Steven R. Daugherty, PhD

• Assistant Professor of Psychology
• Assistant Professor of Preventive Medicine
• Rush Medical College
• Chicago, Illinois

During systemic therapy menopause weight buy cabergoline 0.5 mg on line, monitor for manifestations of depression women's health volunteer opportunities cabergoline 0.25 mg buy overnight delivery, such as lack of interest in personal appearance menstruation after tubal ligation 0.25 mg cabergoline buy with visa, withdrawal from activities women's health boutique torrance generic cabergoline 0.25 mg buy on line, insomnia and lack of appetite women's health center danvers ma cabergoline 0.5 mg buy on line. Depression may arise from the condition being treated or from the use of medicines a ecting the adrenal cortex. Perform a full blood examination, and monitor haemoglobin, serum electrolyte and blood glucose levels during systemic use. Monitor the body and skin carefully, noting colour and character of the skin, distribution of fat and muscle, the presence of bruises, rashes, purpura and petechiae and the condition of hair and nails. Monitor for manifestations of infection, which may occur with medicines that a ect the adrenal cortex. Advise the person to eat foods high in potassium, including fresh and dried fruits, vegetables and nuts. Advise the person not to have any immunisations while taking the medicine unless these have been approved by the doctor. Antacids or other antiulcer agents may be prescribed to lessen the risk of ulceration. If weight gain is an issue after commencement of therapy, a change in the dose or medicine may be warranted. Instruct the person to notify the doctor of fever, cough, sore throat, or injuries that do not heal. Tell the person to avoid contact with people with active respiratory infections, as these medicines suppress the immune system. Teach the person to recognise adverse e ects of these medicines, which may include a moonface, pu y eyelids, dependent oedema, increased bruising, dizziness, bleeding and menstrual irregularity. Evaluate the incidence of adverse e ects, especially when the person is receiving high doses of the medicine over a long period. Systemic use of corticosteroids can lead to a range of serious adverse e ects a ecting uid and electrolyte balance, immunity, metabolism and the integrity of skin and bones. For systemic use of corticosteroids, it is advisable to measure the blood glucose levels, weight, blood pressure and electrolyte levels before treatment and then weekly during the rst month of treatment. The adrenal cortex antagonists spironolactone and eplerenone, as well as the enzyme inhibitor metyrapone can be used in the management of cardiovascular disease, oedema and hyperadrenal states. What parameters should you closely monitor in Mrs Lochdubh, especially in the early stages of this therapy He regularly requires oral glucocorticoid therapy as a part of the management of his asthma attacks. Identify the endocrine agents that act on these endocrine glands or on their target tissues. Describe the actions and properties of the endocrine agents and, in general, the kinds of conditions they are used to treat. In this article the therapeutic uses of hormones from the gonads and their synthetic derivatives are discussed. The applications of hormonal antagonists and medicines that inhibit the synthesis of these hormones are also covered. In the former, oestrogens stimulate the secondary sex characteristics and the menses. Of these women, generally half will experience irregular bleeding in the rst six months of treatment and most will be amenorrhoeic a er 12 months. Oestrogens are available in oral, injectable and intravaginal forms, as well as transdermal patches and subcutaneous implants. Required for normal spermatogenesis; suppresses mammary gland development Feedback e ects exerted Negative feedback exerted on anterior pituitary release of gonadotrophins E ects on reproductive organs Stimulates growth and maturation of the internal and external genitalia and breasts at puberty; maintains adult size and function of the reproductive organs. Examples of the intravaginal formulations include pessaries, creams and an elastic polymer vaginal ring. Administration of the hormone via the transdermal, intranasal, subcutaneous and intravaginal routes avoids the e ects of rst-pass metabolism. In the case of either transdermal application or subcutaneous implant, the hormone is continuously absorbed into the blood, resulting in less uctuation in blood concentration than with daily oral administration. However, the development of skin rashes is common, and adhesiveness may be poor in warmer climates. Common adverse effects A number of adverse e ects are associated with oestrogen-only therapy. Progestogens refer to the group of pharmacological agents with progesteronelike action. For those women who take oestrogen-only replacement therapy, the doctor is encouraged to use the lowest possible dose to produce the desired e ects, in order to reduce the occurrence of adverse e ects. Clinical considerations Oral administration is usually preferred because it is more convenient and less expensive than other routes of administration. Oestrogen patches should be applied to clean, dry and intact skin below the waist or on the upper buttock. If long-term therapy is required for hormone replacement, a progestogen is included to prevent endometrial hyperplasia, which can lead to endometrial carcinoma. Women who have had a hysterectomy are not at risk of endometrial carcinogenic problems and, therefore, do not require the addition of a progestogen. A cyclical form of therapy involves the use of continuous oestrogen, plus a progestogen for 10­14 days each month or for 14 days every three months. A continuous form of therapy involves continuous oestrogen plus continuous progestogen. Importantly, oestrogen replacement therapy does not provide contraceptive protection. It may be advisable to use a low-dose oral contraceptive until menopause occurs and then consider changing to a hormone replacement regimen. If nausea occurs during oestrogen therapy, ask the person to take tablets with food or to try a patch or gel. Tamoxifen is used in the treatment and prevention of breast cancer and toremifene is used in the treatment of breast cancer (see Chapter 80), while raloxifene is used to prevent osteoporosis (see Chapter 64). Mechanism of action Tamoxifen has traditionally been regarded as an antioestrogen. However, it appears to produce a weak oestrogenic e ect on bone, endometrium, coagulation and blood lipid pro le. Compared with oestrogen, raloxifene is associated with a low risk of breast cancer and uterine hyperplasia, and a comparable blood lipid pro le. Common adverse effects Common adverse e ects include hot ushes, thromboembolism, dizziness, gastrointestinal disturbances and leg cramps. Contraindications for use include pregnancy, a history of active thromboembolism and drug hypersensitivity. Clinical considerations Due to the increased risk of thromboembolism with these medicines, people embarking on prolonged travel should be advised to move around at regular intervals. Treatment should be stopped if an illness or injury leads to prolonged immobilisation. People should be advised to inform their doctor if they develop abdominal bleeding, vaginal discharge or pressure in the pelvic region while they are taking tamoxifen. Progestogen-only preparations Progestogens are semisynthetic and synthetic forms of progesterone. Mechanism of action Progestogen-only preparations produce both suppression of ovarian function and inhibition of ovulation. As progestogens promote the development of the endometrium, they can be used in uterine hypoplasia and amenorrhoea associated with a poorly developed endometrium. Progestogen-only preparations are indicated in the treatment of both premenstrual syndrome and threatened/habitual abortion. However, the e ectiveness of progestogen therapy in these conditions has not been convincingly demonstrated. Longer-term injectable or implantable progestogen-only contraceptive preparations, which do not require daily dosing, are also available. An intrauterine implant of levonorgestrel is available in Australia and New Zealand. A disadvantage of this approach is that ovulation may not always be inhibited, increasing the likelihood of conception. Common adverse effects e adverse e ects associated with progestogens are not dissimilar to those observed during oestrogen therapy. Weight gain, raised blood pressure, breast tenderness and nausea have been reported. As some older synthetic progestogens (levonorgestrel and norethisterone) are closely related to the structure of androgens, acne and hirsutism also may be observed. Clinical considerations For maximum protection with progestogen-only contraceptives, the person must take the same dose around the same time each day. Mechanism of action Tibolone is related to the natural sex hormones and has oestrogenic, anti-oestrogenic, androgenic