By V. Bufford.
The significance of coronary atheroma is that individuals with this dis- ease are particularly prone to the development of dysrhythmias during periods of stress when their decreased ability to perfuse areas of the myocardium may result in the development of ectopic electrical foci buy cheap oxytrol 2.5 mg. Deaths may be preceded by the development of classical cardiac chest pain buy oxytrol 2.5 mg with visa, or it may present with sudden collapse and death without warning generic oxytrol 5mg without a prescription. Individuals suffering from significant myocardial hypertrophy resulting from chronic hypertension are also at greater risk during periods of stress. Once again, it is the older age groups that are most commonly affected by essential hypertension, which may also render these individuals susceptible to focal lack of myocardial perfusion during periods of tachycardia. In addition to these two disease processes, there are also rarer diseases or syndromes that may cause sudden death, which are possibly more significant in the context of “deaths in custody” because some of them tend to affect younger age groups in particular. Current research is now focusing on a genetic basis for many other sud- den cardiac deaths in the younger age groups. The examination for these specific gene markers in any sudden death in police custody must now be considered in the absence of other causes of death. Other cardiovascular causes of sudden death, for the most part, are also age related. The rupture of atheromatous aortic aneurysms is a disease almost entirely confined to late-middle and old age, whereas the rarer forms of aorti- tis and collagen diseases of the aorta (11), which may also result in rupture, are more commonly seen in the younger age groups. It is most unusual for deep venous thrombosis of the leg veins to be present in a young active male; however, the association between some types of the combined oral contraceptive pill and the development of thromboses has been known for some time (12) and may render a small sub- group of the female population at greater risk of pulmonary emboli than the general population. Central Nervous System The stress associated with arrest and detention in custody may also have significant effects on the cerebrovascular system and may, in suscep- tible individuals, precipitate intracerebral hemorrhage by the rupture of con- genital or acquired aneurysms or vascular malformations. Ruptured berry aneurysms will result in the development of acute subarachnoid hemorrhages. It is less likely that these intracranial hemorrhages will result in sudden death, but they may result in sudden unconsciousness, which ultimately leads to death. Clearly, the distinction between hemorrhage resulting from a natural disease process and death resulting from trauma will need to be established and a specialist neuropathological examination will be required should death occur. However, it is unlikely that meningitis or encephalitis will present without any prodromal symptoms. Epilepsy is unlikely to develop de novo after arrest and detention, but epilepsy can and does lead to sudden collapse and death, and a pre-existing history of epilepsy is clearly impor- tant. Any individual known to suffer from epilepsy should be monitored with the utmost care and his or her prescribed medication continued. Other forms of intracranial pathology that may lead to sudden death include tumors, both benign and malignant, and such rarities as the develop- ment of colloid cysts of the ventricular system. Endocrine Diabetes mellitus should raise similar concerns to those associated with epilepsy because poorly controlled diabetes occasionally may be the direct cause of sudden death and, through its association with an increased incidence of arterial disease, it is a major factor in the development of coronary artery disease in the younger age groups. At postmortem, consideration must be given in all cases of sudden death in a young individual, particularly when there is a history of diabetes mellitus, to the sampling of the vitreous humor to deter- mine the blood glucose level at the time of death. The samples must be taken as soon after death as possible to avoid postmortem use of the intraocular glucose yielding erroneous results (14). Other Causes There are many other natural disease processes that could theoretically lead to sudden collapse and death. Among them is asthma, a disease that is usually unlikely to lead to sudden death if adequately treated and supervised but that may, if untreated and unsupervised and in stressful circumstances, result in the individual being found dead in their cell. Other disease pro- cesses include the development of hemoptysis, from tuberculosis or pulmo- nary malignancy, or hematemesis, from peptic ulceration or esophageal varices, which can be life threatening and may, because of the bleeding, be considered to be the result of trauma rather than a natural disease process. These cases should present no problem to an experienced pathologist follow- ing a full postmortem examination. Conclusion The significant feature when considering possible natural causes of death of an individual in police custody is that some diseases can lead to rapid col- lapse