Dale Bloomquist, DDS, MS

Administration of the medicine with food may reduce the incidence of gastrointestinal upsets pregnancy workouts buy cabergoline on line amex. As the prostate gland is a ected by diet pregnancy due date predictor order cabergoline 0.5 mg otc, exercise and lifestyle womens health vest generic 0.5 mg cabergoline free shipping, men should examine these factors to reduce the severity of a prostate problem womens health lowell general cheap 0.25 mg cabergoline visa. A nutritious breast cancer her2 positive cabergoline 0.5 mg buy without a prescription, low-fat diet and reasonable exercise are helpful for this condition. Only a short course of valerian should be taken for sleeping problems to prevent the incidence of tolerance or dependence. It must be acknowledged that tolerance and dependence are not proven characteristics of this therapy; however, it is advisable to be cautious. Advise the person to avoid ca eine, nicotine and foods high in sugar and fats in the early evening. This person should not be taking valerian for the time leading up to the anaesthetic administration. Herbs and their extracts can have adverse e ects similar to those of conventional medicines. Most herbal preparations have inconclusive activity in the treatment or prevention of disease. Her health professional recommends that evening primrose could help to relieve her premenstrual symptoms. Joel Smith, a 55-year-old man, has experienced ongoing problems with migraine headaches since adolescence. His medical practitioner recommends that a course of feverfew may help his condition. What medicine education relating to the administration of feverfew would you talk over with Mr Smith How would you evaluate the potential bene ts of raw garlic in a person who is taking it for atherosclerosis Herb Elbs, a 78-year-old man is taking saw palmetto for benign prostate hypertrophy. Over the past few weeks he has been losing weight rapidly, experiencing di culty in breathing, and has endured nausea and vomiting. The doctor then inserts a central venous catheter and prescribes total parenteral nutrition. Seven days after admission, the nurse notices yellow ooze at the insertion site of the central catheter and noti es the doctor. Which serum electrolyte requires monitoring during initiation of treatment with hydroxocobalamin In reviewing what the child eats, the doctor nds that her diet is severely lacking in red meat and fresh green vegetables. Why is the central line changed and daily dressing performed under sterile conditions Why does the doctor want to wait a month before assessing the e ectiveness of therapy She also has hypertension, which is treated with hydrochlorothiazide and atenolol. On further questioning, she informs you that she is also taking ginkgo and ginseng. After visiting her surgeon for a review of her condition, she has commenced a course of therapy with intramuscular hydroxocobalamin for the prevention of vitamin B12 de ciency. Her dose of hydroxocobalamin is administered every three months at the local community health centre. Intravenous ampicillin and gentamicin are also administered to treat any respiratory infection that may be present. A nasogastric tube is inserted through his nasal cavity, and once the position of the tube has been checked, he commences 60 ml/hr of enteral feed. Upon checking the nasogastric tube, the nurse notices that that she is unable to aspirate uid from the tube. What strategies can be implemented to address the problem associated with diarrhoea in relation to enteral feeding What strategies can be implemented to address the problem relating to the inability to aspirate the nasogastric tube Does the information provided with herbal products available over the counter enable safe use Whether the dangerous stranger is a virus, a bacterium, a parasite or a cancerous cell is of no importance-the aim of therapy is to destroy the foreign cell without damaging the normal body cells of the host organism. During a relatively short time, chemotherapy has established itself and become a prominent area of clinical pharmacology. Such is the pace of development that many medicines have already become redundant, either because they have been replaced by safer and more potent compounds, or because drug resistance has emerged. The following chapters explore the nature of the chemotherapeutic agents used to facilitate the eradication of pathogenic organisms from the body. The principles of chemotherapy (Chapter 70) apply not only to the treatment of bacterial infections (Chapters 71, 72 and 73) but also to those caused by multicellular parasites (Chapters 75 and 76), viruses (Chapter 77) and fungi (Chapter 78). In Chapter 80, we demonstrate how these chemotherapeutic principles apply also to the treatment of cancer. A number of medicines can stimulate or boost immunity, while others will inhibit it. In Chapter 79, we examine medicines that modify the function of the immune system. The principles, current procedures and limitations associated with gene therapy are explored in Chapter 81. Gene therapy may also have applications in immune, inflammatory, cardiovascular and endocrine disorders. Outline the main adverse effects of antimicrobial agents and explain why they occur. Describe how microbes acquire resistance to the action of antimicrobial agents, and state some factors that contribute to the development of resistance and how its incidence can be minimised. By identifying and understanding the nature of the causative agent, scientists had an opportunity to develop a cure. In the early part of the 20th century, the search began for medicines that would be effective in treating the infectious diseases responsible for so many human fatalities through the ages. This search has led to the development of many important antimicrobial agents, such as the sulfonamides and the antibiotics. More recently, research has led to the formulation of medicines with efficacy against viral infections. In this article, you are introduced to some general chemotherapeutic principles relating to the actions and effects of antimicrobial agents. To achieve this aim, it must attack and disable some microbial process or structure not present in humans. The mechanism of action of any antimicrobial agent can be classified according to the way in which it exploits these differences. Penicillins, cephalosporins, vancomycin and bacitracin are examples of medicines that work in this way. These are relatively nontoxic antimicrobial agents, as human cells do not possess a cell wall. Disruption of the microbial cell membrane Antimicrobial agents that act through this mechanism affect