and progestogenic activity on selected tissues. It has progestogenic and antioestrogenic activity on the breast, reducing the risk of breast cancer. Common adverse effects Common adverse e ects of tibolone include headache, dizziness and vaginal bleeding. Clinical considerations Tibolone therapy should not be commenced until 12 months a er menstruation has ceased to prevent irregular bleeding. Any bleeding that persists for greater than six months, commences a er six months of treatment or continues a er tibolone is stopped should be investigated. Progestogen formulations are taken continuously: they do not contain inactive (sugar) pills. It is possible, therefore, that two pills may be taken at the same time or on the same day. It should be emphasised that if a pill is taken a er three hours from the usual time, the person is not protected against pregnancy. Additional means of contraception are used for 48 hours if a progestogen-only contraceptive is started a er the rst day of menstruation. Using depot medroxyprogesterone acetate as a contraceptive may be inappropriate if pregnancy is planned within a year, because of a possible delayed return of the normal ovulatory cycle. For women who use this progestogen implant as a contraceptive device, removal within three years is essential because of the risk of a future ectopic pregnancy. Women using a progestogen for hormone replacement and who experience bleeding should have their progestogen dose increased. Alternatively, less frequent withdrawal bleeds can be achieved by using a progestogen for 14 days every three months. Indeed, oral contraceptives are the most e ective form of contraception available, with low failure rates (around 1 per cent). On the plus side, there have been signi cant reductions in the e ective dose of the constituent hormones since the oral contraceptives rst appeared, resulting in relatively mild acute side-e ects. In addition, the packaging and presentation make oral contraceptives easy and convenient to use. Despite these bene ts, it is the long-term e ects that cause the greatest community concern. Studies have shown an increased risk of thromboembolism, heart disease, cerebrovascular accident, atherosclerosis, liver disease, infertility and certain forms of cancer with long-term oral contraceptive use. Moreover, the combination induces changes to the reproductive tract itself, which contribute to the prevention of pregnancy. When administered in combination, progestogens inhibit oestrogen-mediated endometrial cell proliferation and facilitate the secretory phase of uterine development. In this way, progestogens, administered in combination with an oestrogenic agent, o er protection against endometrial cancer when oestrogens are indicated for a woman with an intact uterus. E ects that may result from the action of oestrogens include breast enlargement and tenderness; enhancement of blood clotting; raised heart rate, blood pressure, serum iron levels, blood lipid levels; increased skin pigmentation; and impairment of liver function and bile ow. Common adverse effects e most common adverse e ects are nausea and vomiting, which usually subside with continued use. Less frequent side-e ects are those detailed in the sections on oestrogenonly preparations: breast changes, weight gain, changes in blood pressure, headache, breakthrough bleeding and midcycle spotting, and an increased incidence of vaginal infections. As some of the synthetic progestogens are derived from androgens, acne and hirsutism may occur. Contraindications are as for oestrogen therapy: evidence of thromboembolism, vascular disease, heart or hepatic dysfunction and oestrogen-dependent tumours all preclude the use of the oral contraceptives. Clinical considerations A number of di erent oral contraceptives containing an oestrogen­progestogen combination are available. Generally, they fall into two categories according to whether the dose of progestogen or oestrogen is modi ed during the menstrual cycle. For e ective contraception it is important to take oral contraceptives as directed, with each dose interval no longer than 24 hours. As a further precaution, an additional method of contraception should be used or abstinence practised until seven consecutive doses of hormone have been taken. Alternatively, if there are fewer than seven active doses le, advise the person to nish the active pills in their current pack and to proceed to take the active pills in the new pack. In this situation, inform the person that the menstrual period will usually be delayed until the end of the new pack. If the missed pill is in the seven days a er the inactive pill week and the woman has had unprotected sex during or a er that time, emergency contraception should be sought. If the woman is on a triphasic pill, she may still experience spotting or bleeding despite proceeding to the active pills of the new pack. If one or more doses of the pharmacologically inert tablets are missed, there is no impact on the e ectiveness of the contraception so long as the hormone-containing tablets are started on time.

This action can create problems in cases when it is used as a prophylactic and the individual also becomes infected with a chloroquine-resistant strain of the parasite womens health 6 week meal plan cheap cabergoline 0.25 mg line. This suppression can have dire consequences pregnancy 9th month cabergoline 0.25 mg low price, as active treatment may not be sought quickly enough menstrual juices discount 0.25 mg cabergoline fast delivery. Because of its anti-inflammatory action womens health 5 minute workout purchase cabergoline 0.25 mg without prescription, chloroquine and its derivatives are sometimes used to treat rheumatoid arthritis (see Chapter 41) breast cancer 7 tablet cases buy cabergoline with american express. Care must be taken when administering chloroquine and its derivatives to individuals at risk of developing a prolonged Q-T interval. It is also important to avoid administering other medicines that have a tendency to prolong the Q-T interval together with chloroquine and its derivatives, such as the antidysrhythmic amiodarone, the antiemetic dolasetron and the antibacterial erythromycin. Chloroquine and hydroxychloroquine should be taken with food to reduce stomach irritation. Mechanism of action Pyrimethamine, like the sulfonamides, antagonises folic acid synthesis (see Chapter 71). Common adverse effects Common side-effects of pyrimethamine are headaches, gastrointestinal disturbances and methaemoglobinaemia. Occasionally, agranulocytosis has been reported, and it may be judicious to perform blood counts at intervals during its use. This depression of haemopoiesis can be reversed by giving folic acid, which does not interfere with the action of the drug. Clinical considerations In many parts of the world, antifolate resistance has developed to pyrimethamine. It is, thus, combined with other antimalarial agents, usually a schizontocide, to assist with antifolate resistance. Pyrimethamine is not recommended for malaria prophylaxis because of toxicity and widespread resistance. However, there is far too little quinine in tonic water to have any therapeutic effect, and its only benefit is to impart a pleasantly bitter taste to the drink. Quinine can act as an antidysrhythmic in high doses, although it is not used as such. Because of this effect, care must be taken when it is administered to people with abnormal cardiac rhythms. Mechanism of action Quinine has a mechanism of action similar to chloroquine, to which it is related. Common adverse effects Quinine has some adverse effects, which have had specific names attached to them. The other is blackwater fever, in which haemolysis occurs, causing pyrexia and blood pigments to appear in the urine (hence the name). Clinical considerations Today, quinine is not used often in the treatment of malaria. Cerebral malaria occurs when the parasitaemia is so severe that brain capillaries become blocked, and this can cause agonising headaches, convulsions and death. Occasionally, oral quinine may be combined with other antimalarials to suppress attacks of malaria. During intravenous quinine therapy, it is important to monitor blood glucose levels, blood pressure, visual acuity, and cardiac rate and rhythm. Quinine is not used for prophylaxis because of the high incidence of adverse effects. Care must be taken when administering quinine to individuals at risk of developing a prolonged Q-T interval. It is also important to avoid administering other medicines that have a tendency to prolong the Q-T interval together with quinine, such as amiodarone, dolasetron and erythromycin. Clindamycin (see Chapter 72) can be given in combination with quinine to increase the effectiveness of therapy. The major site of action of primaquine appears to be on mitochondria, where it suppresses their normal role in cell metabolism. As it preferentially kills the hypnozoites, it is useful in preventing