and death with no warning in a young individual who is apparently fit and well immediately before the collapse. There is no method that the police can use to determine which of the individuals they encounter will be suffering from any of these diseases or from a genetic abnormality that may lead to electrical disturbances within the myocardium. Indeed, many of these disease processes can only be diagnosed after complex medical testing and after tak- ing a full medical history. That many of these diseases are rare in the age group that is most likely to be detained in custody places additional burdens on the police officers who are required to care for them and also on the doctors required to examine and treat them in the police station. The difficulties that these cases present to the 336 Shepherd pathologist lie in the need to have an awareness of all of the possible natural causes of sudden death and a careful determination and, if necessary, exclu- sion of all of these causes (cardiac, neurological, and endocrine) before form- ing the conclusion that some other factor has resulted in death. Accidental Trauma It is clear that determining whether trauma is the result of an accident may depend on the “eye of the beholder. All of the injuries or marks found on the body will have to be correlated with witness statements from both the police and any other parties present at the time of the fall. Often the true inter- pretation of many of the injuries and marks found during the postmortem will only become clear when these statements are considered. However, in general terms, accidental trauma can be caused by many events during the course of an arrest. The site and significance of the injuries that are present will depend on the descriptions of the events before, during, and after the arrest. It is essential that all injuries, no matter how apparently trivial, present on a detained individual are carefully documented by the forensic physician who examines the detainee whether at a police station or elsewhere. Contem- poraneous photographs are always extremely helpful in these circumstances. In terms of cause of death, few of the minor injuries will be relevant, but they may provide an indication of the extent and degree of the force that was applied to effect an arrest and, as such, they can be of immense value. All of the injuries must be inter- preted in the light of witness statements and can provide useful corroborative evidence. At low concentrations, the specialized cells of the cerebral cortex are affected, but as the concentration increases, the depressive effects involve the higher areas of the brain, resulting in increasingly disinhibited behavior. Still higher levels of alcohol result in the depressant effects involving the lower levels of brain function, including the vital cardiorespiratory centers in the midbrain and the medulla, predisposing the intoxicated individual to cardiorespiratory depres- sion or arrest. Alcohol levels in excess of 300 mg/dL are considered to be potentially lethal, and although some individuals have survived, usually with medical attention, with higher levels, it should be remembered that some indi- viduals have died with far lower levels of alcohol in their blood stream. However, the effects of alcohol are not confined to the brain; there is also marked peripheral vasodilation, resulting in increased heat loss that may occa- sionally lead to hypothermia. The adverse effects of alcohol on the coronary circulation, particularly when associated with coronary atheroma, may lead to myocardial ischemia and the development of dysrhythmias and sudden death. Alcohol also has marked diuretic effects and, when combined with the ingestion of large quantities of fluid (particularly in beer and lager drinking), it may result in electrolyte disturbances, particularly hyponatremia. The chronic effects of alcohol involve many of the internal organs; alco- holic cardiomyopathy, hepatic steatosis, and cirrhosis are the most common, and all can lead to sudden death. Alcohol may also be a major factor in causing death by predisposing the individual to accidental trauma and by obscuring the effects of that trauma. This is particularly the case in head injuries when the changes in the level of consciousness are attributed to the effects of alcohol rather than an identified or unidentified head injury. Alcohol is also a gastric irritant and may precipitate vomiting when taken in excess. This, combined with the effects of decreased consciousness and the reduced laryngeal reflexes associated with intoxication may result in a signifi- cantly increased risk of aspiration of vomit into the airways and death. These deaths are the result of the intoxicated individual moving into or being placed or left in a position that impedes respiration either by occlusion 338 Shepherd of the external respiratory orifices or the internal airways (particularly the larynx) or restricts the free movement of the chest wall. These positions may result from lying face down on a bed, marked extension or flexion of the neck, or lying across an edge with the head down. Deaths resulting from impairment of respiration in this manner classically result in profound asphyxial changes involving the upper body, and