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Once a specific cause is identified based on specific microbiologic tests buy endep 25 mg overnight delivery treatment 2015, the following further questions should be considered: 1 generic endep 75 mg without a prescription treatment 8th february. If a specific microbial pathogen is identified buy discount endep 10 mg medicine keflex, can a narrower-spectrum agent be substituted for the initial empiric drug? What specific tests (eg, susceptibility testing) should be undertaken to identify patients who will not respond to treatment? For example, is surgery feasible for removal of devitalized tissue or foreign bodies—or drainage of an abscess—into which antimicrobial agents may be unable to penetrate? Is it possible to decrease the dosage of immunosuppressive therapy in patients who have undergone organ transplantation? Is it possible to reduce morbidity or mortality due to the infection by reducing host immunologic response to the infection (eg, by the use of corticosteroids for the treatment of severe Pneumocystis jiroveci pneumonia or meningitis due to Streptococcus pneumoniae)? This use of antimicrobial agents is called empiric (or presumptive) therapy and is based on experience with a particular clinical entity. The usual justification for empiric therapy is the hope that early intervention will improve the outcome; in the best cases, this has been established by placebo-controlled, double-blind prospective clinical trials. For example, treatment of febrile episodes in neutropenic cancer patients with empiric antimicrobial therapy has been demonstrated to have impressive morbidity and mortality benefits even though the specific bacterial agent responsible for fever is determined for only a minority of such episodes. Finally, there are many clinical entities, such as certain episodes of community-acquired pneumonia, in which it is difficult to identify a specific pathogen. In such cases, a clinical response to empiric therapy may be an important clue to the likely pathogen. Frequently, the signs and symptoms of infection diminish as a result of empiric therapy, and microbiologic test results become available that establish a specific microbiologic diagnosis. At the time that the pathogenic organism responsible for the illness is identified, empiric therapy is optimally modified to definitive therapy, which is typically narrower in coverage and is given for an appropriate duration based on the results of clinical trials or experience when clinical trial data are not available. Approach to Empiric Therapy Initiation of empiric therapy should follow a specific and systematic approach. Formulate a Clinical Diagnosis of Microbial Infection Using all available data, the clinician should determine that there is a clinical syndrome compatible with infection (eg, pneumonia, cellulitis, sinusitis). Obtain Specimens for Laboratory Examination Examination of stained specimens by microscopy or simple examination of an uncentrifuged sample of urine for white blood cells and bacteria may provide important immediate etiologic clues. Cultures of selected anatomic sites (blood, sputum, urine, cerebrospinal fluid, and stool) and nonculture methods (antigen testing, polymerase chain reaction, and serology) may also confirm specific etiologic agents. Formulate a Microbiologic Diagnosis The history, physical examination, and immediately available laboratory results (eg, Gram stain of urine or sputum) may provide highly specific information. For example, in a young man with urethritis and a Gram-stained smear from the urethral meatus demonstrating intracellular gram-negative diplococci, the most likely pathogen is Neisseria gonorrhoeae. In the latter instance, however, the clinician should be aware that a significant number of patients with gonococcal urethritis have negative Gram stains for the organism and that a significant number of patients with gonococcal urethritis harbor concurrent chlamydial infection that is not demonstrated on the Gram-stained smear. Determine the Necessity for Empiric Therapy Whether or not to initiate empiric therapy is an important clinical decision based partly on experience and partly on data from clinical trials. Empiric therapy is indicated when there is a significant risk of serious morbidity or mortality if therapy is