Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (697 page)

BOOK: Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis
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Increased In

   CAH caused by 21-hydroxylase deficiency; marked increase is suppressed to normal levels by adequate glucocorticoid therapy.
   Suppressed level reflects adequacy of therapeutic control.
   Androstenedione may be better than 17-hydroxyprogesterone for monitoring therapy because it shows minimal diurnal variation, better correlation with urinary 17-KS excretion, and plasma levels that are not immediately affected by a dose of glucocorticoid.
   Adrenal tumors
   Cushing disease
   Polycystic ovarian disease

Decreased In

   Addison disease
   Any condition that causes partial or complete adrenal or gonadal failure
ANGIOTENSIN II
   Definition
   Angiotensin II is the biologically active product of renin–angiotensin system. It is an oligopeptide of eight amino acids and very strong physiologic vasoconstrictor. The concentration of ACE is highest in the lung, and it had been thought that most angiotensin II formation occurred in the pulmonary circulation. It is now clear, however, that ACE is produced in the vascular endothelium of many tissues; therefore, angiotensin II can be synthesized at a variety of sites, including the kidney, vascular endothelium, adrenal gland, and brain.
   Alternative enzymatic pathways not involving ACE may contribute to angiotensin II production. Angiotensin II binds to its specific receptors and exerts its effects in the brain, kidney, adrenal, vascular wall, and the heart. The actions of circulating angiotensin II contribute to hypertension. This may indirectly influence cardiac function, irrespective of any direct effect on the heart and myocardium.
   Circulating angiotensin II promotes sodium and water reabsorption, increasing intravascular fluid volume, which in turn increases cardiac preload and, therefore, stroke volume. Circulating angiotensin II causes systemic arteriolar vasoconstriction, thereby increasing vascular resistance and cardiac afterload. Angiotensin II also affects the autonomic nervous system, stimulating the sympathetic nervous system and reducing vagal activity. These actions are oriented toward maintaining the blood pressure when the renin–angiotensin system is activated by effective volume depletion.

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