these deaths are ascribed to postural asphyxia. Given the speed with which an individual under the influence of alcohol can die from either the aspiration of vomit or postural asphyxia, it is doubtful if a police station cell is the correct environment for his or her recovery from intoxication. Drugs Drug use is now so ubiquitous in Western society that any examination of a potential detainee by a forensic physician must include a careful evaluation of drug use whether in the past or recently. The skill of the forensic physician will undoubtedly be stretched to the full in the evaluation of the history given, and this is discussed fully in Chapter 10. The failure to identify a drug abuser who then suffers from withdrawal while in custody is just as potentially life-threat- ening as the failure to continue a detainee’s prescribed medication. In terms of deaths in custody, all drug use, whether social, abusive, or therapeutic, is relevant (13), and the possibility that a detainee may have abused just one drug or a combination of drugs with or without alcohol before death must be positively excluded. Some laboratories will also examine samples of bile and/ or liver to detect evidence of previous drug abuse. The management of acute drug intoxication is a matter of clinical judg- ment, but with adequate medical care, it is unlikely that, except in exceptional circumstances, drug intoxication alone will to lead to sudden death in custody. Baton Blows Blows from a baton are usually easily identified because forceful blows produce the classic “tram line”-type injuries on the skin.
Having just one of these conditions increases your risk of disease buy oxytrol 2.5mg free shipping, but having them in combination multiplies the risk signiﬁcantly purchase oxytrol 5mg without prescription. Ac- M cording to research generic 2.5 mg oxytrol fast delivery, those who have three features of metabolic syndrome are nearly twice as likely to have a heart attack or stroke and more than three times as likely to develop heart disease as are those with no features. There is a great deal of research focused on this problem as it is affecting a grow- ing number of our population. According to reports, over half of people over age 60 meet the criteria for metabolic syndrome, and overall about 25 percent of the entire population are classiﬁed as having metabolic syndrome. Researchers believe that insulin resistance is the key underlying cause of this syn- drome and responsible for the metabolic changes that occur. Insulin is the hormone secreted by the pancreas that takes glucose from your blood and moves it into the cells to be used for energy. In people with insulin resistance, cells don’t respond to insulin and glucose can’t enter the cells. The pancreas reacts by releasing more and more insulin to help glucose get into your cells. High insulin levels also promote fat storage around the belly, lead- ing to abdominal obesity. These combined factors greatly increase one’s risk of heart disease, stroke, diabetes, and other conditions. The key to the management of metabolic syndrome and the prevention of its con- sequences is to address insulin resistance. This can be done effectively with lifestyle strategies (diet, exercise, and supplements). Over half of children who are obese have the features of metabolic syn- drome, putting them at signiﬁcant risk of heart disease, diabetes, and premature death. Studies have shown, however, that in as little as 12 weeks, regular exercise and healthy eating can facilitate weight loss and improve blood pressure, cholesterol, and blood sugar. Medications can be used to lower blood pressure, cholesterol, triglycerides, and blood sugar and to improve insulin sensitivity. As discussed below, a low-glycemic diet and regular activity can greatly improve insulin sensitivity and the other features of this syndrome. Cinnamon contains com- pounds that work with insulin to reduce blood sugar levels. It is found in brewer’s yeast, whole grains (especially wheat germ), onions, and garlic. Foods to avoid: • Alcohol can cause either high or low blood sugar depending on how much you drink and if you are eating while drinking. M • Saturated fat (animal products such as meat and dairy) and trans fats (hydrogenated margarine) and deep-fried foods can worsen blood glucose control. Lifestyle Suggestions • Exercise regularly as this can help improve insulin sensitivity and help with weight loss. Aim for 30 minutes to one hour of moderate-intensity activity daily such as brisk walking, cycling, or swimming. Muscle burns more calories than fat and helps your body use blood sugar and insulin more efﬁciently. Try different strength-training exercises that focus on the core muscle groups: chest, back, shoulders, abdominals, and quadriceps. Losing even 5–10 percent of excess weight can help improve insulin sensitivity and reduce blood pressure and cholesterol. Top Recommended Supplements Since metabolic syndrome is a collection of medical disorders, recommendations vary depending on which factors are present. Below are some general recommendations for supplements that address a few of the features of metabolic syndrome. For speciﬁc recom- mendations on supplements for obesity, diabetes, high blood pressure, and