relapses in P. Common adverse effects the adverse effects of primaquine are similar to those of chloroquine, as one would expect owing to its similar chemical structure. Thus, this combination should not be used unless it is considered essential for either treatment or prophylaxis. Clinical considerations Preventive treatment with primaquine is taken at the same time on the same day each week. It is started one week before entering and continued for one week after leaving a malaria-affected area. A complete blood count is required before primaquine therapy to ensure that the person is not suffering from methaemoglobinaemia or haemolytic anaemia. Mechanism of action Its mechanism of action in plasmodia is very different from that in bacteria. The tetracyclines are active only against the pre-erythrocytic and asexual blood stages of P. Common adverse effects Common adverse effects include photosensitivity, gastrointestinal disturbances. Clinical considerations Doxycycline is taken two days before entering and continued for four weeks after leaving a malaria-affected area. It is well absorbed from the gut and should be consumed with a meal and a large glass of fluid. As doxycycline may cause photosensitivity, instruct the person to use a sunscreen and wear protective clothing. It is also useful as monotherapy in the management of Pneumocystis jiroveci pneumonia, a condition that can develop in immunocompromised people (see Chapter 77). Several trials of this combination have shown between 94 and 100 per cent cure rates in different tropical countries, this being vastly superior to all other current treatments. Proguanil is a prodrug but has intrinsic plasmodicidal properties of its own, inhibiting pyrimidine synthesis and, thus, nucleic acid synthesis in the parasites. Common adverse effects When used in combination, the individual dose of each medicine is low and adverse effects are, therefore, uncommon. Proguanil has a remarkably low incidence of adverse effects and is safe in pregnancy; it may be surprising, therefore, that it is not used more often. Clinical considerations Atovaquone is administered together with proguanil to provide synergistic activity against malaria. As prophylactic therapy, it is commenced one to two days before entering and continued for seven days after leaving a malaria-affected area. As dietary fat increases its absorption, the medicine is taken with food to increase its bioavailability. Renal function should be measured before commencing prophylactic proguanil treatment. It was advised that mefloquine be used only in areas where both chloroquine and antifolate resistance had been demonstrated, especially as a prophylactic. Sadly, resistance to this drug is fast becoming widespread, especially in South-East Asia. It also binds to haematin, a breakdown product of haemoglobin that accumulates in the plasmodial cell, and might cause lethal membrane damage. The medicine is effective against blood schizonts and the sexual blood forms of P. The medicine is useful for both prophylaxis and treatment and, like pyrimethamine, can be given weekly. Common adverse effects Adverse effects of mefloquine are usually mild and include dizziness, nausea, diarrhoea and headache. It may also cause anxiousness, confusion, depression, paraesthesia, delirium and stupor. Health professionals, patients and their relatives should be watchful for any developing mental health problems. Clinical considerations When using mefloquine as a prophylactic, administer it at the same time and on the same day of the week. Start mefloquine two to three weeks before entering and continue for two weeks after leaving a malaria-affected area. This medicine can also be given for treatment of malaria after seeking specialist advice. However, as the medicine can cause severe neuropsychiatric reactions, it is more preferable that it is used mainly for prophylactic treatment. Due to its neurological adverse effects, such as paraesthesia, delirium and stupor, people may experience difficulties in performing daily activities for many weeks after a particular dose. People should be advised to consult their doctor if they experience anxiousness, confusion or depression, and they may need to stop taking the medicine. Care must be taken when administering mefloquine to individuals at risk of developing a prolonged Q-T interval. It is also important to avoid administering other medicines together with mefloquine that have a tendency to prolong the Q-T interval, such as amiodarone, dolasetron and erythromycin. Mefloquine is structurally related to quinine, so it should not be used in people with cardiac disease or in pregnant women unless there is no alternative. The increasing incidence of reports of drug resistance to the artemisinins is of concern, especially in South-East Asia. Mechanism of action the artemether­lumefantrine combination acts as a blood schizontocide and as a gametocytocide. Artemether is a prodrug that is converted into the active metabolite dihydroarteminisin. The preparation prevents the breakdown of haem into a non-toxic pigment within the malarial parasite. The combination also inhibits nucleic acid synthesis and is more effective than either drug alone. Common adverse effects Common adverse effects include headache, fever, dizziness and asthenia. Serious adverse effects that have been reported include haemolytic anaemia, hepatitis and cardiac dysrhythmia (associated with Q-T interval prolongation). Clinical considerations People should be monitored for signs of anaemia and liver impairment. Electrocardiogram monitoring is recommended for people with pre-existing symptomatic dysrhythmias or those taking other medicines that prolong the Q-T interval. This combined preparation should not be given concurrently with other antimalarial agents. People need to be reminded that relapse is possible if the preparation is not taken with food. Inform people that they may feel dizzy or drowsy during treatment; if this is the case, they should avoid driving or operating machinery. This medicine is only available in Australia, but its use is restricted through the Special Access Scheme. Mechanism of action Like artemether, artesunate is a prodrug that is converted into the active metabolite dihydroarteminisin. A derivative of artemisinin, artemether, is available in Australia in combination with a drug called lumefantrine. An intravenous bolus is given at three time points, and treatment then follows with a full course of artemether and lumefantrine. A promising novel approach in the management of this condition is the development of malaria vaccines. An examination of the literature shows that researchers are currently trying to target one or more stages of the Plasmodium life cycle for vaccination. Another approach is to develop a vaccine that prevents an infected person from transmitting the disease through a mosquito to another person. Given the extent of malaria in the world and the mortality rate associated with it, we can only hope that these developments prove to be useful therapeutic techniques. Monitor the person for manifestations of toxicity, including convulsions, drowsiness, visual disturbances, headaches, or cardiac or respiratory arrest. If using a pyrimethamine­sulfadoxine combination, monitor for Stevens­Johnson syndrome and toxic epidermal necrolysis during treatment of chloroquineresistant malaria. Assess the person for a history of liver disease, blood disorders, neurological conditions or severe gastrointestinal disease. Monitor the person for manifestations associated with cinchonism that occur with regular quinine use. Manifestations include tinnitus, dizziness, visual problems, gastrointestinal irritation and headache. People on long-term therapy should have regular full blood examinations and liver function tests. Medicine education Advise people travelling to malaria-affected countries to take prophylactic doses of antimalarial therapy before leaving, during the trip and after return. The length of prophylactic treatment varies depending on the antimalarial therapy given. Prophylaxis should be taken regularly at the same time and on the same day each week. Advise the person to see the doctor if a febrile illness develops within 12 months of possible exposure. Advise the person to avoid mosquito bites by using insect repellents and wearing protective clothing. Teach the person to watch out for manifestations of blood dyscrasias, including malaise, fever, sore throat, pallor, and unexplained bruising or bleeding. Advise the person to take oral antimalarial agents after meals to prevent gastric irritation. Advise people on chloroquine to have regular eye examinations, and to report visual changes immediately. Inform the person that an additional dose of antimalarial is required if an oral dose is vomited within one hour of administration. Evaluation Evaluate the effectiveness of drug therapy in preventing or treating malaria, without producing adverse effects.

