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Adverse Effects Signs of toxicity common to vasodilator therapy in general also occur with minoxidil; they are attributable to vasodilation and reflex increases in sympathetic nerve activity antibiotics natural trusted 250 mg zi-factor. These effects do not have great clinical importance antibiotics for pcos acne generic zi-factor 250mg, since minoxidil is almost always administered in combination with a -blocker antibiotic resistant urinary infection buy discount zi-factor 500mg, which antagonizes the indirect cardiac effects. A more troublesome side effect, particularly in women, is the growth of body hair, possibly due to a direct stimulation of the growth and maturation of cells that form hair shafts. Apparently, minoxidil activates a specific gene that regulates hair shaft protein. In any case, this particular side effect has been capitalized upon, and minoxidil is now marketed as Rogaine for the treatment of male pattern baldness. Absorption, Metabolism, and Excretion Peak concentrations of minoxidil in the blood occur 1 hour after oral administration, although the therapeutic effect may take 2 or more hours to manifest. This is probably related to the time it takes to convert minoxidil to minoxidil sulfate. The long duration of action allows the drug to be administered only once or twice a day, a regimen that may be beneficial for compliance. Interestingly, the therapeutic half-life is considerably longer than the plasma half-life. This may be, as has been suggested for hydralazine, a result either of accumulation of the drug and its active metabolite in arterial walls or a longer plasma half-life of the sulfated metabolite, or both. The ultimate disposition of minoxidil depends primarily on hepatic metabolism and only slightly on renal excretion of unchanged drug. Because of this, pharmacological activity is not cumulative in patients with renal failure. The mechanism by which diazoxide relaxes vascular smooth muscle is related to its ability to activate potassium channels and produce a hyperpolarization of the cell membrane. Since tolerance to diazoxide can develop rapidly, it is frequently administered in conjunction with a diuretic. Adverse Effects Absorption, Metabolism, and Excretion Diazoxide lowers blood pressure within 3 to 5 minutes after rapid intravenous injection, and its duration of action may be 4 to 12 hours. Interestingly, if diazoxide is either injected slowly or infused its hypotensive action is quite modest. This is believed to be due to a rapid and extensive binding of the drug to plasma proteins. The plasma half-life is therefore prolonged in patients with chronic renal failure. Since diazoxide is not often used for long-term treatment, toxicities associated with chronic use are rare. The chief concern is the side effects associated with the increased workload on the heart, which may precipitate myocardial ischemia and Na and water retention. These undesirable effects can be controlled by concurrent therapy with a -blocker and a diuretic. Diazoxide may cause hyperglycemia, especially in diabetics, so if the drug is used for several days, blood glucose levels should be measured. When used in the treatment of toxemia, diazoxide may stop labor, because it relaxes uterine smooth muscle. Pharmacological Actions the hemodynamic effects of diazoxide are similar to those of hydralazine and minoxidil. It produces direct relaxation of arteriolar smooth muscle with little effect on capacitance beds. Its administration is, however, associated with a reflex increase in cardiac output that partially counters its antihypertensive effects. Propranolol and other -blockers potentiate the vasodilating properties of the drug.