cholesterol, refer to those sections of this book. Fish oils: Help improve glucose tolerance, reduce triglycerides and cholesterol levels, and reduce inﬂammation. Studies have shown that ﬁsh oils play an important role in protection against heart disease. Studies involving ﬁbre supplements of psyllium, oat bran, and glucomannan have shown beneﬁts for diabet- ics. Studies have shown that it can lower after-meal blood sugar levels, reduce triglycerides, and help promote weight loss. Studies have shown that it can improve blood glucose control and reduce diabetic complications. Vitamin E: Helps improve glucose tolerance and reduce glycosylation (binding of sugar to proteins in blood vessels). It also helps reduce blood clotting, and as an antioxidant, it may M help protect against heart disease. Eat small, frequent meals with low-glycemic, high-ﬁbre carbohydrates, protein, and healthy fats. For some people, migraines are preceded or accompanied by a sensory warning sign, called an aura, such as ﬂashes of light, wavy lines, blind spots, or tingling in M your arm or leg. A migraine attack may last for just a few minutes or continue for up to several days. Episodes can vary in frequency from several times in one week to once every few years. It is thought that migraines may be caused by changes in the nervous system (af- fecting the trigeminal nerve pathway) and by imbalances in neurotransmitters (brain chemicals) such as serotonin, which plays a regulatory role for pain messages going through this pathway. Researchers believe this causes the trigeminal nerve to release substances called neuropeptides, which travel to your brain’s outer covering (meninges) and cause blood vessels to become dilated and inﬂamed. There are drugs that can abort a headache, and various natural products that can reduce the severity and frequency of headaches. An aura may cause you to see sparkling ﬂashes of light, changes in vision (wavy lines and blind spots), tingling, and pins and needles sensation in one arm or leg and, less commonly, weakness or difﬁculty in speaking. Several hours or a day before the headache, some people experience a prodrome—feelings of elation or intense energy, cravings for sweets, thirst, drowsiness, irritability, or depression. The choice of treatment depends on the frequency and severity of your headaches and other existing medical problems. Codeine and other narcotic pain relievers can be addictive and cause constipation and other problems, so they should be used only when absolutely necessary. These drugs are rapid acting and effective in relieving the pain, nausea, and sensitivity to light. Examples include sumatriptan (Imitrex), rizatriptan (Maxalt), naratriptan (Amerge), and zolmitriptan (Zomig). There are drugs that can be taken regularly to prevent migraines (reduce the frequency). Examples include beta-blockers (propranolol), calcium channel blockers (verapamil), and antidepres- sants (amitriptyline and nortriptyline). These drugs can cause serious side effects, so speak to your doctor and pharmacist. Foods to avoid: • Food additives, preservatives, and dyes can trigger migraines (benzoic acid, tartrazine). Limit foods high in salt (snack foods, deli meats) and avoid using the salt shaker. Try an elimination diet to determine if food sensitivities are triggering your migraines (see Appendix D). This relaxation technique uses special equipment to teach you how to monitor and control certain physical responses, such as muscle tension. Do moderate-intensity activities (walking, swimming, and cycling) and warm up slowly because sudden, intense activity can trigger a headache. Record what you ate that day and any 334 factors that you feel could have triggered the event, such as stress, reaction to a smell, or light. This information will also be helpful to your doctor in determining a treatment strategy.
John’s wort can interact with birth control pills buy 2.5mg oxytrol fast delivery, but this interaction is controversial 2.5 mg oxytrol with amex, with three recent (2003-2008) studies finding no reduced contraceptive effect and two 21 showing lowered contraceptive efficacy oxytrol 2.5mg generic. The frequency of interaction is difficult to estimate, and a sixth recent study describes it as "unpredictable. In summary, there appears to be a potential interaction that decreases biologic activity of oral contraceptives, but this may vary depending on the birth control pill formulation and the St. John’s wort formulation (hypericin or hyperforin content) and possibly other factors. The studies are limited by small samples, but this is more than just anecdotal evidence. How likely a woman is to become pregnant from this interaction remains unclear, but there is enough evidence to warrant caution. In real life clinical practice, many people are taking additional medications for co-morbid medical conditions. Therefore, one cannot always generalize the findings from even a randomized study to the potential risks to patients being treated outside of a research trial. The most common adverse effects include gastrointestinal upset, skin reactions, fatigue/sedation, restlessness or anxiety, sexual dysfunction, dizziness, headache, and dry mouth. Studies suggest that side effects occur in 1 to 3% of