NCM 212 4th Unit Pharmacology PDF

NCM 212 4th UNIT PHARMACOLOGY COURSE OUTLINE: G. Neurological Agents G.1 CNS sedatives and hypnotics G.2 Anxiolytics and Psychiatric Agents G.3 CNS stimulants, ADHD and Alzheimer agents G.4 Muscle relaxants and Antiparkinson’s agents G.5 Antiseizures/ Antiepilepsy G.6 Substance abuse – depressant...

NCM 212 4th UNIT PHARMACOLOGY COURSE OUTLINE: G. Neurological Agents G.1 CNS sedatives and hypnotics G.2 Anxiolytics and Psychiatric Agents G.3 CNS stimulants, ADHD and Alzheimer agents G.4 Muscle relaxants and Antiparkinson’s agents G.5 Antiseizures/ Antiepilepsy G.6 Substance abuse – depressants, stimulants, hallucigenics G.7 Autonomic Nervous System agents I. Eye, Ear, Skin Agents I.1 Ophthalmic Agents I.2 Otic Agents I.3 Dermatological agents J. Endocrine Agents J.1 Thyroid, Parathyroid, and Pituitary agents J.2 Insulin & Antidiabetics agents K. Reproductive System agents Male and female sex hormones G. Neurological Agents G.1 CNS sedatives and hypnotics The central nervous system (CNS) It represents the largest part of the nervous system, including the brain and the spinal cord. Together with the peripheral nervous system, it has a fundamental role in the control of behavior. SEDATIVE/HYPNOTICS are medications for induction and maintenance of sleep in people with insomnia. Sedative/hypnotics induce sedation by depressing the central nervous system (CNS), in particular, the sensory cortex of the brain, which is responsible for processing the sensory inputs from the body, such as touch, pain and temperature. It depresses the limbic system of the brain, which regulates emotional and behavioral responses, and reticular formation which regulates sleep and consciousness. - Sedative/hypnotics produce sedation by enhancing the activity of gamma-aminobutyric acid (GABA), a neurotransmitter that inhibits electrical activity in the brain. GABA is known for producing a calming effect. The category of sedative hypnotics includes barbiturates, benzodiazepines, non-benzodiazepines and piperidinediones. Common Terminologies: Sedatives: Drugs cause calmness, relaxation, reduction of anxiety. Sedatives may be referred to as tranquilizers, depressants, anxiolytics, soporifics, sleeping pills, downers, or sedative-hypnotics, including barbiturates, benzodiazepines, zolpidem Hypnotics: Drugs that induce sleep, used in the treatment of severe insomnia, including barbiturates, benzodiazepines, zolpidem Anxiolytics: Drugs used for the treatment of symptoms of anxiety, including benzodiazepines Therapeutic Actions and Indications: a) BARBITURATES Barbiturates were extensively used as “sleeping pills” throughout the first half of the 20th century. They also were used to reduce voluntary inhibition during psychiatric examinations. When taken in high-enough doses, these drugs are capable of producing a deep unconsciousness that makes them useful as general anesthetics. In higher doses, however, they depress the central nervous and respiratory systems to the point of coma, respiratory failure, and death. The use of barbiturates declined after the development in the 1950s of the benzodiazepines. Barbiturates are classified as long-acting, intermediate-acting, short-acting, and ultrashort-acting. The long-acting group includes phenobarbital and mephobarbital, and is used to control seizures in epilepsy. Phenobarbital, introduced in 1912, is still in use. The intermediate-acting barbiturates amobarbital (Amytal), aprobarbital (Alurate), and butabarbital (Butisol) are useful as sleep sustainers for maintaining long periods of sleep. The short-acting barbiturates secobarbital (Seconal) and pentobarbital (Nembutal) are used to induce sleep for those who have difficulty falling asleep. The ultrashort-acting barbiturate, thiopental sodium (Pentothal), is used as a general anesthetic. Pharmacokinetics: It has a slow absorption rate and is moderately protein-bound. The long half-life is mainly because of the formation of active metabolites resulting from liver metabolism. Pharmacodynamics: Pentobarbital and secobarbital are used primarily for sleep induction and for sedation needs. They have a rapid onset with a short duration of action; thus they are considered short-acting barbiturates. The onset of action of pentobarbital is slower when administered intramuscularly (IM) than when administered orally (PO). Pentobarbital increases hepatic enzyme action, thus causing an increased metabolism and decreased effect of drugs such as oral anticoagulants, glucocorticoids, tricyclic antide-pressants, and quinidine. Pentobarbital may cause hepatotoxicity if taken with large doses of acetaminophen. INDICATIONS: Anxiety, Pre-operative sedation, Convulsions, Induced coma MECHANISM OF ACTION: Bind to GABA A receptors ↑ duration of Cl- channel opening; ↑ Cl- influx Membrane hyperpolarization; ↓ neuronal excitability ROUTES OF ADMINISTRATION: PO, IV, IM SIDE EFFECTS: Headache, somnolence (strong desire for sleep), confusion, CNS depression, hallucinations, vertigo (sensation of motion or spinning), nausea, vomiting, diarrhea, asthenia (weakness), ataxia (loss of muscle control), Paradoxical stimulation (effect of a chemical substance that is opposite to what is expected), Tolerance, dependence, and withdrawal symptoms, Stevens- Johnson syndrome (a rare, serious disorder of the skin and mucous membranes, usually a reaction to medication that starts with flu-like symptoms, followed by a painful rash that spreads and blisters). Advise client to report adverse reactions such as hangover. Drug selection or dosage may need to be changed. CONTRAINDICATIONS AND CAUTIONS: Concomitant use with other CNS depressants, hypotension, laryngospasm, bronchospasm. NURSING INTERVENTIONS: Monitor vital signs, especially respiration and blood pressure. Raise bedside rails of older adults and clients who are receiving a hypnotic for the first time. Confusion may occur, and injury may result. Check client's skin for rashes. Skin eruptions may occur in clients taking barbiturates. Recognize that continuous use of a barbiturate might result in drug abuse. Assess client for withdrawal symptoms when barbiturates have been taken over a prolonged period of time and then discontinued. IM injection should be given deep in a large muscle such as the gluteus medius. NOTE: GABA-A agonists (ie: benzodiazepines and barbiturates) reduce cerebral activity, and toxicity from these drugs results in coma. Withdrawal states can precipitate seizures as well as status epilepticus. CLIENT TEACHING: Teach client to use non-pharmacologic ways to induce sleep, such as enjoying a warm bath, listening to music, drinking warm fluids, and avoiding drinks with caffeine for 6 hours before bedtime. Instruct client to avoid alcohol and antidepressant, antipsychotic, and narcotic drugs while taking the barbiturate. Respiratory distress may occur when these drugs are combined. Inform client that certain herbs may interact with CNS depressants such as barbiturates.The herb may need to be discontinued or the drug dose may need to be modified. Advise client not to drive a motor vehicle or operate machinery. Instruct client to take the hypnotic 30 minutes before bedtime. Short-acting hypnotics take effect within 15 to 30 minutes. Can reduce the efficacy of oral contraceptives. Make position changes slowly to reduce effects of orthostatic hypotension. Promptly report flu-like symptoms or a rash which could indicate Stevens-Johnson syndrome. b) BENZODIAZEPINES Benzodiazepines are superior to barbiturates because of the reduced dangers they present to tolerance and addiction, and because they are much less likely to harmfully depress the central nervous system when used at high doses. They also require a much smaller dosage than barbiturates to achieve their effects. The benzodiazepines include chlordiazepoxide (Librium), diazepam (Valium), alprazolam (Xanax), oxazepam (Serax), and triazolam (Halcion). They are intended only for short or medium-term use, since the body develops a tolerance to them and withdrawal symptoms (anxiety, restlessness) develop even in those who have used the drugs for only four to six weeks. Pharmacokinetics: Benzodiazepines are well absorbed through the gastrointestinal (GI) mucosa. Flurazepam is rapidly metabolized in the liver to active metabolites, and it has a long half-life of 45 to 100 hours. Pharmacodynamics: Benzodiazepines are used to treat insomnia by inducing and sustaining sleep. They have a rapid onset of action and intermediate to long acting effects. The normal recommended dose of a benzodiazepine may be too much for the older adult, so half of the dose is recommended initially to prevent overdosing. Alcohol or narcotics taken with a benzodiazepine may cause an additive depressive CNS response. Triazolam (Halcion) may cause rebound insomnia and temazepam (Restoril) may cause euphoria and palpitations. INDICATIONS: Anxiety, Pre-operative sedation, Anesthesia induction, Sedation for mechanical ventilation, Alcohol withdrawal syndrome, Status epilepticus MECHANISM OF ACTION: Bind to GABA A receptors ↑ frequency of Cl- channel opening; ↑ Cl- influx Membrane hyperpolarization; ↓ neuronal excitability ROUTES OF ADMINISTRATION: PO, IV, IM, SC, SL, PR SIDE EFFECTS: Headache, sedation, dizziness, blurred vision, dry mouth, urinary incontinence, constipation, Leukopenia, Paradoxical stimulation, dependence and withdrawal symptoms. CONTRAINDICATIONS AND CAUTIONS: Myasthenia gravis (chronic autoimmune disorder resulting in weakness of the skeletal muscles), Concomitant use with other CNS depressants, Acute narrow-angle glaucoma (eye condition that damages the optic nerve), Pregnancy, breastfeeding. NURSING INTERVENTIONS: Monitor vital signs. Check for signs of respiratory distress, such as slow, irregular breathing patterns. Raise bedside rails of older adults or clients receiving sedative- hypnotics for the first time. Confusion may occur, and injury may result. Observe client for side effects of sedative-hypnotics, such as hangover (residual sedation) light-headedness, dizziness, or confusion. NOTE: GABA-A agonists (ie: benzodiazepines and barbiturates) reduce cerebral activity, and toxicity from these drugs results in coma. Withdrawal states can precipitate seizures as well as status epilepticus. CLIENT TEACHING: Teach client to use non-pharmacologic ways to induce sleep, such as enjoying a warm bath, listening to music, drinking warm fluids such as milk, and avoiding drinks with caffeine after dinner. Instruct client to avoid alcohol and antidepressant, anti-psychotic, and narcotic drugs while taking sedative-hypnotics. Severe respiratory distress may occur when these drugs are combined. Advise client to take sedative-hypnotic before bedtime. Flurazepam takes effect within 15 to 45 minutes. Suggest that client urinate before taking sedative-hypnotic to prevent sleep disruption. Encourage client to check with health care provider about OTC sleeping aids. Drowsiness may result from taking these drugs; therefore caution while driving is advised. Teach the client to monitor for and report side effects. Keep clients who receive parenteral doses in bed for at least three hours to ensure safety. Provide safety measures like raising side-rails and ensuring adequate lighting. Make position changes slowly to reduce effects of orthostatic hypotension (a medical condition wherein a person's blood pressure drops when they are standing up or sitting down). Avoid grapefruit juice if taking alprazolam or midazolam (may inhibit metabolism of drug causing high levels of the drug in your blood, leading to potentially dangerous effects.). c) NON-BENZODIAZEPINES: DRUG NAME: zolpidem (Ambien), zaleplon, eszopiclone (Lunesta) INDICATION: Insomnia MECHANISM OF ACTION: Bind to GABA A receptors ↑ frequency of Cl- channel opening; ↑ Cl- influx Membrane hyperpolarization; ↓ neuronal excitability ROUTES OF ADMINISTRATION: PO SIDE EFFECTS: Headache, Hot flashes, Drowsiness, Anxiety, Nausea, vomiting, Ataxia, Erectile