Back To CoursePathophysiology Textbook
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Jen has taught biology and related fields to students from Kindergarten to University. She has a Master's Degree in Physiology.
'Salt' is often used as a synonym for 'flavor.' And indeed, the common sodium chloride that we shake, sometimes too liberally, onto our food makes the bland taste good. But sodium is also an essential nutrient, one that the body carefully regulates and keeps in balance with other electrolytes, especially potassium. In a condition called hyperaldosteronism (or sometimes just aldosteronism), the body makes too much of the steroid hormone aldosterone. As we'll see, aldosterone plays a major role in sodium, water, and potassium balance.
Let's start by reviewing just a little about this hormone and its pathway. Recall that aldosterone is part of a hormone system called the renin-angiotensin-aldosterone system, or RAAS. This system plays a large role in maintaining blood pressure. When the kidney senses low blood pressure, it secretes an enzyme called renin, which helps activate the hormone angiotensin. The final form of angiotensin stimulates the adrenal cortex, the outer layer of the adrenal gland, to release aldosterone.
Aldosterone is the steroid hormone that stimulates kidneys to absorb sodium ions. It also causes the kidneys to retain water (which happens by osmosis, since water follows high concentrations of solutes like sodium) and to excrete potassium and hydrogen ions. These actions raise blood pressure.
In addition to low blood pressure, aldosterone production is triggered by plasma acidosis (high concentration of hydrogen ions in the blood) and high potassium levels. When released, aldosterone binds to receptors in the nephron's distal tubule, turning on the sodium/potassium pumps there. Aldosterone isn't 'shut off' via a negative feedback loop. Instead, it stops being made when the body has absorbed enough sodium ions.
But what happens when the body makes too much aldosterone? And how does this condition happen in the first place?
Hyperaldosteronism (recall that 'hyper' means 'above') occurs any time the body makes too much aldosterone. It can be divided into two categories, primary and secondary.
Primary hyperaldosteronism results when something in the adrenal gland goes wrong. Sometimes called Conn's syndrome, primary hyperaldosteronism usually results from tumors of the adrenal gland called adenomas. Adrenal adenomas are benign - that is, they are non-cancerous - and form when adrenal epithelial cells don't stop dividing. These extra cells 'go rogue' and secrete aldosterone even when not stimulated by the RAAS.
Primary hyperaldosteronism can occur even when no adrenal tumor exists. This is termed idiopathic adrenal hyperplasia, which is a bit of a mouthful. It has a simple definition, though: an increased number of cells (there's 'hyper' again) in the adrenal gland for no determined reason.
These two classifications make up the majority of cases of primary hyperaldosteronism, with genetic conditions and cancerous adrenal tumors making up many of the rest of the cases.
Secondary hyperaldosteronism occurs when aldosterone secretion is cause by something other than the adrenal gland itself. Usually, this form of aldosteronism is associated with hypertension (high blood pressure) due to either some sort of kidney failure or tumors that secrete renin, kicking off the RAAS pathway. Liver cirrhosis, heart failure, and other conditions characterized by chronic low blood pressure (and therefore consistently trigger the RAAS) can also cause this type of aldosteronism.
Whatever the cause of hyperaldosteronism, the effects of the disease are similar. Let's go back to our picture of the nephron to see what happens when there's a lot of uncontrolled aldosterone floating around. The first thing that happens is that the RAAS is suppressed because sodium uptake is increased. Since the aldosterone acts on the distal tubule to increase sodium and water uptake into the blood and to force potassium and hydrogen excretion into the urine, there is a higher than normal blood sodium level called hypernatremia and a lower than normal blood potassium level called hypokalemia. (Notice how the letter 'K,' the chemical symbol for potassium, is right in that term, as well as the prefix 'hypo' - which means below or under, like a hypodermic needle goes below the skin.) Loss of hydrogen ions to the urine means the blood pH will also be basic, or alkaline.
It's not surprising, then, that the primary symptom of uncontrolled salt and water resorption into the blood is high blood pressure (hypertension). Hyperaldosteronism shares many symptoms with chronic hypertension, like heart failure and stroke. What might be a little surprising is that there is very little edema (tissue swelling) associated with hyperaldosteronism. Instead, many of the symptoms presented are due to changes in sodium and potassium. Recalling that these ions are needed for healthy nervous system function, an upset in their balance leads to headache and constipation, general fatigue and weakness, and, if left untreated, heart arrhythmias, seizures, and coma.
In diagnosing aldosteronism, a key value is a high aldosterone-to-renin ratio; remember that the body suppresses renin when sodium and potassium balance is achieved. Serum values for this are aldosterone of over 14 ng/dL, with plasma renin activity being less than 2 ng/mL/hr. Hypokalemia manifests itself in a serum potassium level of less than 3.6 mEq/L, while serum sodium will be slightly elevated - about 143-147 mEq/L.
A CT scan or MRI is used to find and measure adrenal adenoma. If a tumor is causing the problem, then it's generally removed by laparoscopic surgery, and any remaining hypertension is treated with drugs. If the cause is not adenoma (and this includes cases of idiopathic hyperplasia), then a salt-restricted diet and medication are used to restore water and potassium balance. Diuretics are used to counteract excess water absorption, and aldosterone blockers, like spironolactone, prevent too much sodium absorption and restore potassium uptake. If primary aldosteronism is detected early, the prognosis is excellent.
Treatment of secondary hyperaldosteronism is directed at solving whatever is at its root; prognosis of this type of disorder depends on the underlying cause.
Let's review. In hyperaldosteronism, the body makes too much of the steroid hormone aldosterone. Aldosterone is a major component of the hormone system used to regulate water balance, the renin-angiotensin-aldosterone system. Aldosterone's job is to stimulate the kidneys to absorb sodium ions. It also causes the kidneys to retain water and to excrete potassium and hydrogen ions. In addition to low blood pressure, aldosterone production is triggered by plasma acidosis (high concentration of hydrogen ions in the blood) and high potassium levels.
Hyperaldosteronism can be divided into two categories: primary, in which there is a problem with the adrenal gland, and secondary, in which too much aldosterone is secreted for other reasons. The main causes of primary hyperaldosteronism are:
Secondary hyperaldosteronism is largely caused by high blood pressure.
Excess aldosterone suppresses the RAAS and causes too much sodium and water to be reabsorbed into the bloodstream and potassium and hydrogen ions to be excreted into the urine. This causes the bloodstream to be hypernatremic (high in sodium) and hypokalemic (low in potassium). Other symptoms include headache, weakness, seizures, and coma.
In addition to lab tests that show hypernatremia and hypokalemia, CT or MRI are used to confirm or rule out adrenal tumors. The key value in hyperaldosteronism, however, is a high ratio of aldosterone to plasma renin activity. Treatment of aldosteronism depends on the cause and usually involves laparoscopic surgery for adenoma, followed by drugs to relieve hypertension and to restore potassium and sodium balance.
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Back To CoursePathophysiology Textbook
20 chapters | 274 lessons