patients and that this percentage is similar to placebo (and less than standard antidepressant 24 drugs). John’s wort includes: sensitivity to sunlight (danger of severe sunburn), rare, under 1% risk, and generally in light-skinned people or with use of antibiotics or birth control pills. Mischoulon and Rosenbaum report 17 cases of psychosis, but lesser disturbance is difficult to quantify. At these higher doses, Saint John’s wort causes more side effects, similar to Zoloft and increases the risk of interactions with medications. In the absence of a standardized formulation, dosages can only be considered as approximations. John’s wort and comparative assessment with other drugs -- require further investigation, as do the systematic tracking, reporting and quantification of adverse effects. John’s Wort for Depression – An Overview and Meta-analysis of Randomized Clinical Trials,” British Medical Journal 313(7052):253-258 (1996). John’s Wort: A Critical Evaluation of the Evidence for Antidepressant Effects,” in Natural Medications for Psychiatric Disorders: Considering the Alternatives, co-edited by David Mischoulon, M. On the two primary outcome measures, neither sertraline nor H perforatum was significantly different from placebo. Adverse-effect profiles for H perforatum and sertraline differed relative to placebo. John’s Wort with Oral Contraceptives: Effects on the Pharmacokinetics of Norethindrone and Ethinyl Estradiol, Ovarian Activity and Breakthrough Bleeding,” Contraception 71(6):402-8 (2005). It is available without a prescription in the United States and some other countries. Recent studies have shown promising potential for treatment of dementia, but those studies are preliminary and small. Accompanying use of a mood stabilizer is essential if there is any indication of mania or bipolar disorder. If it were not for the expense and the lack of insurance reimbursement, it would be preferred over most prescription antidepressants. It has been approved as a prescription drug for depression in Germany, Italy, Spain and Russia, and has been in use in Europe for over three decades. It functions as a methyl group donor, similar to folate, described in another chapter of this outline. They reviewed sixteen open trials, thirteen double-blind, placebo- controlled studies and nineteen double-blind controlled trials in comparison to standard 2 anti-depressants. However, they note that in the 2010 adjunctive use trial cited below, in which Dr. They also caution that use of a mood stabilizer is essential if there is any indication of mania or bipolar disorder. They are silent on adjunctive use, although the subsequent 2010 article co-authored by Mischoulon (below) supports adjunctive use. They point out that there is a wide range in dose requirements for response depending on the medication being augmented and the characteristics of the people receiving treatment. Doses will vary depending on the dose and effect of the antidepressant and the individual’s characteristics Larger and longer term studies are needed to confirm and extend the evidence of efficacy and absence of significant adverse drug interactions. Participants receiving the formulation demonstrated a clinically significant delay in decline in the Dementia Rating Scale and clock-drawing test as compared to those receiving placebo. Brown, Gerbarg and Mischoulon all dissent from the concern expressed about adjunctive use (see discussion above under that title) and levadopa. A careful psychiatric evaluation is the appropriate way to make this diagnosis Mild and transient anxiety, insomnia, loose bowels and heartburn are the only physical effects noted by Fugh-Berman and Cott. It is also better tolerated by elderly people and by people on medications that compromise liver function. Folate and omega-3 essential fatty acids are dealt with in separate chapters of this outline. However, they all caution that consumers who are elderly or frail, or have significant medication sensitivities, significant anxiety, serious gastrointestinal problems, or other serious medical conditions, should work up to these dosages. Consumers should be wary of purchasing “bargain brands,” because they are often of poor quality with less active ingredients. They should not be stored in the refrigerator to avoid condensation within the blister pack. Mischoulon concludes that it is one of the safer of the natural products available for mood disorders, and previous evidence is supportive of its use for depression and anxiety. These side effects are usually moderate and often abate or disappear once a steady dosage is achieved. One researcher cautions that absent testing, tryptophan cannot be presumed to be safe, but others advise that while prescription tryptophan is now safe, consumers should be careful about purchasing non-prescription tryptophan. Tryptophan, an amino acid, is a precursor of serotonin and has been used since the 1970s to increase brain levels of serotonin. Small, mostly uncontrolled studies have shown positive effects in some depressed patients, but others have not. The reason proposed for the equivocal effects is that tryptophan by itself may be insufficient to boost serotonin levels. There are also considerable data suggesting that tryptophan depletion