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Pharmacotherapy for adults with alcohol use disorders in outpatient settings: a systematic review and meta-analysis asthma without status asthmaticus singulair 10 mg with amex. Heterogeneity of alcohol use disorder: understanding mechanisms to advance personalized treatment asthmatic bronchitis 3 times order singulair from india. Alcohol abuse: critical pathophysiological processes and contribution to disease burden asthma symptoms 8 days order generic singulair. Consistency of retrospective reports of DSM-IV criterion A traumatic stressors among substance use disorder patients asthma symptoms or anxiety purchase singulair 5mg without prescription. A review of the interactions between alcohol and the endocannabinoid system: implications for alcohol dependence and future directions for research. Alcohol consumption, drinking patterns, and ischemic heart disease: a narrative review of meta-analyses and a systematic review and meta-analysis of the impact of heavy drinking occasions on risk for moderate drinkers. Long-term efficacy, tolerability and safety of nalmefene as-needed in patients with alcohol dependence: a 1-year, randomised controlled study. Profound decreases in dopamine release in striatum in detoxified alcoholics: possible orbitofrontal involvement. Converging patterns of alcohol use and related outcomes among females and males in the United States, 2002 to 2012. Alcohol intake and risk of stroke: a dose-response metaanalysis of prospective studies. The first state is dependence, or "physical" dependence, produced when there is progressive pharmacological adaptation to the drug resulting in tolerance. If the drug is abruptly stopped, a withdrawal syndrome ensues in which the adaptive responses are now unopposed by the drug. The appearance of withdrawal symptoms is the cardinal sign of "physical" dependence. Addiction, the second abnormal state produced by repeated drug use, occurs in only a minority of those who initiate drug use; addiction leads progressively to compulsive, out-of-control drug use. Activation of these circuits motivates normal behavior, and most humans simply enjoy the experience without being compelled to repeat it. For some (16% of those who try cocaine), the experience produces strong conditioned associations to environmental cues that signal the availability of the drug or the behavior. The individual becomes drawn into compulsive repetition of the experience, focusing on the immediate pleasure despite negative long-term consequences and neglect of important social responsibilities. The distinction between dependence and addiction is important because patients with pain sometimes are deprived of adequate opioid medication by their physician simply because they have shown evidence of tolerance or they exhibit withdrawal symptoms if the analgesic medication is stopped or reduced abruptly. The most recent revision of the classification system (Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition; see American Psychiatric Association, 2013) makes a clear distinction between normal tolerance and a drug use disorder involving compulsive drug seeking. Origins of Substance Use Disorders Most of those who initiate use of a drug with addiction potential do not develop a drug use disorder. Many variables operate simultaneously to influence the likelihood that a beginning drug user will lose control and develop an addiction. Agent (Drug) Variables Reinforcement refers to the capacity of drugs to produce effects that make the user wish to take them again. The more strongly reinforcing a drug is, the greater is the likelihood that the drug will be abused. Reinforcing properties of drugs are associated with their capacity to increase neuronal activity in brain reward areas (see Chapters 13 and 14). Cocaine, amphetamine, ethanol, opiates, cannabinoids, and nicotine reliably increase extracellular fluid DA levels in the ventral striatum, specifically the nucleus accumbens region. Despite strong correlative findings, a precise causal relationship between DA and euphoria/ dysphoria has not been established, and other findings emphasize additional roles of 5HT, glutamate, NE, endogenous opioids, and GABA in mediating the reinforcing effects of drugs. When coca leaves are chewed, cocaine is absorbed slowly; this produces low cocaine levels in the blood and few, if any, behavioral problems. Simply inhaling the vapors produces blood levels comparable to those resulting from intravenous cocaine owing to the large surface area for absorption into the pulmonary circulation following inhalation. Thus, inhalation of crack cocaine is much more addictive than chewing, drinking, or sniffing cocaine. This does not imply that the pharmacological addiction liability of nicotine is twice that of cocaine. Rather, there are other variables listed in Table 24-1 in the categories of Agent. Centers for Disease Control and Prevention CNS: central nervous system DA: dopamine DAT: dopamine transporter DEA: Drug Enforcement Agency DMT: N, N-dimethyltryptamine DOM: dimethoxymethylamphetamine EEG: electroencephalogram FDA: U. The risk of addiction is specific to the drug indicated and refers to the percentage who met criteria for addiction among those who reported having used the agent at least once. Comparative epidemiology of dependence on tobacco, alcohol, controlled substances and the inhalants: basic findings from the National Comorbidity Survey. The National Institute on Drug Abuse conducted a related study in 2014: available at. Polymorphism of genes that encode enzymes involved in absorption, metabolism, and excretion of a drug and its receptor-mediated responses may contribute to the effects of the drug across the addiction cycle.