dysfunction, Tolerance, dependence, and withdrawal symptoms. CONTRAINDICATIONS AND CAUTIONS: Concomitant use with other CNS depressants CLIENT TEACHING: Teach the client to monitor for and report side effects Avoid hazardous activities like driving until response is known Provide safety measures like raising side-rails and ensuring adequate lighting Take only if able to get a full night’s sleep (7–8 hrs) Dangerous sleep behaviors like sleep-walking may occur d) PIPERIDINEDIONES: An antipsychotic agent used in the treatment of schizophrenia. Used for the treatment of insomnia. The piperidinediones resemble barbiturates. These sedative-hypnotics were introduced in the mid-1950s and include glutethimide, which has effects similar to the short-acting barbiturates. These drugs were marketed to be non-addictive; however, they can be addictive and can cause severe adverse reactions, such as vasomotor collapse, serious blood dyscrasias (aplastic anemia), and allergic reactions. Over the past decade, the use of the piperidinedione group has declined. G.2 PSYCHIATRIC AGENTS AND ANXIOLYTICS What is PSYCHOSIS? Psychosis is disconnection from reality. People may have false beliefs or experience things that aren’t real. Psychosis isn’t a condition. It’s a term that describes a collection of symptoms. Two important types of psychosis include: Hallucinations. These are when parts of your brain mistakenly act like they would if your senses (vision, hearing, touch, smell and taste) picked up on something actually happening. An example of a hallucination is hearing voices that aren’t there (auditory hallucination). Delusions. These are false beliefs that someone holds onto very strongly, even when others don’t believe them or there’s plenty of evidence that a belief isn't true. For example, people with delusions of control believe someone is controlling their thoughts or actions remotely. Antipsychotic drugs don't cure psychosis but they can help to reduce and control many psychotic symptoms, including: delusions and hallucinations, such as paranoia and hearing voices, anxiety and serious agitation. All antipsychotics work by changing how your brain uses certain signals known as neurotransmitters.  ANTIPSYCHOTICS are also known as neuroleptics or psychotropics. Neuroleptic refers to any drug that modifies psychotic behavior thus exerting an antipsychotic effect. Antipsychotics are divided into two major categories: typical (or traditional) and atypical. The typical antipsychotics, introduced in 1952, are subdivided into phenothiazines and nonphenothiazines, which include butyrophenones, dibenzoxazepines, dihydroindolones, and thioxanthenes. The phenothiazines and thioxanthenes block norepinephrine, causing sedative and hypotensive effects early in treatment. The butyrophenones block only the neurotransmitter dopamine. The second category of antipsychotics is the atypical agents. Clozapine, discovered in the 1960s and made available in Europe in 1971, was the first atypical antipsychotic agent. It was not marketed in the United States until 1990 because of adverse hematologic reactions. Atypical antipsychotics are effective for treating schizophrenia and other psychotic disorders for clients who do not respond to or are intolerant of typical antipsychotics. Because of the decreased side effects, atypical antipsychotics may be used as first time therapy instead of traditional typical antipsychotics. While both generations are effective, the newer medications in general have several advantages over the older ones, including: fewer side effects such as trembling or stiffening of muscles, and less risk of developing Tardive Dyskinesia (a disorder that results in involuntary repetitive body movements, which may include grimacing, sticking out the tongue or smacking the lips). What conditions do antipsychotics treat? Schizophrenia (serious mental health condition- disconnection from reality, including hallucinations and delusions) Bipolar disorder (mental illness that causes unusual shifts in a person's mood, energy, activity levels, and concentration) Mania (abnormally happy mental state, typically characterized by exaggerated feelings of happiness, lack of inhibitions, racing thoughts, less need for sleep, talkativeness, risk taking, and irritability). Major depressive disorder with psychotic features. Delusional disorder. Severe agitation. Borderline personality disorder (mental health condition marked by extreme mood fluctuations) Dementia (term for several diseases that affect memory, thinking, and the ability to perform daily activities) Delirium (altered state of consciousness, characterized by episodes of confusion) Substance-induced psychotic disorder. Providers may treat other conditions with antipsychotics, but those drugs aren’t their main treatment. These conditions include: Tourette syndrome Huntington’s disease (is a condition that damages nerve cells in the brain causing them to stop working properly). Parkinson’s disease Lesch-Nyhan syndrome (rare metabolic disorder that occurs mostly in boys that causes brain and behavior problems). Obsessive-compulsive disorder (an anxiety disorder in which you have frequent unwanted thoughts that cause you to perform repetitive behaviors) PSYCHIATRIC AGENTS: Mechanisms of Action: Antipsychotics block the actions of dopamine and thus may be classified as dopaminergic antagonists. There are five subtypes of dopamine receptors: D1 through D5. All antipychotics block the D2, (dopaminergic) receptor, which in turn promotes the presence of EPS (Extrapyramidal Syndrome), resulting in pseudoparkinsonism. The first-generation antipsychotics work by inhibiting dopaminergic neurotransmission; their effectiveness is best when they block about 72% of the D2 dopamine receptors in the brain. They also have noradrenergic, cholinergic, and histaminergic blocking action. The atypical antipsychotics have a weak affinity for D2 receptors and a stronger affinity to D4 receptors, and they block the serotonin receptor. These agents cause fewer EPS than the typical (phenothiazines) antipsychotic agents, which have a strong affinity to the D2 receptors. Adverse Reactions: A) Extrapyramidal Syndrome Pseudoparkinsonism, which resembles symptoms of Parkinson's disease, is a major side effect of typical antipsychotic drugs. Symptoms of pseudoparkinsonism or EPS include stooped posture, mask-like face, rigidity, tremors at rest, shuffling gait, pill-rolling motion of the hand, and bradyknesia (slowness of movement and speed). When clients take high-potency typical antipsychotic drugs, these symptoms are more pronounced. Clients who lake low-strength antipsychotics, such as chlorpromazine (Thorazine), are not as likely to have symptoms of pseudo-parkinsonism as those who take uphenazine (Prolixin). Characteristics of Pseudoparkinsonism, Acute dystonia, Akathisia, and Tardive Dyskinesia PSYCHIATRIC AGENTS: Adverse Reactions B) Neuroleptic Malignant Syndrome Neuroleptic malignant syndrome (NMS) is a rare but potentially fatal condition that is associated with antipsychotic drugs. NMS symptoms involve muscle rigidity, sudden high fever, altered mental status, blood pressure fluctuations, tachycardia, dysrhythmias, seizures, rhabdomyolysis, acute renal failure, respiratory failure, and coma. Treatment of NMS involves immediate withdrawal of antipsychotics, adequate hydration, hypothermic blankets, and administration of antipyretics, benzodiazepines, and muscle relaxants, such as dantrolene (Dantrium). TYPICAL ANTI-PSYCHOTIC: a) Phenothiazines In 1952, chlorpromazine hydrochloride (Thorazine) was the first phenothiazine introduced for treating psychotic behavior in clients in psychiatric hospitals. The phenothiazines are subdivided into three groups: aliphatic, piperazine, and piperidine, which differ mostly in their side effects. The aliphatic phenothiazines produce a strong sedative effect, decreased blood pressure, and may cause moderate EPS (pseudoparkinsonism). Chlorpromazine (Thorizine) is in the aliphatic group and may produce pronounced orthostatic hypotension. An example of a phenothiazine anti-psychotic drug used to manage psychosis is fluphenazine (Prolixin). Pharmacokinetics: The oral absorption of fluphenazine is rapid and is not affected by food. This drug is strongly protein bound and has a long half-life; therefore, the drug may accumulate. Fluphenazine is metabolized by the liver, and crosses the blood-brain barrier and placenta. Pharmacodynamics: Fluphenazine is prescribed primarily for psychotic disorders. This drug has anticholinergic properties and should be cautiously administered to clients with glaucoma, especially narrow-angle glaucoma. Because hypotension is a side effect of these phenothiazines, any antihypertensives that are simultaneously administered can cause an additive hypotensive effect. Narcotics and sedative-hypnotics administered simultaneously with these phenothiazines can cause an additive CNS depression. Antacids decrease the absorption rate of both drugs and all phenothiazines, therefore they should be given 1 hour before or 2 hours after administering a phenothiazine The onset of action for fluphenazine hydrochloride is 1 hour, with a duration rate of 6 to 8 hours. e.g. FLUPHENAZINE (PIPERAZINE PHENOTHIAZINE) Therapeutic Effects/Uses To manage symptoms of psychosis including schizophrenia Mode of Action: Blocks dopamine receptors in the brain and controls psychotic symptoms. Contraindication: Hypersensitivity, subcortial brain damage, blood dyscrasias, renal or liver damage, coma Side Effects: Sedation, dizziness, headache, dry mouth, nasal congestion, blurred vision, photosensitivity, nausea, constipation, urinary retention, polyuria, peripheral edema Adverse Reactions: Hypotension, tachycardia, tardive dyskinesia, impaired thermoregulation, extrapyramidal symptoms, convulsions Life-threatening: Agranulocytosis (a life-threatening condition that involves having severely low levels of white blood cells) TYPICAL ANTI-PSYCHOTIC: b) Nonphenothiazines: The many groups of nonphenothiazine antipsychotics include butyrophenone, dibenzoxazepines, dihydroindolone, and thioxanthene. In the butyrophenone group, a frequently prescribed nonphenothiazine is haloperidol (Haldol), whose pharmacologic behavior is similar to that of the phenothiazines. Haloperidol is a potent antipsychotic drug in which the equivalent prescribed dose is smaller than drugs of lower potency (e.g., chlorpromazine). Long- acting preparations, such as haloperidol decanoate (Haldol) and fluphenazine decanoate (Prolixin), are given for slow release via injection every 2 to 4 weeks. Administration precautions should be taken to prevent soreness and inflammation at the injection site. Because of the viscous, liquid medication, a dry, large-gauge needle (e.g., 21-gauge) should be used for administration in a deep muscle with the Z-track method. Pharmacokinetics: Haloperidol is absorbed well through the gastrointestinal (GI) mucosa. It has a long half-life and is highly protein bound, so the drug may accumulate. Pharmacodynamics: Haloperidol alters the effects of dopamine by blocking the dopamine receptors; thus sedation and EPS may occur. Dosages need to be decreased in older adults because of decreased liver function and potential side effects. Haloperidol has anticholinergic activity; thus care should be taken when administering it to clients with a history of glaucoma. e.g. HALOPERIDOL (NON-PHENOTHIAZINE) Therapeutic Effects/Uses: To treat acute and chronic psychoses, to treat children with severe behavior problems who are combative, to suppress narcotic withdrawal symptoms, to treat schizophrenia resistant to other drugs, to treat Tourette's syndrome (a neurological disorder that may cause sudden unwanted and uncontrolled rapid/repeated movements or vocal sounds called tics), to treat symptoms of dementia in older adults. Mode of Action: Alteration of the effect of dopamine on CNS; mechanism for antipsychotic effects are unknown. Contraindications: Narrow-angle glaucoma, severe renal, hepatic, cardiovascular diseases, bone marrow depression, Parkinsons Disease, blood dyscrasias, CNS depression, subcortial brain damage. Side Effects: Sedation, extrapyramidal symptoms, orthostatic hypotension, headache, photosensitivity, dry mouth and eyes, blurred vision. Adverse Reactions: Tachycardia, seizures, urinary retention, tardive dyskinesia Life-threatening: Laryngospasm, respiratory depression, cardiac dysrhythmias, neuromalignant syndrome. TYPICAL ANTI-PSYCHOTIC: Side Effects and Adverse Reactions: (PHENOTHIAZINE AND NONPHENOTHIAZINE) The most common side effect for all antipsychotics is drowsiness. Many of the antipsychotics have some anticholinergic effects, such as dry mouth, increased heart rate, urinary retention, and constipation. Blood pressure decreases with the use of antipsychotics; aliphatics and piperidines cause a greater decrease in blood pressure than the others. EPS are most prevalent with the phenothiazines, butyrophenones, and thioxanthenes and include pseudoparkinsonism, akathisia, dystonia, and tardive dyskinesia. EPS can begin 5 to 30 days after initiation of antipsychotic therapy. Anticholinergic drugs may be given to control EPS. High dosing or long tern use of some antipsychoticscan cause blood dyscrasias (blood cell disorders), such as agranulocytosis. White blood cell (WBC) count should be closely monitored and reported if there is an extreme decrease in the WBCs. Dermatologic side effects seen early in drug therapy are pruritus and marked photosensitivity. Clients are urged to use sunscreen, hats, and protective clothing and to stay out of the sun. Drug Interactions: Because phenothiazine lowers the seizure threshold, dosage adjustment of an anticonvulsant may be necessary. Antipsychotics interact with alcohol, hypnotics, sedatives, narcotics, and benzodiazepines to potentiate the sedative effects of antipsychotics. Use of antihypertensives can cause an additive hypotensive effect. Antipsychotics should not be given with other antipsychotic or antidepressant drugs except to control psychotic behavior for selected individuals who are refractory to drug therapy. When discontinuing antipsychotics, the drug dosage should be reduced gradually to avoid sudden recurrence of psychotic symptoms. TYPICAL ANTI-PSYCHOTIC: NURSING INTERVENTIONS Monitor vital signs. Orthostatic hypotension is likely to occur. Remain with client while he or she takes the medication to ensure compliance because some clients hide drugs. Avoid skin contact with liquid concentrates to prevent contact dermatitis. Liquid must be protected from light and should be diluted with fruit juice. Administer oral doses with food or milk to decrease gastric irritation. Administer by IM route deep into the muscle because the drug irritates fatty tissue. Do not inject into subQ tissue. Check blood pressure for marked decrease 30 minutes after drug is injected. Do not mix in same syringe with heparin, pentobarbital, cimetidine, or dimenhydrinate. Chill suppository in the refrigerator for 30 minutes before removing foil wrapper. Observe for extrapyramidal syndrome (EPS): acute dystonia (spasms of the tongue, face, neck, and back), akathisia (restlessness, inability to sit still, foot-tapping), pseudoparkinsonism (muscle tremors, rigidity, shuffling gait, and tardive dyskinesia (lip smacking, protruding and darting tongue, and constant chewing movement). Assess for symptoms of neuroleptic malignant syndrome (NMS): increased fever, pulse, and blood pressure, muscle rigidity; increased creatine phosphokinase and WBC count; altered mental status acute renal failure; varying levels of consciousness; pallor; diaphoresis; tachycardia; and dysrhythmias. Record urine output. Urinary retention may result. Monitor serum glucose level. TYPICAL ANTI-PSYCHOTIC: CLIENT TEACHING Instruct client to take the drug exactly as ordered. In schizophrenia and other psychotic disorders, antipsychotics do not cure the mental illness but do prevent symptoms. Compliance with drug regimen is extremely important. Inform client that medication may take 6 weeks or longer to achieve full clinical effect. Caution client not to consume alcohol or other CNS depressants such as narcotics; these drugs intensify the depressant effect on the body. Recommend client not to abruptly discontinue the drug. Seek advice from the health care provider before making any changes in dosage. Encourage client to read labels on OTC preparations. Some are contraindicated when taking antipsychotics. Teach smoking cessation because smoking increases the metabolism of some antipsychotics. Encourage client to talk with the health care provider regarding family planning. The effect of antipsychotics on the fetus is not fully known; however, there may be teratogenic effects (congenital disabilities) on the fetus. Explain to client that phenotisine passes into breast milk. This could cause drowsiness and unusual muscle movement in the baby. Encourage client to obtain laboratory tests on schedule. WBCs are monitored for 3 months, especially during the start of drug therapy. Leukopenia or decreased WBCs, may occur. Be alert to symptoms of malaise, fever, and sore throat, which may be an indication of agranulocytosis (severely low levels of white blood cells). ATYPICAL ANTI-PSYCHOTIC: (Serotonin/Dopamine Antagonists) A new category for antipsychotics was marketed in the United States in the early 1990s. This group, atypical antipsychotics, differs from the typical/traditional antipsychotics because the atypical agents are effective in treating both positive and negative symptoms of schizophrenia. They are also not likely to cause EPS or tardive dyskinesia. The four atypical drugs available include clozapine (Clozaril), risperidone (Risperdal), olanzapine (Zyprexa), and quetiapine (Seroquel). Clozapine (Clozaril) was the first atypical antipsychotic agent used to treat schizophrenia and other psychoses. It does not cause acute EPS, although tremors and occasional rigidity have been reported. The serious adverse reaction of clozapine is agranulocytosis, a decrease in the production of granulocytes, which results in a decrease in the body's defense mechanism and seizures. Currently it is only indicated for the treatment of severely ill schizophrenic clients who have not responded to traditional antipsychotic drugs. The WBC count needs to be closely monitored; if the WBC (leukocytes) level falls below 3000 mm', clozapine should be discontinued. Another atypical agent used to treat positive and negative symptoms of schizophrenia is risperidone (Risperdal). Its action is similar to that of clozapine, and the occurrence of EPS and tardive dyskinesia is low. It does not cause agranulocytosis. These medicines work by decreasing: Mood swings, Depression, Mania, Severe aggressive outbursts, Psychosis, Agitation, Tics Administration: Atypical antipsychotics are available in immediate-release injectable (IM), long-acting injectable (IM), and orally disintegrating tablets in addition to the customary oral tablets. None of the atypical antipsychotics are administrated intravenously. Immediate-release injectables are used in emergencies when a patient is highly agitated or acutely psychotic, including olanzapine and ziprasidone. The long-acting injectables include aripiprazole, olanzapine, paliperidone, and risperidone, administered at 2 to 4-week intervals. Oral dosing is the preferred course of administration in most patients. The orally disintegrating tablets include aripiprazole, asenapine, clozapine, olanzapine, and risperidone, identical to the standard tablets regarding absorption and bioavailability. Adverse Effects: Atypical antipsychotics can cause adverse effects of weight gain, hyperlipidemia, diabetes mellitus, QTc prolongation, extrapyramidal side effects, myocarditis, agranulocytosis, cataracts, and sexual adverse effects (reduced libido). Contraindications: The few contraindications to the use of antipsychotic drugs include tardive dyskinesia, parkinsonism, and neuroleptic malignant syndrome. Caution is necessary when using antipsychotics in the presence of a prolactinoma (tumor of the pituitary gland). What do you monitor with atypical antipsychotics? Obtain baseline and periodic monitoring of BMI, waist circumference, HbA1c, fasting plasma glucose, and fasting lipids, as major adverse effects of atypical antipsychotics can include weight gain, glucose intolerance, elevation of blood lipids, and cardiac abnormalities. Common side effects include: – Dry mouth – Weight gain – Sleepiness/sedation – Sunburn when exposed to the sun – Stomach upset, constipation – Dizziness, headache Occasional side effects: – Drooling – Cannot sit still/restlessness – Slowing of movements and making less facial expressions – Difficulty with sexual functioning – Menstrual cycle irregularities – Enlargement of the breasts or breast discharge in men or women Serious side effects: – Stiffness or muscle spasms in the tongue, jaw, or neck – Seizures (Seizures have been reported in 3% of clients taking the drug) – Increased thirst and urination – Chest pain, dyspnea on exertion, signs/symptoms of orthostatic hypotension, palpitations, or shortness of breath. Recommended Actions: 1. Advise patient to take medication as directed. 2. Watch for anything different/change in status of the individual and for signs of medication side effects/ Teach clients to recognize and manage side effects. 3. Avoid hazardous activities; take medication in the evening. Provide safety measures to client to minimize the injuries like raising side rails, adequate lighting. 4. Adequate and continuous monitoring of client. 5. This drug may require several weeks to obtain desired effects. 6. Patients should be advised regarding the possibility of extrapyramidal symptoms and that abrupt withdrawal may cause dizziness, nausea and vomiting, uncontrolled movements of mouth, tongue, or jaw. 7. Promptly report flu like symptoms. Seek medical attention if the side effects are serious. ANXIOLYTICS: Anxiolytics, or antianxiety drugs, are primarily used to treat anxiety and insomnia. The major group of anxiolytics are the benzodiazepines (a minor tranquilizer group). Long before benzodiazepines were prescribed for anxiety and insomnia, barbiturates were used. Benzodiazepines are considered more effective than barbiturates because they enhance the action of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter within the CNS. Benzodiazepines have fewer side effects and may be less dangerous in overdosing. A certain amount of anxiety may make one more alert and energetic; however, when the anxiety is excessive, it could be disabling, and anxiolytics may be prescribed. The action of anxiolytics resembles that of the sedative-hypnotics but not that of the antipsychotics. There are two types of anxiety: primary and secondary. Primary anxiety is not caused by a medical condition or by drug use; secondary anxiety is related to selected drug use or medical or psychiatric disorders. The anxiolytics are not usually given for secondary anxiety unless the medical problem is untreatable, severe, and causes disability. In this case, an anxiolytic could be given for a short period to alleviate any acute anxiety attacks. These agents treat the symptoms but do not cure them. Long-term use of anxiolytics is discouraged because tolerance develops within weeks or months, depending on the agent. ANXIOLYTICS: BENZODIAZEPINES Benzodiazepines have multiple uses, such as anticonvulsants, sedative-hypnotics, preoperative drugs, and anxiolytics. Most of the benzodiazepines are used mainly for severe or prolonged anxiety; examples include chlordiazepoxide (Librium), diazepam (Valium), clorazepate dipotassium (Tranxene), lorazepam (Ativan), alprazolam (Xanax), prazepam (Centrax), and halazepam (Paxipam). The most frequently prescribed benzodiazepine is lorazepam (Ativan). Many of the benzodiazepines are used for more than one purpose. Benzodiazepines are lipid