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Drugs commonly assigned to this body image 480 mg bactrim with mastercard, and to some extent buy 960 mg bactrim otc, minor stimulant ef- class include lysergic acid diethylamide (LSD), mesca- fects. Sometimes the dreamlike quality of the experi- line (derived from the peyote cactus), and psilocybin ence produces relaxation, good humor, and a sense of (derived from a mushroom). For this reason the term is sometimes used in- the use of the hallucinogen may have drug-induced anx- terchangeably with psychedelic or psychotomimetic, the iety, panic, or even paranoid ideation. The loss of indi- latter term representing the CNS effects beyond the hal- viduality can be perceived as a disintegration of the per- lucination itself. Even if the drug lucinogen are inadequate, but it should be used to signify experience initially is euphoric, tremendous mood substances that consistently produce changes in sensory swings can occur and suddenly plunge the abuser into perception, thought, and mood. These negative phe- drug that reliably produces alterations in perceptions as nomena are not always precipitated by an unexpected a primary effect. Drugs that should not be included are or sudden frightful event but can be a function of the la- those that produce alterations in sensory perception bile mood induced by the drug. Other types of classified as an hallucinogen if it has other properties as hallucinations are possible. Several drugs that reliably alter mood at low doses volves the belief by the individual that the (altered) sen- and produce altered sensory perceptions at slightly sations and perceptions actually represent reality. These drugs that also reliably lated drugs retains the ability to test reality versus illu- produce differing degrees of CNS stimulation in a dose- sion and knows that the experience is not real. Thus, the 418 IV DRUGS AFFECTING THE CENTRAL NERVOUS SYSTEM typical drug-induced hallucinatory state would be more Tolerance and Dependence appropriately termed a pseudohallucination, though Tolerance to the effects of hallucinogens develops rap- real hallucinations are possible. In fact, a high degree of tolerance can be produced chotomimetic changes are those considered to be after as few as three to four daily doses of drug. These effects are somewhat more Generally, the abuser self-imposes the requirement for variable than the hallucinatory effects or changes in a 2- to 3-day drug-free period before another drug ses- sensory perception. Additionally, there is a tremendous degree of LSD, they seem to be more common with other specific cross-tolerance between the hallucinogens, so other hallucinogens, such as MDMA and MDA. LSD-like hallucinogens cannot be abused during the MDMA (XTC, or ecstasy) possesses hallucinogenic drug-free period either. One danger with the stimulant activity similar to that of mescaline but also produces subclass of hallucinogens is rapid development of toler- stimulant activity similar to that of amphetamine. Despite ity to communicate with others, increases the degree of the apparent overlap of effects with stimulant drugs, intimacy one feels toward others in the surroundings, in- however, there is no cross-tolerance with the CNS stim- creases self-esteem and mood, and generally appears ulants such as amphetamine. One during drug abstinence, nor is there a tremendous crav- residual effect of abuse is the MDMA hangover, which ing for drug during the drug-free period. Therefore, is the occurrence on the second day after abuse of clearly no dependence is attributed to the hallucinogens. Typically, a dose of 75 mg produces the pri- mary psychotomimetic effects, while a dose of 150 mg Treatment Strategies produces LSD-like effects, and a dose of 300 mg pro- The difference between the abused and the lethal dose duces amphetaminelike CNS stimulation. The amphet- of LSD is very large, so little pharmacological interven- aminelike stimulation of the CNS and periphery is tion is necessary. The effects Treatment of PCP intoxication also involves limiting that can be produced by stimulatory doses of hallucino- external stimuli, minimizing lighting, noise, and unneces- gens include tachycardia, hypertension, and arrhyth- sary physical contact. It induces a wide variety of psychotomimetic and hallucinatory effects during emergence from anes- Mechanism of Action thesia. At a low dose, individuals believe they are thinking the hallucinogens is the activation of the 5-HT2-receptor. Other happiness, though (especially at higher doses) the indi- drugs, such as MDMA, induce the release of endogenous vidual can vacillate between euphoria and depression. At higher doses the stimulatory effects are more pronounced and the likelihood of tremendous mood swings more likely. INHALANTS At near anesthetic doses, it produces more typical de- pressant effects, including motor incoordination, Volatile chemicals and gases that produce behavioral ef- catalepsy, vacant stare, or even amnesia. The two derivatives are referred to as drugs in that it is confined primarily to juveniles and China White and are 900 and 1,100 times as potent as young adults. Meperidine has also been used as a template trous oxide by young medical professionals who have for preparing synthetic heroin, the end product being ready access to this agent. However, MPPP is sometimes contaminated with the Deaths occur occasionally by individuals inhaling ni- side reaction product 1-methyl,4-phenyl-1,2,3,6-tetra- trous oxide alone.

