Nursing NR 565Week 7 review Nursing NR 565Week 7 review

Nursing NR 565Week 7 review Nursing NR 565Week 7 review Week 7 review  Management of Bipolar Disorder (BPD) o Drugs from other classes that can be used to treat BPD BPD is treated with three major groups of drugs: mood stabilizers, antipsychotics, and antidepressants. In addition, benzodiazepines are frequently used for sedation. Mood Stabilizers Mood stabilizers are drugs that (1) relieve symptoms during manic and depressive episodes, (2) prevent the recurrence of manic and depressive episodes, and (3) do not worsen symptoms of mania or depression or accelerate the rate of cycling. The principal mood stabilizers are lithium and two drugs originally developed for epilepsy: divalproex sodium (valproate) and carbamazepine. These drugs are the mainstays of treatment. The pharmacology of lithium and the antiepileptic drugs is discussed later. Antipsychotics In patients with BPD, antipsychotic drugs are given to help control symptoms during severe manic episodes, even if psychotic symptoms are absent. Although antipsychotics can be used alone, they are usually employed in combination with a mood stabilizer. For reasons discussed later, the second-generation antipsychotics (e.g., olanzapine, risperidone) are generally preferred to the firstgeneration agents (e.g., haloperidol). Antidepressants Antidepressants may be needed during a depressive episode. However, in patients with BPD, antidepressants are almost always combined with a mood stabilizer because of the long-held belief that, when used alone, antidepressants may elevate mood so much that a hypomanic or manic episode will result. However, data indicate that the risk for inducing mania may be much lower than previously thought. Nonetheless, the current guidelines suggest continuing the traditional practice of using an antidepressant only if a mood stabilizer is being used as well. Although antidepressants have been studied extensively in patients with major depression, research is still lacking in patients with BPD. At this time there are insufficient data on which to base drug selection. Even so, experts do have theirpreferences. Among clinicians with extensive experience in BPD, the following are considered antidepressants of choice: bupropion (Wellbutrin), venlafaxine (Effexor XR), and the selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine (Prozac) and sertraline (Zoloft). One thing we do know is that the use of tricyclic antidepressants (TCAs) appears to promote more incidents of mania; therefore TCAs are not recommended in the treatment of BPD.  o Drug Interactions ▪ Lithium Drug Interactions Diuretics. Diuretics promote sodium loss and can thereby increase the risk for lithium toxicity. Toxicity can occur because renal excretion of lithium is reduced in the presence of low sodium, causing lithium levels to rise. Nonsteroidal antiinflammatory drugs. Nonsteroidal antiinflammatory drugs (NSAIDs) can increase lithium levels by as much as 60%. By suppressing prostaglandin synthesis in the kidney, NSAIDs can increase renal reabsorption of lithium (and also sodium), causing lithium levels to rise. NSAIDs known to increase lithium levels include ibuprofen (Motrin, others), naproxen (Naprosyn), piroxicam (Feldene), indomethacin (Indocin), and celecoxib (Celebrex). Interestingly, aspirin (the prototype NSAID) and sulindac (Clinoril) do notincrease lithium levels. Accordingly, if a mild analgesic is needed, aspirin or sulindac would be a good choice. Anticholinergics o Monitoring ▪ Lithium Monitoring plasma lithium levels. Measurement of plasma lithium levels is an essential component of treatment. Lithium levels must be kept below1.5 mEq/L; levels greater than this can produce signifcant toxicity. Lithum levels should range from 0.4 to 1 mEq/L. Generally levels should be between 0.6 and 0.8 mEq/L. Levels of 0.8 to 1mEq/L may be more effective but carry a greater risk of adverse effects. Blood for lithium determinations should be drawn in the morning, 12 hours after the evening dose. During maintenance therapy, lithium levels should be measured every 3 to 6 months.  - Management of Major Depressive Disorder o Know example drugs ▪ SSRIs Citalopram (Celexa) Escitalopram (lexapro, cipralex) Fluoxetine (Prozac, Sarafem) Fluvoxamine (Luvox) Paroxetine (Paxil, Pexeva) Sertraline (Zoloft) Vortioxetine (Trintellix) o Adverse Effects ▪ Venlafaxine Venlafaxine Venlafaxine (Effexor XR), the first SNRI available, is approved for major depression, generalized anxiety disorder, social anxiety disorder, and panic disorder. The drug produces powerful blockade of NE and 5-HT reuptake and weak blockade of dopamine reuptake. The relationship of these actions to therapeutic effects is uncertain. Venlafaxine does not block cholinergic, histaminergic, or α1-adrenergic receptors. Despite impressions that venlafaxine may be superior to SSRIs, when compared directly in clinical trials, the drugs were about equally effective—and SSRIs are probably safer.Venlafaxine is well absorbed after oral administration, in both the presence and absence of food. In the liver, much of each dose is converted to desvenlafaxine, an active metabolite. The half-life is 5 hours for the parent drug and 11 hours for the active metabolite. Venlafaxine can cause a variety of adverse effects. The most common is nausea (37% to 58%), followed by headache, anorexia, nervousness, sweating, somnolence, and insomnia. Dose-dependent weight loss may occur secondary to anorexia. Venlafaxine can also cause dose-related sustained diastolic hypertension; blood pressure should be monitored. Sexual dysfunction may occur too. Some patients experience sustained mydriasis, which can increase the risk for eye injury in those with elevated intraocular pressure or glaucoma. Like the SSRIs, venlafaxine can cause hyponatremia, especially in older adult patients taking diuretics. Like all other antidepressants, venlafaxine may increase the risk for suicide, especially in children and young adults. The combined use of venlafaxine with MAOIs and other serotonergic drugs (see Table 27.3) increases the risk for serotonin syndrome, a potentially fatal reaction. If the clinical situation demands, venlafaxine may be cautiously combined with an SSRI or another SNRI. However, combined use with an MAOI is contraindicated. Accordingly, MAOIs should be withdrawn at least 14 days before starting venlafaxine. When switching from venlafaxine to an MAOI, venlafaxine should be discontinued 7 days before starting the MAOI. As with the SSRIs, the use of venlafaxine late in pregnancy can result in a neonatal withdrawal syndrome, characterized by irritability, abnormal crying, tremor, respiratory distress, and possibly seizures. Symptoms, which can be managed with supportive care, generally abate within a few days. Abrupt discontinuation can cause an intense withdrawal syndrome. Symptoms include anxiety, agitation, tremors, headache, vertigo, nausea, tachycardia, and tinnitus. Worsening of pretreatment symptoms may also occur. Withdrawal symptoms can be minimized by tapering the dosage over 2 to 4 weeks. Warn patients not to stop venlafaxine abruptly. ▪ Monoamine Oxidase InhibitorsAdverse effects Central nervous system stimulation. MAOIs cause direct CNS stimulation (in addition to exerting antidepressant effects). Excessive stimulation can produce anxiety, insomnia, agitation, hypomania, and even mania. Orthostatic hypotension. Despite their ability to increase the NE content of peripheral sympathetic neurons, the MAOIs reduce blood pressure when administered in usual therapeutic doses. Patients should be informed about signs of hypotension (dizziness, lightheadedness) and advised to sit or lie down if these occur. Also, they should be informed that hypotension can be minimized by moving slowly when assuming an erect posture. MAOIs reduce blood pressure through actions in the CNS. The following sequence has been proposed: (1) Inhibition of MAO increases the NE content of neurons within the vasomotor center. (2) When NE is released, it binds to postsynaptic α receptors on neurons within the vasomotor center, thereby decreasing the firing rate of sympathetic nerves that control vascular tone. (3) This reduction in sympathetic activity results in vasodilation, causing blood pressure to fall. Hypertensive crisis from dietary tyramine. Although the MAOIs normally produce hypotension, they can be the cause of severe hypertension if the patient eats food that is rich in tyramine, a substance that promotes the release of NE from sympathetic neurons. Hypertensive crisis is characterized by severe headache, tachycardia, hypertension, nausea, vomiting, confusion, and profuse sweating—possibly leading to stroke and death. Before considering the mechanism by which hypertensive crisis is produced, let's consider the effect of dietary tyramine under drug-free conditions. In the absence of MAO inhibition, dietary tyramine is not a threat. Much of the tyramine in food is metabolized by MAO in the intestinal wall. Furthermore, as shown in Fig. 27.3A, any dietary tyramine that gets through the intestinal wall intact will then pass directly to the liver through