A virus employs at least some of the existing metabolic machinery in the host cell for its own use breast cancer 3a survival rates order cabergoline pills in toronto. It is breast cancer 49ers gear buy cheap cabergoline 0.25 mg on-line, therefore menopause the musical san francisco best 0.5 mg cabergoline, very difficult to come up with a medicine that can destroy the virus without affecting the host cell fsh 80 menopause order cabergoline canada. Most antiviral agents target the differences that exist between viral nucleic acids or enzymes women's health center medford oregon generic 0.25 mg cabergoline free shipping, and those of the human host. Influenza is a much more serious viral infection than the common cold and epidemics of influenza often result in deaths, mainly in infants and older people. The virus that causes influenza mutates rapidly, and pharmaceutical companies continually have to develop new therapeutic agents. Preventive therapeutic strategies are very important in the management of influenza. The classification is based on which human membrane glycoprotein the virus uses to infect host cells. One of the most important contemporary public health concerns is the possibility that viruses that induce respiratory tract infection and other infectious diseases in animals can jump the species barrier and infect humans. The most likely sources of infection are animals living in close proximity to humans-for example, farm animals such as pigs and poultry. These viruses are considered particularly pathogenic to humans and might spark infectious diseases at epidemic or pandemic level. The H5N1 strain of influenza virus is considered a major public health threat due to its high degree of virulence and lability with respect to mutation rate. To reach the superficial cells of the respiratory tract, zanamivir must be given as an aerosol, using a specifically designed diskhaler. Oseltamivir can be given orally and is slightly better than zanamivir in warding off an attack of influenza but, unfortunately, has a greater potential for adverse effects. Common adverse effects Adverse effects of zanamivir are rare, but may include bronchospasm, dyspnoea and allergic reactions. The most common adverse effects of oseltamivir are transient nausea and/or vomiting associated with the first dose. Clinical considerations It is important that these medicines are taken soon after the onset of infection for maximum benefit. Mechanism of action the influenza virus affects only the superficial cells of the respiratory tract and, like all virus particles, has to enter the cells to induce an infection. As specific inhibitors of neuraminidase, zanamivir and oseltamivir prevent viral penetration. For prophylaxis of influenza, oseltamivir is taken on alternate days for five days and should be taken within two days of exposure with an infected person. It should be noted that protection against influenza lasts for only as long as oseltamivir is taken. However, it is recommended that an annual influenza vaccine (see Chapter 79) be given to prevent infection in high-risk people rather than using oseltamivir. High-risk individuals include older people, and those people with cardiovascular disease, asthma, immune suppression and chronic obstructive pulmonary disease. Zanamivir is given by inhalation twice a day for five days and it significantly reduces the duration of infection by up to 60 hours. Advise the person to read the instructions for the diskhaler inhalation device carefully. If the person has a respiratory disorder that requires a bronchodilator, the bronchodilator should be used before zanamivir. The entire five-day course of treatment should be completed even if the person is starting to feel better and symptoms have improved. Prophylactic zanamivir treatment involves a once-daily inhalation for 10 days; however, this treatment can be extended for up to 28 days. Prophylactic treatment is usually limited to situations where there are poor vaccination rates and communities are at risk of developing influenza. It is recommended that healthy people should not take oseltamivir or zanamivir to shorten the duration of influenza illness. Instead, they should be recommended to have the influenza vaccine for that particular season. In addition, prophylactic use of oseltamivir or zanamivir may increase predisposition to infection by preventing seroconversion. Interestingly, the threat of an epidemic of swine or bird flu has led the governments of a number of countries to stockpile antiviral drugs like oseltamivir. Oseltamivir is considered one of the few drugs effective against the H5N1 and H1N1 strains of influenza virus. Animal studies have cast doubt over whether standard dose regimens would be effective enough to save people infected with the most virulent strains of the virus. Furthermore, a recent review on the effectiveness of these medicines in the management of influenza in children indicated that these drugs shortened the median duration of the infection by only 0. Mechanism of action Amantadine is a very specific antiviral agent in that it is active against only the influenza A virus. When a virus enters a cell, and before it can proceed with its multiplication, it must first uncoat itself. Amantadine appears to prevent the uncoating procedure, and this mechanism of action helps to show why it acts mainly as a prophylactic. It is also suggested that amantadine may prevent viral penetration and inhibit viral assembly. The success rate can be in the order of 90 per cent in preventing influenza infections. Common adverse effects As mentioned in Chapter 37, amantadine has many adverse effects. Thus, it is not used routinely in the prevention of influenza but only in people who are at high risk such as those who are immunocompromised and older adults in whom influenza can be fatal. When used in older adults, the dose is normally half that which a younger person would take. This dose alteration is because amantadine is mainly excreted unchanged by the kidneys and, where renal output is impaired, blood concentrations will rapidly rise to toxic levels. Clinical considerations Use amantadine cautiously in older people, and in people with seizure disorders, heart disease, peripheral oedema, hepatic disease or renal impairment. If postural hypotension occurs, instruct the person not to stand suddenly from a lying position or to change position too quickly. When considering stopping the medicine, reduce the dose gradually because of the risk of neuroleptic malignant syndrome, which can