soluble and are absorbed readily from the GI tract. They are highly protein bound (80% to 98%). Benzodiazepines are primarily metabolized by the liver and excreted in urine, so the drug dosage for clients with liver or renal disease should be lowered accordingly to avoid possible cumulative effects. Traces of benzodiazepine metabolites could be present in the urine for weeks or months after the person has stopped taking the drug. Pharmacokinetics: Lorazepam is highly lipid-soluble, and the drug is rapidly absorbed from the GI tract. The drug is highly protein-bound, and the half-life is 10 to 20 hours. Pharmacodynamics: Lorazepam acts on the limbic, thalamic, and hypothalamic levels of the CNS. The onset of action is 15 to 30 minutes by mouth and 1 to 5 minutes by IV. The serum levels of most oral doses of benzodiazepines peak in 2 hours. NURSING INTERVENTIONS: Observe client for side effects of anxiolytics. Recognize that drug tolerance and physical and psychologic dependency can result with most anxiolytics. Recognize that anxiolytic dosages should be less for older adults, children, and debilitated persons than for middle-age adults. Monitor vital signs, especially blood pressure and pulse; orthostatic hypotension may occur. Encourage the family to be supportive of client. CLIENT TEACHING: Advise client not to drive a motor vehicle or operate dangerous equipment when taking anxiolytics. Instruct client not to consume alcohol or CNS depressants such as narcotics while taking an anxiolytic. Teach client ways to control excess stress and anxiety, such as relaxation techniques. Inform client that effective response may take 1 to 2 weeks. Encourage client to follow drug regimen and not to abruptly stop taking the drug after prolonged use because withdrawal symptoms can occur. Instruct client to arise slowly from the sitting to standing position to avoid dizziness from orthostatic hypotension. G.3 CNS STIMULANTS, ADHD and ALZHEIMER AGENTS  Numerous drugs can stimulate the central nervous system (CNS), but the medically approved use of these drugs is limited to the treatment of attention deficit/hyperactivity disorder (ADHD) in children, narcolepsy, obesity and the reversal of respiratory distress. The major group of CNS stimulants includes amphetamines and caffeine, which stimulate the cerebral cortex of the brain; analeptics and caffeine, which act on the brainstem and medulla to stimulate respiration; and anorexiants, which act to some degree on the cerebral cortex and on the hypothalamus to suppress appetite. The amphetamines and related anorexiants are greatly abused. Long-term use of amphetamines can produce psychologic dependence and tolerance. Gradually increasing a drug dose and then abruptly stopping the drug may result in depression and withdrawal symptoms. Attention deficit/hyperactivity disorder (ADHD) might be caused by a disregulation of the transmitters-serotonin, norepinephrine, and dopamine. ADHD occurs primarily in children, usually before the age of 7, but may continue through the teenage years. The incidence of ADHD is three to seven times more common in boys than in girls. Characteristic behaviors include inattentiveness, inability to concentrate, restessness (fidgety), hyperactivity (excessive and purposeless activity), inability to complete tasks, and impulsivity. AMPHETAMINES: (CNS STIMULANTS) Amphetamines stimulate the release of the neurotransmitters -norepinephrine and dopamine-from the brain and the sympathetic nervous system (peripheral nerve terminals). The amphetamines cause euphoria and alertness; however, they can also cause sleeplessness, restlessness, tremors, and irritability.The half-life of amphetamines varies from 4 to 30 hours. Amphetamines are prescribed for narcolepsy, and in some cases for ADHD, when amphetamine-like drugs are ineffective. Amphetamine (Adderall) has been effective for controlling ADHD. Dextroamphetamine (Dexedrine) and methamphetamine (Desoxyn) may also be prescribed for some ADHD clients. Methylphenidate (Ritalin), dexmethylphendate (Focalin), and pemoline (Cylert), amphetamine-like drugs, are given to increase the child's attention span and cognitive performance (e.g., memory, reading) and to decrease impulsiveness, hyperactivity, and restlessness. Methylphenidate and pemoline are also used to treat narcolepsy. Pemoline should not be considered a first-line drug for ADHD because it can cause hepatic failure. There is less potential abuse of pemoline than methylphenidate; thus it is classified as a controlled- substance schedule (CSS) IV drug. Side Effects and Adverse Reactions: Amphetamines can cause adverse effects in the central nervous, cardiovascular, gastrointestinal (Gl), and endocrine systems. The side effects and adverse reaction include restlessness, insomnia, tachycardia, hypertension, cardiac dysrhythmias, dry mouth, anorexia, weight loss, diarrhea or constipation, and impotence. Amphetamine-Like Drugs for ADHD and Narcolepsy: Narcolepsy is a sleep disorder that makes people very drowsy during the day. People with narcolepsy find it hard to stay awake for long periods of time. It is a chronic neurological disorder that affects the brain's ability to control sleep- wake cycles. They fall asleep suddenly, which can cause serious problems in their daily routine. Methylphenidate (Ritalin), dexmethylphendate (Focalin), and pemoline (Cylert), amphetamine-like drugs, are given to increase the child's attention span and cognitive performance (e.g., memory, reading) and to decrease impulsiveness, hyperactivity, and restlessness. Methylphenidate and pemoline are also used to treat narcolepsy. Pemoline should not be considered a first-line drug for ADHD because it can cause hepatic failure. Pharmacokinetics: Methylphenidate and pemoline are well absorbed from the GI mucosa. Although pemoline has a longer half-life than methylphenidate, the drugs are usually administered to children once a day before breakfast. Pharmacodynamics: Methylphenidate and pemoline help to correct ADHD by decreasing hyperactivity and improving attention span. These drugs may also be prescribed for treating narcolepsy. These amphetamine-like drugs are considered more effective in treating ADHD than amphetamines, except for Adderall. Amphetamines are generally avoided because they have a higher potential for abuse, habituation, and tolerance. Sympathomimete drugs, such as decongestants, enhance the actions of methylphenidate and pemoline. Antihypertensives and barbiturates can decrease the action of these drugs. NURSING INTERVENTIONS: Monitor vital signs. Report irregularities. Record height, weight and growth of children. Observe client for withdrawal symptoms (e.g., nausea, vomiting, weakness, headache). Monitor client for side effects (e.g., insomnia, restlessness, nervousness, tremors, irritability, tachycardia, elevated blood pressure). Report findings. CLIENT TEACHING: Instruct client to take drug 30 to 45 minutes before meals, because food affects the absorption rate. Direct client to avoid alcohol consumption. Encourage the use of sugarless gum to relieve dry mouth. Teach client to monitor weight twice a week and to report weight loss. Advise client to avoid driving and using hazardous equipment when experiencing tremors, nervousness, or increased heart rate. Instruct client not to abruptly discontinue the drug; the dose must be tapered off to avoid withdrawal symptoms. Consult health care provider before modifying the dose. Explain to client or family that long-term use may lead to drug abuse. Encourage client to read the labels on OTC products because many contain caffeine. A high caffeine plasma level could be fatal. Teach nursing mother to avoid taking all CNS stimulants. These drugs pass into the breast milk and can cause the infant to be hyperactive or restless. Direct family to seek counseling for children with attention deficit/hyperactivity disorder. Drug therapy alone is not an appropriate therapy program. Amphetamine and amphetamine-like drugs should not be taken in the evening or before bedtime because insomnia may result. These drugs should not be given within 6 hours before sleep. Instruct parents to provide children with a nutritional breakfast because drug may have anorexic effects. Teach client about drug side effects and the need to report tachycardia and palpitations. Monitor children for onset of Tourette's syndrome. ALZHEIMERS DISEASE: Alzheimer's disease is an incurable dementia illness characterized by chronic, progressive neurodegenerative conditions with marked cognitive dysfunction. The onset occurs between ages 45 and 65. Alzheimer's disease is distinguished from other forms of dementia by characteristic changes in the brain that are visible only upon microscopic examination during autopsy. Brains affected by Alzheimer's disease often show presence of the following: Fiber tangles within nerve cells (neurofibrillary tangles) & clusters of degenerating nerve endings (neuritic plaques). The causes of Alzheimer's disease are not yet fully understood, but probably include a combination of age-related changes in the brain, like shrinking, inflammation, blood vessel damage, and breakdown of energy within cells, which may harm neurons and affect other brain cells. Alzheimer's drugs might be one strategy to help slow or manage memory loss, thinking and reasoning problems, and day-to-day function. While Alzheimer's drugs don't cure the disease, they can improve quality of life and help prolong independence. These drugs may help reduce or control some cognitive and behavioral symptoms. Cholinesterase inhibitors prevent the breakdown of acetylcholine, a brain chemical believed to be important for memory and thinking. TACRINE: Tacrine (Cognex), an AChE (acetylcholinesterase) inhibitor, is prescribed to improve cognitive function for clients with mild to moderate Alzheimer's disease. This drug increases the amount of ACh (acetylcholine) at the cholinergic synapses. Tacrine tends to slow the disease process. Only 30% of clients have an effective response to tacrine, and even for those it has a short-lasting effect. Pharmacokinetics: Tacrine is absorbed faster through the GI tract without food. Because it has a relatively short half-life, tacrine is given four times a day, and the dose is gradually increased. Pharmacodynamics: Tacrine has been somewhat successful in improving memory in the early phase of Alzheimer's disease. The onset of action is 0.5 to 1.5 hours: peak action is 2 hours. However, the duration of action is prolonged to 24 to 36 hours; thus side effects should be closely monitored. This drug is contraindicated for clients with liver disease because hepatotoxicity may occur. Cumulative drug effect is likely to occur in older adults and in clients with liver and renal dysfunction. NURSING INTERVENTIONS: Maintain consistency in care. Assist client in ambulation and activity. Check for side effects related to the continuous use of AChE inhibitors. Record vital signs periodically. Note signs of bradycardia and hypotension. Monitor client's behavioral changes and record improvement or decline. CLIENT TEACHING: Explain to client and family members the purpose for the prescribed drug therapy. Teach the time for drug dosing and the schedule for increasing drug dosing to the family member responsible for client's medications. Inform client and family member that client should rise slowly to avoid dizziness and loss of balance. G.4 ANTIPARKINSONS AGENTS and MUSCLE RELAXANTS Parkinsonism (Parkinson's disease), a chronic neurologic disorder that affects the extrapyramidal motor tract (which controls posture, balance, and locomotion), is considered a syndrome (combination of symptoms) because of its three major features: rigidity, bradykinesia (slow movement), and tremors. Rigidity (abnormally increased muscle tone) increases with movement. Postural changes caused by rigidity and bradykinesia include the chest and head thrust forward with the knees and hips flexed, a shuffling gait, and the absence of arm swing. Other characteristic symptoms are masked facies (no facial expression), involuntary tremors of the head and neck, and pill-rolling motions ot the hands. The tremors may be more prevalent at rest. Parkinsonism is caused by an imbalance of the neurotransmitters dopamine (DA) and acetylcholine (ACh). It is marked by degeneration of neurons that originate in the substantia nigra of the midbrain and terminate as the basal ganglia of the extrapyramidal motor tact. When dopamine levels decrease, it causes irregular brain activity, leading to problems with movement and other symptoms of Parkinson's disease. The reason for the degeneration of neurons is unknown. Drugs used to treat parkinsonism reduce the symptoms or replace the dopamine deficit. These drugs fall into five categories: (1) anticholinergics, which block the cholinergic receptors; (2) dopaminergics, which convert to dopamine; (3) dopamine agonists, which stimulate the dopemine receptors; (4) MAO-B inhibitor, which inhibits the monoamine oxidase-B (MAO-B) enzyme that interferes with dopamine: and (5) COMT inhibitors, which inhibit the catechol-O-methyltransferase enzyme that inactivates dopamine. 