withheld until a specific pathogen is detected by the clinical laboratory. In other settings, empiric therapy may be indicated for public health reasons rather than for demonstrated superior outcome of therapy in a specific patient. For example, urethritis in a young sexually active man usually requires treatment for N gonorrhoeae and Chlamydia trachomatis despite the absence of microbiologic confirmation at the time of diagnosis. Because the risk of noncompliance with follow-up visits in this patient population may lead to further transmission of these sexually transmitted pathogens, empiric therapy is warranted. Institute Treatment Selection of empiric therapy may be based on the microbiologic diagnosis or a clinical diagnosis without available microbiologic clues. If no microbiologic information is available, the antimicrobial spectrum of the agent or agents chosen must necessarily be broader, taking into account the most likely pathogens responsible for the patient’s illness. Pharmacologic factors include (1) the kinetics of absorption, distribution, and elimination; (2) the ability of the drug to be delivered to the site of infection; (3) the potential toxicity of an agent; and (4) pharmacokinetic or pharmacodynamic interactions with other drugs. Knowledge of the susceptibility of an organism to a specific agent in a hospital or community setting is important in the selection of empiric therapy. Pharmacokinetic differences among agents with similar antimicrobial spectrums may be exploited to reduce the frequency of dosing (eg, ceftriaxone, ertapenem, or daptomycin may be conveniently given once every 24 hours). Finally, increasing consideration is being given to the cost of antimicrobial therapy, especially when multiple agents with comparable efficacy and toxicity are available for a specific infection. Changing from intravenous to oral antibiotics for prolonged administration can be particularly cost-effective.
It is thus contraindicated in the elderly diction potential of the opioids while retaining the anal- patient and those with renal or liver disease buy endep australia medicine keri hilson lyrics. The use erally attributed to an interaction at the - and to a of sedatives in combination with propoxyphene can be lesser extent the -opioid receptor purchase endep 25mg mastercard treatment yellow tongue. In addition discount endep 50 mg without prescription hair treatment, the metabolism of the drug is in- Interaction at the -receptor increases the sedative creased in smokers due to induction of liver enzymes. The euphoric effects are due to in- Thus, smokers may require a higher dose of the drug for teraction with the -receptor. Propoxyphene enhances the effects of both chotomimetic side effects of the drugs are attributed to warfarin and carbamazepine and may increase the tox- interaction at the -receptor. Other con- duce excitatory effects related to the sympathetic dis- traindications are similar to those for morphine. Similarly, it is contraindicated in epileptic Pentazocine patients because it decreases seizure threshold. In addi- Pharmacological Effects tion, in head trauma patients, it can increase intracranial Pentazocine (Talwin) is a potent analgesic with an- pressure and brain injury. It incom- with psychoses is contraindicated because of its psy- pletely blocks the effects of morphine in such patients chotomimetic side effects. This combination pro- However, the drug will retain its analgesic potency duces heroinlike subjective effects, and heroin addicts when administered orally, since naloxone is not active use it in the absence of heroin. Pentazocine produces as much respiratory de- pentazocine in combination with alcohol or barbitu- pression as morphine but does not produce the same rates greatly enhances its sedative and respiratory de- degree of constipation or the biliary constriction ob- pressant effects. Unlike morphine, penta- Tolerance and Dependence zocine increases heart rate and blood pressure by re- Tolerance to the analgesic effects of pentazocine de- leasing norepinephrine. The onset of action occurs within approxi- Butorphanol (Stadol) is chemically related to levor- mately 15 minutes, and the half-life is 2 to 3 hours. As an opioid antagonist it is nearly 30 times as thus has a high ﬁrst-pass effect following oral administra- potent as pentazocine and