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Precisely timed alterations in the secretion of these hormones are responsible for coordinating the structural and secretory changes that occur throughout the menstrual cycle purchase genuine florinef on line gastritis diet 974. Estrogens Biosynthesis and Elimination Females In premenopausal women purchase florinef once a day gastritis diet 2012, the ovary is the principal source of estrogen purchase 40 mg betapace otc. During the follicular phase of the menstrual cycle, estrogens are synthesized by ovarian follicles; during the luteal phase, estrogens are synthesized by the corpus luteum. In the periphery, some of the estradiol secreted by the ovaries is converted into estrone and estriol, hormones that are less potent than estradiol itself. Estrogens are eliminated by a combination of hepatic metabolism and urinary excretion. In the human male, small amounts of testosterone are converted into estradiol and estrone by the testes. Activating these surface receptors produces a rapid response—more rapid than can be produced by activating nuclear receptors. Physiologic and Pharmacologic Effects Effects on Primary and Secondary Sex Characteristics of Females Estrogens support the development and maintenance of the female reproductive tract and secondary sex characteristics. These hormones are required for the growth and maturation of the uterus, vagina, fallopian tubes, and breasts. Estrogens have a profound influence on physiologic processes related to reproduction. During the follicular phase of the menstrual cycle, estrogens promote (1) ductal growth in the breast, (2) thickening and cornification of the vaginal epithelium, (3) proliferation of the uterine epithelium, and (4) copious secretion of thickened mucus from endocervical glands. In addition, estrogens increase vaginal acidity (by promoting local deposition of glycogen, which is then acted on by lactobacilli and corynebacteria to produce lactic acid). At the end of the menstrual cycle, a decline in estrogen levels can bring on menstruation. However, it is the fall in progesterone levels at the end of the cycle that normally causes breakdown of the endometrium and resultant menstrual bleeding. However, final transformation of the breast for milk production requires the combined influence of estrogen, progesterone, and human placental lactogen. Under normal conditions, bone undergoes continuous remodeling, a process in which bone mineral is resorbed and deposited in equal amounts. The principal effect of estrogens on the process is to block bone resorption, although estrogens may also promote mineral deposition. During puberty, the long bones grow rapidly under the combined influence of growth hormone, adrenal androgens, and low levels of ovarian estrogens. When estrogen levels grow high enough, they promote epiphyseal closure and thereby bring linear growth to a stop. Cardiovascular Effects Cardiovascular disease is much less common in premenopausal women. For example, estrogen receptors in the vascular smooth muscle respond to activation by decreasing vasoconstriction. Activation of estrogen receptors in vessel endothelium results in the production of nitric oxide, which results in vasodilation and increased perfusion.

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Oxygen supply is increased with vasodilators purchase florinef us chronic gastritis lasts, which prevent or relieve coronary artery spasm buy florinef 0.1mg without a prescription gastritis diet öööţüôřäţęă. Overview of Therapeutic Agents Vasospastic angina is treated with two groups of drugs: calcium channel blockers and organic nitrates 50 mg indocin visa. Beta blockers and ranolazine, which are effective in stable angina, are not effective in variant angina. As with stable angina, therapy is symptomatic only; drugs do not alter the underlying pathology. Organic Nitrates The organic nitrates are the oldest and most frequently used antianginal drugs. P ro t o t y p e D r u g s Drugs for Angina Pectoris Organic Nitrate Nitroglycerin Beta Blockers Propranolol Metoprolol Calcium Channel Blockers Verapamil Nifedipine Drug That Increases Myocardial Efficiency Ranolazine Nitroglycerin Nitroglycerin has been used to treat angina since 1879. Despite availability of newer antianginal agents, nitroglycerin remains the drug of choice for relieving an acute anginal attack. For our purposes, the most important aspect of this sequence is the conversion of nitrate to its active form—nitric oxide—in the presence of a sulfhydryl source. Mechanism of Antianginal Effects Stable Angina Nitroglycerin decreases the pain of exertional angina primarily by decreasing cardiac oxygen demand. Oxygen demand is decreased as follows: by dilating veins, nitroglycerin decreases venous return to the heart and thereby decreases ventricular filling; the resultant decrease in wall tension (preload) decreases oxygen demand. In patients with stable angina, nitroglycerin does not appear to increase blood flow to ischemic areas of the heart. Second, when nitroglycerin is injected directly into coronary arteries during an anginal attack, it does not relieve pain. Both observations suggest that pain relief results from effects of nitroglycerin on peripheral blood vessels—not from effects on coronary blood flow. Variant Angina In patients with variant angina, nitroglycerin acts by relaxing or preventing spasm in coronary arteries. Pharmacokinetics Absorption Nitroglycerin is highly lipid soluble and crosses membranes with ease. Because of this property, nitroglycerin can be administered by uncommon routes (sublingual, buccal, transdermal) as well as by more conventional routes (oral, intravenous). Metabolism Nitroglycerin undergoes rapid inactivation by hepatic enzymes (organic nitrate reductases). When nitroglycerin is administered orally, most of each dose is destroyed on its first pass through the liver. Principal adverse effects—headache, hypotension, and tachycardia—occur secondary to vasodilation. In the meantime, headache can be reduced with aspirin, acetaminophen, or some other mild analgesic. Pooling decreases venous return to the heart, which reduces cardiac output, causing blood pressure to fall.

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However cheap florinef 0.1mg visa gastritis foods to eat list, if a vasodilator is combined with a beta blocker discount florinef 0.1 mg overnight delivery gastritis diet juice, reflex tachycardia will be minimal purchase venlor 75 mg. Dosing For each drug in the regimen, dosage should be low initially and then gradually increased. As a result, sympathetic reflexes offer less resistance to the hypotensive effects of therapy. Individualizing Therapy Patients With Comorbid Conditions Comorbid conditions complicate treatment. Two conditions that are especially problematic—renal disease and diabetes—are discussed here. Preferred drugs for patients with these and other comorbid conditions are shown in Table 39. Drugs to avoid in patients with specific comorbid conditions are summarized in Table 39. Verapamil Diltiazem Coronary artery Hydralazine Reflex tachycardia induced by hydralazine can precipitate an anginal disease attack. Post–myocardial Hydralazine Reflex tachycardia induced by hydralazine can increase cardiac infarction work and oxygen demand. Diuretics Renal K -sparing diuretics+ Use of these agents can lead to dangerous accumulations of insufficiency K supplements+ potassium. Diabetes Thiazides Thiazides and furosemide promote hyperglycemia, and beta blockers mellitus Furosemide suppress glycogenolysis and can mask signs of hypoglycemia. Furosemide Hyperkalemia K -sparing diuretics+ These drugs cause potassium accumulation. Furosemide Collagen Hydralazine Hydralazine can precipitate a lupus erythematosus–like syndrome. Nephrosclerosis secondary to hypertension is among the most common causes of progressive renal disease. Pathophysiologic changes include degeneration of renal tubules and fibrotic thickening of the glomeruli, both of which contribute to renal insufficiency. Hence, in the absence of contraindications, all patients should get one of these drugs. In patients with advanced renal insufficiency, thiazide diuretics are ineffective, hence a loop diuretic should be employed. In diabetic patients, as in nondiabetic patients, beta blockers and diuretics can decrease morbidity and mortality. Keep in mind, however, that beta blockers can suppress glycogenolysis and mask early signs of hypoglycemia and therefore must be used with caution.