Air Pollution Industrial activity has polluted the outdoor air with a number of chemicals known to be hazardous to human health antibiotic resistance arises due to quizlet order zi-factor without prescription. These include a variety of gases antibiotic gastritis buy zi-factor 500 mg on-line, such as carbon monoxide infection breastfeeding purchase 100mg zi-factor otc, ozone, and the oxides of sulfur and nitrogen. Natural products such as pollen, anthrax spores, and animal dander can elicit toxic reactions on inhalation or skin contact. The inhalation of asbestos, silica, or coal dust can cause pneumoconiosis, which may develop into serious lung disease. The size of the particle, ventilatory rate, and depth of breathing will determine the extent of pulmonary deposition. Food Additives and Contaminants Thousands of substances are added to foods to enhance their marketability (appearance, taste, texture, etc. Microbial or fungal contamination of food, either during processing or storage, can introduce potent toxins into food. Metals Characteristics of toxicity for a number of metals are presented in Table 7. While the exact tissue and molecular site of the toxic action of each metal is different, toxicity generally results from interaction of the metal with specific functional groups on macromolecules in the cell. These groups include sulfhydryl, carboxyl, amino, phosphoryl, and phenolic moieties. Interactions of such groups with metals can lead to disruption of enzyme activities and transport processes and eventually the types of reactions they undergo. Particulate matter associated with most emissions promotes the conversion of sulfur dioxide to the more toxic sulfuric acid and facilitates deposition in the deep lungs. Occupational exposure to solvents occurs in cleaning, degreasing, painting, and gluing. Exposure to solvents is generally through inhalation of vapors, although direct skin contact also occurs. The concentration of solvent in air is determined by the vapor pressure of the solvent, the ambient temperature, and the effectiveness of ventilation systems. These factors and the rate of pulmonary air exchange will affect the extent of exposure. Solvents are generally lipid-soluble, and therefore they are readily absorbed across the skin. Solvents often undergo bioactivation and may cause systemic toxicity as a result of the formation of reactive intermediates. Common targets for pesticides include insects, weeds (herbicides), fungi, and rodents. Poisoning from pesticides often affects professional exterminators, agricultural workers, and consumers (Table 7. Inorganic *Representative toxicities are presented; for most metals, other symptoms of toxicity may be demonstrated. Nature of the toxicities is dependent on level of exposure, whether the exposure is acute or chronic, and the route of exposure. In general, toxicity is related to the form of the metal (inorganic, organic, or elemental), the route of exposure, and the route of excretion. Herbicides and Rodenticides Herbicidal activity generally consists of interference with plant-specific biochemical reactions.
When taken at the onset of chest pain infection night sweats purchase generic zi-factor canada, the effects of nitroglycerin appear within 2 to 5 minutes; however antibiotics muscle pain order zi-factor cheap online, the true duration of action is difficult to establish in patients with secondary angina antibiotics quiz nursing buy zi-factor without a prescription, since the onset of pain causes patients to reduce their physical activity, and this alone can ameliorate the symptoms. Thus, further wellcontrolled clinical studies are necessary to establish the effectiveness of sulfhydryl-containing compounds at preventing or reversing nitrate tolerance. Industrial exposure to organic nitrates induces both tolerance and physical dependence. The state of dependence becomes manifest when exposure to nitrates is withdrawn suddenly. For example, munitions workers who have become dependent on nitroglycerin have been reported to undergo angina, myocardial infarction, or even sudden death following removal from contact with nitroglycerin. Some of these patients showed symptoms of ischemic heart disease, even though their coronary arteriography was judged to be normal. Since it is possible that coronary vasospasm plays a role in the pathogenesis of angina that occurs in nitrate-dependent individuals, these patients should be cautioned to watch for increased chest pain when they withdraw from medication or discontinue their exposure. An effective dose of nitrate usually produces a fall in upright systolic blood pressure of 10 mm Hg and a reflex rise in heart rate of 10 beats per minute. Larger changes than these should be avoided, because a reduction in myocardial perfusion and an increase in cardiac oxygen requirements may actually exacerbate the angina. Since nitrite ions oxidize the iron atoms of hemoglobin and convert it to methemoglobin, there may be a loss in oxygen delivery to tissues. While methemoglobinemia does not follow therapeutic doses of organic nitrates, it can be observed after overdosage or accidental poisoning. Cautions Chest pain that is not relieved by two