has one-fortieth the potency tion; its half-life differs considerably from patient to pa- of naloxone. Its potency is 7 gation to glucuronides in the liver terminates the effects times that of morphine and 20 times that of pentazocine of pentazocine. It produces exci- Pentazocine is indicated for relief of moderate pain tatory effects and sedation and precipitates withdrawal in patients not receiving large doses of opioids. Although generally ad- used as premedication for anesthesia and as a supple- ministered parenterally because of its low bioavailabil- ment to surgical anesthesia. The nasal spray is Adverse Effects indicated for the relief of postoperative pain and mi- The most common side effect of pentazocine is se- graine headache. Nasal administration of butorphanol decreases the Respiratory depression and increased heart rate, body onset of action to 15 minutes and decreases the ﬁrst- temperature, and blood pressure accompany overdose. Naloxone is effective in reducing the respiratory de- Generally the patient sprays a set dose of 1 mg per hour pression but requires the use of higher doses than for for 2 hours. The morphinelike, it does reduce the craving for morphine abuse potential following such administration has not and for the stimulant cocaine. Thus, buprenorphine is a been extensively studied, although it is thought to be potential new therapy for the treatment of addiction to small. Adverse effects, contraindications, and drug interac- Dezocine tions are similar to those for pentazocine and morphine. The onset of Nalbuphine activity and potency as an analgesic are comparable to Nalbuphine (Nubain) is a mixed agonist–antagonist that those of morphine. Although the drug requires glu- is similar in structure to both the antagonist naloxone curonidation during metabolism, patients with hepatic and the agonist oxymorphone. As an an- fects (analgesia, respiratory depression, sedation, and so tagonist, dezocine is more potent than pentazocine. As on) are similar to those produced by pentazocine, nal- an agonist, dezocine produces analgesia and respiratory buphine produces fewer psychotomimetic effects. It dif- depression (which is readily reversed by naloxone), but fers from pentazocine in that it has far greater antagonist unlike pentazocine, it has little if any effect on the car- than agonist effect. It is used Dezocine is indicated as an analgesic for moderate much as pentazocine is, that is, for moderate to severe to severe pain. Nalbuphine’s abuse potential is less than that of codeine Contraindications and adverse effects of the drug are and propoxyphene, although tolerance and dependence similar to those described for morphine. Drug interactions and contraindications are Opioid Antagonists similar to those for pentazocine and morphine. Naloxone and naltrexone are pure opioid antagonists Buprenorphine synthesized by relatively minor changes in the morphine structure.
The most common adverse effects associated with enfuvirtide therapy are local injection site reactions discount endep uk symptoms of a stranger, consisting of painful erythematous nodules buy endep overnight delivery medications and pregnancy. No drug-drug interactions have been identified that would require the alteration of the dosage of concomitant antiretroviral or other drugs 75 mg endep with amex medicine bow. The absorption of maraviroc is rapid but variable, with the time to maximum absorption generally being 1–4 hours after ingestion of the drug. Maraviroc has excellent penetration into the cervicovaginal fluid, with levels almost four times higher than the corresponding concentrations in blood plasma. There appears to be no cross-resistance with drugs from any other class, including the fusion inhibitor enfuvirtide. Potential adverse effects of maraviroc include cough, upper respiratory tract infections, muscle and joint pain, diarrhea, sleep disturbance, and elevations in serum aminotransferases. Hepatotoxicity has been reported, which may be preceded by a systemic allergic reaction (ie, pruritic rash, eosinophilia, or elevated IgE); discontinuation of maraviroc should be prompt if this constellation occurs. Myocardial ischemia and infarction have been observed in patients receiving maraviroc; therefore caution is advised in patients at increased cardiovascular risk. To date, however, there has been