can increase depressive symptoms in patients with major depression and seasonal affective disorder. Subsequent reversal of depression with intravenous tryptophan supports the notion of an antidepressant effect. Its use declined dramatically when tryptophan was banned, but it is making a strong comeback. There are no published studies of these uses, with the exception of Lake and Spiegel’s reference to insomnia treatment. Lake and Spiegel state that, “doses up to 600 mg have been shown to be effective in treating 7 insomnia but may increase the incidence of vivid dreams. Serotonin syndrome may theoretically occur with any drug that affects the serotonin system. Gastrointestinal effects are usually moderate and often abate or disappear once a steady dosage is achieved, and Lake and Spiegel recommend an enteric coating to minimize gastrointestinal side effects. Most patients had arthralgia (73%), rash (50%), cough or dyspnea (59%), peripheral edema (59%) elevated aldolase levels (46%) and elevated liver function tests (43%). Fugh-Berman cautions that absent testing, tryptophan cannot be presumed to be safe. However, excluding the one established contamination case, according to a 2004 review by Das et al. Research needs to consider long-term as well as short-term effects and needs to catch up with consumer use. Three of the eight sources discussing valerian decline to recommend its use for sleep disorders, citing inadequate evidence, despite its traditional use in the United States, Europe and Japan. In the sleep laboratory, the effects of valerian were not significantly different from those of placebo, and a 2007 meta-analysis concluded that no rigorous studies had found any significant effect of valerian on sleep. There is not enough scientific evidence to determine whether valerian works for anxiety (the sources are split 3 to 3 on the use of valerian for anxiety) or for other conditions, such as headaches, depression, menopausal symptoms, sedation, irregular heartbeat and trembling.
Hydantoins (phenytoin discount 5 mg oxytrol with mastercard, mephenytoin proven oxytrol 5 mg, ethotoin) These treat grand mal (tonic-clonic) seizures and psychomotor seizures purchase oxytrol 2.5 mg free shipping. Barbiturates (Phenobarbital, mephobarbital, primidone) These are used for treating grand mal and acute episodes or status epilepticus; meningitis, toxic reactions, and eclampsia Succinimides (ethosuximide) These are used to treat absence seizures and may be used in combination with other anticonvulsants. Oxazolidones (trimethadione) This is used to treat petit mal seizures and may be used in combination with other drugs or singly for treating refractory petit mal seizures. Benzodiazepines (diazepam, clonazepam) These are effective in controlling petit mal seizures. Carbamazepine This is effective in treating refractory seizure disorders that have not responded to other anticonvulsant therapies. It is also used to control grand mal and partial seizures and a combination of these seizures. Valproate (valproic acid) This is used to treat petit mal, grand mal, and mixed types of seizures. It can suppress the sodium influx by binding to the sodium channel pro- longing the channel’s inactivation and preventing neurons from firing. Antipsychotics Psychosis is a disorder that is characterized by a number of symptoms. These include difficulty processing information and reaching a conclusion; experienc- ing delusions or hallucinations; being incoherent or in a catatonic state; or demonstrating aggressive violent behavior. Schizophrenia is a chronic psychotic disorder where patients exhibit either positive or negative symptoms. Positive symptoms are exaggeration of normal function such as agitation, incoherent speech, hallucination, delusion, and paranoia. Negative symptoms are characterized by a decrease or loss of motiva- tion or function such as social withdrawal, poor selfcare, and a decrease in the content of speech. Psychosis is caused by an imbalance in the neurotransmitter dopamine in the brain. Antipsychotic medication, also known as dopamine antagonists, block the D2 dopamine receptors in the brain thereby reducing the psychotic symptoms. A number of antipsychotic medications block the chemoreceptor trigger zone and vomiting (emetic) center of the brain. Although blocking dopamine improves the patient’s thought processes and behavior, it can cause side effects. These include symptoms of Parkinsonism (see Parkinsonism previously dis- cussed in this chapter). Patients who undergo long-term treatment for psychosis using antipsychotic medications also might be prescribed drugs to treat the symptoms of Parkinsonism. The typical category of antipsychotic med- ication is further subdivided into phenothiazines and nonphenothiazines. Phenothiazines block norepinephrine causing sedative and hypotensive effects early in treatment. Nonphenothiazines include butyrophenone haloperidol (Haldol) whose phar- macologics are similar to phenothiazines as it alters the effects of dopamine by blocking the dopamine receptor sites. Included in this group are prochlorperazine (Compazine), fluphenazine (Prolixin), perphenazine (Trilafon), and trifluoperazine (Stelazine). These have replaced sedatives that were traditionally used