cause fever, muscle rigidity, rhabdomyolysis, profuse sweating and tachycardia. Humans do not have the reverse transcriptase enzyme; however, these enzyme inhibitors can slightly affect other enzymes involved in human nucleic acid metabolism. These groups of antiretrovirals are used in combination therapy because of the tendency for the rapid development of drug resistance. Zidovudine was originally synthesised in the 1960s as a cytotoxic agent for use in tumour chemotherapy but was never used as such. Common adverse effects Zidovudine is not without some severe adverse effects, such as bone marrow suppression. Adverse effects associated with stavudine include peripheral sensory neuropathy, pancreatitis and hepatotoxicity. Clinical considerations Zidovudine is a prodrug and is converted by a series of kinase reactions into a triphosphate metabolite. In addition, this medicine is available as a combination tablet preparation with lamivudine or with lamivudine and abacavir. Neutropoenia commonly occurs about six to eight weeks after starting treatment, and anaemia commonly occurs four to six weeks after starting treatment. It is, therefore, important to monitor these effects and avoid giving concomitant myelosuppressive medicines. Blood Reverse transcriptase inhibitors Most reverse transcriptase inhibitors are nucleosides. The general mechanism of action of the group will be described followed by more detailed information about specific medicines. General mechanism of action the mechanism of action of this drug family is fairly specific to the group of viruses known as retroviruses. The need for blood transfusions will depend on the severity of anaemia and the blood count. People are advised to inform their doctor if they develop extreme tiredness, pale skin, bleeding, sore throat, infection or weakness. Considering the nature of the disease, bone marrow suppression is not a desirable consequence, but the remission from the disease is usually preferential. Peripheral neuropathy experienced with stavudine is dose related and usually responds to prompt withdrawal of the medicine. It may be possible to recommence stavudine at a lower dose without recurrence of neuropathy. Advise people to inform their doctor if they develop numbness, a burning sensation or tingling in their hands and feet. Elevated liver transaminase levels usually resolve a few weeks after stopping treatment. People should be monitored for the elevated enzyme levels that occur in pancreatitis. In Australia, it is formulated as a single ingredient medicine and in combination with other antiviral agents, such as emtricitabine, or emtricitabine and efavirenz. Common adverse effects the major adverse effects of didanosine include peripheral neuropathy and pancreatitis. Tenofovir commonly causes nausea, vomiting, diarrhoea, headache and hypophosphataemia. There is the risk of pancreatitis, lactic acidosis and renal failure during tenofovir therapy. Clinical considerations Didanosine has a comparatively long half-life, which enables a once- or twice-daily dose. Didanosine enteric-coated capsules should be taken on an empty stomach about 30 minutes before food. Monitor regularly for peripheral neuropathy, as shown by numbness or burning in the hands or feet. Peripheral neuropathy usually improves if didanosine is stopped, after which it can be recommenced at a lower dose. Pancreatitis is dose related and usually resolves one to three weeks after stopping treatment. Tenofovir is available as a single medicine preparation, which is taken daily with food to prevent gastrointestinal symptoms. Tenofovir is also available as a fixed-dose combination preparation with emtricitabine, which is taken daily with food. Tenofovir is also available as a combination product with emtricitabine and efavirenz, which is taken at bedtime on an empty stomach. The fixed-dose preparation involving tenofovir, emtricitabine and efavirenz is not suitable if creatinine clearance is less than 50 mL per minute. Creatinine clearance and serum phosphate levels need to be checked at baseline and during therapy, especially for those people with a history of renal impairment or who are also taking medicines that may cause nephrotoxicity. There is evidence that tenofovir may raise the blood levels of other antiviral agents by interfering with their renal excretion. It is not recommended as monotherapy but as a part of combined antiviral drug therapy. Common adverse effects Common adverse effects include lactic acidosis, hepatotoxicity, gastrointestinal disturbances, lipodystrophy, headaches and skin hyperpigmentation. At-risk people include women, and individuals who are obese or have received prolonged nucleoside antiviral drug exposure. Common adverse effects Adverse effects of lamivudine therapy include pancreatitis (more likely to occur in children), musculoskeletal pain, lactic acidosis, altered fat distribution and enlarged liver. When using lamivudine, liver enzymes are monitored for at least four months after discontinuation of therapy in people with chronic hepatitis B. This medicine should not be used in children with a history of pancreatitis or with risk factors for developing pancreatitis. If needed, the tablets can be crushed with a small amount of liquid or semi-solid food such as yoghurt. Clinical considerations Hypersensitivity reactions occur in about 8 per cent of people taking abacavir, usually within the first six weeks of therapy. Common symptoms of hypersensitivity reactions include fever, gastrointestinal pain, nausea, vomiting, diarrhoea, lethargy, malaise, myalgia, arthralgia, dyspnoea, sore throat and cough. Therapy should not be recommenced after a hypersensitivity reaction because of the risk of life-threatening hypotension. Non-nucleoside reverse transcriptase inhibitors Mechanism of action Delavirdine, efavirenz, etravirine, nevirapine and rilpivirine are non-nucleoside inhibitors that non-competitively bind to the reverse transcriptase enzyme to completely inactivate it. At the time of writing, delavirdine and rilpivirine were available only in Australia. Common adverse effects the main adverse effect of these medicines is a skin rash which, if severe, warrants withdrawal of the medicine, as fatal skin reactions may occur. Hepatotoxicity (and elevated transaminase levels), abnormal dreams and depression can develop. Along with severe rash, these adverse reactions are the most common reasons for discontinuation of therapy. Gastrointestinal upset, alterations in body fat and fever have been observed during therapy.