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Natural sleep produces a decrease in the sensitivity of the medullary center to CO2 asthma short definition cheap singulair line, and the depressant effects of morphine and sleep are at least additive definition asthma bronchiale im kindesalter generic 10mg singulair overnight delivery. Obstructive sleep apnea is considered to be an important risk factor for increasing the likelihood of fatal respiratory depression asthma and pregnancy singulair 10 mg line. Elderly patients are at greater risk of depression because of reduced lung elasticity asthma treatment cycle discount singulair 5mg visa, chest wall stiffening, and decreased vital capacity. Opiates may cause a greater depressant action in patients with chronic cardiopulmonary or renal diseases because they can manifest a desensitization of their response to increased CO2. Enhanced depression can also be noted in patients with COPD and sleep apnea secondary to diminished hypoxic drive. Because pain stimulates respiration, removal of the painful condition (as with the analgesia resulting from the therapeutic use of the opiate) will reduce the ventilatory drive and lead to apparent respiratory depression. Neuroendocrine Effects the regulation of the release of hormones and factors from the pituitary is under complex regulation by opiate receptors in the HPA axis. Broadly considered, morphine-like opioids reduce the release of a large number of HPA hormones (Armario, 2010). Sex Hormones In males, acute opiate therapy reduces plasma cortisol, testosterone, and gonadotrophins. Inhibition of adrenal function is reflected by reduced cortisol production and reduced adrenal androgens (DHEA). In both males and females, chronic therapy can result in endocrinopathies, including hypogonadotrophic hypogonadism. In men, this may result in decreased libido and, with extended exposure, reduced secondary sex characteristics. Prolactin release from the anterior pituitary is under inhib- itory control by DA released from neurons of the arcuate nucleus. MOR agonists act presynaptically on these DA-releasing terminals to inhibit DA release and thereby increase plasma prolactin. The effects of opiates on ADH Comparative Respiratory Effects of Different Opiates Numerous studies have compared morphine and morphine-like opioids with respect to their ratios of analgesic to respiratory-depressant activities, and most have found that when equianalgesic doses are used, there is no significant difference. Maximal respiratory depressant effects occur more rapidly with more lipid-soluble agents. Agents that have persistent kinetics, such as methadone, must be carefully monitored, particularly after dose incrementation. Respiratory depression produced by any opiate agonist can be readily reversed by delivery of an opiate antagonist. Opiate antagonist reversal in the somnolent patient is considered to be indicative of an opiate-mediated depression. It is important to remember that most opiate antagonists have a relatively short duration of action compared to an agonist such as morphine or methadone, and fatal "renarcotization" can occur if vigilance is not exercised. These hormones are synthesized in the perikarya of the magnocellular neurons in the paraventricular and supraoptic nuclei of the hypothalamus and released from the posterior pituitary (Chapter 42). KOR agonists inhibit the release of oxytocin and ADH and cause prominent diuresis. Note, however, that agents such as morphine may yield a hypotension secondary to histamine release; this would, by itself, promote ADH release. Miosis the MOR agonists induce pupillary constriction (miosis) in the awake state and block pupillary reflex dilation during anesthesia. The parasympathetic outflow from the Edinger Westphal nucleus activates parasympathetic outflow through the ciliary ganglion to the pupil, producing constriction. Opiates block this GABAergic interneuron-mediated inhibition, leading to increased parasympathetic outflow (Larson, 2008). At high doses of agonists, the miosis is marked, and pinpoint pupils are pathognomonic; however, marked mydriasis will occur with the onset of asphyxia. While some tolerance to the miotic effect develops, addicts with high circulating concentrations of opioids continue to have constricted pupils. Therapeutic doses of morphine increase accommodative power and lower intraocular tension in normal and glaucomatous eyes (Larson, 2008). Seizures and Convulsions In older children and adults, moderately higher doses of opiates produce EEG slowing. In the newborn, morphine can produce epileptiform activity and occasionally seizure activity (Young and da Silva, 2000). Several mechanisms are likely involved in these excitatory actions: Inhibition of inhibitory interneurons. Morphine-like drugs indirectly excite certain groups of neurons, such as hippocampal pyramidal cells, by inhibiting the inhibition otherwise exerted by GABAergic interneurons (McGinty, 1988). Opiates may interact with receptors coupled through both inhibitory and stimulatory G proteins, with the inhibitory coupling but not the excitatory coupling showing tolerance with continued exposures (King et al. The metabolites of several opiates (morphine-3-glucuronide, normeperidine) have been implicated in seizure activity (Seifert and Kennedy, 2004; Smith, 2000).
