Mineralcorticoid Excess
Thu, 12/27/2007 - 00:19 — oxygen
Mineralcorticoid Excess
clinical causes
clinical manifestations
anesthetic management
Primary aldosteronism:
-unilateral adrenal adenoma
-bilateral adrenal hyperplasia
-adenoma carcinoma
Secondary aldosteronism:
-congestive heart failure
-cirrhosis
-nephrotic syndrome
-hypertension
-hypervolemia
-muscle weakness
-metabolic alkalosis
-hypokalemia
Fluid disturbance:
-hypervolemia, secondary to increased Na+ reabsorption and H20 following
-assess orthostatic hypotension
-PAC helps to assess LV filling pressures (LVEDP)
electrolyte disturbance
-hypokalemia
Treatment with spirinolactone:
-aldosterone antagonist
-K+ sparring
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Comments
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The remainder is called
The remainder is called intracellular fluid.
In some animals, including mammals, the extracellular fluid can be divided into two major subcompartments, interstitial fluid and blood plasma. The extracellular fluid also includes the transcellular fluid; making up only about 2.5 percent of the ECF.actually i was surfing net to get data related to my projects of 1z0-051 exam | 70-272 exam | 117-101 exam and in the meantime came here...And find this post different one!
U can analyze that what i am
U can analyze that what i am gonna add about it ,"Apparent mineralocorticoid excess (AME) is an autosomal recessive cause of hypertension and hypokalaemia which responds to glucocorticoid treatment. It results from mutations in the HSD11B2 gene, which encodes the kidney isozyme of 11β-hydroxysteroid dehydrogenase.
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11β-hydroxysteroid dehydrogenase in a normal patient inactivates circulating cortisol to the less-active metabolite cortisone. The inactivating mutation leads to elevated local concentrations of cortisol in the kidney. Cortisol at high concentrations can cross-react and activate the mineralocorticoid receptor, leading to aldosterone-like effects in the kidney. This is what causes the hypokalemia, hypertension, and hypernatremia associated with the syndrome."
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