no evidence of an increased risk of either malignancy or infection in patients receiving maraviroc. As a class, these agents tend to be well tolerated, with headache and gastrointestinal effects being the most commonly reported adverse events. Other nervous system (including neuropsychiatric) effects are often reported but are milder and less frequent than with efavirenz. Dolutegravir should be taken 2 hours before or 6 hours after taking cation-containing antacids or laxatives, sucralfate, oral iron supplements, oral calcium supplements, or buffered medications. For this reason, co-administration with dofetilide is contraindicated and close monitoring, with potential for dose adjustment, is recommended for co-administration with metformin. Current evidence suggests that dolutegravir retains activity against some viruses resistant to both raltegravir and elvitegravir. Hypersensitivity reactions characterized by rash, constitutional findings, and sometimes organ dysfunction, including liver injury, have been reported and may be life-threatening. Other reported side effects include elevations in serum aminotransferases and the fat redistribution syndrome. Elvitegravir is therefore available only as a component of a fixed-dose combination, with cobicistat, emtricitabine, and tenofovir. Cobicistat can inhibit renal tubular secretion of creatinine, causing increases in serum creatinine that may not be clinically significant; in the fixed-dose formulation it may be difficult to distinguish between cobicistat effect and tenofovir- induced nephrotoxicity. The recommendation is that the fixed-dose combination elvitegravir/cobicistat/tenofovir/emtricitabine should not be initiated in patients with calculated creatinine clearance < 70 mL/min and should be discontinued in those with creatinine clearance < 50 mL/min; discontinuation should be considered if the serum creatinine increases by 0. For example, since concurrent use of rifampin substantially decreases raltegravir concentrations, the dose of raltegravir should be increased. Since polyvalent cations (eg, magnesium, calcium, and iron) may bind integrase inhibitors and interfere with their activity, antacids should be used cautiously and ingestion separated by at least 4 hours from raltegravir. The chewable tablets may contain phenylalanine, which can be harmful to patients with phenylketonuria. Although virologic failure has been uncommon in clinical trials of raltegravir to date, in vitro resistance requires only a single point mutation (eg, at codons 148 or 155). The low genetic barrier to resistance emphasizes the importance of combination therapies and of adherence. Potential adverse effects of raltegravir include insomnia, headache, dizziness, diarrhea, nausea, fatigue, and muscle aches. Increases in pancreatic amylase, serum aminotransferases, and creatine kinase (with rhabdomyolysis) may occur. Severe, potentially life-threatening and fatal skin reactions have been reported, including Stevens-Johnson syndrome, hypersensitivity reaction, and toxic epidermal necrolysis. Interferon alfa appears to function by induction of intracellular signals following binding to specific cell membrane receptors, resulting in inhibition of viral penetration, translation, transcription, protein processing, maturation, and release, as well as increased host expression of major histocompatibility complex antigens, enhanced phagocytic activity of macrophages, and augmentation of the proliferation and survival of cytotoxic T cells. Interferon alfa-2a and interferon alfa-2b may be administered either subcutaneously or intramuscularly; half-life is 2–5 hours, depending on the route of administration. Alfa interferons are filtered at the glomerulus and undergo rapid proteolytic degradation during tubular reabsorption, such that detection in the systemic circulation is negligible. The use of pegylated (polyethylene glycol-complexed) interferon alfa-2a and pegylated interferon alfa-2b results in slower clearance, longer terminal half-lives, and steadier concentrations, thus allowing for less frequent dosing. Renal elimination accounts for about 30% of clearance, and clearance is approximately halved in subjects with impaired renal function; dosage must therefore be adjusted.
- Complete physical exam
- In the eye, adhesion of the iris to the lens can lead to glaucoma.
