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Pregnancy outcome following anticonvulsant agent overdoses has been published in one isolated case report order 1 mg finax amex symptoms narcolepsy. A case of carbamazepine megadose in attempted suicide with more than 10 g of carbamazepine during early preg- nancy resulted in a fetus with a large meningomyelocele and frontal lobe necrosis that was electively aborted buy cheap finax 1mg on line treatment 4 addiction. The mother recovered without complication following nonspe- cific therapy and coma for 5 days (Little et al generic finax 1mg with mastercard symptoms 1 week before period. Damage to the embryo or fetus is probable because the two anticonvulsants listed (phenytoin order finax 1 mg fast delivery treatment narcolepsy, carbamazepine) are known human teratogens. Anticonvulsant agents have no specific antidote, and supportive therapy should be given. Near-therapeutic amounts of these drugs cross the placenta and achieve significant concentrations in the fetus. It is known that phenytoin may induce fetal hepatic enzymes, but the effects of a potentially toxic dose are unknown. Phenytoin’s half-life ranges from 8–60 h and is dose dependent because each individual has a threshold plasma concentration beyond which the drug exhibits zero-order kinetics (Arnold and 272 Drug overdoses during pregnancy Gerber, 1970; Kostenbauder et al. Details of the clinical course of pregnancy after overdoses of any of these agents have not been pub- lished. It is known that signif- icant amounts of these drugs cross the placenta to reach near-therapeutic levels in the fetus. Camphorated oil Camphor, a gastrointestinal irritant and central nervous system stimulant, was used in four suicide attempts during pregnancy that have been published (Blackmon and Curry, 1957; Jacobziner and Raybin, 1962; Riggs et al. Uniformly, maternal seizures occurred and should apparently be expected with camphor ingestion. The fourth pregnancy was compromised by preeclampsia, abruptio placenta, and other serious complications, and the infant died less than 1 h after delivery. Clinical experience with camphor overdose is very limited and no specific antidote is available. Therefore, the nonspecific antidote regimen should be given and supportive therapy provided. Even limited experience with gravid women who have ingested cam- phor is sufficient to begin antiseizure medication as a component of the antidote regi- men in anticipation that seizures may ensue. Turpentine and ammonia No details of the course of pregnancy following poisoning with these nondrug chemi- cals have been reported. No specific antidote to these poisons is available and nonspe- cific antidote regimens and supportive therapy should be given. Quinine overdose An attempt to induce abortion should be suspected when quinine overdose is encoun- tered in pregnant women. Among 70 published cases of pregnant women taking quinine at Summary 273 high doses in an attempt to induce abortion suggest the drug may be teratogenic (Dannenberg et al. At least 11 women died as a result of quinine overdose and many who did not expire experienced toxic effects of the drug. No fewer than 41 infants with major congenital anomalies were born to women who took large doses of quinine during pregnancy. Causality cannot be proven using these data because the information comprised of only case reports. Nonetheless, large doses of quinine appear to pose an increased risk of some specific abnormalities that parallel toxicity from the drug often seen in adults. Eighteen of 60 infants (30 percent) born to women who ingested large amounts of quinine during pregnancy were congenitally deaf (Dannenberg et al. Ototoxicity is a common and well-documented complication of quinine therapy in adults. Large doses of quinine during the first trimester of pregnancy are anecdotally associ- ated with major congenital anomalies, including central nervous system anomalies (especially hydrocephalus or otolithic damage), limb defects, cardiac defects, and gas- trointestinal tract anomalies (Nishimura and Tanimura, 1976). No characteristic pattern of anomalies or syndrome was identified, and the association of these anomalies with maternal quinine ingestion remains empirically uncertain, but seems plausible. Nonspecific antidote treatment and supportive therapy should be given because no specific antidote for quinine overdose is available. Ergotamine overdose Overdose of ergotamine during pregnancy was published in a case report of a woman at 35 weeks’ gestation who took 10 tablets of ergotamine tartrate in a suicide gesture. Two hours later uterine contractions began with no relaxation between contractions. Two weeks after the over- dose, a macerated stillbirth with no gross abnormality was delivered. Impaired placen- tal perfusion and fetal anoxia associated with ergotamine was speculated to have caused the fetal death (Au et al. Spontaneous onset of preterm labor following ingestion of ergot also occurred with therapeutic levels of the drugs, but at usual therapeutic levels prematurity was the only complication, and there were no fetal deaths. Two antidotes to ergot alkaloid overdose (prazosin and nitroprusside) are now available that were unavailable to patients described above (Au et al. Nitroprusside should be avoided during pregnancy because it conjugates to cyanide and accumulates in the fetal liver. If there is no specific antidote, a nonspecific aggressive treatment should be instituted as early as possible (see Appendix). Homicide and other injuries as causes of maternal death in New York City, 1987 