1) ANTICHOLINERGICS: Anticholinergics are parasympatholytics that inhibit the release of acetylcholine. Anti-cholinergics are used to treat drug-induced parkinsonism, or pseudoparkinsonism, a side effect of the antipsychotic drug group phenothiazines. Examples of anticholinergics used for parkinsonism include trihexyphenidyl (Artane), benztropine (Cogentin), biperiden (Akineton), procyclidine (Kemadrin), ethopropazine (Parsidol), and orphenadrine (Norflex). NURSING INTERVENTION: Monitor vital signs, urine output, and bowel sounds. Increased pulse rate, urinary retention, and constipation are side effects of anticholinergics. Observe for involuntary movements. CLIENT TEACHING: Advise client to avoid alcohol, cigarettes, caffeine, and aspirin to decrease gastric acidity. Suggest that client relieve dry mouth with hard candy, ice chips, or sugarless chewing gum. Anticholinergics decrease salivation. Suggest that client use sunglasses in direct sun because of possible photophobia. Advise client to void before taking the drug to minimize urinary retention. Advise client who takes an anticholinergic to control symptoms of parkinsonism to have routine eye examinations to determine the presence of increased intraocular pressure, which indicates glaucoma. Clients who have glaucoma should not take anti-cholinergics. 2) DOPAMINERGICS: Carbidopa-Levodopa The first dopaminergic drug was levodopa (L-dopa), introduced in 1961. Levodopa is the most effective drug for diminishing the symptoms of Parkinson's disease. Its major benefit is increased mobility. Because dopamine cannot cross the blood-brain barrier, levodopa, a precursor of dopamine that can cross the blood-brain barrier, was developed. Because of the side effects of levodopa and the fact that so much of the levodopa is metabolized before reaching the brain, an alternative drug, carbidopa, was developed to inhibit the enzyme dopa decarboxylase. By inhibiting the enzyme in the peripheral nervous system, more levodopa reaches the brain. The carbidopa is combined with levodopa in a ratio of 1 part carbidopa to 10 parts levodopa. NURSING INTERVENTIONS: Monitor client's vital signs and electrocardiogram. Orthostatic hypotension may occur during early use of levodopa and bromocriptine. Instruct the client to rise slowly to avoid faintness. Check for weakness, dizziness, or syncope, which are symptoms of orthostatic hypotension. Administer carbidopa-levodopa (Sinemet) with low-protein foods. High-protein diets interfere with drug transport to the CNS. Observe for symptoms of parkinsonism. CLIENT TEACHING: Advise client not to abruptly discontinue the medication. Rebound parkinsonism (increased symptoms of parkinsonism) can occur. Inform client that urine may be discolored and will darken with exposure to air. Perspiration also may be dark. Explain that both are harmless but that clothes may be stained. Advise client with diabetes that the blood sugar level should be checked with an OTC reagent and not done through urine testing. Instruct client to report side effects and symptoms of dyskinesia. Explain to client that it may take weeks or months before the symptoms are controlled. Suggest to client that taking levodopa with food may decrease GI upset; however, food will slow the drug absorption rate. Advise client to avoid vitamins that contain vitamin B6 (pyridoxine) and foods rich in vitamin B6, such as beans (lima, navy, kidney) and cereals. Advise client who takes high doses of selegiline to avoid foods high in tyramine, such as aged cheese, red wine, cream, yogurt, chocolate, bananas, and raisins. 3) DOPAMINE ANTAGONISTS: Other dopaminergics called dopamine antagonists stimulate the dopamine receptors. For example- amantidine hydrochloride (Symmetrel) is an antiviral drug that acts on the dopamine receptors. It may be taken alone or in combination with levodopa or an anticholinegic drug. Initially, amantadine produces improvement in symptoms of parkinsonism in approximately two thirds of the clients; however, this improvement is usually not sustained because drug tolerance develops. Amantadine can also be used to treat drug-induced parkinsonism. Bromocriptine mesylate (Parlodel) acts directly on the dopamine receptors in the central nervous system (CNS), cardiovascular system, and gastrointestinal (GI) tract. Bromocriptine is more effective than amantadine and the anticholinergics, however it is not as effective as levodopa. Clients who cannot tolerate levodopa are frequently given bromocriptine. Bromocriptine may be given with levodopa or carbidopa- levodopa. 4) MAO-B INHIBITOR: The enzyme monoamine oxidase-B (MAO-B) causes catabolism (breakdown) of dopamine. Selegiline inhibits MAO-B, thus prolonging the action of levodopa. It may be ordered for newly diagnosed clients with Parkinson's disease. The use of selegiline could delay levodopa therapy by a year. It decreases "on-off" fluctuations. Large doses of selegiline may inhibit MAO-A, an enzyme that promotes the metabolism of tyramine in the Gl tract. Ingestion of foods high in tyramine, such as aged cheese, red wine, and bananas, if they are not metabolized by MAO-A, can cause a hypertensive crisis. Severe adverse drug interactions can occur between selegiline and various tricyclic antidepressants (TCA) or selective serotonin reuptake inhibitors (SSRIs). 5) COMT INHIBITORS: The enzyme catechol-O-methyltransferase (COMT) inactivates dopamine. When taken with a levodopa preparation, COMT inhibitors increase the amount of levodopa forcentration in the brain. Tolcapone (Tasmar) was the first COMT inhibitor taken with levodopa for advanced Parkinson's disease. This drug can affect liver cell function, therefore serum liver enzymes should be closely monitored. Precautions for Drugs Used to Treat Parkinson's Disease: The common side effects of anticholinergics include dry mouth and dry secretions, urinary retention, constipation, blurred vision, and an increase in pulse rate. Mental effects, such as restlessness and confusion, may occur in the older adult. GI disturbances are common because dopamine stimulates the chemoreceptor trigger zone (CTZ) in the medulla, which stimulates the vomiting center. Taking the drug with food can decrease nausea and vomiting: however, food slows the absorption rate. Dyskinesia (impaired voluntary movement) may occur with high levodopa dosages. Cardiovascular side effects include orthostatic hypotension and increased heart rate during early use of levodopa. Cardiac dysrythmias may occur as the levodopa dosages are increased. Psychosis (paranoia) and increased libido are additional side effects of increased levodopa dosages. Amantadine has few side effects, but they can intensify when the drug is combined with other antiparkinson drugs. Orthostatic hypotension, confusion, urinary retention, and constipation are common side effects of amantadine. MUSCLE RELAXANTS: Muscle relaxants relieve muscular spasms and pain associated with traumatic injuries and spasticity from chronic debilitating disorders (e.g. MS, strokes [cerebrovascular accident], cerebral palsy, head and spinal cord injuries). Spasticity results from increased muscle tone from hyper-excitable neurons caused by increased stimulation from the cerebral neurons or lack of inhibition in the spinal cord or at the skeletal muscles. The centrally acting muscle relaxants depress neuron activity in the spinal cord or brain and act directly on the skeletal muscles. Pharmacokinetics: Carisoprodol is well absorbed from the GI tract. Pharmacodynamics: Carisoprodol alleviates muscle spasm associated with acute painful musculoskeletal conditions. When carisoprodol is taken with alcohol, sedative-hypnotics, barbiturates, or tricyclic antidepressants (TCAs), increased central nervous system (CNS) depression occurs. The onset of action, peak concentration time, and duration of action for carisoprodol is short. Side Effects and Adverse Reactions: The side effects from centrally acting muscle relaxants include drowsiness; dizziness; lightheadedness; headaches, and occasional nausea, vomiting, diarrhea, and abdominal distress. Cyclobenzaprine and orphenadrine have anti-cholinergic effects. CLIENT TEACHING: Instruct client that the muscle relaxant should not be abruptly stopped. Drug should be tapered over 1 week to avoid rebound spasms. ・ Advise the dient not to drive or operate machinery when taking muscle relaxants. These drugs have a sedative effect and can cause drowsiness. Inform client that most of the centrally acting muscle relaxants for acute spasms are usually taken for no longer than 3 weeks. Teach client to avoid alcohol and CNS depressants. If muscle relaxants are taken with these drugs, CNS depression may be intensified. Warn client that these drugs are contraindicated for pregnant women or nursing mothers. Check with the health care provider. Tell client to report side effects of the muscle relaxant, such as nausea, vomiting, dizziness, faintness, headache, and diplopia. Dizziness and faintness are most likely caused by orthostatic hypotension. Educate the client to take muscle relaxants with food to decrease GI upset. G.5 ANTI-SEIZURES/ ANTI-EPILEPSY  Epilepsy is a chronic, recurrent neurological disorder of the brain characterized by repeated seizures. A seizure is defined as a sudden alteration of behavior due to a temporary change in the electrical functioning of the brain. Normally, the brain continuously generates tiny electrical impulses in an orderly pattern. These impulses travel along neurons — the network of nerve cells in the brain — and throughout the whole body via chemical messengers called neurotransmitters. In epilepsy, the brain's electrical rhythms have a tendency to become imbalanced, resulting in recurrent seizures. Drugs used for epileptic seizures are called antiseizure drugs, anti-convulsants, or antiepileptic drugs (AEDs). Antiseizure drugs stabilize nerve cell membranes and suppress the abnormal electric impulses in the cerebral cortex. These drugs prevent seizures but do not eliminate the cause or provide a cure. Antiseizure drugs are classified as central nervous system (CNS) depressants. With the use of antiseizure drugs, seizures are controlled in approxImately 70% of patients. Because of the possible long-term side effects of the drugs, it is common clinical practice to consider drug withdrawal after an individual has been in remission (seizure free) for three or more years. Many types of antiseizure drugs are used to treat seizures, including the hydantoins (phenytoin), long-acting barbiturates (phenobarbital, primidone), succinimides (ethosuximide), benzodiazepines (diazepam, clonazepam), iminostilbanes (carbamazepine), and valproate (valproic acid). Antiseizure drugs are not indicated for all types of seizures. For example, phenytoin is effective in treating