because they have fewer and less potent side effects, especially if an overdose of the medication is given to the patient. Anxiolytics are prescribed when the patient’s anxiety reaches a level where the patient becomes disabled and is unable to perform normal activities. Anxiolytics have a sedative-hypnotic effect on the patient, but not an antipsychotic effect. Primary anxiety is not caused by a medical condition or drug use but may be sit- uational. Anxiolytics are usually not administered for secondary anxiety unless the sec- ondary cause is severe or untreatable. Benzodizepines include chlordiazepoxide (Librium), diazepam (Valium), chlorazepatge dipotassium (Tranxene), oxazepam (Serax), lorazepam (Ativan), and alprazolam (Xanax). Depression About 20% of Americans are depressed; however, one-third receives medical or psychiatric help for their depression. Depression is characterized by mood changes and loss of interest in normal activities. Patients who are depressed might have insomnia, fatigue, a feeling of despair, and an inability to concen- trate. Depression is caused by a number of factors including genetic predisposition, social and environmental factors, and biologic conditions such as insufficient monoamine neurotransmitter (norepinephrine and serotonin). Causes of major depression can include genetic predisposition, social and environmental factors, and biologic conditions. Antidepressants are used to treat depressions, however they also can mask sui- cidal tendencies (Table 15-3). They do not cause hypotension, sedation, anticholinergic effects, or cardiotoxi- city. A n t i c h o l i n e r g i c I n s o m n i a / C a t e g o r y e f f e c t S e d a t i o n H y p o t e n s i o n G I d i s t r e s s C a r d i o t o x i c i t y S e i z u r e s A g i t a t i o n T r i c y c l i c A n t i d e p r e s s a n t s A m i t r i p t y l i n e ( E l a v i l ) + + + + + + + + + + + – + + + + + + + – C l o m i p r a m i n e ( A n a f r a n i l ) + + + + + + + + + + – + + + + + + – D e s p r a m i n e ( N o r p r a m i n ) + + + + + – + + + + + D o x e p i n ( S i n e q u a n ) + + + + + + + + + – + + + + – I m i p r a m i n e ( T o f r a n i l ) + + + + + + + + + + + + + + + + + N o r t r i p t y l i n e ( A v e n t y l ) + + + + + – + + + + + – P r o t r i p t y l i n e ( V i v a c t i l ) + + + + + + – + + + + + T r i m i p r a m i n e ( S u r m o n t i l ) + + + + + + + + + + – + + + + + + – S e l e c t i v e S e r o t o n i n R e u p t a k e I n h i b i t o r s F l u o x e t i n e ( P r o z a c ) – + – + + + – 0 / + + + F l u v o x a m i n e ( L u v o x ) – + + – + + + – – + + P a r o x e t i n e ( P a x i l ) – + – + + + – – + + S e r t r a l i n e ( Z o l o f t ) – + – + + + – – + + T a b l e 1 5 - 3. The enzyme monoamine oxidase inactivates norepinephrine, dopamine, epinephrine, and serotonin. Examples of these drugs includes isocarboxazid (Marplan), phenelzine sulfate (Nardil), and tranycypromine sulfate (Parnate). A list of drugs utilized in the treatment of depression is provided in the Appendix. Summary There are many medications that either interfere with impulses transmitted over the neural pathways or stimulate those impulses. Medications that interfere with impulses are called inhibitors and usually compete with neurotransmitters for receptor sites. That is, the medication gets to the receptor site before the neurotransmitters blocking the neurotransmitters from delivering the impulse to the receptor site. There are four major groups of medications that stimulate the central nervous system. Caffeine also stimu- lates the cerebral cortex and stimulates respiration by acting on the brain stem and medulla. Anorexiants inhibit appetite by stimulating the cerebral cortex and the hypothalamus. There are seven broad classifications of medications that depress the central nervous system. These are sedative-hypnotics, general and local anesthetics, anal- gesics, narcotic analgesics, anticonvulsants, antipsychotics, and antidepressants. Sedative-hypnotics diminish the patient’s physical and mental responses without affecting the patient’s consciousness. Local anesthetics block pain at the site where the medication is administered without affecting the patient’s consciousness. Narcotic analgesics are drugs that reduce pain and produce a state of stupor or drowsiness by blocking the transmission of pain signals in the brain. Psychosis is a disorder that is characterized by one of a number of symptoms such as difficulty processing information and reaching a conclusion. The next chapter continues our exploration of drugs that affect the central nervous system by examining narcotic agonists. Patients who experience migraines (a) can be treated with a combination of migraine medications. Selective blockers affect specific receptors while non-selective blockers affect multiple receptors. A local anesthetic blocks pain at the site where the medication is admin- istered without affecting the patient’s consciousness. The pill may be a narcotic agonist that blocks transmission of impulses from the site of the injury to the area of the brain that interprets pain. This chapter explores pain and how healthcare providers assess pain and manage pain.
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