the hepatic portal circulation. When in the liver, tyramine isimmediately inactivated by MAO there. Hence, as long as intestinal and hepatic MAO is functioning, dietary tyramine is prevented from reaching the general circulation and therefore is devoid of adverse effects. o Food & Drug Interactions Monoamine Oxidase Inhibitors (MAOIs) Foods That Can Interact With Monoamine Oxidase Inhibitors Foods That Contain Tyramine Category Foods With High Tyramine Content Foods With Little or No Tyramine Vegetables Avocados, especially if overripe; fermented bean curd; fermented soybean; soybean paste Most vegetables Fruits Figs, especially if overripe; bananas, in large amounts Most fruits Meats Meats that are fermented, smoked, or otherwise aged; spoiled meats; liver, unless very fresh Meats that are known to be fresh (exercise caution in restaurants; meat may not be fresh)Sausages Fermented varieties: bologna, pepperoni, salami, others Nonfermented varieties Fish Dried or cured fish; fish that is fermented, smoked, or otherwise aged; spoiled fish Fish that is known to be fresh; vacuum-packed fish, if eaten promptly or refrigerated only briefly after opening Milk, milk products Practically all cheeses Milk, yogurt, cottage cheese, cream cheese Foods with yeast Yeast extract (e.g., Marmite, Bovril) Baked goods that contain yeast Beer, wine Some imported beers, Chianti wine Major domestic brands of beer, most wines Other foods Protein dietary supplements; soups (may contain protein extract); shrimp paste; soy sauce Foods That Contain Nontyramine Vasopressors Food CommentsChocolate Contains phenylethylamine, a pressor agent; large amounts can cause a reaction Fava beans Contain dopamine, a pressor agent; reactions are most likely with overripe beans Ginseng Headache, tremulousness, and manic-like reactions have occurred Caffeinated beverages Caffeine is a weak pressor agent; large amounts may cause a reaction  • MAOIs must not be dispensed to patients considered incapable of rigid adherence to dietary restrictions.  • Before an MAOI is dispensed, the patient must be fully informed about the hazard of ingesting tyramine-rich foods.  • The patient must be given a detailed list of foods and beverages to avoid.  • The patient should be instructed to avoid all drugs not specifcally approved by the prescriber. o Suicide Risks and Considerations ▪ Safety measuresBlack Box Warning Suicide Risk With Antidepressant Drugs Patients with depression often think about or attempt suicide. During treatment with antidepressants, especially early on, the risk for suicide may actually increase. Concerns about antidepressant-induced suicide apply mainly to children, adolescents, and adults younger than 25 years. Patients should be informed about the symptoms of hypertensive crisis (headache, tachycardia, palpitations, nausea, vomiting, sweating) and instructed to seek immediate medical attention if these develop. In addition to tyramine, several other dietary constituents (e.g., caffeine, phenylethylamine) can precipitate hypertension in patients taking MAOIs. Foods that contain these compounds are listed in Table 27.5. Patients should be instructed to avoid them. Depression. MAOIs are equal to SSRIs and TCAs for relieving depression. However, because MAOIs can be hazardous, they are generally reserved for patients who have not responded to SSRIs, TCAs, and other safer drugs. Nonetheless, there is one group of patients—those with atypical depression—for whom MAOIs are the treatment of choice. As with other antidepressants, beneficial effects do not reach their peak for several weeks. o Administration and Cessation of Medication Considerations ▪ Selective serotonin reuptake inhibitors (SSRIs) Patient EducationWithdrawal Syndrome Abrupt discontinuation of selective serotonin reuptake inhibitors can cause a withdrawal syndrome. Symptoms include dizziness, headache, nausea, sensory disturbances, tremor, anxiety, and dysphoria. These begin within days to weeks of the last dose and then persist for 1 to 3 weeks. Resumption of drug use will make symptoms subside. The withdrawal syndrome can be minimized by tapering the dosage slowly.  