through 1991. No tocolytic agent is uni- versally effective, although more than 100 000 pregnancies will receive tocolysis ther- apy. Pregnant women treated with tocolytics are at increased risk for serious cardiopulmonary com- plications that are directly attributed to the tocolytic drug. Tocolytic therapy invariably occurs outside embryogenesis, so congenital anomalies are not an issue. The primary concern is for adverse maternal, fetal, and neonatal effects (Sanchez-Ramos et al. The three principal indications that guide the use of tocolysis in the treatment of preterm labor are: (1) prophylaxis, (2) acute therapy, and (3) maintenance. Instances do exist when exposure to tocolytic agents occurs during organogenesis, and is used for other indications: terbutaline (asthma), indomethacin (pain), and nifedipine (hypertension). Use for these indications is discussed in the chapters on antiasthma (Chapter 5), analgesic (Chapter 8), and cardiovascular drugs (Chapter 3), respectively. Pharmacokinetics of tocolytic drugs Pharmacokinetic data on tocolytic drugs in pregnancy are limited to five studies of four drugs (Table 15. Half-life and steady-state concentrations are generally not different between pregnant and nonpregnant states. Beta-adrenergic receptor agonists Ritodrine and terbutaline are beta-agonist drugs, structurally related to epinephrine, and are used as tocolytics. This type of tocolytic binds to beta-adrenergic receptors on the outer myometrial cell membrane and acti- vates adenylate cyclase. Another pathway is the phosphorylation of myosin light chain kinase which inactivates the enzyme, thus inhibiting subsequent phosphorylation of the myosin light chain. Maternal metabolic abnormalities (gluconeogenesis, hypokalemia, and hyper- glycemia), as well as cardiopulmonary complications (tachycardia, hypotension, arrhyth- mias, myocardial ischemia, pulmonary edema) are associated with beta-agonist tocolyt- ics (Box 15. Every beta-agonist is associated with pulmonary edema and occurs among as many as 5 percent of gravidas who took any of these drugs (Boyle, 1995; McCombs, 1995). Maternal tocolytic therapy has been associated with neonatal hypoglycemia and tachycardia. Several fetal and neonatal cardiovascular adverse effects are associated with beta-sympathomimetic therapy (Katz and Seeds, 1989) (Box 15. Decreases in the systolic/diastolic ratios of the umbilical artery have been reported in patients using either terbutaline or ritodrine (Brar et al. By 1979, ritodrine was available as a tocolytic agent in 23 foreign countries (Barden, et al.

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Its first branches are to the sinoatrial node and the right ventricular outflow (conus) purchase finax 1mg with amex treatment jerawat di palembang. It supplies the right ventricle with branches as it circles the grove inferiorly and posteriorly discount 1 mg finax mastercard treatment under eye bags. On the posterior surface of the heart it supplies the area of the atrioventricular node and branches to both ventricles order finax 1 mg with visa symptoms non hodgkins lymphoma. The posterior descending buy finax 1mg online medicine song 2015, arising from either vessel, gives arterial supply to both sinoatrial and atrioventricular nodes. The coronary arteries are terminal vessels, which means they do not have collateral branches under normal circumstances. The first slide shows dynamic real-time ultrasound images recorded in a child at 30 frames per second. The ultrasound now passes from the cardiac apex and permits accurate Introduction To Cardiac & Tomographic Anatomy Of The Heart - Norman Silverman, M. The subsequent slides show tomograms, which are the interactive data, showing the power of tomographic techniques in a real anatomic case. The use of computerized tomography and magnetic resonance imaging and dynamic 3 dimensional spatial reconstruction techniques are the tools of modern medicine. In order to study the heart the student must have an intimate knowledge of basic cardiac anatomy, with this introduction and references provide. As much of cardiac study uses tomographic methods, this course provides an opportunity through on-line methods for study of tomographic anatomy and its clinical applications Positive Inotropic Agents - James Whitlock, M. Understand the autonomic and hormonal compensatory changes that heart failure evokes. Pay special attention to the mechanisms of its beneficial and adverse effects, its effects on cardiac rhythm, and the effects of potassium ion and calcium ion on digoxin action. Learn the pharmacology of (1) beta adrenergic receptor agonists and (2) inhibitors of phosphodiesterase-3. Understand the autonomic and hormonal compensatory changes that occur when the heart fails. Understand the vicious cycles in cardiovascular function that accompany the changes and that make heart failure worse. Understand the rationale for using various drug groups to alter preload, afterload, and contractility in patients with heart failure. Approximately 30,000 babies with heart defects are born each year in the United States. In severity, congenital defects span a spectrum from those which are potentially lethal in the first few days of life to those with minor hemodynamic significance and which are often found incidentally in adult autopsies. With current diagnostic procedures and recent advances in medical and surgical therapy, many of the complications of these defects can be treated and/or prevented, thus markedly increasing survival and adding to the quality of life for the majority of patients. To better understand the