membrane transport into and out of the microbe. These medicines are more toxic systemically than the previous group, as some human cells. Inhibition of cell wall synthesis Most bacteria possess a cell wall to protect them from the osmotic influences of the external environment. As new proteins need to be manufactured before cell division, inhibition of this process halts microbial population growth. These medicines exploit structural differences between human and bacterial ribosomes or enzymes involved in nucleic acid synthesis. However, at higher doses they can be quite toxic to human cells, which also need to synthesise proteins. Logically, an antimicrobial agent that is effective against only a few species is a narrowspectrum medicine. For instance, penicillin G is regarded as a narrow-spectrum antibiotic as it is effective only against Gram-positive bacteria and a limited number of other microbes, whereas the tetracyclines are effective against both Gram-positive and Gram-negative bacteria, mycoplasma, chlamydiae and some protozoa, and are, therefore, considered broad-spectrum antibiotics. The terms narrow- and broad-spectrum should never be confused with drug potency or efficacy. In fact, a narrow-spectrum antimicrobial agent, effective against only a few species, may be more efficacious than a broadspectrum medicine in treating a particular infectious agent. Without folic acid, the bacteria cannot produce the proteins necessary for growth. The selectivity of these medicines derives from the fact that many microbes must synthesise their own folic acid, whereas humans can use folic acid present in their diet. The sulfonamides and trimethoprim are examples of medicines with this mechanism of action (see Chapter 71). However, we often observe a number of adverse effects common to a variety of antimicrobial agents, such as gastrointestinal and central disturbances, as well as allergic reactions. These include the gut-associated problems of superinfection and antibiotic-associated colitis, hypersensitivity and drug resistance. An unwanted effect of a bactericidal medicine is that microbial cell death may result in endotoxins being released into surrounding tissues or even the general circulation. As a general rule, medicines that inhibit the formation of a cell wall or disrupt the cell membrane are bactericidal medicines, while those medicines that inhibit protein synthesis or interfere with metabolic processes are bacteriostatic. This kind of classification system is not without problems, as some bacteriostatic medicines are bactericidal at higher doses. Superinfection Some of the microbes that live in the gastrointestinal tract as natural flora may be susceptible to the action of an orally administered antimicrobial agent. As a result, the balance of pathogenic and nonpathogenic gut flora, maintained through competition for resources, is disturbed. Certain pathogenic organisms then proliferate to a point where a serious secondary illness arises-a superinfection. Common organisms include staphylococci, Candida albicans and Gram-negative bacteria. Fortunately, such a state occurs infrequently and is usually associated with prolonged therapy. Common manifestations include the appearance of a rash, local itchiness and diarrhoea. Oral candidiasis is a painless condition, with whitish lesions that can involve the lips, tongue, throat and the buccal surface of the cheeks. Hypersensitivity reactions Hypersensitivity reactions are triggered by an interaction of preformed antibodies or immune cells with specific antigens. This formation of antibodies is not surprising, as some of these substances are defensive secretions made by, or derived from, other living organisms. In fact, we may possess antibodies to a particular antibiotic without ever having received it as clinical treatment. This process occurs because there are residual amounts of antibiotics in the meat we eat. We might also inhale airborne particles of antibiotics when visiting our local pharmacy or someone in hospital. However, in some individuals these antibodies can trigger a life-threatening type I (anaphylactic) hypersensitivity reaction if they come into contact with the antigenic substance a second time. Allergies to penicillins and other related medicines are relatively common in our community. Health professionals play an important role in identifying people allergic to such medicines and treating reactions when they occur. All it takes is an appreciation that hypersensitivity to a particular class of antimicrobial agents has been commonly reported. Remember, it is easier to prevent a hypersensitivity reaction from occurring than it is to treat one when it happens. The anaerobic bacterium Clostridium difficile is known to induce this condition, but can be controlled by vancomycin therapy. The condition also responds well to treatment with the nonsteroidal anti-inflammatory drugs (see Chapter 41) or the resin cholestyramine (see Chapter 45), the latter binding to and causing the elimination of the toxic particles. Antidiarrhoeal agents, such as loperamide, codeine or diphenoxylate with atropine, should not be administered if antibiotic-associated colitis is suspected because this can lead to possible retention of toxin and worsening of colitis. Antimicrobial resistance Acquired resistance to the action of antimicrobial agents by a previously sensitive strain of microorganism is a major problem associated with the effectiveness of pharmacological therapy of infectious diseases. It is a continual source of confusion to students as to whether it is the microbe that develops resistance to the drug or whether the drug develops resistance to the microbe. It is important to understand that it is the microbe that develops resistance to the drug. First, within a population of microbes, one microbe undergoes a spontaneous mutation that may code for the production of a lytic enzyme, which inactivates the antimicrobial agent. Another means is through the spontaneous exchange of genetic material between microbes, not necessarily of the same strain, which code for resistance to specific antimicrobial agents or between microbes and bacteriophages. The vectors of this information are called plasmids- packets of spare nucleic acids that are transferred from one microbial cell to another through conjugation. In these examples, the progeny of the cells have a distinct advantage over the rest of the population sensitive to the drug, as they will have inherited a kind of protection against its action. Examination of the affected wall reveals diffuse pseudomembranous plaques-hence its former name, pseudomembranous colitis.