tonic-clonic and partial seizures but is not effective in treating absence seizures. Action of Antiseizure Drugs: Antiseizure drugs work in one of three ways: (1) by suppressing sodium Influx through the drug binding to the sodium channel when it is inactivated, which prolongs the channel inactivation and thereby prevents neuron firing: (2) by suppressing the calcium influx, which prevents the electric current generated by the calcium ions to the T- type calcium channel; or (3) by increasing the action of GABA, which inhibits neurotransmitters throughout the brain. The drugs that suppress sodium influx are phenytoin, fosphenytoin, carbamazepine, oxcarbazepine, valproic acid, topiramate, zonisamide, and lamotrigine. Valproic acid and ethosunimide are examples of drugs that suppress calcium influx. Examples of drug groups that enhance the action of GABA are barbiturates, benzodiazepines and tiagabine. Gabapentin promotes GABA release. Pharmacokinetics: Phenytoin is slowly absorbed from the small intestine. It is a highly protein-bound. With a small to average drug dose, the half-life of phenytoin averages approximately 22 hours, but the range can be from 7 to 60 hours. Pharmacodynamics: The pharmacodynamics of orally administered phenytoin include onset of action within 30minutes to 2 hours, peak serum concentration in 1.5 to 3 hours, and a duration of 6 to 12 hours. The onset of action tor intravenous (IV) administration is with minutes, peak action is 10 to 30 minutes, and the duration is up to 12 hours. Types of seizures: Generalized tonic-clonic seizure or Grand mal seizure. This type of seizure has people crying out, falling on the ground, jerking around, experiencing muscle spasms, and generally losing consciousness. This is accompanied by fatigue afterwards. Absence Seizures or “Petit mal” seizures, are staring spells that start suddenly and may be mistaken for simple daydreaming. The person having an absence seizure will typically stop moving and stare in one direction for 15 seconds or less. Focal seizure or Partial seizure begins in one side of the brain. Status epilepticus is a seizure that lasts longer than 5 minutes, or if you have more than one seizure without returning to a normal level of consciousness between episodes. Call for emergency help if: A seizure lasts 5 minutes or longer. One seizure occurs right after another without the person regaining consciousness or coming to between seizures. Breathing becomes difficult or the person appears to be choking. Very long seizures (those lasting 30 minutes or longer) are dangerous and even increase the risk of death. Side Effects and Adverse Reactions: The adverse effects of hydantoins include psychiatric effects such as depression, suicidal ideation, Stevens-Johnson syndrome, ventricular fibrilation, and blood dyscrasias such as thrombocytopenia (low platelet count) and leukopenia (low white blood cell count). Injection site reactions, such as purple glove syndrome (swollen, discolored, and painful extremities that may require amputation), may occur. Patients on hydantoins for long periods might have elevated blood glucose (hyperglycemia) that results from the drug inhibiting the release of insulin. Less severe side effects include nausea, vomiting, gingival hyperplasia (overgrowth of gums or reddened gums that bleed easily), constipation, drowsiness, headaches, slurred speech, confusion, and nystagmus (constant, involuntary, cyclical movement of the eyeball). Drug Interactions: Drug interaction is common with hydantoins because they are highly protein bound. Hydantoins compete with other drugs (e.g., anti-coagulants, aspirin) for plasma protein-binding sites. The hydantoins displace anticoagulants and aspirin, causing more free-drug avalability and increasing their activity. Nursing Interventions: Monitor serum drug levels of antiseizure medication to determine therapeutic range (10 to 20 mcg/mL). Encourage patient's compliance with medication regimen. Monitor patient's complete blood count (CBC) levels for early detection of blood dyscrasias. Use seizure precautions (environmental protection from sharp objects) for patients at risk for seizures. Determine whether the patient is receiving adequate nutrients; phenytoin may cause anorexia, nausea, and vomiting. Advise female patients who are taking oral contraceptives and antiseizure drugs to use an additional contraceptive method. CLIENT TEACHING: Advise patients not to drive or perform other hazardous activities when initiating antiseizure therapy because drowsiness may occur. Counsel female patients contemplating pregnancy to consult with a health care provider because phenytoin and valproic acid may have a teratogenic effect (can cause birth defects or abnormalities in fetus). Monitor serum phenyton levals closely during pregnancy because seizures tend to become more frequent due to increased metabolic rates. Warn patients to avoid alcohol and other CNS depressants because they can cause an added depressive effect. Explain to patients that cartain herbs can interact with antiseizure drugs, and dose adjustment may be required. Encourage patients to obtain a medical alert identifcation card, medical alert bracelet, or tag that indicates their diagnosis and drug regimen. Teach patients not to abruptly stop drug therapy but rather to withdraw the prescribed drug gradually under medical supervision to prevent seizure rebound (recurrence of seizures) and status epilepticus. Counsel patients about the need for preventive dental checkups. Wam patients to take their prescribed antiseizure drug, get laboratory tests as ordered, and keep follow-up visits wim health care providers. Teach patients not to self-medicate with over-the-counter (OTC) drugs without first consulting a health care provider. Advise patients with diabetes to monitor serum glucose levels more closely than usual because phenytoin may inhibit insulin release, causing an increase in glucose level. G.6 SUBSTANCE ABUSE, DEPRESSANTS, STIMULANTS, HALLUCIGENICS  Most drugs are used safely and within prescribed guidelines, but it is possible for all drugs to be misused or abused. Drug misuse generally refers to indiscriminate use of a chemical substance or its use for purposes other than for which it is intended. Drug abuse refers to an overindulgence of a chemical substance that results in a negative impact on the psychologic, physical, or social functioning of an individual. Chronic abuse of a drug may lead to addiction. Drug addiction is a complex disease of the central nervous system (CNS) characterized by a compulsive, uncontrolled craving for and dependence on a substance to such a degree that cessation causes severe emotional, mental, or physiologic reactions. Current research indicates that most addictive drugs increase the availabily of dopamine and other neurotransmitters in the "pleasure" area of the mesolimbic system of the brain. This area has been identified as the brain reward system, an ancient system that creates the sensation of pleasure for certain behaviors necessary for survival such as eating and sexual behavior. Central Nervous System (CNS) depressants are medicines that include sedatives, tranquilizers, and hypnotics. These drugs can slow brain activity, making them useful for treating anxiety, panic, acute stress reactions, and sleep disorders. CNS depressants cause drowsiness; sedatives are often prescribed to treat sleep disorders like insomnia and hypnotics can induce sleep, whereas tranquilizers are prescribed to treat anxiety or to relieve muscle spasms. Misuse of prescription CNS depressants can lead to problem use, known as a Substance Use Disorder (SUD), which takes the form of addiction in severe cases. Long-term use of prescription CNS depressants, even as prescribed by a doctor, can cause some people to develop a toleranc.. A SUD develops when continued use of the drug leads to negative consequences such as health problems or failure to meet responsibilities at work, school, or home, but despite all that the drug use continues. Some examples of CNS depressants grouped by their respective drug class are: Benzodiazepines diazepam (Valium®) clonazepam (Klonopin®) alprazolam (Xanax®) triazolam (Halcion®) estazolam (Prosom®) Non-Benzodiazepine Sedative Hypnotics zolpidem (Ambien®) eszopiclone (Lunesta®) zaleplon (Sonata®)  When people overdose on a CNS depressant, their breathing often slows or stops. This can decrease the amount of oxygen that reaches the brain, a condition called hypoxia. Hypoxia can have short and long-term mental effects and effects on the nervous system, including coma and permanent brain damage. Those who have become addicted to a prescription CNS depressant and stop using the drug abruptly may experience a withdrawal. Withdrawal symptoms include: seizures; shakiness; anxiety; agitation; insomnia; overactive reflexes; increased heart rate, blood pressure, and temperature; hallucinations; and severe cravings. People addicted to prescription CNS depressants should not attempt to stop taking them on their own. Withdrawal symptoms from these drugs can be severe and—in the case of certain medications-potentially life-threatening. How can people get treatment for prescription CNS depressant addiction? People addicted to these medications should undergo medically supervised detoxification because the dosage they take should be tapered gradually. Counseling can help people through this process. One type of counseling, cognitive-behavioral therapy, focuses on modifying the person's thinking, expectations, and behaviors while improving ways to cope with life's stresses. Prescription stimulants are medicines generally used to treat attention-deficit hyperactivity disorder (ADHD) and narcolepsy. Prescription stimulants increase the activity of the brain chemicals dopamine and norepinephrine. Dopamine is involved in the reinforcement of rewarding behaviors. Norepinephrine affects blood vessels, blood pressure and heart rate, blood sugar, and breathing. Prescription stimulants increase alertness, attention, and energy. Their misuse, including overdose, can also lead to psychosis, anger, paranoia, heart, nerve, and stomach problems. These issues could lead to a heart attack or seizures. Misuse of prescription stimulants can lead to a substance use disorder (SUD), which takes the form of addiction in severe cases. Long-term use of stimulants, even as prescribed by a doctor, can cause a person to develop a tolerance. An SUD develops when continued use of the drug causes issues, such as health problems and failure to meet responsibilities at work, school, or home. Common drug examples are: dextroamphetamine (Dexedrine®) dextroamphetamine/amphetamine combination product (Adderall®) methylphenidate (Ritalin®, Concerta®). Short-Term Effects: People who use prescription stimulants report feeling a "rush" (euphoria) along with the following: increased blood pressure and heart rate increased breathing decreased blood flow increased blood sugar opened-up breathing passages - When people overdose on a prescription stimulant, they most commonly experience several different symptoms, including restlessness, tremors, overactive reflexes, rapid breathing, confusion, aggression, hallucinations, panic states, abnormally increased fever, muscle pains and weakness. At high doses, prescription stimulants can lead to a dangerously high body temperature, an irregular heartbeat, heart failure, and seizures. - If a person develops an SUD and stops use of the prescription stimulant, he or she can experience withdrawal. Withdrawal symptoms include fatigue, depression, and sleep problems. - Behavioral therapies can be effective in helping people stop prescription stimulant misuse, including cognitive-behavioral therapy and contingency management. Hallucinogens are a class of drugs that cause hallucinations—profound distortions in a person’s perceptions of reality. Hallucinogens can be found in some plants and mushrooms (or their extracts) or can be man-made, and