pathophysiology of these congenital cardiac lesions, one must first understand the special features of the fetal circulation and the multitude of hemodynamic, hormonal and biochemical changes which occur during and after birth. The fetus exists within the fetal membranes (chorion and amnion) and uterus, bathed in amniotic fluid. While it has been shown that the fetus does have respiratory movements, gas exchange does not occur via the lungs. The placenta performs these important functions in the fetus, however, since the placenta is removed from the circulation at birth, there are several important transitions which must occur between the fetal, newborn and adult cardiovascular systems. Most of our current knowledge about the fetal circulation has been obtained from animal studies, with pioneering studies in the fetal lamb performed by Dr. However, more recently the Fetal Circulation & Congenital Heart Disease - Daniel Bernstein, M. There are several important differences between the fetal cardiovascular system and that of the infant or adult: 1. The fetal myocardium has a lower density of sympathetic nerve endings and lower density of ß- adrenergic receptors than does the adult myocardium and these receptors are less effectively coupled to downstream effectors such as adenylyl cyclase. Although the fetus does have the ability to increase heart rate and stroke volume in response to sympathetic stimulation, this capacity is blunted when compared to the adult. Both in vivo and in vitro studies demonstrate that the fetal myocardium has different contractile properties than that of the adult, although the significance of this is still the subject of some debate. Morphologically, the fetal myocardium has a higher ratio of interstitial space to myocytes, and myocytes are more randomly oriented as opposed to the parallel arrangement of the adult heart. The fetal myocardium also has a less well-developed T-tubule system than the adult, so that extension of the sarcoplasmic reticulum in proximity to muscle fibers is not as extensive. Additionally, the fetal heart relies on extracellular calcium entering via sarcolemmal calcium channels for triggering contraction as opposed to the adult heart where most of the calcium for activation comes from calcium-induced calcium release from the sarcoplasmic reticulum. Length-tension (or pressure-volume) curves in fetal sheep myocardium demonstrate higher resting tension and lower active tension than adult curves (Figure 1), indicating less compliance than the adult heart. These early studies suggested to investigators that the ability of the fetal heart to utilize the Frank-Starling mechanism to increase stroke volume is significantly diminished compared with the adult heart. When saline was infused, the fetal cardiac output increased only about 30% compared with a 200% increase seen in the adult. However, these studies failed to account for the fact that by changing preload with large volume infusions, the investigators were also increasing afterload. The fetal heart is very sensitive to changes in afterload, and these increases were part of the reason why fetal cardiac output appeared to be blunted in response to volume. Subsequent studies, controlling for changes in afterload, have shown that the fetal heart does respond to changes in preload, although perhaps still less well than the adult heart. The clinical significance of this finding is that lesions which result in volume loading of the fetal heart (e. There are major histological differences between the fetal, newborn and adult pulmonary vascular beds. The extent of smooth muscle lining intra-acinar pulmonary arteries changes with advancing age. Since the placenta supplies oxygen to the fetus, there is no reason for a large amount of blood flow through the pulmonary circulation; it is the chronic constriction of the pulmonary vessels that maintains a high resistance in the fetal pulmonary circulation. Endothelin may also play a role, as blockade of endothelin A receptors also decreases pulmonary resistance in the fetus. Thus, with a very vasoconstricted pulmonary bed, only 7-8 percent of total fetal cardiac output flows to the lungs. With advancing gestational age, an increase in the number of pulmonary vessels associated with lung growth gradually increases the pulmonary vascular cross- sectional area and gradually decreases pulmonary vascular resistance, although pulmonary resistance remains quite high until the time of birth (Figure 3-1). In the early embryo, metabolic exchange occurs by diffusion, but as the fetus grows diffusion becomes inadequate to meet cellular metabolic needs, and thus the circulatory system develops during the first trimester. With the development of the fetal circulation, oxygen transport by hemoglobin becomes progressively more important. Since hemoglobin is the major carrier of oxygen in blood, alterations in hemoglobin concentration and/or oxygen affinity will have a large effect on oxygen delivery to the tissues. In the fetus, hemoglobin concentration increases with age (Figure 2a), and at term is actually higher than in the adult; this high level of hemoglobin is important to the fetus in that it allows more oxygen to be carried to the tissues. The top figure shows chanes in hemoglobin tetramers, the bottom changes in the individual globin subunits. In addition to a change in total hemoglobin concentration, hemoglobin in the fetus also undergoes an evolution in oxygen affinity (Figure 2). As seen in Figure 2b, early in gestation several minor hemoglobin constituents appear, but by the second month the major hemoglobin is Hgb F.

