By Andrzej Bartke, Andrew Constanti
This textbook has been written essentially for undergraduate scholars of pharmacy, toxicology, and drugs who require a concise reference e-book on easy endocrine functionality and disorder.
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Additional info for Basic Endocrinology for Students of Pharmacy and Allied Health Sciences
5. Low levels of plasma cortisol, associated with high levels of ACTH. Adrenal autoantibodies may also be present in the serum. 6. Increased skin pigmentation (lack of cortisol leads to an increase in plasma ACTH levels due to release from negative feedback; note that ACTH has MSH-like activity: see p. 11); the pigmentation is particularly prominent around scars, skin creases, elbows, knees and buttocks, the nipple area and the gums. Low plasma cortisol levels with low levels of ACTH would be expected in patients with secondary hypoadrenalism; low cortisol/high ACTH levels are also seen in cases of congenital adrenal hyperplasia, where enzyme defects occur in cortisol biosynthesis (see below).
Glucocorticoids are known to inhibit the synthesis and release of these important inflammatory mediators by suppressing the activity of the enzyme phospholipase A2 (PLA2), involved in the formation of arachidonic acid from cell membrane phospholipid (phosphatidyl choline). This effect is mediated indirectly via the induction of a phosphoprotein lipocortin-1, that inhibits PLA2 activity, and also directly by inhibition of inducible PLA2 synthesis. Inhibition of the production of cyclo-oxygenase-2 (COX-2), an inducible form of the enzyme responsible for conversion of arachidonic acid to pro-inflammatoryprostaglandins has also been recently demonstrated.
G. nicotine, morphine (and other opiates), angiotensin II, prostaglandin E2 and noradrenaline. Alcohol, however, inhibits AVP release (alcohol-induced diuresis). An increase in blood volume can also evoke the release of a 28 amino acid peptide from atrial muscle fibres, termed atrial natriuretic peptide (ANP) that causes an increase in the excretion of Na + and water by the kidneys (natriuresis) and vasodilatation. The heart itself can therefore behave as an important endocrine organ! Accordingly, ANP inhibits the secretion of AVP by the posterior pituitary, and may therefore contribute to the volume control of AVP release.