Common adverse effects Common adverse reactions of these medicines include hypotension menopause neuropathy order cabergoline 0.25 mg on line, bradycardia diagnosis women's health issues buy discount cabergoline on-line, headache breast cancer jewelry discount cabergoline 0.25 mg free shipping, dizziness and gastrointestinal upset women's health issues 2012 cheap 0.5 mg cabergoline with amex. Use -blockers cautiously in people with diabetes women's health clinic johnson county discount cabergoline 0.5 mg, respiratory or hepatic disease, and in older people. Monitor blood glucose levels closely in people with diabetes because these medicines may mask signs of hypoglycaemia. However, -selective blockers such as metoprolol have been shown to be safe in people with type 2 diabetes. Before beginning treatment with -blockers, make sure that the person has a sitting systolic blood pressure above 85 mm Hg, and has no peripheral oedema or ventricular dysrhythmia. Any hypotension is treated by reducing rst the dose of diuretic or other vasodilator drugs before reducing dose of the -blocker. Interactions have been noted with digoxin, calcium channel antagonists and insulin. Clinical considerations For some people with chronic heart failure, carvedilol has been shown to produce a relative reduction in risk of death by 35 per cent. Bene ts from drug therapy may take around four months to become apparent, so adherence with treatment during this time is essential. Similar to other -blocker therapy, carvedilol should not be commenced unless the person has a sitting systolic blood pressure over 85 mm Hg, and has no peripheral oedema or ventricular dysrhythmias. Clinical trials have shown that this combination improves survival in heart failure. Glyceryl trinitrate or sodium nitroprusside can be used in the short-term management of severe chronic heart failure. In combination, there is synergistic interaction (see Chapter 16) such that there is potentiation of the vasodilator e ect. Common adverse effects e peripheral vasodilators may induce hypotension, ushing, headache and tachycardia. Mechanism of action Carvedilol is a non-selective -blocker with 1 antagonist activity. Further to this, the -blocking e ect counteracts the re ex tachycardia triggered by the vasodilating response. Common adverse effects Common adverse reactions are associated with adrenergic receptor blockade: orthostatic hypotension, bradycardia, dizziness and syncope. Patients need to be monitored for any signs that their heart failure is worsening. Tolerance to nitrates can occur with continuous exposure; ensure a nitrate-free period of about 10­12 hours each day. Advise people that they should remove a transdermal patch at a designated time during the day to enable a 10­12-hour nitrate-free period. Glyceryl trinitrate is the preferred intravenous vasodilator in severe heart failure and is usually administered for a short period. Sodium nitroprusside can also be used in this case, especially when accompanied by severe hypertension. In fact, the generic term digitalis is o en used to represent all cardiac glycosides used in the clinical setting. Mechanism of action Cardiac glycosides act by in uencing the movement of ions into and out of the myocardial bres, as well as by altering the activity of the autonomic nervous system. Stores of calcium within the myocardium are released and the membrane becomes more permeable to this ion. Stronger myocardial contraction improves cardiac e ciency, boosting cardiac output. Any change in heart rate is known as a chronotropic e ect; a decreased rate is a negative chronotropic e ect. An increase in this interval allows more time for the ventricles to ll with blood. In summary, the therapeutic e ects of the cardiac glycosides, positive inotropy and negative chronotropy, are directed towards increasing the e ciency of the heart in order to improve cardiac output. Increased blood ow will reduce tissue congestion and, in the kidneys, promote urine formation. However, supporters suggest that further bene ts ow on through a reduction in anxiety and apprehension as a function of judicial administration of morphine in this situation. Today they have been relegated to secondline therapy, used in combination with other medicines in selected patients. It is particularly useful in people with heart failure who are experiencing atrial brillation or when the symptoms cannot be controlled with the combinations described above. The net result of these e ects is that sodium accumulates within the myocardial cell. The cardiac glycosides also elevate intracellular calcium levels by 3 opening membrane calcium channels, and 4 triggering the release of calcium ions from intracellular storage sites. The net result of the latter e ects is that the force of myocardial contraction is enhanced. Moreover, cardiac glycosides stimulate the chemoreceptor trigger zone in the brain, which is linked to the medullary vomiting centre, to produce nausea and vomiting. Anorexia and diarrhoea are consequences of direct gastrointestinal irritation by these medicines. With such a narrow margin of safety, the toxic potential of the drug may be realised at plasma levels previously regarded as therapeutic. In heart failure, it is advisable that lower concentrations of digoxin are used, namely 0. Due to this potential toxicity and individual di erences in drug pharmacokinetics, it is necessary to assay plasma drug levels soon a er treatment. Before administering the loading dose, obtain baseline observations for heart rate and rhythm, blood pressure, renal function and electrolyte (especially potassium) levels. Digoxin toxicity may occur in susceptible individuals, including the older person, and those with electrolyte disturbances, hypothyroidism and hypoxia. In particular, hypokalaemia, hypomagnesaemia, hypercalcaemia, acidosis and hypoxia increase the risk for digoxin toxicity. Blood levels for digoxin are taken immediately before or at least six hours a er the dose is administered. According to the laws of pharmacokinetics (see Chapter 15), it takes approximately ve half-lives to reach a plateau in the plasma. With constant dosing of digoxin, this would take more than a week of therapy in people with normal renal function. If the therapeutic e ects are required more quickly, a dosing regimen of a large loading dose followed by smaller maintenance doses can be implemented. Digoxin can cause drug interactions relating to its ability to slow cardiac conduction, resulting in bradycardia. Administration with other medicines that also cause bradycardia may lead to additive e ects. Mechanism of action Ivabradine lowers heart rate by selective inhibition of diastolic depolarisation within sinoatrial node. At therapeutic doses, its action does not a ect ventricular repolarisation, cardiac contractility or conduction. Common adverse effects Common adverse reactions include cardiac dysrhythmias, headaches, blurred vision, dizziness, vertigo and gastrointestinal disturbances. Another side e ect commonly reported a ects visual function, due to cross-reaction with the generation of a similar current through the retina. People should be informed that their vision could be blurred and they may see bright areas of light especially if there are sudden changes in light intensity. People should be warned not to drive if they are a ected by the changes in light intensity. Intravenous infusions of dobutamine can be used in the management of chronic cardiac failure. Mechanism of action Dobutamine produces a positive inotropic e ect by stimulating 1 receptors on the myocardium, inducing a rise in cardiac output. Dobutamine is a direct-acting medicine that induces very little change in heart rate unless it is administered at high doses. A positive chronotropic e ect may be therapeutically counterproductive as it increases the work, and therefore the oxygen demand, of an ailing heart. Dobutamine also has 2 agonist action and a mix of 1 agonist and antagonist activity. Common adverse effects Common adverse reactions include an increase in heart rate and ventricular ectopic beats. Clinical considerations When dobutamine is used in combination with a -blocker its agonist e ects dominate, whereas when used with an -blocker, its agonist e ects predominate. Before dopamine is administered, any acidosis, hypercapnia or hypoxia is corrected, because these conditions can reduce the e ectiveness of dopamine or increase the incidence of adverse e ects. Before initiating treatment with dopamine agonists, hypovolaemia is corrected with the use of plasma volume expanders, such as Haemaccel and saline. Solutions should be administered through a central venous catheter or large peripheral vein, such as the antecubital fossa, to minimise the risk of digital necrosis. Titrate the dose against