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Summary: This woman was given a minimal test at our office buy finax 1 mg overnight delivery treatment pneumonia, just to remove her cancer purchase finax 1mg with amex medications used to treat fibromyalgia. Hopefully purchase finax 1 mg mastercard symptoms 3 days before period, she has removed the propanol from her lifestyle and carried out the parasite program buy 1 mg finax with mastercard medicine 4h2 pill. Lenora Wilson Colon Cancer Lenora Wilson is a 55 year old woman whose main problem, she said, was ovarian cancer. Instead she went to Ann Wigmore Foundation for 2 weeks and changed diet to vegetarian. But it came back recently; her doctor used the cancer marker Ca 125 to monitor it. Two years later a different doctor found it quite abnormal, and she got cold knife conization. Calcium slightly low Drink 2% milk, 3 glasses/day; magne- sium (300 mg) 1/day; Vit D (by pre- scription from dentist 50,000) 1- 2/week forever. Summary: Mary came from several states away and had only 16 days to accomplish her goal: to avoid a hysterectomy. We hope she will eventually do a liver cleanse to lose the weight she suddenly gained. I was out of wormwood so I started her on quassia (see Recipes), rather than have her merely wait until it arrived. She will switch to wormwood and the usual parasite killing program now that it has arrived. Summary: This woman did not come in for health problems but only because she was worried about cancer, since her husband had died of it. Indeed, her intuition was right, but very quickly she removed all of the cancer, even though she substituted quassia for our regular parasite recipe. She has probably not returned for financial reasons (she lives on Social Security). Her good attitude will probably bring her back quickly if she has a health problem. The intestinal fluke was in the liver as usual, with a stage present in the breast. The first priority was to eliminate the cancer, although her purpose in coming to the office was her high blood pressure and ringing in the head. Hopefully, she will return free of her cancer, so we can pursue her other health prob- lems. Three weeks later He has had top right wisdom tooth pulled (#1), it had an abscess. His blood test sug- gested parasites (high platelet count) and Fasciolopsis was found. He acted quickly to clear up his Staph aureus infection by having a wisdom tooth pulled. Later we noticed a common lung infection, Pneumocystis, but he still could not stop smoking. At the last visit he had picked up the intestinal fluke again, probably from eating rare meat but he had no solvents in his body. This explains why the parasite stayed in the intestine and did not move to his liver or lungs. This bout with lung cancer was missed by his medical doctor whom he continues to see regularly. Perhaps if his medical doctor had also seen the cancer, he would have quit smoking. He and his wife have been neglectful of the parasite program and other restrictions. Richard England Lymphoma In Bone Richard England has 2 preschool children and a wife who brought him here. Due to his resentment at being “dragged” in by his wife, I tested only for Fasciolopsis and Sheep liver fluke. His young children sat quietly in their chairs during the appointment, sensing the grave danger their father was in. But he made jokes about my technical com- petence and devices instead of listening. A friend who had gone through our cancer program successfully tried to encourage him at home. He was always talking about his exceptional oncologist and the great rapport and team work in the hospital. His wife would have gladly moved from their fossil fuel contaminated home or turned the furnace off and put in an electric space heater till they could sell the home. So I began with a conversation with her husband in the office instead of with her. The chronology of her illness was: 6 months ago she had arthritis; 3 months ago it became more serious; 1½ months ago walking was very painful; 1¼ months ago she needed a walker; 4 weeks ago she could not walk. Her clinical doctor diagnosed rheumatoid arthritis and treated her with a steroid. They put steel reinforcement in one leg and cut out the cancerous part in the other leg. She will have another week of this but her doctor let him know they could only expect a short remission, if any. I discussed my approach with her husband, reassuring him that I did not controvert any clinical treatment. She was using a walker and had visible pain, but she was interested in my approach. They have a lot of electronic equipment in house, but no copier; computer is on porch. She is wearing a metal partial denture; she will not wear it at night and change this to plastic soon. She has been using Efferdent for cleaning her teeth; she will switch to grain alcohol. She is not on any supplements except magne- sium (300 mg) 1/day and Vitamin B6 (500 mg) 1/day. Her friend who is cooking for her said she would eat only noodles with any enjoyment. We are adding Vitamin D, prescribed by dentist (50,000 u) 1/day for 30 days for pain and to help healing. She thinks the kidney herbs were instrumental in her suddenly feeling “like my old self. We are now starting a regimen of: 6 caps per week only; then 5 days/week; then 4 days/week; then 2 caps per week indefinitely. She is not using any as- sistance with walking and sits down easily on a chair by herself without discomfort. One week later She is not using her cane and is sitting comfortably on a chair without a cushion. Start on 07 (a commercial preparation of chlo- rine dioxide) and peroxy (17½ % hydrogen peroxide). Her husband and friends supported her and were not negative about alternative therapy. She had a particularly difficult time killing all the parasite stages but pursued the program diligently without being discouraged and quitting. She has had kidney infections (pain over kidney, frequency of very yellow urine, dizziness, ears are shut).

Not surprisingly order finax 1mg with mastercard medicine 4h2 pill, they have the capacity to be ideal starting points in the drug discovery process finax 1mg visa 20 medications that cause memory loss. However discount finax 1mg mastercard symptoms bowel obstruction, there are a number of major problems that must be con- fronted when exploiting peptides or proteins as lead compounds for drug discovery order finax 1mg mastercard medications like prozac. Peptides are often too flexible (thus binding with too many receptors, leading to toxicity). Despite these obvious deficiencies, peptides have a number of properties that make them attractive as starting points in drug design: 1. Peptides contain numerous stereogenic (chiral) centers (an excellent starting point when designing stereoselective drugs). Peptides can have their conformation and geometries easily optimized by energy minimization calculations using current computational methods (e. Peptides function as neurotransmitters and hormones and thus are good starting materials when designing bioactive molecules. Since peptides are ideal starting molecules that cannot be turned into successful peptidic drugs, the specialty area of peptidomimetic chemistry has emerged. The goal of pep- tidomimetic chemistry is to design small, conformationally constrained, non-peptidic organic molecules that possess the biological properties of a peptide. Hopefully, this will retain the strength of the peptide as a putative drug while eliminating the problems. There are two approaches whereby peptidomimetic chemistry can achieve this design goal. In Step A, the smallest bioactive fragment of the larger peptide is identified; in Step B, a process such as an alanine scan is used to identify which of the amino acids are impor- tant for bioactivity; in Step C, individual amino acids have their configuration changed from the naturally occurring L-configuration to the unnatural D-configuration (in an attempt to make the peptide less “naturally peptidic”); in Step D, individual amino acids are replaced with atypical unnatural amino acids and amino acid mimics; in Step E the peptide is cyclized to constrain it con- formationally; finally, in Step F, fragments of the cyclic peptide are replaced with bioisosteres in an attempt to make a non-peptidic organic molecule. Next, this segment is then rebuilt isosteric fragment by isosteric fragment, gradually replacing each portion of the molecule in a stepwise fashion. For example, the amide bond may be replaced by a bioisosterically equivalent amide bioisostere. In this fashion, an equivalent but non- peptidic organic molecule drug eventually emerges. An alternative approach is a little less plodding and perhaps a little more elegant. Next, an educated guess (hopefully based on some exper- imental data) is made to suggest which portion of the peptide is the pharmacophore. The geometries of the functional groups within the pharmacophore are then measured from the theoretical and experimental studies of the peptide’s geometry and conformation. For example, these data may show that the peptide pharmacophore contains a carboxylate group located 4. Using these precise data, databases of known organic molecules are then computation- ally searched to identify an organic molecule with similar functional groups held in the same position in three-dimensional space. These include nucleic acids, lipids, and carbohydrates, which are discussed in detail in chapter 8. Likewise, there is a need to develop small organic molecules as mimetics of these other endogenous molecules. Although not as clearly defined as peptidomimetic chemistry, ultimately, “nucleotidomimetic” or “carbohydromimetic” chemistries may eventually emerge as new design strategies for lead compound identification. An alternative is to exploit molecules that are endogenous to other life forms (animal or plant) but do not naturally occur within humans. Such molecules would be classed as exogenous from the perspective of drug design for humans. Digitalis for congestive heart failure was first isolated from the foxglove plant. Various antibiotics (penicillin) and anticancer