In this section women's health questions menopause cabergoline 0.5 mg with mastercard, medicines are discussed that are used in the treatment of motion sickness menopause bleeding symptoms cheap 0.25 mg cabergoline amex, in ammation and allergy menstrual disorder 0.5 mg cabergoline with visa, problematic pregnancies women's health center logansport in buy cabergoline 0.25 mg with visa, myocardial ischaemia and hypertension womens health 6 week boot camp purchase 0.5 mg cabergoline with amex. You will be introduced to a number of key groupings of chemical mediators, their physiological roles are described and their pharmacological manipulation explained. Traditionally, the way in which the nervous and endocrine systems function is nicely contrasted. Hormones are made in and released from endocrine glands directly into the bloodstream in order to communicate with distant target tissues, whereas neurotransmitters are released from nerves and interact with short-range targets. Hormones are generally thought to produce their responses relatively slowly and for a prolonged period compared with neurotransmitters. It has become apparent that this classi cation system, although useful in many respects, is an oversimpli cation. Non-nervous cells can produce chemical mediators that act at short range on a near target and produce e ects relatively rapidly. Examples of local hormones are histamine and prostaglandins, which both play key roles in in ammation. You may already be aware that serotonin is a neurotransmitter with a key role in the control of mood and behaviour (see Chapter 36). It is also produced by non-nervous cells in the periphery and is regarded as a paracrine secretion (see Chapter 31). Indeed, the other mediators examined in this section, nitric oxide and the endothelins (see Chapter 32), can also be synthesised by nerve cells and by non-nervous peripheral cells alike. A cell may also secrete a chemical mediator that acts within the con nes of a localised region, such as a lesion, or even upon itself. Generally speaking, it is better to regard the classi cation of chemical mediators in a less rigid way than was proposed originally. You should keep in mind that there may be signi cant overlap in the roles of chemical mediators and in the types of cells that release them. In some contexts, a chemical mediator may act as a neurocrine secretion and in others be regarded as a paracrine secretion or autacoid. Another important concept related to chemical mediator function is that of modulation. A train of impulses is transmitted towards the brain along the sensory pathway, triggered by neurotransmitter release at the synapse. Neighbouring cells release chemical mediators, such as prostaglandins, which increase the frequency of nerve impulse transmission, making the perception of the sensation stronger. In this instance, the prostaglandins are chemical modulators that have a ected nervous system function. Peptides are implicated in cardiovascular function, pain transmission, in ammation, neurotransmission, gastrointestinal regulation and endocrine communication. Indeed, they can function as neurocrine, endocrine, paracrine and autocrine mediators. From a pharmacological perspective, peptide mediators are attracting a lot of attention. Analogues and antagonists of these peptides have been, and are being, investigated as therapeutic agents. More recently the use of selected peptides to enhance sporting performance has attracted controversy. In peptide pharmacology, the physiological properties of the peptide can be altered by a slight manipulation of its structure. As an example, changing one or two amino acids in human insulin creates an insulin analogue. Although it retains the same functional characteristics of insulin, the altered chemical properties of the analogue means that it can be released from the injection site much faster or very much slower than regular insulin (see Chapter 61). It is also possible to substitute amino acids within a sequence in order to turn a peptide mediator into an antagonist. However, it must be said that peptide medicines may be of only limited use in clinical practice. Nevertheless, there are many situations where peptide mediators are targeted in the treatment of common diseases. Mediators may be classi ed as neurocrine, endocrine, paracrine or autocrine secretions. Chemical modulators modify cell-to-cell communication without activating the actual cell response. Peptide mediators are involved in a diverse range of physiological and pathophysiological processes. Advances in peptide pharmacology are being made, but their use as medicines may be limited. Compare and contrast the characteristics of neurocrine, endocrine, paracrine and autocrine mediators. Histamine is widely distributed in mammalian tissues and, as histo means tissue, it is aptly named. It is found in most body cells but is especially plentiful in the lungs, skin and the gastrointestinal tract wall. In these sites it is mainly contained within mast cells, cells that are involved in in ammatory and allergic reactions. Histamine is synthesised from the amino acid histidine, but the rate of production varies greatly depending on location and functional role. It plays a major role in modulating allergic and hypersensitivity reactions and is an important mediator in the regulation of the secretion of gastric acid in the stomach. In addition, it is a neurotransmitter in the brain, and is considered a neuromodulator with both central and peripheral actions. Histamine receptors are G-protein-coupled receptors linked to second messenger systems. H1 receptors act via activation of phospholipase C, raising the production of inositol triphosphate and increasing the availability of intracellular calcium. H1 Receptors are found on the endothelium, on mucussecreting cells, in the brain and on peripheral nerve endings. Activation of H1 receptors associated with the endothelium induces increased permeability. It is a common belief that this e ect occurs in capillaries, but this is incorrect. In the brain, H1 receptors are associated with increased wakefulness and appetite suppression. When stimulated, histamine receptors on peripheral nerve endings cause itching, burning and pain. H2 Receptors are found mainly in the parietal cells of the stomach and their activation can cause the release of signi cant amounts of gastric acid. Activation of either type of histamine receptor triggers dilation of vessels in vascular beds. However, H1 receptors mediate a rapid, short-lived response, whereas the response at H2 receptors is slow and prolonged. In regard to non-vascular smooth muscle (such as the intestines and bronchioles), H1 receptor stimulation tends Table 30. In the heart, stimulation of the H2 receptors is positively chronotropic (induces increased heart rate). On the other hand, stimulation of the H1 receptors is positively chronotropic and inotropic (induces an increased force of contraction). H3 Receptors are located presynaptically on a variety of nerve terminals and have a role in autoinhibition-that is, a feedback mechanism designed to inhibit the release of transmitter from the axon terminal. Although some of these antigenic compounds are actually innocuous, in many people they can induce adverse reactions. In susceptible persons, the local release of histamines in the nasal epithelia, due to , for example, pollen grains, can lead to hay fever or allergic rhinitis. In severe cases, an immediate, systemic allergic reaction called anaphylaxis can, without treatment, lead to death within minutes. Anaphylaxis is a medical emergency that usually responds to treatment if it is administered quickly enough. It is important that health professionals who are involved with the administration of medicines or in immunisation programs be competent in the management of anaphylaxis, as prompt action is lifesaving. In anaphylaxis, these mediators can lead to a massive vasodilatory response, with resultant hypotension causing shock and perhaps death. At the same time bronchoconstriction can lead to laboured breathing and, if allowed to continue unabated, asphyxiation. As there are a number of mediators involved in this systemic reaction, the use of antihistamines alone in the treatment is not satisfactory. Since noradrenaline is not an e ective