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Access to the lung or medi- astinum is then gained though the intercostal space bactrim 960mg discount, which can be opened out considerably owing to the elasticity of the thoracic cage generic 480 mg bactrim with amex. The diaphragm The diaphragm is the dome-shaped septum dividing the thoracic from the abdominal cavity. It comprises two portions: a peripheral muscular part which arises from the margins of the thoracic outlet and a centrally placed aponeurosis (Fig. The right crus arises from the front of the bodies of the upper three lumbar vertebrae and intervertebral discs; the left crus is only attached to the first two verte- brae. The arcuate ligaments are a series of fibrous arches, the medial being a thickening of the fascia covering psoas major and the lateral of fascia overly- ing quadratus lumborum. The fibrous medial borders of the two crura form a median arcuate ligament over the front of the aorta. The central tendon, into which the muscular fibres are inserted, is trefoil in shape and is partially fused with the undersurface of the pericardium. The diaphragm receives its entire motor supply from the phrenic nerve (C3, 4, 5) whose long course from the neck follows the embryological migration of the muscle of the diaphragm from the cervical region (see below). Injury or operative division of this nerve results in paralysis and elevation of the corresponding half of the diaphragm. Radiographically, paralysis of the diaphragm is recognized by its eleva- tion and paradoxical movement; instead of descending on inspiration it is forced upwards by pressure from the abdominal viscera. The sensory nerve fibres from the central part of the diaphragm also run in the phrenic nerve, hence irritation of the diaphragmatic pleura (in pleurisy) or of the peritoneum on the undersurface of the diaphragm by subphrenic collections of pus or blood produces referred pain in the corre- sponding cutaneous area, the shoulder-tip. The peripheral part of the diaphragm, including the crura, receives sensory fibres from the lower intercostal nerves. The thoracic cage 15 Oesophagus Inferior vena cava Left phrenic nerve Right phrenic nerve Vagi Right splanchnic Aorta nerve Left splanchnic nerve Subcostal nerve Transverse abdominis muscle Quadratus lumborum muscle Sympathetic trunk Psoas major muscle Fig. The three major orifices, from above downwards, transmit the inferior vena cava, oesophagus and aorta. Openings in the diaphragm The three main openings in the diaphragm (Figs 10, 11) are: 1the aortic (at the level of T12) which transmits the abdominal aorta, the thoracic duct and often the azygos vein; 2the oesophageal (T10) which is situated between the muscular fibres of the right crus of the diaphragm and transmits, in addition to the oesopha- gus, branches of the left gastric artery and vein and the two vagi; 3the opening for the inferior vena cava (T8) which is placed in the central tendon and also transmits the right phrenic nerve. In addition to these structures, the greater and lesser splanchnic nerves (see page 49) pierce the crura and the sympathetic chain passes behind the diaphragm deep to the medial arcuate ligament. The development of the diaphragm and the anatomy of diaphragmatic herniae The diaphragm is formed (Fig. The septum transversum is the mesoderm which, in early develop- ment, lies in front of the head end of the embryo. With the folding off of the head, this mesodermal mass is carried ventrally and caudally, to lie in its 16 The Thorax Fig. This drawing shows the four elements contributing to the diaphragm—(1) the septum transversum, (2) the dorsal mesentery of the oesophagus, (3) the body wall and (4) the pleuroperitoneal membrane. During this migra- tion, the cervical myotomes and nerves contribute muscle and nerve supply respectively, thus accounting for the long course of the phrenic nerve (C3, 4 and 5) from the neck to the diaphragm. With such a complex embryological story, one may be surprised to know that congenital abnormalities of the diaphragm are unusual. However, a number of defects may occur, giving rise to a variety of con- genital herniae through the diaphragm. These may be: 1through the foramen of Morgagni; anteriorly between the xiphoid and costal origins; 2through the foramen of Bochdalek— the pleuroperitoneal canal— lying posteriorly; 3through a deficiency