What do patients need to know about starting and stopping SSRIs? *** ▪ MAOIs  What patient type would be appropriate for MAOIs? The MAOIs are second- or third-choice antidepressants for most patients. Although these drugs are as effective as the SSRIs and TCAs, they are more hazardous. The greatest concern is hypertensive crisis, which can be triggered by eating foods rich in tyramine. At this time, MAOIs are drugs of choice only for atypical depression. Three MAOIs (isocarboxazid [Marplan], phenelzine [Nardil], and tranylcypromine [Parnate]) are administered orally, and one (selegiline [Emsam]) is administered by transdermal patch. o Baseline Data Needed to prescribe and strategies to minimize adverse effects for the following: (you will use each option only one on the exam) ▪ SSRI/SNRI: check sodium level ▪ Tricyclic Antidepressants: check EKG ▪ MAOIs :BP - Management of Panic Disorder o Medications used to treat▪ Exam will note mg in choices but if you know the med, the mg will be irrelevant. Treatment Between 70% and 90% of patients with PD respond well to treatment. Two modalities may be employed: drug therapy and CBT. Combining drug therapy with CBT is more effective than either modality alone. As a rule, patients experience rapid and signifcant improvement. Drug therapy helps suppress panic attacks, whereas CBT helps patients become more comfortable with situations and places they’ve been avoiding. Additional beneft can be derived from avoiding caffeine and sympathomimetics (which can trigger panic attacks), avoiding sleep deprivation (which can predispose to panic attacks), and doing regular aerobic exercise (which can reduce anxiety). Drug therapy should continue at least 6 to 9 months. Stopping sooner is associated with a high rate of relapse. Antidepressants PD responds well to all four classes of antidepressants: SSRIs, SNRIs, tricyclic antidepressants (TCAs), and MAOIs. With all classes, full benefits take 6 to 12 weeks to develop. Owing to better tolerability, SSRIs are generally preferred. The basic pharmacology of the antidepressants is discussed in Chapter 27. Selective serotonin reuptake inhibitors. The SSRIs are first-line drugs for PD. At this time, only three SSRIs— fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft)—are approved for this condition. However, the other SSRIs appear just as effective. The SSRIs decrease anticipatory anxiety, avoidance behavior, and the frequency and intensity of attacks. Furthermore, SSRIs decrease panic attacks regardless of whether the patient is actually depressed. However, if the patient does have coexisting depression, antidepressants will benefit the depression and PD simultaneously. Common side effects include nausea, headache, insomnia, weight gain, and sexual dysfunction. In addition, SSRIs can increase anxiety early in treatment. (SSRI) Fluoxetine (Prozac) –10mg once a day (SSRI) Paroxetine (Paxil) – 10 mg once a day(SSRI) Sertraline (Zoloft) – 25mg once a day  - Management of social anxiety disorder (SAD)  o What medications can be used ▪ On a routine basis versus on an as needed basis Treatment SAD can be treated with psychotherapy, drug therapy, or both. Studies indicate that psychotherapy—both cognitive and behavioral—can be as effective as drugs. However, a combination of psychotherapy plus drugs is likely to be more effective than either modality alone. The SSRIs are considered frst-line drugs for most patients. These drugs are especially well suited for patients who fear multiple situations and are obliged to face those situations on a regular basis. Only two SSRIs—paroxetine (Paxil) and sertraline (Zoloft)—are approved for SAD, but available data indicate that the other SSRIs are effective also. Initial effects take about 4 weeks to develop; optimal effects are seen in 8 to 12 weeks. Patients should be informed that benefts will be delayed. Benzodiazepines (e.g., clonazepam [Klonopin, Rivotril ], alprazolam [Xanax]) are an option for some patients. These drugs are well tolerated and their benefts are immediate, unlike those of the SSRIs. As a result, benzodiazepines can provide rapid relief and can be used PRN. Accordingly, these drugs are well suited for people whose fear is limited to performance situations and who must face those situations only occasionally. The usual dosage is 1 to 3 mg/day for clonazepam and 1 to 4mg/day for alprazolam. Propranolol (Inderal) and other β blockers can beneft patients with performance anxiety. When taken 1 to 2 hours before a scheduled performance, beta blockers can reduce symptoms caused by autonomic hyperactivity (e.g., tremors, sweating, tachycardia, palpitations). Doses are relatively small—only 10 to 80mg for propranolol.