bronchodilator due to its low e cacy on 2 receptors, it is not indicated in the treatment of this reaction. However, the intravenous route is preferred if hypovolaemic shock is present or the response following other routes of administration is not adequate. If given subcutaneously, absorption can be erratic; therefore, subcutaneous injection is not recommended. It should not be administered in the buttocks as this site does not allow for e ective absorption compared to the anterolateral thigh site. Adrenaline should be administered slowly and the electrocardiogram needs to be regularly monitored. Only clinical experience will determine which route to use, depending on the severity of the reaction. Many people who are allergic to insect stings, certain foods or the like carry adrenaline in a pen-like syringe or autoinjector for self-administered intramuscular injection in case of an emergency. Adrenaline autoinjectors need to be stored in the dark between 15 and 25 degrees Celsius, but they do not need to be refrigerated. Corticosteroids are o en given to stabilise the immunological cells causing the problem (see Chapter 62). Corticosteroids have been shown to be more e ective than the antihistamines in the management of allergic rhinitis. However, antihistamines do produce bene cial e ects in the treatment of urticaria. H2 receptor antagonists, whose clinical use is in disorders associated with excessive gastric acid secretion, are discussed in Chapter 56. Apart from treating allergies, H1 antihistamines are useful in the treatment of nausea, especially travel or motion sickness. Mechanismofaction e term antihistamine is usually reserved for drugs acting at the H1 receptor. Historically they have been considered to be receptor antagonists, but the current thinking is that they act as inverse agonists (see Chapter 17). In other words, there is some degree of constitutive activity associated with these receptors without the presence of histamine. Azelastine, cetirizine, levocarbastine, levocetirizine, loratadine, desloratadine and fexofenadine are second-generation antihistamines. Cetirizine, considered the most potent H1-antihistamine, has the added advantage of inhibiting eosinophil migration to in ammatory sites, minimising the in ammatory response by another mechanism. Interestingly, the tricyclic antidepressant doxepin (see Chapter 36) is a very potent H1 antihistamine. It has been used in the management of refractory allergic conditions, such as chronic urticaria. Finding one that does not adversely a ect an individual may involve trial and error. Cetirizine, loratadine, desloratadine and fexofenadine are reputedly less likely to cross the blood­brain barrier. Even though cetirizine is relatively lipophobic, it crosses the blood­ brain barrier in about 15 per cent of people and, thus, is more likely to induce drowsiness than the other secondgeneration antihistamines. People taking any antihistamine should be warned of concurrent drowsiness and told, if so a ected, not to drive or operate hazardous machinery. Some antihistamines, such as promethazine and trimeprazine, are excellent at promoting drowsiness. Although the second-generation antihistamines tend not to produce sedation in most people, they may still produce drowsiness in a small percentage of users. Generally speaking, apart from drowsiness, antihistamines are well-tolerated medicines. Some rst-generation antihistamines have antagonist activity at muscarinic receptors (see Chapter 28). Resting state G-protein-coupled H1 receptor Cell membrane Phospholipase C Inactive state B. Histamine present Histamine Active state 2nd messenger production Inactive state C. When used topically, antihistamines can themselves be antigenic and elicit an allergic reaction. Combinations of H1 and H2 antihistamines may eventually be used for conditions such as an allergic itch. Clinicalconsiderations e main use of H1 antihistamines, and indeed the most e ective use, is in the management of a number of acute allergic conditions where histamine release has a prominent role, such as rhinitis, urticaria and conjunctivitis. Some argue that antihistamines have a place as adjuvant therapy in bronchial asthma. However, corticosteroids (see Chapter 62) have been shown to be more e ective than the antihistamines in the management of chronic and severe allergic conditions. Most of the rst-generation antihistamines have a short duration of action (around six hours), whereas most of the second-generation agents have a more prolonged action (12­24 hours). Loratadine acts faster than fexofenadine and has a longer half-life, which on paper makes it a better alternative. As mentioned earlier, antihistamines are quite e ective as sedatives in premedication before surgery. Sedating antihistamines should not be used in children younger than two years of age, as they have been associated with increased risk of adverse e ects such as dizziness, blurred vision and lack of coordination.

In heart failure women's health clinic young nsw buy cabergoline online from canada, they have been shown to reduce mortality and hospitalisation rates women's health center statesville nc order cheapest cabergoline and cabergoline. Common adverse effects Common adverse reactions of these medicines include hyperkalaemia women's health clinic yuma arizona 0.25 mg cabergoline free shipping, nausea menopause jealousy cabergoline 0.5 mg purchase amex, hypotension and diarrhoea pregnancy 24 weeks discount cabergoline 0.5 mg mastercard. Other adverse e ects associated with spironolactone are skin rashes and blood dyscrasias, as well as endocrine imbalances resulting in increased breast development (gynaecomastia) in men and menstrual irregularities in women. Spironolactone is also used in the treatment of hirsutism in women when non-pharmacological therapy has failed, in heart failure and in primary hyperaldosteronism. It is important to note that older adults are more susceptible to postural hypotension, renal impairment and hyperkalaemia during this treatment. Endocrine and blood irregularities also need to be monitored during spironolactone therapy. Its diagnostic value, therefore, lies in di erentiating the level at which dysfunction of the pituitary­adrenocortical axis has occurred. Common adverse effects Common adverse reactions include gastrointestinal disturbances, dizziness and headache. Contraindications for use are hypersensitivity and conditions characterised by adrenocortical insu ciency. Clinical considerations In people where the function of the adrenal cortex or anterior pituitary is severely impaired, metyrapone can induce transient adrenal insu ciency, which can be overcome by administering a glucocorticoid. As prolonged therapy can also induce hypertension, blood pressure should be monitored. Mechanism of action Metyrapone prevents the synthesis of the glucocorticoid hormones hydrocortisone (cortisol), corticosterone and aldosterone within the adrenal cortex itself. Caution should be used when administering corticosteroids in people with these conditions, as they may intensify. Corticosteroids should not be used in people who have a systemic fungal infection or who are on immunosuppressant therapy. It needs to be noted that these contraindications to systemically administered corticosteroids are not applicable when corticosteroids are used as replacement therapy. These medicines should be weaned slowly and not stopped abruptly; adrenal crisis may otherwise result. Wear gloves to apply topical preparations on people to prevent absorption through your skin. Use care when moving and positioning immobilised people to prevent fractures and bruising. An increase in glucocorticoid therapy is required during illness and times of stress, such as during surgery and with infection. These medicines may cause infection, which may manifest as changes in the vital signs. Changes can include a fast, thready pulse, increased respirations and lowered blood pressure. Other manifestations of oedema may include a moonface, pu y eyelids and dependent oedema of the arms, legs and sacral area. During systemic therapy, monitor for manifestations of depression, such as lack of interest in personal appearance, withdrawal from activities, insomnia and lack of appetite. 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.

