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CRF-secreting neurons are wide- down-regulated by antidepressant drugs order v-gel 30 gm without a prescription, thus allowing in- spread in the CNS purchase v-gel 30gm amex, and CRF apparently functions as a neuro- CHAPTER 10 DRUGS FOR MOOD DISORDERS: ANTIDEPRESSANTS AND MOOD STABILIZERS 165 transmitter and mediator of the endocrine, autonomic, immune, stimulate the CNS can cause manic and hypomanic behaviors and behavioral responses to stress as well as a releasing that are easily confused with schizophreniform psychoses. Hypothalamic CRF is part of the hypothalamic-pituitary-adrenal (HPA) axis, which becomes hyperactive in depression. As a result, there is increased se- ANTIDEPRESSANT DRUGS cretion of CRF by the hypothalamus, adrenocortiocotropic hormone (ACTH) by the anterior pituitary, and cortisol by Drugs used in the pharmacologic management of depressive the adrenal cortex. The increased cortisol (part of the nor- disorders are derived from several chemical groups. Older mal physiologic response to stress) is thought to decrease antidepressants include the tricyclic antidepressants (TCAs) the numbers or sensitivity of cortisol receptors (down- and the monoamine oxidase inhibitors (MAOIs). This view is supported drugs include the selective serotonin reuptake inhibitors by animal studies indicating that antidepressant drugs re- (SSRIs) and several individual drugs that differ from TCAs, store the ability of cortisol receptors to bind with cortisol. General characteristics of antidepres- This alteration of cortisol receptors takes about two weeks, sants include the following: the approximate time interval required for the drugs to im- • All are effective in relieving depression, but they differ prove symptoms of depression. Secretion of both hypothala- • All must be taken for 2 to 4 weeks before depressive mic and extrahypothalamic CRF apparently returns to nor- symptoms improve. Many antidepressants and other drugs are me- Additional Factors tabolized by the 2D6 or 3A4 subgroup of the enzymes. Additional factors thought to play a role in the etiology of Thus, antidepressants may interact with each other and depression include the immune system, genetic factors, and with a wide variety of drugs that are normally metabo- environmental factors. Immune cells (eg, T lymphocytes and B lymphocytes) produce cytokines (eg, interleukins, interferons, and tumor necrosis factor), which affect neurotransmission. Possible Mechanisms of Action mechanisms of cytokine-induced depression include in- creased CRF and activation of the HPA axis, alteration of Although their actions are still being studied in relation to monoamine neurotransmitters in several areas of the brain, newer information about brain function and the etiology of or cytokines functioning as neurotransmitters and exerting mood disorders, antidepressant drugs apparently normalize direct effects on brain function. Changes endings, the molecules that are not bound to receptors are nor- have been identified in CRF, the HPA axis, and the noradren- mally inactivated by reuptake into the presynaptic nerve fibers ergic neurotransmission system, all of which are activated as that released them or metabolized by monoamine oxidase part of the stress response. Most antidepressants prevent the reuptake of multiple a hypersensitive or exaggerated response to later stressful neurotransmitters; SSRIs selectively inhibit the reuptake of events, including mild stress or daily life events.