- Management of anxiety Recommended duration of treatment o Long term treatment options: For long-term management, buspirone and the antidepressants are preferred. Because GAD is a chronic disorder, initial drug therapy should be prolonged, lasting at least 12 months and possibly longer. Unfortunately, even after extended treatment, drug withdrawal frequently results in relapse. Hence, for many patients, drug therapy must continue indefnitely. Because therapeutic effects are delayed, buspirone is not suitable for PRN use or for patients who need immediate relief. Buspirone has no abuse potential and thus may be especially appropriate for patients known to abuse alcohol or other drugs. Because it lacks depressant properties, buspirone is an attractive alternative to benzodiazepines in patients who require long-term therapy but cannot tolerate benzodiazepineinduced sedation and psychomotor slowing. Buspirone is labeled only for short-term treatment of anxiety. However, the drug has been taken for as long as a year with no reduction in beneft. Long-term use of benzodiazepines carries a risk for physical dependence. Withdrawal symptoms include panic, paranoia, and delirium. These can be especially troubling for patients with GAD. Furthermore, they can be confused with a return of pretreatment symptoms. Accordingly, clinicians must differentiate between a withdrawal reaction and relapse. To minimize withdrawal symptoms, benzodiazepines should be tapered gradually—over a period of several months. If relapse occurs, treatment should resume.  - Side effects of both 1st generation Patents should be informed about signs of hypotension (lightheadedness, dizziness) and advised to sit or lie down if these occur. In additon, patents should be informed that hypotension can be minimized by moving slowly when assuming an erect posture. Patents should be warned against partcipatng in hazardous actvites (e.g., driving) untl sedatve effects diminish. Sedation. Sedation is common during the early days of treatment but subsides within a week or so. Neuroleptic-induced sedation is thought to result from the blockade of histamine-1 (H1) receptors in the CNS. Daytime sedation can be minimized by giving the entire daily dose at bedtime. Neuroendocrine effects. Antipsychotics increase levels of circulating prolactin by blocking the inhibitory action of dopamine on prolactin release. Elevation of prolactin levels promotes gynecomastia (breast growth) and galactorrhea in up to 57% of women. Up to 97% of women experience menstrual irregularities. Gynecomastia and galactorrhea can also occur in males. Because prolactin can promote growth of prolactin-dependent carcinoma of the breast, neuroleptics should be avoided in patients with this form of cancer. (It should be noted that, although FGAs can promote the growth of cancers that already exist, there is no evidence that FGAs actually cause cancer.) Seizures. First-generation agents can reduce seizure threshold, thereby increasing the risk for seizure activity. The risk for seizures is greatest in patients with seizure disorders. These patients should be monitored, and, if loss of seizure control occurs, the dosage of their antiseizure medication must be increased. Sexual dysfunction. First-generation agents can cause sexual dysfunction in women and men. In women, these drugs can suppress libido and impair the ability to achieve orgasm. In men, FGAs can suppress libido and cause erectile and ejaculatory dysfunction; the incidence is 25% to 60%. Drug-induced sexual dysfunction can make treatment unacceptable to sexually active patients, thereby leading to poor adherence. A reduction in dosage or switching to a high-potency FGA mayreduce adverse sexual effects. Patients should be counseled about possible sexual dysfunction and encouraged to report any problems. Agranulocytosis. Agranulocytosis is a rare but serious reaction. Among the FGAs, the risk is highest with chlorpromazine and certain other phenothiazines. Because agranulocytosis severely compromises the ability to fight infection, a white blood cell (WBC) count should be done whenever signs of infection (e.g., fever, sore throat) appear. If agranulocytosis is diagnosed, the neuroleptic should be withdrawn. Agranulocytosis will then reverse. Severe dysrhythmias. Four FGAs—chlorpromazine, haloperidol, thioridazine, and pimozide—pose a risk for fatal cardiac dysrhythmias. The mechanism is prolongation of the QT interval, an index of cardiac function that can be measured with an electrocardiogram (ECG). Drugs that prolong the QT interval increase the risk for torsades de pointes, a dysrhythmia than can progress to fatal ventricular fibrillation. To reduce the risk for dysrhythmias, patients should undergo an ECG and serum potassium determination before treatment and periodically thereafter. In addition, they should avoid other drugs that cause QT prolongation, as well as drugs that can increase