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Diuretics cause a significant reduction in mortality and the risk of worsening heart failure asthma symptoms without wheezing purchase 10 mg singulair overnight delivery, as well as an improvement in exercise capacity asthma definition hyperbole buy singulair 5mg without prescription. Although furosemide is the most commonly used loop diuretic for the treatment of heart failure asthma x-ray image discount singulair 10mg with amex, patients with heart failure have fewer hospitalizations and better quality of life with torsemide than with furosemide asthma severity classification singulair 5mg otc, perhaps because of its more reliable absorption and due to other ancillary pharmacological effects (Buggey et al. Although diuretics are used widely for treatment of hypertension (see Chapter 28), in patients with normal renal function, Na+-K+-2Cl- symport inhibitors are not considered first-line diuretics for the treatment of hypertension. This is due to the lower antihypertensive efficacy of loop diuretics in such patients and the lack of data demonstrating a reduction in cardiovascular events. However, in patients with a low GFR (<30 mL/min) or with resistant hypertension, loop diuretics are the diuretics of choice. The edema of nephrotic syndrome often is refractory to less-potent diuretics, and loop diuretics often are the only drugs capable of reducing the massive edema associated with this renal disease. Loop diuretics also are employed in the treatment of edema and ascites of liver cirrhosis; however, care must be taken not to induce volume contraction. In patients with a drug overdose, loop diuretics can be used to induce forced diuresis to facilitate more rapid renal elimination of the offending drug. Loop diuretics, combined with isotonic saline administration to prevent volume depletion, are used to treat hypercalcemia. Consequently, loop diuretics combined with hypertonic saline are useful for the treatment of life-threatening hyponatremia. Loop diuretics also are used to treat edema associated with chronic kidney disease, in which the dose-response curve may be right shifted, requiring higher doses of the loop diuretic. Loop diuretics, particularly furosemide, acutely increase systemic venous capacitance and thereby decrease left ventricular filling pressure. This effect, which may be mediated by PGs and requires intact kidneys, benefits patients with pulmonary edema even before diuresis ensues. High doses of inhibitors of Na+-K+-2Cl- symport can inhibit electrolyte transport in many tissues. This effect is clinically important in the inner ear and can result in ototoxicity, particularly in patients with preexisting hearing impairment. This may manifest as hyponatremia or extracellular fluid volume depletion associated with hypotension, reduced GFR, circulatory collapse, thromboembolic episodes, and, in patients with liver disease, hepatic encephalopathy. If dietary K+ intake is not sufficient, hypokalemia may develop, and this may induce cardiac arrhythmias, particularly in patients taking cardiac glycosides. Increased Mg2+ and Ca2+ excretion may result in hypomagnesemia (a risk factor for cardiac arrhythmias) and hypocalcemia (rarely leading to tetany). Loop diuretics should be avoided in postmenopausal osteopenic women, in whom increased Ca2+ excretion may have deleterious effects on bone metabolism. Loop diuretics can cause ototoxicity that manifests as tinnitus, hearing impairment, deafness, vertigo, and a sense of fullness in the ears. Ototoxicity occurs most frequently with rapid intravenous administration and least frequently with oral administration. To avoid ototoxicity, the rate of furosemide infusions should not exceed 4 mg/min. Ethacrynic acid appears to induce ototoxicity more often than do other loop diuretics and should be reserved for use only in patients who cannot tolerate other loop diuretics. Loop diuretics also can cause hyperuricemia (occasionally leading to gout) and hyperglycemia (infrequently precipitating diabetes mellitus) and can increase plasma levels of LDL cholesterol and triglycerides while decreasing plasma levels of HDL cholesterol. Other adverse effects include skin rashes, photosensitivity, paresthesias, bone marrow depression, and GI disturbances. Contraindications to the use of loop diuretics include severe Na+ and volume depletion, hypersensitivity to sulfonamides (for sulfonamide-based loop diuretics), and anuria unresponsive to a trial dose of loop diuretic. The class now includes diuretics that are benzothiadiazine derivatives (thiazide or thiazide-type diuretics) and drugs that are pharmacologically similar to thiazide diuretics but differ structurally (thiazide-like diuretics). Thiazide diuretics inhibit NaCl transport in the DCT; the proximal tubule may represent a secondary site of action. Free energy in the electrochemical gradient for Na+ is harnessed by a Na+-Cl- symporter in the luminal membrane that moves Cl- into the epithelial cell against its electrochemical gradient. Thiazide diuretics inhibit the Na+-Cl- symporter (called ENCC1 or TSC) that is expressed predominantly in kidney and localized to the apical membrane of DCT epithelial cells. Mutations in the Na+-Cl- symporter cause a form of inherited hypokalemic alkalosis called Gitelman syndrome. Some thiazide diuretics also are weak inhibitors of carbonic anhydrase, an effect that increases HCO3 and phosphate excretion and probably accounts for their weak proximal tubular effects. Inhibitors of Na+-Cl- symport increase K+ and titratable acid excretion by the same mechanisms discussed for loop diuresis. However, uric acid excretion is reduced following chronic administration by similar mechanisms discussed for loop diuretics. In addition, thiazides may be transported from the basolateral compartment to the luminal compartment via the OAT4 antiporter in the apical membrane (Palmer, 2011; see Chapter 5). Acute effects of inhibitors of Na+-Cl- symport on Ca2+ excretion are variable; when administered chronically, thiazide diuretics decrease Ca2+ excretion.
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