careful monitoring of the cardiac rate and rhythm, arterial blood pressure, arterial blood gases, pulmonary artery pressure and urine output. Levosimendan is a member of a class of medicines known as the calcium sensitisers. It acts to enhance the binding of calcium ions to troponin, which is associated with the thin cardiac myo lament. Common adverse effects Common adverse e ects of these medicines include dysrhythmias, hypotension, headache and chest pain. During milrinone therapy it is important to monitor cardiac rate and rhythm, arterial blood pressure, arterial blood gases, pulmonary artery pressure and urine output, and to titrate responses according to the response achieved with these parameters. Similarly, milrinone is not compatible with solutions containing sodium bicarbonate. Mechanism of action Milrinone is a relatively selective phosphodiesterase inhibitor in vascular and cardiac muscle. Indeed, there are subtle chemical di erences in the conformation of the phosphodiesterases in di erent cell types that a ord therapeutic selectivity. A loop diuretic is included in the treatment plan to control uid retention and congestive symptoms. If the person remains moderately or severely symptomatic despite this treatment, spironolactone can be commenced as well. If the person has atrial brillation with a rapid ventricular rate, digoxin is used as rst-line therapy. Due to the risk of thromboembolism, treatment with the anticoagulant warfarin is also recommended in people with heart failure who have atrial brillation, mitral stenosis or in those with severe le ventricular dysfunction who have previously had an embolic episode, or those who have had a myocardial infarction (see Chapter 48). I Assess the person for coronary occlusion, as digoxin is usually contraindicated in this condition. Use digoxin with caution in people with renal impairment or potassium disturbances. Report a pulse rate that has reduced by more than 25­30 beats/min below the baseline value or is below 60 beats/min. Assess for clinical symptoms of fatigue, oedema and dyspnoea, because these are indicative of heart failure. However, they are non-speci c symptoms and the diagnosis should be con rmed by an echocardiogram. Assess for risks of thromboembolism in people with heart failure, which includes those with atrial brillation, mitral stenosis or severe left ventricular dysfunction who have previously had an embolic episode. Assess whether the person is taking medicines that can worsen the symptoms of heart failure. Other medicines to avoid during heart failure include the calcium channel blockers verapamil and diltiazem; some antidysrhythmics, such as quinidine and ecainide; tricyclic antidepressants and some antipsychotics. The person will not experience the adverse e ects associated with medicines used for the treatment of heart failure. Doses in the lower range and slower titration may be needed for people with signi cant renal impairment or if hypotension is present. Advise the person to lie or sit down for two to four hours after this initial dose. Start with an extremely low dose of the -blocker, and increase the dose very gradually. Due to the risk of thromboembolism in people with heart failure, especially those who have atrial brillation, mitral stenosis or in those with severe left ventricular dysfunction who have previously had an embolic episode, or those who have had a myocardial infarction recently, treatment with warfarin is recommended. Check with the doctor prior to administration if the pulse is less than 60 beats/min. Assess the electrocardiogram and chest X-ray periodically to determine the e ect of the medicine used to treat heart failure. Digoxin has a low therapeutic index, where the toxic e ects occur close to the therapeutic range for the medicine. Hypo- or hyperkalaemia should be treated prior to administering digoxin to prevent cardiac rhythm disturbances. If serum potassium levels are not within normal limits prior to administration, notify the doctor and withhold the administration of digoxin. Symptoms of heart failure should be closely monitored by the person, and if symptoms worsen. Instruct the person on the adverse reactions attributed to medicines used in heart failure and to notify the doctor immediately if they occur.

Cabergoline 0.5 mg purchase online. 6 Effective Yoga Asanas For PCOD & Hormonal Imbalance.

More speci cally menstrual vomiting and diarrhea cheap cabergoline 0.5 mg free shipping, verapamil should not be combined with -blockers womens health haven buy genuine cabergoline line, especially in people with systolic ventricular dysfunction breast cancer research foundation 0.25 mg cabergoline otc, because of the additive negative e ect on cardiac conduction and the high risk of heart block and profound bradycardia menstrual ibs discount cabergoline 0.5 mg amex. Diltiazem can be given cautiously with -blockers because it has less negative inotropic e ect than verapamil menstrual like cramping in late pregnancy buy 0.5 mg cabergoline overnight delivery. Treatment with calcium channel antagonists should not be withdrawn abruptly, as this process may exacerbate the angina. Nifedipine and felodipine, which have relatively short half-lives, are available as controlled-release preparations to prolong their duration of action and enable oncedaily dosing. On the other hand, amlodipine, which has a relatively long half-life, can be given as a once-daily dose without the need to administer a controlled-release preparation. Short-acting preparations of nifedipine may cause re ex tachycardia, which can exacerbate ischaemic heart disease. Peripheral oedema associated with these medicines does not need to be treated with diuretics, which may put the patient at risk of volume depletion. About 10 per cent of people are slow metabolisers who require very low doses of perhexiline. As perhexiline has a low therapeutic index, serious adverse e ects may occur if the plasma concentration is not carefully monitored. A blood sample for perhexiline should be taken a er three to ve days of treatment to determine whether there is evidence of slowed metabolism. Subsequent samples need to be taken at monthly intervals until the desired e ect is achieved. However, it also has a novel action as a potassium channel opener or potassium channel activator. Cerebral ischaemia can arise from a meningeal haemorrhage associated with a head injury. A stroke can result from an obstruction to the cerebral vasculature by a thrombus or embolism, or from a cerebral haemorrhage. Oedema Mechanism of action Nimodipine is a calcium channel blocker which, due to its structural di erences from the other members of this group, is relatively selective for cerebral blood vessels. Nimodipine has been shown to increase cerebral blood ow, particularly to damaged areas of the brain and to areas with restricted circulation. It readily crosses the blood­brain barrier to interact with cerebral blood vessels. Common adverse effects e adverse reactions that accompany the use of nimodipine are similar to those observed during therapy with other calcium channel antagonists. Common adverse e ects include hypotension, headache, skin rash, nausea, abnormal liver tests and cardiac dysrhythmias. Clinical considerations Nimodipine is available in oral and intravenous formulations. It is highly lipid-soluble, is absorbed from the oral route rapidly and is relatively una ected by the presence of food in the gut. When administering nimodipine by intravenous infusion, polyvinyl chloride giving sets should not be used because of adsorption of the active substance on plastic. Polyethylene potassium channels in the muscle membrane, it allows an e ux of potassium. Common adverse effects Common adverse e ects include headache, facial ushing, nausea, vomiting, dizziness and weakness. Nicorandil is contraindicated in people with cardiogenic shock, le ventricular failure and hypotension. Clinical considerations Headaches occur commonly following initiation of nicorandil therapy. If commenced early a er onset of cerebrovascular symptoms, nimodipine is of bene t. Nimodipine can increase the risk of heart failure when administered with -blockers. One of the causes of impotence involves an impairment of blood ow through the penis during sexual stimulation. Impotence is a common complication associated with radical prostatectomy, spinal cord injury and diabetes mellitus. For a signi cant number of men with this kind of impotence, erectile function can be restored by improving penile tissue perfusion. A number of medicines, sildena l (Viagra), alprostadil, tadala l, vardena l and papaverine, can be used to manage erectile dysfunction. Sildena l, tadala l and vardena l are grouped together as phosphodiesterase inhibitors. People without impotence have asked their local