they are commonly divided into two broad categories: classic hallucinogens (such as LSD) and dissociative drugs (such as PCP). When under the influence of either type of drug, people often report experiencing rapid, intense emotional swings and seeing images, hearing sounds, and feeling sensations that seem real but are not. Classic hallucinogens are thought to produce their perception-altering effects by acting on neural circuits in the brain that use the neurotransmitter serotonin. Specifically, some of their most prominent effects occur in the prefrontal cortex—an area involved in mood, cognition, and perception—as well as other regions important in regulating arousal and physiological responses to stress and panic. Long-Term Effects of Hallucinogens are: Persistent psychosis: Visual disturbances, Disorganized thinking, Paranoia, Mood disturbances, Hallucinogen Persisting Perception Disorder (HPPD): Hallucinations, Other visual disturbances (such as seeing halos or trails attached to moving objects) There is no established treatment for HPPD, in which flashbacks may occur spontaneously and repeatedly although less intensely than their initial occurrence. Some antidepressant and antipsychotic drugs can be prescribed to help improve mood and treat psychoses. Psychotherapy may also help patients cope with fear or confusion associated with visual disturbances or other consequences of long-term LSD use. Classic Hallucinogens: LSD (d-lysergic acid diethylamide)—also known as acid, blotter, doses, hits, microdots, sugar cubes, trips, tabs, or window panes—is one of the most potent mood and perception altering hallucinogenic drugs. Psilocybin(4-phosphoryloxyN,N-dimethyltryptamine)—also known as magic mushrooms, shrooms, boomers, or little smoke—is extracted from certain types of mushrooms found in tropical and subtropical regions of South America, Mexico, and the United States. Dissociative drugs cause their effects by disrupting the actions of the brain chemical glutamate at certain types of receptors—called N-methyl-D-aspartate (NMDA) receptors—on nerve cells throughout the brain. Glutamate plays a major role in cognition (including learning and memory), emotion, and the perception of pain. PCP also alters the actions of dopamine, a neurotransmitter responsible for the euphoria and “rush” associated with many abused drugs. Dissociative drugs can produce visual and auditory distortions and a sense of floating and dissociation (feeling detached from reality) in users. Use of dissociative drugs can also cause a user to experience anxiety, memory loss, and impaired motor function, including body tremors and numbness. These effects,depends on the amount of the drug taken. In addition, different dissociative drugs can produce a variety of distinct and dangerous effects. For example, at moderate to high doses, PCP can cause a user to have seizures or severe muscle contractions, become aggressive or violent, or even experience psychotic symptoms similar to schizophrenia. At moderate to high doses, ketamine can cause sedation, immobility, and amnesia. Examples of dissociative drugs are: PCP (Phencyclidine)— also known as ozone, rocket fuel, love boat, hog, embalming fluid, or superweed—was originally developed in the 1950s as a general anesthetic for surgery. While it can be found in a variety of forms, including tablets or capsules, it is usually sold as a liquid or powder. DXM (Dextromethorphan)—also known as robo—is a cough suppressant and expectorant ingredient in some over-the- counter (OTC) cold and cough medications that are often abused by adolescents and young adults. The most common sources of abused DXM are “extra-strength” cough syrup. Ketamine—also known as K, Special K, or cat Valium—is a dissociative currently used as an anesthetic for humans as well as animals. Much of the ketamine sold on the street has been diverted from veterinary offices. Research shows that repeated use of PCP can lead to tolerance and the development of a substance use disorder that includes a withdrawal syndrome when drug use is stopped. Other effects of long-term PCP use include persistent speech difficulties, memory loss, depression, suicidal thoughts, anxiety, and social withdrawal. Opioids are a broad group of pain-relieving medicines that work with your brain cells. Opioids can be made from the poppy plant — for example, morphine (Duramorph, MS Contin). Or opioids can be made in a laboratory — for example, fentanyl (Actiq and Fentora). Other opioids include codeine, hydrocodone (Vicodin), oxycodone (OxyContin, Roxybond). Opioid medicines travel through the blood and attach to opioid receptors in brain cells. This blocks pain messages and can boost feelings of pleasure. When used as directed by your doctor, opioid medicines safely help control severe pain, such as pain you may have after surgery. But there are risks when the medicines aren't used correctly. Early symptoms of withdrawal include: Agitation Anxiety Muscle aches Increased tearing Insomnia Sweating Late symptoms of withdrawal include: Abdominal cramping Diarrhea Dilated pupils Nausea Vomiting G.7 AUTONOMIC NERVOUS SYSTEM AGENTS  The autonomic nervous system (ANS) is essential for survival and is responsible for the body’s involuntary activities such as cardiovascular, gastrointestinal, and thermoregulatory homeostasis. The ANS is divided into two major branches: the sympathetic nervous system (SNS), which controls the “fight or flight” responses, and the parasympathetic nervous system (PNS), which oversees the body’s maintenance functions including digestion. Drugs can affect this system, either boosting or blocking its effects. These drugs work by interacting with specific receptors, mimicking or inhibiting natural chemicals in our body. A) ADRENERGIC DRUGS Adrenergic drugs are medications that stimulate certain nerves in your body. They do this either by mimicking the action of the chemical messengers epinephrine and norepinephrine, or by stimulating their release. Many of these medications are used in critical care and emergency settings. Changes in heart rate and blood pressure are the most common side effects. How do they work? Adrenergic drugs stimulate the nerves in your body’s sympathetic nervous system (SNS). This system helps regulate your body’s reaction to stress or emergency. During times of stress, the SNS releases chemical messengers from the adrenal gland. These chemical messengers act on your body to increase heart rate, sweating, and breathing rate and to decrease digestion. This is sometimes called the “fight or flight” response. EPINEPHRINE: Its main use involves the treatment of anaphylaxis. This is a severe allergic reaction that can affect a person’s breathing. An injection of epinephrine can help open up your airway so you can breathe. Other uses of epinephrine include: Asthma attacks. An inhaled form of epinephrine can help treat or prevent severe asthma attacks. Cardiac arrest. An epinephrine injection may restart your heart if your heart has stopped pumping. Infection. If you have a severe infection and aren’t producing enough catecholamines, you may need to be given epinephrine through an intravenous line (IV). Anesthesia. Adding epinephrine to local anesthetics can make them last longer. NOREPINEPHRINE Healthcare professionals sometimes use norepinephrine to treat septic shock, a severe infection that can lead to organ failure. This infection tends to cause dangerously low blood pressure. Norepinephrine given through an IV can help constrict blood vessels, increasing blood pressure. Epinephrine and norepinephrine are two neurotransmitters that also serve as hormones, and are very similar neurotransmitters and hormones. They belong to a class of compounds known as catecholamines. Epinephrine has slightly more of an effect on your heart, while norepinephrine has more of an effect on your blood vessels. Types of adrenergic drugs and their uses: a) Bronchodilators Bronchodilators open up the bronchial tubes, or air passages. These adrenergic drugs act on the beta receptors directly. When they bind with beta-2 receptors, they cause the airways leading to the lungs to open up. This helps improve breathing in patients with respiratory diseases such as: asthma chronic obstructive pulmonary disease (COPD) emphysema bronchitis Examples of bronchodilators include: albuterol formoterol levalbuterol olodaterol salmeterol b) Vasopressors Vasopressors stimulate smooth muscle contraction in the blood vessels. This causes your blood vessels to become narrow. This effect also causes your blood pressure to increase. Increasing blood pressure can help treat shock. Narrowing blood vessels can help stop bleeding. It can also help keep anesthetics (drugs that numb your body) from spreading by closing off nearby blood vessels. Certain vasopressors may also be used for colds or allergies. They can shrink the swollen blood vessels in the mucous membranes of your nose. These drugs are often referred to as nasal decongestants. Examples of vasopressors include: ephedrine epinephrine dopamine phenylephrine pseudoephedrine oxymetazoline c) Cardiac stimulators Cardiac stimulators can be used to stimulate and restore the heart beat. They’re used if your heart stops beating suddenly because of electrocution, suffocation, or drowning. When this happens, epinephrine can be injected directly into your heart to help make it start beating again. Adrenergic drugs may be given for the treatment of the following: Hypovolemic and septic shock Moderately severe to severe episodes of hypotension Control of superficial bleeding during surgical and dental procedures of the mouth, nose, throat, and skin Cardiac decompensation and arrest Allergic reactions (anaphylactic shock, angioneurotic edema) Temporary treatment of heart block Adverse reactions: Cardiac arrhythmias (bradycardia and tachycardia) Headache Nausea and vomiting Increased blood pressure (which may reach dangerously high levels) Precautions: These drugs are used cautiously in patients with coronary insufficiency, cardiac arrhythmias, angina pectoris, diabetes, hyperthyroidism, occlusive vascular disease, or prostatic hypertrophy. Patients with diabetes may require an increased dosage of insulin. Adrenergic drugs are used with extreme caution during pregnancy. Contraindications: Adrenergic drugs are contraindicated in patients with known hypersensitivity. Isoproterenol is contraindicated in patients with tachyarrhythmias, tachycardia, or heart block caused by digitalis toxicity, ventricular arrhythmias, and angina pectoris. Dopamine is contraindicated in those with pheochromocytoma (adrenal gland tumor), unmanaged arrhythmias, and ventricular fibrillation. Epinephrine is contraindicated in patients with narrow-angle glaucoma. Norepinephrine is contraindicated in patients who are hypotensive from blood volume deficits. Midodrine causes severe hypertension in the patient who is lying down (supine); therefore, it is used for orthostatic hypotension only when the patient is considerably impaired. Alpha-adrenergic blocking agents or Alpha blockers lower blood pressure by keeping a hormone called norepinephrine from tightening the muscles in the walls of smaller arteries and veins. As a result, the blood vessels remain open and relaxed. This improves blood flow and lowers blood pressure. Alpha blockers also relax other muscles throughout the body. So, these medicines are sometimes used to improve urine flow in older men with prostate problems. Common side effects might include: Dizziness, Headache, Fast or pounding heartbeat, Weakness. Examples of alpha blockers used to treat high blood pressure include: Doxazosin (Cardura), Prazosin (Minipress), Terazosin. Beta-adrenergic receptor antagonists or Beta-blockers are a family of agents that are widely used to treat hypertension, angina pectoris and cardiac arrhythmias. Beta-blockers are also used for migraine prophylaxis, to treat anxiety, to prevent essential tremor, and to block the side effects of