levels of these four FGAs. Black Box Warning Antipsychotic Drugs When used off-label to treat older adult patients with dementia-related psychosis, all antipsychotics (FGAs and SGAs) approximately double the rate of mortality. Most deaths result from heart-related events (e.g., heart failure, sudden death) or from infection (mainly pneumonia). Because antipsychotics are not approved for treating dementia-related psychosis, and because doing so increases the risk for death, such use is not recommended. Signs of withdrawal and extrapyramidal symptoms in neonates. Neonates exposed to antipsychotic drugs (first or second generation) during the third trimester of pregnancy may experience EPSs and signs of withdrawal. Symptoms include tremor, agitation, sleepiness, difficulty feeding, severe breathing difficulty, and altered muscle tone (increased or decreased). Fortunately, the risk appears low. Neonates who present with EPSs or signs of withdrawal should be monitored. Some will recover within hours or days, butothers may require prolonged hospitalization. Despite the risk to the infant, women who become pregnant should not discontinue their medication without consulting the prescriber. Patient Education Sun Exposure and Dermatitis Patients should be warned against excessive exposure to sunlight and advised to apply a sunscreen and wear protective clothing. Handling antipsychotics can cause contact dermatitis in patients and health care workers. Dermatitis can be prevented by avoiding direct contact with these drugs.  Side effects of 2nd generation antipsychotics Metabolic side effects Weight gain, tachycardia, diabetes, dislipidemia, sedation, ortho hypotension  - Management of Insomnia o What type of patient scenario would be appropriate for administration of the following drugs? ▪ Trazodone : insomnia, help with sleep, not highly addictive, prolong sleep duration ▪ Zaleplon : short term insomnia, rapid onset and short duration ▪ Flurazepam ▪ Zolpidem: falling a sleep o Know Examples for the major drug classes ▪ Benzodiazepine: diazepam, valium,Ativan, Xanax, lorezapam ▪ Benzodiazepine-like Drug: ambien, zolpidiem, lunesta ▪ Zolpidem: ▪ Melatonin Receptor Agonist : Ramelteon For the following herbal medications, you will need to know how they interact with conventional drugs and common problems that can happen with each one.o Kava: hepatoxicity, liver transplant, avoid alcohol o Ginkgo biloba: Several case reports suggest that glucosamine may increase the risk for bleeding. Therefore, patients taking antiplatelet drugs (e.g., aspirin) or anticoagulants (e.g., warfarin and heparin) should probably avoid this product. warfarin, heparin, can increase bleeding, avoid in patients’ risk for seizures, headache, dizziness o Echinacea: By stimulating the immune system, echinacea can oppose the effects of immunosuppressant drugs. Conversely, by suppressing immune function (in response to long-term use), echinacea can compromise drug therapy of tuberculosis, cancer, and HIV infection. o St.John’swort: St. John's wort is known to interact adversely with many drugs— and the list continues to grow. Three mechanisms are involved: induction of cytochrome P450 enzymes, induction of P-glycoprotein, and intensification of serotonin effects. Considered one by one, the following may be said: reduce the effects of oral contraceptoves, skin reactions, dry mouth, restlessness, insomnia o Gingerroot: Ginger can inhibit production of thromboxane by platelets and can, hence, suppress platelet aggregation. Accordingly, ginger can increase the risk for bleeding in patients receiving antiplatelet drugs (e.g., aspirin) or anticoagulants (e.g., warfarin and heparin) or other drugs that inhibit clotting such as the direct thrombin and factor xa inhibitors. Ginger can lower blood sugar and, hence, may potentiate the hypoglycemic effects of insulin and other drugs for diabetes. o Flaxseed: Flaxseed may reduce the absorption of conventional medications. Therefore, it should be taken 1 hour before or 2 hours after these drugs. o Black cohosh: Black cohosh may potentiate the hypotensive effects of antihypertensive drugs as well as the hypoglycemic effects of insulin and other drugs for diabetes. Black cohosh may potentiate the effects of estrogens used for hormonetherapy. Because it may cause liver inflammation, black cohosh may increase the risk for liver damage when taken with other drugs that may harm the liver. Medications you will need to know for the prescription writing questions include: o Azithromycin o Erythromycin o Tinidazole o Benzathine Penicillin o Acyclovir