of the whole central tendon (occasionally such a hernia may be traumatic in origin); 4through a congenitally large oesophageal hiatus. Far more common are the acquired hiatus herniae (subdivided into sliding and rolling herniae). These are found in patients usually of middle age where weakening and widening of the oesophageal hiatus has occurred (Fig. In the sliding hernia the upper stomach and lower oesophagus slide upwards into the chest through the lax hiatus when the patient lies down or bends over; the competence of the cardia is often disturbed and peptic juice can therefore regurgitate into the gullet in lying down or bending over. This may be followed by oesophagitis with consequent heartburn, bleeding and, eventually, stricture formation. In the rolling hernia (which is far less common) the cardia remains in its normal position and the cardio-oesophageal junction is intact, but the fundus of the stomach rolls up through the hiatus in front of the oesopha- gus, hence the alternative term of para-oesophageal hernia. The movements of respiration During inspiration the movements of the chest wall and diaphragm result in an increase in all diameters of the thorax. This, in turn, brings about an increase in the negative intrapleural pressure and an expansion of the lung tissue.

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At the more complicated parasympathetic ganglia bactrim 480 mg low price, there is a simple presynaptic synapses cheap bactrim 960mg on-line, the release of ACh from preganglionic neurons to postsynaptic cell relationship; in others, the presyn- results in the appearance of complex postsynaptic po- aptic to postsynaptic cell relationship may involve neu- tential changes consisting of several temporally ar- rons interposed between the presynaptic and postsy- ranged components. At There is considerable diversity among nicotinic some autonomic ganglia, the SIF cell is a true interneu- acetylcholine receptors, and at least one source of this ron, receiving afferent innervation from preganglionic diversity is the multiplicity of acetylcholine receptor cholinergic neurons and forming efferent synapses with genes. At other autonomic ganglia, its cle are different from those in autonomic ganglia and function is not completely understood, but the SIF cell the central nervous system. Excitatory and Inhibitory Potentials Unlike the receptors at postganglionic neuroeffector junctions or at skeletal neuromuscular junctions, both The interaction of ACh with the postsynaptic nicotinic types of cholinergic receptors, that is, nicotinic and mus- receptor results in depolarization of the membrane, an 141 142 II DRUGS AFFECTING THE AUTONOMIC NERVOUS SYSTEM influx of Na and Ca through a neuronal nicotinic re- existence of these receptors provides a wide variety of ceptor channel, and the generation of the fast EPSP. Agonists This change in postsynaptic potential is principally re- for these receptors most likely reach the ganglia through sponsible for the generation of the propagated action the circulation. For simplic- eral presynaptic terminals innervate a single ganglion ity, the figure has been divided into a type A synapse, cell, and several preganglionic axon terminals must which includes SIF cells, and a type B synapse, which fire simultaneously for transmission to take place. The drugs the type of receptor mediating the response, and the pri- either interact with the nicotinic–cholinergic receptor mary transmitter or mediator that activates the receptor. Interaction of ACh with the postsynaptic ganglionic cell muscarinic receptor is responsible for slowly devel- GANGLIONIC STIMULANTS oping depolarization, the slow EPSP, which has a longer latency than the fast EPSP and a duration of 30 to 60 A variety of agents, including nicotine, lobeline, and di- seconds. The slow EPSP is due to inhibition of a voltage- methylphenyl piperazinium (DMPP), can stimulate gan- dependent K current called the M current, and inhibi- glionic nicotinic receptors. First, drugs such as nicotine that both M4 and M5) have been identified using functional stud- stimulate and block ganglionic receptors have proved ies and at least five subtypes (m1,m,m,m,2 3 4 and m5) valuable as an aid in identifying and localizing postgan- identified by molecular cloning techniques. In this case, acti- Mechanism of Ganglionic Stimulation vation of a muscarinic receptor