- Coronary angiography
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Parasympathetic function is not altered order endep 75mg otc medicine clipart, a fact that with a diuretic when therapy with a single agent is not sat- distinguishes guanethidine from the ganglionic blocking isfactory buy endep 10mg on line medicine remix. The half-life From a hemodynamic viewpoint buy endep 10 mg lowest price medicine quetiapine, there are several of guanethidine is 5 days, with about one-seventh of the obvious advantages to using a -blocker in combination total administered dose eliminated per day. Reﬂex-mediated cardiac stimulation elimination contributes to the cumulative and pro- is a common feature of vasodilator treatment and longed effects of the drug. Guanethidine reduces blood pressure by its ability A -blocker will reduce the cardiac stimulation and thus to diminish vascular tone; both the arterial and venous preserve the effectiveness of the vasodilator. The result- the vasodilator will prevent the increase in peripheral ing venous pooling contributes to orthostatic hypoten- vascular resistance that occurs on initiation of treatment sion, a prominent feature of guanethidine treatment. Furthermore, vasodilator treatment The reduction in blood pressure is more prominent initiates reﬂexes that lead to an increase in plasma renin when the patient is standing than recumbent. This event re- creased venous return and the inability of sympathetic quires two successive steps: (1) transfer of norepineph- nerve impulses to release enough transmitters to stimu- rine across the neuronal membrane into the cytosol by late the heart occur during the early stages of guanethi- an energy-dependent carrier-mediated active process, dine therapy. In addition to impairing norepinephrine storage and A common and troublesome side effect is postural thereby enhancing its catabolism, reserpine impairs the hypotension. Sexual impotence does occur, and male vesicular uptake of dopamine, the immediate precursor patients may have difﬁculty ejaculating. Since dopamine must be taken up unopposed parasympathetic activity include such gas- into the adrenergic vesicles to undergo hydroxylation trointestinal disturbances as diarrhea and increased gas- and form norepinephrine, reserpine administration im- tric secretion. The combined effects of Guanethidine may aggravate congestive heart fail- the blockade of dopamine and norepinephrine vesicular ure or actually precipitate failure in patients with mar- uptake lead to transmitter depletion. This central pheochromocytoma because the drug may release cate- transmitter depletion is responsible for the sedation and cholamines from the tumor. The depletion of brain amines also may contribute dine is also to be avoided, since this combined drug to the antihypertensive effects of reserpine. As with other sympathetic certain other adrenomimetic drugs, that is, biotransfor- depressant drugs, tolerance to the antihypertensive ef- mation and neuronal uptake. Dangerously high concen- fects of reserpine can occur, owing to a compensatory trations of catecholamines at receptor sites are possible. Reserpine, amitriptyline) and some phenothiazines block the sym- therefore, should be used in conjunction with a diuretic. Conversely, toms of agitated psychotic states and who may be unable guanethidine competitively inhibits the uptake of drugs to tolerate therapy with phenothiazine derivatives. Reserpine treat- ment, therefore, is contraindicated in patients with a his- tory of severe depression. Because of the increased gas- tial invades the sympathetic nerve terminal, a portion of tric secretion, reserpine is contraindicated for patients 20 Antihypertensive Drugs 235 with peptic ulcer. In patients with little cardiac reserve, The orally effective ganglionic blocking agents in fact reserpine must be administered with caution because of are not recommended for the treatment of primary hy- its ability to interfere with sympathetic stimulation of pertension. The drug blocks the action of tyrosine hydroxylase, the rate- limiting enzyme in the synthesis of catecholamines. The ul- timate action of the drug is to decrease the production Two important antihypertensive agents, -methyldopa of catecholamines. Although the details of their actions may differ nal tract and is excreted in the urine largely as un- in some respects, their antihypertensive activity is ulti- changed drug. It is useful for preopera- -Methyldopa tive treatment and for long-term therapy when surgery The spectrum of activity of -methyldopa (Aldomet) is not feasible. Current The basis for the antihypertensive activity of the gan- evidence suggests that for -methyldopa to be an anti- glionic blockers lies in their ability to block transmis- hypertensive agent, it must be converted to -methyl- sion through autonomic ganglia (Fig. This ac- norepinephrine; however, its site of action appears to be tion, which results in a decrease in the number of in the brain rather than in the periphery. Systemically ad- impulses passing down the postganglionic sympathetic ministered -methyldopa rapidly enters the brain, (and parasympathetic) nerves, decreases vascular tone, where it accumulates in noradrenergic nerves, is con- cardiac output, and blood pressure. Unfortunately, Absorption, Metabolism, and Excretion blockade of transmission in both the sympathetic and parasympathetic systems produces numerous untoward Approximately 50% of an orally administered dose of responses, including marked postural hypotension, -methyldopa is absorbed from the gastrointestinal blurred vision, and dryness of mouth, constipation, par- tract.
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