Clinical considerations e freedom from adverse e ects in most instances and the e ectiveness make sumatriptan a valuable addition to the pharmacopoeia of migraine treatments women's health clinic ut austin cabergoline 0.25 mg free shipping. Sumatriptan given subcutaneously is useful in the treatment of the agonising pain of cluster headaches pregnancy yoga pants purchase generic cabergoline online. Sumatriptan is speedily absorbed a er oral administration but is subject to a high hepatic rst-pass e ect breast cancer zumba pants purchase generic cabergoline from india, so a comparatively large dose must be given orally pregnancy test positive cabergoline 0.5 mg purchase on line. If given by subcutaneous injection its onset of action is fast womens health worcester quality 0.25 mg cabergoline, and this may be the preferred route of administration for many patients. It is available for self-administration in pre lled syringes with an automatic injection device. Injection of sumatriptan can be accompanied by pain at the injection site and by transient ushing in various parts of the body. A nasal spray is available for patients who cannot manage self-injection but must not be used in asthmatics, as bronchoconstriction may occur. Rizatriptan can be given as a lingual wafer to be dissolved on the tongue; the other triptans are taken orally. It is important to point out that rizatriptan wafers contain aspartame and are thus precluded from use in phenylketonuria. Zolmitriptan can cause prolongation of the Q-T interval on the electrocardiogram and should not be combined with other medicines that prolong the Q-T interval, such as amiodarone. Ergotamine is prepared from ergot, a fungal product obtained from Claviceps purpurea, a contaminant of cereal grains, especially rye. Many civilisations were aware that ingestion of rye occasionally led to severe disorders of the body, the most dramatic e ect being gangrene of the extremities, with subsequent mummi cation of the limbs. Partial agonist activity on the -adrenoreceptors accounts for the vasoconstriction and the gangrene associated with the use of ergotamine described above. Ca eine enhances the absorption of ergotamine, and is o en included in antimigraine preparations to speed up the onset of action. Ca eine also potentiates the action of analgesics that may have been given concurrently. Common adverse effects An unfortunate property of ergotamine is its ability to stimulate the chemoreceptor trigger zone, an area of the brain that can initiate vomiting (see Chapter 58); as migraine is o en accompanied by nausea, the problem may be compounded. Ergotamine is available as an inhalant for pulmonary absorption; this may be useful in nauseous individuals in whom rectal administration is undesirable. Most of the peripheral adverse reactions of ergotamine are due to its vasoconstrictor e ect on arterioles (peripheral coldness and cyanosis), and overdosing can lead to gangrene. Even though ergotamine has a short half-life of about two hours, it can bind to arterioles and its e ect can last for more than 24 hours. Rare cases of brotic complications have been associated with long-term continuous therapy with this medicine. Clinical considerations As too much ergotamine can lead to a headache, care must be taken not to increase the dose, as this can cause a worsening of the condition, with the resultant adverse consequences of the excess ergotamine. It is recommended that the minimum e ective oral dose be established by titrating ergotamine over successive attacks. Advise the person to cease treatment if problems occur, such as numbness in the ngers and toes, chest pain or shortness of breath. As ergotamine stimulates uterine contractions (see Chapter 59), it could be disastrous if used in pregnancy. Sumatriptan should not be given with ergotamine, as the potential for excessive vasoconstriction exists. Continuous use of these medicines requires monitoring for signs of brotic disorders. Contraindications to ergot alkaloids, which include various types of vascular disease, should be closely observed. Treatment with ergotamine should be for no more than a week at a time in order to prevent a severe withdrawal syndrome. Triptans are generally e ective in more than half of the individuals su ering from an acute migraine attack, and are e ective in improving associated symptoms of an attack, including photophobia, nausea and vomiting. Neither ergot alkaloids nor triptans are recommended for use in children under 12 years because bene t has not been established. Migraine prophylaxis is usually suitable only for patients who experience more than two attacks per month. Selected -blockers, such as propranolol, nadolol, timolol or atenolol (see Chapter 27), are sometimes e ective in preventing attacks. Calcium channel blockers, such as nifedipine and verapamil (see Chapters 46 and 47), have also been used with some success. Tricyclic antidepressants, such as amitriptyline (see Chapter 36), taken at night, are o en helpful. Up to 600 mg of aspirin daily may be e ective in controlling frequent attacks; more than this can exacerbate them. General clinical considerations of migraine treatment Non-pharmacological measures, which include rest, sleep and relaxation techniques, should be considered rst. Some argue that their e ectiveness and relatively mild adverse e ect pro le make them suitable candidates as a rst-line choice for this condition. Mechanism of action At this stage the mechanisms of action of topiramate and sodium valproate in migraine prophylaxis is unclear. Common adverse effects Common adverse e ects associated with topiramate therapy include fatigue, paraesthesias, dizziness, speech problems, gastrointestinal upset, nausea, weight loss, drowsiness and impairment in memory/concentration. Clinical considerations Topiramate has been shown to be as e ective as -blockers in reducing the frequency of migraine attacks. Unfortunately, the use of topiramate is limited by its ability to cause weight loss, fatigue, and mood and memory problems. It takes a number of days for the prophylactic e ect to develop, suggesting that the therapeutic bene t may be associated with the accumulation of an active and more potent metabolite. Methysergide has no therapeutic bene t in the treatment of an acute migraine attack. Common adverse effects e adverse e ects pro le of methysergide is not favourable due to the incidence of an in ammatory brosis which, although rare, can be life-threatening. Due to these side-e ects, people normally take this medicine for no more than six months at a time, and medicine holidays are given for one or two months if treatment needs to be continued. Clinical considerations e person is advised not to drive or operate machinery if feeling drowsy. Methysergide is considered only if other preventive drug measures fail because of its potential to produce severe adverse e ects. Stop the treatment if the person experiences numbness and tingling of ngers or