agents (taxol) are derived from natural product sources. There is good reason to be optimistic about the potential future usefulness of such exogenous compounds as a continuing source of potential lead compounds. With many thousands of years of trial-and-error by evolution on her side, Mother Nature is a vastly superior experimentalist to any mere human organic chemist. Amphibian evolution has enabled the biosynthesis of antibacterial peptides on the skins of frogs so that they can avoid infections as they swim through stagnant swamp waters; peptides such as these could be a good starting point for the peptidomimetic design of novel antibacterial agents. Reptile evolution has culminated in the biosynthesis of neuroactive venoms for pur- poses of hunting and defense; these molecules have been fine-tuned by evolution as agents specific for neurotransmitter receptors. Plant evolution has culminated in a wide variety of biomolecules that affect any animal that may choose to eat them: it is bio- logically advantageous for some plants to be eaten so that their seeds can be dispersed in the stool of the animal that ate them; conversely, it is biologically advantageous for other plants to produce noxious chemicals to decrease the likelihood of their being eaten. Because of these diverse biological activities, any of these non-human biosyn- thetic molecules could, in principle, be a lead compound for human drug discovery. Another promising feature of animal- or plant-based natural products is that they are a superb source of molecular diversity. As a synthetic chemist, Nature is much more creative and is not constrained to the same finite number of synthetic reactions typically employed by human synthetic organic chemists. Furthermore, when developing compound libraries for high throughput screening (see section 3. Although ethnopharmacology, the scientific investigation of natural products, folk medicine, and traditional remedies, has led to some bona fide drugs (e. However, natural products have always been and still are an inexhaustible source of drug leads as well as drugs. From each of these sources, extracts conducted with solvents with different polar- ities will yield different natural products. This complex extraction system ensures the identifica- tion of all possible candidate molecules from a plant source. Several research institutes and well-established groups (notably the Scripps Institute of Oceanography and the University of Hawaii) are producing some very promis- ing results in this field. The isolation of prostaglandins from a coral was one of the more startling recent discoveries in marine pharmacology. An extension of natural products chemistry is the biochemical information derived from the study of metabolic pathways, enzyme mechanisms, and cell physiological phenomena; this research has revealed exploitable differences between host and para- site (including malignant cells), and between normal and pathological function in terms of these parameters. The large and fertile area of antimetabolite (metabolic inhibitors) and parametabolite (metabolic substitutes) chemistry is based on such stratagems, and has found use in the field of enzyme inhibition and in conjunction with nucleic acid metabolism. The design of drugs based on biochemical leads remains a highly sophis- ticated endeavor, light-years removed from the random screening of sulfonamide dyes in which it has its origin. However, of the approximately 10200 “small” organic molecules that could theoretically exist in our world (1052 of which are drug- like molecules), many would be purely synthetic substances that do not occur naturally. The concept of rational drug design (in contrast to its logical counterpart, irrational drug design) implies that the disease under consideration is understood at some funda- mental molecular level and that this understanding can be exploited for purposes of drug design. Such an understanding would facilitate the design of purely synthetic mol- ecules as putative drugs. Although this ideal of rational drug design has been pursued for many years (see section 3. Recognizing its chemical similarity to iodine, French physicians immediately exploited it as an iodine alternative for the treat- ment of numerous conditions, including syphilis and thyroid goitre. Although no bene- ficial effects were reported for either bromine or its potassium salt, their widespread use persisted and eventually the depressant effect of potassium bromide on the nervous system, so-called ivresse bromurique, was recognized. However, it was a report in the German literature concerning bromide’s ability to induce impotence and hyposexuality, rather than ivresse bromurique, which lead to its discovery as an anticonvulsant. In 1857, Sir Charles Locock, the physician accoucheur to Queen Victoria, ascrib- ing to the then prevalent view that epilepsy arose from excessive sexuality, introduced bromide as an anaphrodisiac to suppress the supposed hypersexuality of epileptics.

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