or three tablets within 30 minutes may be due to an acute myocardial infarction. In addition, nitrate administration may result in an increase in intracranial pressure, and therefore, these drugs should be used cautiously in patients with cerebral bleeding and head trauma. Adverse Effects Vascular headache, postural hypotension, and reflex tachycardia are common side effects of organic nitrate therapy. Fortunately, tolerance to nitrate-induced headache develops after a few days of therapy. Postural hypotension and tachycardia can be minimized by proper dosage adjustment and by instructing the patient to sit -Adrenoceptor Blocking Agents -Adrenoceptor blockade is a rational approach to the treatment of angina pectoris, since an increase in sympathetic nervous system activity is a common feature in acute anginal attacks. Based on their ability to reduce oxygen demand, all -blockers tested so far have also been shown to be effective in the treatment of second- 17 Antianginal Drugs 201 ary angina. Propranolol is the prototype of this class of compounds -Blockers approved for clinical use in secondary angina in the United States include propranolol and nadolol (Corgard), compounds that block both 1- and 2-adrenoceptors equally, while atenolol (Tenormin) and metoprolol (Lopressor) are cardioselective 1receptor antagonists. Mechanism of Action the myocardial response to exercise includes an increase in heart rate and myocardial contractility. Propranolol and other -adrenoceptor blockers antagonize the actions of catecholamines on the heart and thereby attenuate the myocardial response to stress or exercise. The resting heart rate is reduced by propranolol, but not to the same extent as is the decrease in exercise-induced tachycardia. Overall, propranolol reduces myocardial oxygen consumption for a given degree of physical activity. Although the mechanisms responsible for this antihypertensive effect are not completely understood, they are thought to involve (1) a reduction in cardiac output, (2) a decrease in plasma renin activity, (3) an action in the central nervous system, and (4) a resetting of the baroreceptors. Thus, propranolol may exert a part of its beneficial effects in secondary angina by decreasing three of the major determinants of myocardial oxygen demand, that is, heart rate, contractility, and systolic wall tension. Propranolol and other -blockers also have been shown to produce an increase in oxygen supply to the subendocardium of ischemic areas. Because subendocardial blood flow and flow distal to severe coronary artery stenosis occur primarily during diastole, this increase in diastolic perfusion time, due to the bradycardiac effect of propranolol and other -blockers, would be expected to increase subendocardial blood flow to ischemic regions.
Vasopressin and Oxytocin Historically vasopressin and oxytocin treatment for uti home remedies zi-factor 100mg fast delivery, two nonapeptides antibiotic 3 day dose order zi-factor with amex, were the first peptide "neurohormones" to be considered; they are stored in the neurohypophysis and released into the bloodstream upon an appropriate stimulus antibiotics resistance discount zi-factor 500mg amex. In the periphery, oxytocin stimulates the contraction of epididymal and uterine smooth muscle (see Chapter 62) and vasopressin (antidiuretic hormone) facilitates the reabsorption of water from the kidney tubules. In addition to these well-accepted roles as neurohormones, there is convincing evidence that these compounds function as neurotransmitters; they both possess potent inhibitory actions on neurohypophyseal neurons. Endogenous Opioid Peptides A seminal discovery during the 1960s and 1970s was the presence of endogenous substances in mammalian brain that appeared to possess the pharmacological qualities of morphine and other opioid analgesics. It had been known for quite awhile that most "drug receptors" were in fact receptors for endogenous transmitters. It was surprising, therefore, when tissue from mouse brain was shown to avidly bind opioids, such as morphine and heroin, in a stereoselective manner. As Avram Goldstein, one of the pharmacologists involved in discovering the endogenous opioids, noted, "It seemed unlikely, a priori, that such highly stereospecific receptors should have been developed by nature to interact with alkaloids from the opium poppy. It is likely that the endogenous opioid peptides coexist in neurons with other nonopioid neurotransmitters. The initial hope that these endogenous agents or synthetic derivatives of them would be found to retain the analgesic activity of the opioids but be devoid of respiratory depression and/or addictive properties has now somewhat abated. Location of the Blood-Brain Barrier the capillaries of the brain are the most likely location of the blood-brain barrier. Brain capillaries differ in several important respects from capillaries in other body locations. For example, the endothelial cells of brain capillaries are so closely joined to each other that passage of substances cannot readily occur through the intercellular clefts between adjacent cells; furthermore, brain capillaries do not contain fenestrae (pores). Fenestrae