toes, chest pain or shortness of breath. Serotonin antagonists ere are a number of medicines acting on serotonergic receptors that are helpful in migraine prophylaxis. In general, these medicines are serotonergic antagonists or antiserotonergic agents. Intuitively, this e ect appears somewhat at odds with the knowledge that serotonin agonists are useful in the treatment of acute migraine attacks. Pizotifen also has appetite-stimulating properties, which may lead to weight gain. Clinical considerations Pizotifen is generally well tolerated; however, it may cause transient drowsiness or weight gain. General clinical considerations of migraine prophylaxis In using -blockers for migraine prophylaxis, it is important to commence with a low dose and gradually titrate higher to achieve the required response. Contraindications to the use of -blockers include asthma, chronic obstructive pulmonary disease, atrioventricular block and peripheral vascular disease. When testing the e ectiveness of di erent prophylactic preparations, it is important to try one medicine at a time, increasing the dose gradually and attempting treatment for about three to six months. Assess the person for contraindications of ergotamine medicines and methysergide, including hepatic or renal disorders, as these medicines are metabolised in the liver and also eliminated by the kidneys. Ergot alkaloid medicines and methysergide should not be given to a pregnant woman or to a woman contemplating pregnancy, because of possible harm to the fetus. Assess the person for valvular heart disease, pulmonary, urinary tract or collagen disease when placed on methysergide. Methysergide can cause a rare brosis of the pulmonary tissue, retroperitoneal area or cardiac valves. I Monitor and document aspects of the migraine attack, including severity, duration, location, frequency, aggravating factors and alleviating factors. Monitor additional characteristics, such as the presence of an aura, nausea, vomiting, visual changes, slowness of thought, drowsiness, vertigo and mood changes. Preventive therapies should be used one at a time over a period of about three to six months to adequately determine the e ectiveness of a particular medicine. The medicine should be withdrawn slowly to prevent any rebound migraines before another medicine is commenced. Remember that ergotamine preparations are not well absorbed, despite the route of administration. Ergotamine preparations are administered about two hours before an attack or immediately at the onset. The combination of triptan medicines with serotoninlike medicines should be avoided because it is possible that this combination can result in serotonin toxicity. Zolmitriptan, which is part of the triptan group, can cause prolongation of the Q-T interval on the electrocardiogram; therefore, it should not be combined with other medicines that prolong the Q-T interval, such as amiodarone. People on methysergide should not be on this medicine for more than six months at a time and should have medicine holidays lasting one to two months. People on ergot alkaloid medicines should report coldness, numbness or tingling of the extremities. Administer ergot alkaloid medicines and methysergide with meals to alleviate symptoms of nausea and vomiting. Encourage the person to maintain a diary to record the medicines used, doses, responses to treatment, adverse e ects, and any event that may have caused or aggravated a migraine attack. I -Blockers used for migraine prophylaxis include propranolol, atenolol and metoprolol. A trial for six months is considered to determine the possible e ectiveness of treatment. However, the person should be advised not to operate machinery or to drive if feeling drowsy. The potent ergot alkaloid derivative methysergide has serious risks associated with it and, therefore, should be reserved for preventing migraine headaches that are not responding to other preparations. Ergotamine should not be used for more than two days per week because of the possibility of dependence and rebound headaches. Sumatriptan and other triptans should not be administered with ergotamine because of an increased predisposition to coronary vascular disease. Neuronal hyperactivity and chemical mediator release are thought to have an important role in the pathophysiology of this condition. Acute migraine attacks are treated with cerebral vasoconstrictors, which include serotonin agonists. Medicines used for this purpose include -blockers, calcium channel antagonists and serotonin antagonists. Mohamed Allaraz, a 65-year-old man with angina, also su ers from severe migraine attacks. Why is the triptan sumatriptan an unsuitable form of treatment for his migraine condition Jack McDonnell, aged 55 years, has peripheral vascular disease and su ers from migraine attacks, which occur approximately once every two months. Give two reasons why you would not recommend a course of the serotonin antagonist methysergide for him. John Chung, aged 44 years, has experienced regular migraine attacks requiring preventive therapy with the serotonin antagonist pizotifen. His doctor now wants to withdraw the medicine because the frequency of attacks has reduced considerably. What medicine education can you o er a person who wants to decrease the frequency of migraine attacks by resorting to non-pharmacological therapy List the physiological parameters that require monitoring during general anaesthesia. Throughout the centuries people have striven to conquer the pain associated with surgical procedures. Operative procedures have always been limited in their success by two main factors: postoperative infections and the agonising pain that occurred during the procedures. If a person did not succumb to the operative procedure, death from a postoperative infection usually ensued. Their main limitation was that to produce insensitivity to pain, deep sleep or unconsciousness was necessary and the amount of the substances needed to do this would be potentially fatal. It was not until the 1840s that surgical anaesthesia became possible, with the introduction of three medicines in quick succession: chloroform, ether and nitrous oxide. These three substances, on inhalation, quickly lead to unconsciousness, and surgical anaesthesia results. Nitrous oxide is still one of the most widely used gaseous anaesthetics, and diethyl ether (ether) is still used occasionally. Chloroform is rarely used today because of its toxicity, but other, newer halogenated hydrocarbons, such as iso urane, are common. However, the intravenous anaesthetics are taking primacy of place in surgery because they induce and maintain safe and reliable general anaesthesia. Stage 1-Analgesia Pain is the rst sense to be abolished and consciousness is still retained. Operating room personnel should be aware of this when induction with anaesthetic gases is used. Comments passed between sta may be recalled later by the person, and these could cause embarrassment on both sides.