on the SIF cells results in the release of a catecholamine; this in turn activates a Nicotine, lobeline, trimethylammonium, and DMPP receptor on the postganglionic cell, leading to the slow stimulate all autonomic ganglia by simple combination IPSP. The catecholamine most frequently released from with ganglionic nicotinic receptors on the postsynaptic SIF cells appears to be dopamine. This leads to membrane depolarization, an EPSP, lasting for 1 to 2 minutes, can be seen at some influx of sodium and calcium ions, and the generation of ganglionic synapses. These agents produce general stimulation now well established that there are a large number of of autonomic ganglia and a complex pattern of mixed peptides in the ganglia, including luteinizing hormone– sympathetic and parasympathetic responses. In addition to the cholinergic and adrenergic recep- Activation of nicotinic receptors on the plasma mem- tors on autonomic ganglion cells, there also appear to be brane of the cells of the adrenal medulla leads to the exo- receptors for a variety of excitatory and inhibitory sub- cytotic release of epinephrine and norepinephrine; stimu- stances, including angiotensin, bradykinin, histamine, lation of nicotinic receptors at the neuromuscular 5-hydroxytryptaimine (serotonin), and substance P. For simplicity, it has been divided into a type A synapse containing interneurons or small intensely fluorescent (SIF) cells and a type B synapse lacking interneurons. In the type A synapse, ACh is released from the preganglionic neuron and activates nicotinic and muscarinic receptors on the SIF cells (when present), leading to the release of a catecholamine, presumably dopamine. The insert depicts the temporal postganglionic action potential, consisting of a fast excitatory postsynaptic potential (EPSP) due to activation of nicotinic receptors by ACh, a slow inhibitory postsynaptic potential (IPSP) due to dopamine or another catecholamine activating the appropriate receptor, and a slow EPSP due to activation by ACh of an M1 muscarinic cholinergic receptor on the postganglionic nerve cell body. In this case, ACh activates both nicotinic receptors leading to the fast EPSP and muscarinic receptors leading to the slow IPSP and slow EPSP. Stimulation of nicotinic receptors in adren- ganglionic transmission produced by most ganglionic ergic nerve terminals leads to the release of norepineph- blocking agents, that is, a nondepolarizing competitive rine; and activation of nicotinic chemoreceptors in the antagonism, the blockade produced by nicotine consists aortic arch and carotid bodies causes nausea and vomit- of two phases. After a few seconds, however, this discharge stops and transmission is Mechanism of Ganglionic Blockade blocked. At this time, antidromic stimuli fail to induce an Large doses of nicotine produce a prolonged blockade action potential. Unlike the blockade of fail to respond to the administration of any ganglionic 144 II DRUGS AFFECTING THE AUTONOMIC NERVOUS SYSTEM stimulant, regardless of the type of receptor it activates. Central Nervous System The main reason for the loss of electrical or receptor- The actions of nicotine on the central nervous system mediated excitability during a period of maintained de- are the result of a composite of stimulatory and depres- polarization is that the voltage-sensitive sodium channel sant effects. These can include tremors, convulsions, res- is inactivated and no longer opens in response to a brief piratory stimulation or depression, and release of antid- depolarizing stimulus. Nausea and emesis all ganglionic stimulants that are not nicotinic, such as are frequently observed after the initial use of nicotine histamine, angiotensin, bradykinin, and serotonin, be- in the form of tobacco smoke. This is in contrast to the Phase 1 is followed by a postdepolarization phase effects of nicotine on the cardiovascular system, where (phase 2) during which only the actions of nicotinic re- tolerance develops much more slowly. The main factor responsible for phase 2 block Additional effects of nicotine include an increase in gas- appears to be desensitization of the receptor to ACh, tric acid secretion and an increase in the tone and motil- which causes transmission failure. These effects are pro- duced because of the predominance of cholinergic input Pharmacological Actions of Nicotine to these effector systems.