doctor for a prescription in response to claims that their sexual performance will be enhanced, and it has managed to corner a lucrative market in a relatively short time. Clinical considerations Before prescribing these medicines, it is important to consider whether the man being treated has a cardiovascular disorder. Possible risks and bene ts need to be examined carefully for people with coexisting uncontrolled hypertension, stroke or myocardial infarction over the past six months, heart failure or severe hypotension. Sildena l has a half-life of three to ve hours and reaches peak blood levels within two hours of administration. In order to achieve the maximal therapeutic bene t, it is recommended that administration take place one hour before intercourse. Unlike sildena l, administration of tadala l with food does not appear to impair oral absorption. It is subject to signi cant rst-pass e ects and the rate of absorption is slowed with a high-fat meal. Sildena l may cause visual disturbances, and these medicines can induce dizziness. Men should be advised that if these adverse e ects occur, they are not to drive or operate machinery. Common adverse effects Common adverse e ects include headache, ushing, dyspepsia and hypotension. It can be used also as palliative therapy to maintain a patent (open) ductus arteriosus in neonates with congenital heart defects. Mechanism of action A er injections into the penis, alprostadil directly relaxes the smooth muscle of the spongy tissue (the corpora cavernosa and corpus spongiosum) and dilates the cavernosal arteries. As a result, the spaces in the spongy tissue enlarge and blood ow into the penis is increased. Penile erection occurs within minutes of administration, and its duration is dose dependent. In the ductus arteriosus, alprostadil is believed to relax the vascular smooth muscle. Common adverse effects e most common adverse e ect is a painful penis, but this is not usually a barrier to the continued use of the medicine. Men treated with alprostadil who have an erection for more than four hours should be instructed to seek medical help. In neonates with congenital heart problems, the most common adverse e ects are apnoea, ushing, bradycardia, fever, seizures and hypotension. Clinical considerations As a naturally occurring prostaglandin, alprostadil is rapidly metabolised. Until recently the drug has been available only via injection directly into the corpus cavernosum of the penis, a technique that initially needs careful, supervised training. Alprostadil is available for intracavernosal injection as a powder for reconstitution. Erectile dysfunction of a neurogenic or psychogenic origin usually requires a lower initial dose compared to that associated with vascular causes. A er reconstitution, the remaining solution may be refrigerated, but not frozen, for use up to 24 hours later. Venous channels compress in response to these haemodynamic changes, allowing engorgement of the penis. In order to keep its e ects localised to the penis, papaverine is administered as an intracavernosal injection. Common adverse effects Common adverse e ects include local reactions at the injection site, such as pain, a burning sensation, bruising, blistering and loss of sensation. Men who have used this medicine have reported priapism, and di culty in reaching orgasm and ejaculation. Clinical considerations A medical practitioner usually administers the rst dose, when the process for self-administration is explained. It is not currently available in Australia, but is marketed for this indication in New Zealand. Mechanism of action Yohimbine is an -adrenergic antagonist that is selective for 2 receptors. It is able to cross the blood­brain barrier, where it blocks presynaptic 2 receptors. When blocked, additional transmitter is released, resulting in increased sympathetic out ow and stimulation of central adrenergic pathways. Common adverse effects As a centrally acting 2 antagonist, yohimbine can lead to adverse e ects, such as increases in blood pressure, heart rate, motor activity, mania and anxiety. Mechanism of action Papaverine can be used as a spasmolytic agent due to its capacity to relax smooth muscle. However, some researchers question its e cacy in the treatment of sexual dysfunction. It is contraindicated in people with either renal or liver disease, and drug interactions have been noted when used concomitantly with the tricyclic antidepressants or the phenothiazine antipsychotic agents. General clinical considerations of medicines used to treat erectile dysfunction Men who do not have potency problems should be discouraged from using these medicines because they run a greater risk of priapism (prolonged erection). Due to the potential for adverse e ects with these medicines, regular medical reviews are required. Some conditions predispose individuals to priapism, including sickle cell anaemia, myeloma and leukaemia. If an erection lasts more than two hours, individuals are advised to take oral pseudoephedrine. Emergency treatment is essential if an erection lasts longer than four hours, and involves aspiration of 20­50 mL blood from the corpus cavernosum. C the potassium channel opener nicorandil acts to enhance potassium e ux across the membrane, resulting in hyperpolarisation and altered calcium ion availability. An electrocardiogram is performed to determine changes to cardiac trace and the area of heart muscle a ected. Assess vital signs so that baseline pulse and blood pressure can be compared with subsequent observations. For -blockers, assess the patient history for congestive cardiac failure, heart block, asthma, diabetes, liver and renal diseases. For calcium channel blockers, assess the person for congestive cardiac failure, severe hypotension and cardiogenic shock. Use of nitrates is contraindicated in men prescribed sildena l, tadala l, vardena l or alprostadil. Monitor chest pain following administration of the medicine to determine e ectiveness. Ensure that the correct method is used when administering glyceryl trinitrate by the sublingual or transdermal route (see Chapter 7, Tables 7. The person will have normal blood pressure if administered medicine for hypertension. The person with chest pain, after administration of medicine, will be free from anginal pain. For the man administered sildena l, tadala l, vardena l or alprostadil, the aim will be to achieve normal erectile function. Men should be assessed for cardiovascular risk before being prescribed sildena l, tadala l, vardena l or alprostadil. Treatment should be avoided in severe heart disease, hypotension, recent stroke or myocardial infarction, and known degenerative retinal disorders. Instruct the person on the use of sublingual or transdermal preparations of glyceryl trinitrate (see Chapter 7, Tables 7. Instruct the person on the correct storage requirements for glyceryl trinitrate tablets. Explain to the person that a glyceryl trinitrate tablet is used if chest pain occurs. When chest pain occurs, the person should sit down, allow a tablet to dissolve under the tongue, wait ve minutes and, if relief is not obtained, repeat the dose. Wait ve minutes and, if needed, repeat the dose again for a maximum of three tablets. Advise the person not to withdraw the medicine abruptly, as this will result in rebound ischaemia, re ex tachycardia and pain. If withdrawal is required, this process is carried out gradually over a few weeks. Encourage the person to have regular dental examinations, and to oss and brush regularly. To administer nifedipine sublingually or intrabuccally, instruct the person to chew the capsule to break it, and to guide the contents across to the cheek or under the tongue. Driving or using machinery is not advised during the early stages of verapamil therapy because it may cause light-headedness and dizziness. Advise the person to change position slowly to avoid dizziness (see Chapter 11, Table 11. The man having papaverine injections should be advised to rise slowly from a sitting or lying position because the injection may make him feel dizzy. He should tell his doctor if he experiences penile pain, or develops nodules or bending of the penile shaft.

References

• Allardice JT, Allwright GJ, Wafula JM, et al: High prevalence of abdominal aortic aneurysm in men with peripheral vascular disease: screening by ultrasonography, Br J Surg 75:240- 242, 1988.
• Serra-Majem L, Roman B, Estruch R. Scientific evidence of interventions using the Mediterranean Diet: a systematic review. Nutr Rev 2006;64:S27-47.
• Chang C, Dughi J, Shitabata P, et al: Air embolism and the radial arterial line. Crit Care Med 16:141, 1988.
• Grossfeld GD, Tigrani VS, Nudell D, et al: Management of a positive surgical margin after radical prostatectomy: decision analysis, J Urol 164(1):93n99, 2000.