Evaluation Evaluate the effectiveness of the medicine regimen womens health fitness us diet order genuine cabergoline line, as shown by the negative result of the sputum test for acid-fast bacilli pregnancy updates cabergoline 0.25 mg order free shipping. Implementation Monitor tissue cultures of the microorganism regularly until the leprosy is treated women's health center richmond va buy cabergoline online now. Monitor the person for a full blood examination menstrual relief purchase 0.5 mg cabergoline with amex, platelet count breast cancer organization order cabergoline 0.25 mg on line, and serum creatinine and urea levels. Treatment of leprosy usually requires the administration of at least two antileprotic agents. Standard treatment Evaluation Evaluate the effectiveness of drug therapy, as shown by the disappearance of skin lesions and negative tissue cultures. The successful treatment of tuberculosis relies on multidrug use and prolonged therapy. Leprosy is caused by Mycobacterium leprae and is still a common disease in developing countries. Medicines used to treat these conditions are termed first-line or second-line; the second-line agents being used in cases of non-effectiveness of, or severe adverse effects to , the first-line agents. How does this influence the effectiveness of the action of these medicines in the treatment of tuberculosis You get a panicky call from his daughter because the family is concerned that his reddish urine means he is bleeding from the kidneys. Which drugs form part of the bactericidal phase and which ones the sterilising phase Outline the mechanisms of action of: · oxidising agents · alkylating agents · detergents · phenols · alcohols · heavy metals · dyes with antimicrobial activity · tea-tree oil · honey. State the indications for use of the various types of antiseptics and disinfectants. Discuss the problems associated with the various types of antiseptics and disinfectants. Antiseptics and disinfectants play an important role in health care and help prevent many nosocomial infections. Antiseptics are used to kill or inhibit the growth of microorganisms on the human being, while disinfectants are used to do the same on inanimate surfaces. Most disinfectants are only partially successful in killing or denaturing microorganisms. Antiseptics are never able to sterilise completely and cannot be relied on to produce asepsis. The other main difference between antiseptics and disinfectants is that disinfectants are generally more toxic than antiseptics. Some disinfectants are similar chemicals to antiseptics but are used at a much higher concentration, which would be an irritant to living tissue. The efficacy of both antiseptics and disinfectants is still measured by comparing them with the original antiseptic used by Dr Lister, phenol. Each compound is evaluated by comparing its killing effect on a bacterium, usually Salmonella spp. This group is very susceptible to being oxidised to what is known as a disulfide bridge, ­S­S­. If this happens, the enzyme will be inactivated and the organism will die, or at least be immobilised. Chlorine, being much stronger than iodine, is mainly used as a disinfectant, while iodine is used as an antiseptic. Because it is so toxic, chlorine-containing compounds that release the element slowly are usually employed as disinfectants. A chlorine-containing mixture that has been used as an antiseptic is Eusol (Edinburgh University solution), a dilute solution of chlorinated lime, which was still used in wound dressings, and in ear, nose and throat surgery. However, the use of this agent on wounds has shown that capillary damage can occur, which delays the healing process and reduces its usefulness as an antiseptic. Iodine is very widely known as a solution in alcohol called tincture of iodine, which is still used occasionally. But as anyone who has had this applied to a graze or cut will know, its initial stinging effect can be quite uncomfortable. Iodine, nevertheless, is still one of the most commonly used antiseptics in a form known as an iodophor, the most common iodophor being povidone-iodine. The iodine concentration in povidoneiodine solution is at a much lower concentration than in its tincture. When iodine oxidises an enzyme, it is reduced to the iodide ion, which is inactive as an antiseptic. Povidone-iodine in solution is in equilibrium, as shown in the following equation. If iodine is removed by being reduced to iodide, more povidone-iodine will convert to free iodine to maintain the equilibrium: Povidone-iodine povidine + iodine Povidone-iodine is available in many different preparations for antiseptic use. These include an alcoholic If the coefficient is calculated at less than 1, the agent is superior to phenol, and the lower the coefficient, the better. Unfortunately, the results obtained from this test are not always applicable to the clinical setting. This lack of application occurs because nosocomial infections are caused by bacteria very often not used in the test. Many of the chemicals used as antiseptics or disinfectants are inactivated by substances like proteins, which are often present on areas to be treated. Antiseptics and disinfectants are classified according to their mode of action, which is usually chemical in nature. Some disinfectants are commonly found about the household and are similar to those employed in hospitals and clinics. In this article, reference will be made only to the brand names commonly used in a clinical setting. It is also available as an antiseptic solution, cream or ointment for household first-aid purposes. There is strong evidence that povidone-iodine can delay wound healing and generally it is not recommended for such uses. As mentioned in Chapter 78, povidone-iodine has antifungal properties, and is used as pessaries or as a douche in vaginal candidiasis as well as in other vaginal infections. It may also have some antiviral properties and is available as a gargle to treat pharyngitis and as a topical cold sore preparation. Cadexomer iodine is a complex involving a polysaccharide polymer with iodine cross-linked in its structure. Wound exudate causes the iodine to be released over a 72-hour period, thereby reducing the bacterial levels in the wound. It is also a very suitable oxidising agent for dealing with severe algal overgrowth in swimming pools. This is released from the peroxide in a manner similar to that of chlorine from the hypochlorites and iodine from povidone-iodine. When hydrogen peroxide breaks down, oxygen bubbles are produced, which