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Liver damage resulting from chronic abuse of ethanol In moderation purchase bactrim 960mg with mastercard, however bactrim 480mg lowest price, there is no evidence that the ju- can impair metabolism of a variety of drugs. Other Body Systems The ethanol content in the urine is normally about 130% of the blood concentration and is quite constant; In general, ethanol in low to moderate amounts, is rela- the expired air contains about 0. A moderate amount ethanol level, a concentration that also is remarkably of ethanol causes peripheral vasodilation, especially of consistent. On the other hand, ethanol consumption in high Mechanism of Action concentrations, as found in undiluted spirits, can induce A great deal of attention has been focused on a class of hemorrhagic lesions in the duodenum, inhibit intestinal proteins termed the ligand-gated ion channels as being brush border enzymes, inhibit the uptake of amino important to the mechanism of action of alcohol. This flux of ions largely determines the degree of ability to inhibit secretion of antidiuretic hormone from neuronal activity. Two distinct types of ligand-gated the posterior pituitary, which leads to a reduction in re- ion channels are particularly sensitive to concentrations nal tubular water reabsorption. Ethanol produces a number of depressant effects on Ethanol intoxication is probably the best-known form the myocardium. A seri- themselves and others, particularly if they attempt to ous clinical entity, alcoholic cardiomyopathy, has also drive or operate machinery. Ethanol intoxi- hibition of gastric secretion and irritation of the gastric cation is sometimes mistakenly diagnosed as diabetic mucosa. Ethanol irritates the entire gastrointestinal coma, schizophrenia, overdosage of other CNS depres- tract, which may lead to constipation and diminished sant drugs, or skull fracture. Other pathological effects in- monly associated with excessive ethanol consumption is clude pancreatitis and peripheral neuropathy. Hypothermia gonadal failure is often found in both men and women, frequently results, with body temperature falling toward accompanied by low blood levels of sex hormones. This problem can be A variety of pathological problems involving the particularly severe in the elderly, who normally have CNS have been described in chronic alcoholics, the difficulty regulating their body temperature. Brain damage from chronic the hangover, a condition characterized by headache, ethanol consumption can be especially severe in the nausea, sweating, and tremor. The fetal alcohol syndrome has three primary features: microcephaly, prenatal growth Treatment for Acute Intoxication deficiency, and short palpebral fissures. Other character- Generally, no treatment is required for acute ethanol in- istics include postnatal growth deficiency, fine motor toxication. Allowing the individual to sleep off the ef- dysfunction, cardiac defects, and anomalies of the exter- fects of ethanol ingestion is the usual procedure. A definite risk of producing Hangovers are treated similarly; that is, no effective fetal abnormalities occurs when ethanol consumption remedy exists for a hangover, except for controlling the by the mother exceeds 3 oz daily, the equivalent of amount of ethanol consumed. For example, prompt treat- ment is required if the patient is in danger of dying of Treatment for Alcoholism respiratory arrest, is comatose, has dilated pupils, is hy- pothermic, or displays tachycardia. The immediate concern in the treatment of alcoholics is Treatment for severe ethanol overdose is generally detoxification and management of the ethanol with- supportive. Once the patient is detoxified, long- lieved by intravenous administration of hypertonic term treatment requires complete abstinence, psychiatric mannitol. Hemodialysis can accelerate the removal of treatment, family involvement, and frequently support ethanol from the body. If ethanol is taken after disulfiram administration, blood acetalde- hyde concentrations increase 5 to 10 times, resulting in Alcoholism vasodilation, pulsating headache, nausea, vomiting, se- Alcoholism is among the major health problems in most vere thirst, respiratory difficulties, chest pains, orthosta- countries. In certain tive drugs, is expressed as drug-seeking behavior and is cases, marked respiratory depression, cardiac arrhyth- associated with a withdrawal syndrome that occurs after mias, cardiovascular collapse, myocardial infarction, abrupt cessation of drinking. The ethanol withdrawal acute congestive heart failure, unconsciousness, convul- syndrome is characterized by tremors, seizures, hyper- sions, and sudden death have been reported. Hepatic fatty infiltration and cirrhosis are common ticraving drugs, for example serotonin uptake inhibitors, 416 IV DRUGS AFFECTING THE CENTRAL NERVOUS SYSTEM dopaminergic agonists, and opioid antagonists. The only of the most abundant receptors in the CNS, and its dis- treatment that has shown considerable promise is one tribution within the brain reflects the pharmacological that uses the opioid antagonist naltrexone. High receptor densities in the extrapyramidal motor system and the cerebellum are consistent with the actions of cannabinoids on many MARIJUANA forms of movement.

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