are prominent in many capillaries, especially those in renal glomeruli and in the chorioid plexus. The ability of a drug to leave a capillary by diffusion appears to be directly related to the number of capillary pores. Compared with capillaries at other sites, brain capillaries also appear to possess very few pinocytotic vesicles, which are believed to play a role in the transport of large molecules through capillary walls. Brain capillaries contain many more mitochondria than do other capillaries, and it is probable that the mitochondria supply energy for active transport of watersoluble nutrient substances into the brain. A large number of lipid-insoluble endogenous substances are known to be transported into the brain. In the brain capillary, the intercellular clefts are sealed shut by tight junctions. Exchange of compounds between the circulation and the brain must take place in the cells of the capillary wall, the major barriers of which are the inner and outer plasma membranes of the capillary endothelial cells. The concentration in the brain of these bioactive substances appears to be carefully regulated. On the other hand, the biochemical precursors of these transmitters can pass relatively easily, although usually by active transport, from the blood to the brain, and this ensures an adequate supply of locally synthesized transmitters. By and large, the precursors are inactive biologically or have only minimal biological activity. Therefore, a sudden increase in blood concentration of these substances would have little effect on brain levels. Peptide transmitters will not readily penetrate the brain from the circulation, and they are synthesized in the brain. Certain small areas, including the area postrema beneath the floor of the fourth ventricle, an area in the preoptic recess, and portions of the floor of the third ventricle surrounding the stalk of the pituitary, appear to be devoid of this barrier. The ability of the blood-brain barrier to exclude entry of a number of drugs into the brain has several therapeutic implications. Many drugs, most notably certain antibiotics, are relatively excluded from the brain.
Antigenic shift: Abrupt change due to genetic reassortment with an unrelated strain antibiotic ophthalmic ointment purchase zi-factor 100 mg visa. It spreads by respiratory droplets or contact with contaminated surfaces and hands antibiotics for sinus infection contagious cheap zi-factor 250 mg without a prescription. Antigenic variants of influenza virus are caused by antigenic shift and antigenic drift antibiotic resistance examples order zi-factor 500mg mastercard. Clinical Symptoms Major cause of local infections of respiratory tract with constitutional symptoms. Its mechanism of action as an antiparkinsonian agent remains poorly understood, but it is thought to act as a partial dopamine agonist. Both are specific for influenza A virus but are not prescribed owing to toxicity and high rates of resistance. Vaccine Natural immunity toward a single influenza strain is long lasting and is provided by IgA of the respiratory tract. The flu vaccine is contraindicated for those with severe egg allergy, although in some cases it may still be safely given under the supervision of an allergist. It contains three influenza strains (2As and 1B), and is approved for use in individuals older than 6 months of age, both healthy people and those with chronic medical conditions. It is approved for use in healthy people 5 years to 49 years of age who are not pregnant. Flu vaccines do not protect against flulike illnesses caused by noninfluenza viruses. Pneumonia: Young children, immunocompromised patients, and elderly people in nursing homes are particularly susceptible. In some epidemics (depending on the viral strain), pregnant women are at high risk as well. More commonly acquired from bat, raccoon, and skunk bites than from dogs in the United States. Following local inoculation, the virus progresses to the peripheral nervous system and reaches the central nervous system by way of retrograde axonal transport after binding to nicotinic acetylcholine receptors. The incubation period may be 3 months or longer; hence, the rabies virus is considered a slow virus. The wound is cleaned and the patient is administered human rabies immunoglobulin and the rabies vaccination, which is a killed-virus vaccine. Characteristic cytoplasmic inclusions (arrows) in neurons infected by rabies virus. The segmented genome allows for switching of various segments among viruses within the same family. Pathogenesis the virus is spread via the fecal-oral route and possibly the respiratory route. The mechanism is intestinal villous destruction and atrophy with decreased reabsorption of sodium and water, with consequent copious, osmotic diarrhea. Clinical Symptoms the major clinical findings are vomiting, diarrhea, fever, and dehydration. Because most patients have large quantities of virus in stool, the direct detection of viral antigen is the method of choice for diagnosis. The previous version, RotaShield, was removed from the market after being linked to intussusception in children (Figure 103).
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