may contribute to its cleansing action. Unfortunately, many organisms and human cells produce an enzyme called catalase, which breaks down hydrogen peroxide rapidly and causes it to lose its effectiveness. It can be as a skin antiseptic, to disinfect contact lenses and, occasionally, a dilute solution is used as a mouthwash for gingivitis and other oral infections. Hydrogen peroxide is often available in dilutions named after the amount of free oxygen they can release. The concentration used for disinfecting inanimate objects varies between 3% and 6%, and the concentration used for an antiseptic is 1. Hydrogen peroxide is a strongly reactive chemical (very strong preparations are actually used as rocket fuel), and care must be taken with its use as, for example, 100-volume solution is corrosive to skin. Bottles of hydrogen peroxide should be made of dark glass and stored at a low temperature because the release of oxygen on exposure to light or heat may cause the bottle to explode. The other peroxide in common use is benzoyl peroxide, an ingredient of many formulations used to treat acne. Clinical considerations Iodine solutions and powders should be shaken well before using because the various components have a tendency to separate out. Although 6% hydrogen peroxide solution may be placed on sloughy skin that requires debridement, it should be avoided on healthy skin. When using a benzoyl peroxide preparation, wash the affected area first with mild soap and warm water, and pat dry. It is also important to avoid contact with hair or coloured fabric because discolouration may occur. Most of the alkylating agents are very toxic to all living organisms and are, thus, reserved for the decontamination of inanimate materials. Compounds such as the gas ethylene oxide are so efficient that they are useful for sterilising objects such as endoscopes, which heat would damage. Traces of this substance left on materials have resulted in thrombophlebitis and tracheitis. The other two alkylating agents in common use are formaldehyde solution (formalin) and glutaraldehyde. Formaldehyde is a noxious chemical and very harmful to living tissues; therefore, its use is reserved for sterilising laboratory materials and for the decontamination of infected glassware. Glutaraldehyde is not quite as noxious as formaldehyde and is less damaging to living tissue. Nevertheless, glutaraldehyde has been reported to cause asthma attacks, conjunctivitis and rhinitis in persons often exposed to it. Clinical considerations When using ethylene oxide, ensure that the gas has dispersed from surgical instruments to prevent tissue toxicity. Gloves should be used if handling formaldehyde and glutaraldehyde to prevent skin contact. Care should also be taken to ensure that individuals do not inhale these noxious chemicals because they can be quite irritating to respiratory passages. The simplest of these are the anionic detergents (the negative ion is the detergent part and they are normally sodium or potassium salts of long-chain fatty acids), or simple soaps, which are only weakly antiseptic. The anion associated with the cation is usually a halide and, in the case of cetrimide, a bromide. The cationic detergents have good penetrating power and cause disruption to the cell membrane of bacteria and other microorganisms in the same way that dishwashing detergents dissolve or emulsify fats. All the cationic compounds, such as cetrimide, are relatively free of adverse reactions; skin sensitivities and/or allergies are rare. The other common cationic detergents used as antiseptics and/ or disinfectants are benzalkonium chloride, cetalkonium chloride and cetylpyridinium chloride. They are of interest not because they are used to kill bacteria but because they are used to kill spermatozoa. It is one of the most widely used antiseptics today because it has a very high therapeutic index. The advantages of chlorhexidine are that it can be used over a wide range of pH values and it is not inhibited greatly by the presence of organic material, such as pus. Its range of uses as an antiseptic are many, and there are even more preparations available with chlorhexidine than with the cationic antiseptics. As either the gluconate or hydrochloride, it is present in many cleansing soaps and scrubs, skin antiseptic creams, mouthwashes, gargles and throat lozenges. When used often as a mouthwash, staining of the teeth can occur and it can lead to gingival bleeding. Contact is avoided with eyes, middle ear and brain meninges because it might cause tissue irritation. For the same reason, cetrimide should not be used as an enema or in body cavities. Any diluted solutions of cetrimide must be discarded after use because diluted solutions are associated with overgrowth of microorganisms. When using a nonoxynol preparation, additional applications are required each time intercourse is repeated. If a diaphragm is used with a nonoxynol preparation, it should remain in place for six to eight hours after intercourse to allow for the full spermicidal effect. Several of these topical contraceptive treatments are applied using a vaginal applicator. Chlorhexidine may cause skin and hypersensitivity reactions, which warrants discontinued use. Discard any remaining solution after applying chlorhexidine to wounds to prevent overgrowth of microorganisms. Since then its use has waned, even though external use on adults is considered acceptable. Phenols exert their action by disrupting cell membranes, and they are protein denaturants. The cresols are used mainly as disinfectants because they are quite irritating to skin. Thymol is viewed by some as having a pleasant taste and smell and is, therefore, incorporated in many mouthwashes, but probably at too low a concentration to be of much value. Resorcinol is an ingredient of some acne and other skin preparations; it is mildly keratolytic as well as antiseptic. Triclosan has a spectrum of efficacy similar to that of chlorhexidine, except that it is not very effective against Pseudomonas aeruginosa, a common cause of nosocomial infections. As a general antiseptic, triclosan is incorporated in many soaps, facial washes, shampoos and acne preparations. Another group of phenolic compounds have an important part to play in pharmaceutical preparations. They are effective at very low concentrations and appear to be devoid of systemic toxic effects at a concentration of about 0. They are used as preservatives in many ointments, creams and oral liquid preparations.

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