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In HF generic v-gel 30gm mastercard, it is given concomitantly with a and endothelin receptor antagonists order v-gel 30 gm free shipping, are also presented. In atrial dysrhythmias, digoxin slows the rate of ventricular contraction (negative chronotropic effect). Negative chro- Digoxin notropic effects are probably caused by several factors. First, digoxin has a direct depressant effect on cardiac conduction Digoxin (Lanoxin) is the only commonly used digitalis gly- tissues, especially the atrioventricular node. In the following discussion, the terms digitalization creases the number of electrical impulses allowed to reach the and digitalis toxicity refer to digoxin. Third, increased efficiency of myocardial contraction and vagal stimulation decrease com- General Characteristics pensatory tachycardia that results from the sympathetic ner- When digoxin is given orally, absorption varies among avail- vous system response to inadequate circulation. Lanoxicaps, which are liquid-filled cap- sules, and the elixir used for children are better absorbed than Indications for Use tablets. With tablets, the most frequently used formulation, differences in bioavailability are important because a person The clinical uses of digoxin are management of HF, atrial fib- who is stabilized on one formulation may be underdosed or rillation, and atrial flutter. Digoxin may be used in acute or overdosed if another formulation is taken. Differences are at- chronic conditions, for digitalization, or for maintenance tributed to the rate and extent of tablet dissolution rather than therapy. In addition to drug dosage forms, other factors that may decrease digoxin absorption include the Contraindications to Use presence of food in the GI tract, delayed gastric emptying, malabsorption syndromes, and concurrent administration of Digoxin is contraindicated in severe myocarditis, ventricu- some drugs (eg, antacids, cholestyramine). It also crosses the placenta, and serum lev- syndrome (risk of fatal dysrhythmias), electrolyte imbal- els in neonates are similar to those in the mother. Digoxin cir- ances (hypokalemia, hypomagnesemia, hypercalcemia), and culates mainly in a free state, with only 20% to 30% bound renal impairment. How- Administration and Digitalization ever, toxicity may occur at virtually any serum level. Most (60% to 70%) of the digoxin is excreted unchanged Digoxin is given orally or intravenously (IV). Dosage must be reduced in the presence of be given intramuscularly, this route is not recommended be- renal failure to prevent drug accumulation and toxicity.

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Lidocaine may be used to treat ventricular dysrhythmias Hepatic impairment increases plasma half-life of several precipitated by cardiac surgery or digitalis toxicity v-gel 30 gm with visa. Class I antidysrhythmic drugs discount v-gel 30gm otc, and dosage usually should be re- or III drugs are usually started in a hospital setting, at lower duced. These include disopyramide, flecainide, lidocaine, dosage ranges, because of prodysrhythmic effects. Prodys- mexiletine, moricizine, procainamide, propafenone, quini- rhythmia is more common in children with structural heart dine, and tocainide. In general, serum levels Dosages of adenosine and ibutilide are unlikely to need should be monitored with class IA and IC drugs and IV lido- reductions in clients with hepatic impairment. Class III drugs are used in pediatrics mainly to treat life-threatening refractory tachydysrhythmias. Use in Critical Illness As in adults, most antidysrhythmic drugs and their metabolites are excreted through the kidneys and may accu- Critically ill clients often have multiple cardiovascular and mulate in children with impaired renal function. They may also have refractory dysrhythmias that re- quire strong, potentially toxic antidysrhythmic drugs. Thus, Cardiac dysrhythmias are common in older adults, but in gen- antidysrhythmic drugs are often given IV in critical care eral only those causing symptoms of circulatory impairment settings for rapid reversal of a fast rhythm. Compared IV or oral drugs may be given to prevent recurrence of the with younger adults, older adults are more likely to experi- dysrhythmia. Cautious use is required, and in preventing, recognizing, and treating conditions that predis- dosage usually needs to be reduced to compensate for heart pose to the development of serious dysrhythmias (eg, elec- disease or impaired drug elimination processes. If dysrhythmias cannot be prevented, early recognition and treatment are needed. Overall, any antidysrhythmic drug therapy in critically ill Use in Renal Impairment clients is preferably performed or at least initiated in critical care units or other facilities with appropriate equipment and Antidysrhythmic drug therapy in clients with renal impair- personnel. For example, nurses who work in emergency de- ment should be very cautious, with close monitoring of drug partments or critical care units must be certified in cardio- effects (eg, plasma drug levels, ECG changes, symptoms that pulmonary resuscitation and advanced cardiac life support may indicate drug toxicity). With ACLS, the American Heart Association and dysrhythmic drugs and their metabolites. As a result, decreased others have developed algorithms to guide drug therapy of renal perfusion or other renal impairment can reduce drug dysrhythmias. As a general rule, dosage of bretylium, digoxin, disopyramide, flecainide, lidocaine, moricizine, pro- Home Care cainamide, propafenone, quinidine, sotalol, and tocainide should be reduced in clients with significant impairment of Clients receiving chronic antidysrhythmic drug therapy are renal function.