hyperthyroidism. Common side effects are bradycardia, fatigue, dizziness, depression, memory loss, insomnia, impotence, cold limbs and, less commonly, severe hypotension, heart failure and acute bronchospasm. Examples are: Acebutolol, Atenolol, Betaxolol, Bisoprolol, Carvedilol, Esmolol, Labetalol, Metoprolol, Nadolol, Nebivolol, Penbutolol, Pindolol, Propranolol, Sotalol, Timolol Contraindications and Cautions: Allergy to any component of the drug. Bradycardia and heart blocks. Can be worsened by slowed heart rate & conduction. Hepatic impairment. Can alter metabolism of drugs. Asthma. Exacerbated by loss of norepinephrine’s effect of bronchodilation. Shock or heart failure. Can become worse with loss of sympathetic reaction Lactation. Potential effects on neonates. NURSING CONSIDERATION: Monitor patient response to therapy (improvement in blood pressure and heart failure). Monitor for adverse effects (e.g. CV changes, headache, GI upset, liver failure). Avoid using with other alpha-blockers. Advise patients to change positions slowly. Patient should take the medication at the same time each day. Cholinergic drugs mimic the activity of the parasympathetic nervous system. They are also called parasympathomimetic drugs. They are a class of drugs that affect acetylcholine, one of the major neurotransmitters in the nervous system. Acetylcholine, the primary neurotransmitter of the parasympathetic nervous system (PNS), can be excitable or inhibited, is stored at the end of cholinergic neurons and can act on the muscarinic or nicotinic receptors. Activation of these nerves is sometimes called the rest-and-digest response. There are two broad categories of cholinergic drugs: direct-acting and indirect- acting. Examples of direct-acting cholinergic agents include choline esters (acetylcholine, methacholine, carbachol, bethanechol) and alkaloids (muscarine, pilocarpine, cevimeline). Indirect-acting cholinergic agents increase the availability of acetylcholine at the cholinergic receptors. These include reversible agents (physostigmine, neostigmine, pyridostigmine, edrophonium, rivastigmine, donepezil, galantamine) and irreversible agents (echothiophate, parathion, malathion, diazinon, sarin, soman). * Micturition (voiding of urine) is both a voluntary and involuntary act. Urinary retention (not caused by a mechanical obstruction, such as a stone in the bladder) results when micturition is impaired. Treatment of urinary retention with direct-acting cholinergic drugs causes contraction of the bladder smooth muscles and passage of urine. * Myasthenia gravis is a disease that involves rapid fatigue of skeletal muscles because of the lack of ACh released at the nerve endings of parasympathetic nerves. * Glaucoma is a disorder of increased pressure within the eye caused by an obstruction of the outflow of aqueous humor. Treatment of glaucoma with an indirect-acting cholinergic drug produces miosis (constriction of the iris). This opens the blocked channels and allows the normal passage of aqueous humor, thereby reducing intraocular pressure. Adverse Reactions: Topical administration usually produces few adverse effects, but a temporary reduction of visual acuity (sharpness) and headache may occur. General adverse reactions include the following: Nausea, diarrhea, abdominal cramping Salivation Flushing of the skin Cardiac arrhythmias and muscle weakness Contraindications: These drugs are contraindicated in patients with known hypersensitivity to the drugs, asthma, peptic ulcer disease, coronary artery disease, and hyperthyroidism. Bethanechol is contraindicated in those with mechanical obstruction of the GI or genitourinary tracts. Patients with secondary glaucoma, iritis, corneal abrasion, or any acute inflammatory disease of the eye should not use the ophthalmic cholinergic preparations. Precautions: These drugs are used cautiously in patients with hypertension, epilepsy, cardiac arrhythmias, bradycardia, recent coronary occlusion, and megacolon. The safety of these drugs has not been established for use during pregnancy or lactation, or in children.  Cholinergic blocking drugs are also called anticholinergic drugs, cholinergic blockers, or parasympatholytic drugs. Acetylcholine (ACh) is the primary neurotransmitter in the parasympathetic branch of the autonomic nervous system. Cholinergic blocking drugs block the action of the neurotransmitter ACh in the parasympathetic nervous system. Anticholinergic drugs can treat a variety of conditions, including chronic obstructive pulmonary disease (COPD), bladder conditions, and gastrointestinal disorders. Atropine is currently the only widely used anticholinergic drug. Other common examples include meclizine, scopolamine, ipratropium and oxybutynin (Ditropan). Two types of receptors are found in the parasympathetic nervous b ranch: muscarinic and nicotinic receptors. Cholinergic blocking drugs can specifically target one of these types of receptors. For example, antispasmodic drugs used to treat an overactive urinary bladder work by inhibiting the action of the muscarinic receptors in the parasympathetic nervous system. As a result, the detrusor muscle of the bladder does not contract, which prevents the sensations of urinary urgency. Yet, an antispasmodic drug has no effect on skeletal muscles, because it does not inhibit the nicotinic receptors in the parasympathetic nervous system. Anticholinergics can help treat various health conditions including: antidote for insecticide poisoning and cholinergic crisis respiratory disorders, such as bronchospasm and COPD overactive bladder and incontinence asthma symptoms of Parkinson’s disease, such as tremor cardiovascular disease gastrointestinal symptoms allergies pre operative and preanesthetic application emergency treatment of bradychardia and atrioventricular heartblock with hypotension Use of anticholinergic agents may result to these adverse effects: *mydriasis- dilation of the pupil *dysuria- painful urination *cycloplegia- paralysis of the ciliary muscle of the eye CONTRAINDICATIONS: dementia glaucoma hyperthyroidism rapid or irregular heartbeat enlarged prostate depression schizophrenia Pregnancy INTERACTIONS: Antihistamines, antiparkinsonisms, MAOIs, TCAs. These drugs also have anticholinergic effects so incidence of anticholinergic effects increases. Phenothiazines. Decreased effectiveness of this drug. Burdock, rosemary, turmeric. Risk for exacerbated anticholinergic agents PRECAUTIONS: Remain hydrated when taking anticholinergics because they decrease sweating, which may increase the risk of overheating. Taking too many anticholinergics can result in anticholinergic toxicity. Use of these drugs among pregnant women is not allowed because they can cross placenta and cause adverse effects to the fetus. Dose adjustment is needed for older adults as this age group is also more susceptible to drug side effects. They are more likely to have toxic levels of the drug because of renal or hepatic impairments. DEMENTIA WARNING: Long-term use of anticholinergics, as well as use of these drugs in older people, has been linked with an increased risk of dementia. NURSING CONSIDERATIONS: Monitor patient response (e.g., blood pressure, ECG, urine output) for changes that may indicate need to adjust dose. Ensure proper administration of the drug to ensure effective use and decrease the risk of adverse effects. Provide comfort measures (e.g., sugarless lozenges, lighting control, small and frequent meals) to help patient cope with drug effects. Provide patient education about drug effects and warning signs to report to enhance knowledge about drug therapy and promote compliance. Monitor patient response to therapy (improvement in condition being treated). Monitor for adverse effects (e.g., photophobia, heat intolerance, urinary retention). Evaluate patient understanding on drug therapy. CLIENT TEACHING: I. EYE, EAR & SKIN AGENTS I.1 OPTHALMIC AGENTS Eye (ophthalmic) medications are used to treat a variety of common conditions, such as result to injury, allergies, dry eyes, viral or bacterial infections, macular degeneration and glaucoma. Following proper procedures will ensure patients receive the maximum effect of the eye medication, reduce waste, and ensure safe administration of the medication. Forms of Eye Instillations: Medications administered via the eye come prepared in a variety of forms, including drops, ointments, and medication disks. Generally, eye instillations should be used within thirty days of opening, unless otherwise indicated by the manufacturer. Expired eye instillations should never be used because they can become less effective or contaminated over time. Eye Drops- Liquid solutions commonly used to treat conditions such as dry eyes, conjunctivitis (pink eye), glaucoma, red eyes, or itchiness are known as eye drops. They may be ordered as a prescription or found over the counter, depending on the symptoms and complexity of the condition. The medication bottle should always be assessed before use to ensure the medication is indicated for ophthalmic use. Eye Ointments- Greasy, semisolids that use body warmth to melt into tiny drops that rest between the eyeball and eyelid are known as eye ointments. Typically, eye ointments are thicker than eye drops and will stay in the eye longer. Topical Anesthetics: Topical anesthetics are used in selected aspects of a comprehensive eye examination and in a variety of ophthalmic procedures. Ophthalmic anesthetics act by locally blocking the pain signals at the eyes nerve endings. The two most common topical ophthalmic anesthetic are proparacaine hydrochloride (HCI) and tetracaine HCI. Both medications, available in solutions, are administered as drops. Ophthalmic anesthetics should be administered by a trained clinician. Anti-infectives: Antlinfectives are frequently used for eye infections. Conjunctivitis- an inflammation of the membrane (conjunctiva) covering the eye and inner eyelids, is the most common eye condition. Conjunctivitis is also called "pink eye" and can occur because of bacteria, virus, and allergens. Bacterial conjunctivitis usually requires anti-infective therapy to either kill or inhibit the spread of bacteria. Before administering ophthalmic antiinfectives, the nurse should screen the patient for previous allergic reactions. Noninfectious conjunctivitis and local skin and eye irritation are possible side effects of ophthalmic antiinfective drugs. ANTIBACTERIALS: ANTIBACTERIALS: ANTIBACTERIALS: ANTIBACTERIALS: Acanthamoeba keratitis is a rare but serious eye infection that occurs due to a single-celled organism called an amoeba. These are present in bodies of water, the soil, and the air. Acanthamoeba parasites infect the cornea, the transparent covering of the eye. Without treatment, Acanthamoeba keratitis can lead to severe pain, and in some cases, loss of vision. Although anyone can develop the infection, in the United States, most infections develop in those who wear contact lenses. Anti-inflammatories: Inflammatory conditions of the eye not related to infectious pathogens often require treatment with anti- inflammatory drugs. If the inflammation is secondary to a bacterial or fungal infection, an antibiotic or antifungal agent is included in the medication regime. Opthalmic Non Steroidal Antiinflammatory drugs (NSAIDs) such as dicoflenac sodium and ketorelac tromethamine inhibit miosis by preventing the formation of ocular prostaglandins. Most of these drugs are used for management or prevention of ocular inflammation before and after eye surgery. Unlike corticosteroids, NSAIDs do not affect intraocular pressure (IOP). However, ocular NSAIDs can increase bleeding tendencies and delay corneal healing. Ophthalmic Corticosteroids such as dexamethasone and prednisolone acetate are another type of antinflammatory. Corticosteroids are used to treat a number of eye conditions, such as allergic conjunctivitis, herpes zoster keratitis, corneal abrasion, postoperative ocular inflammation, and optic neuritis. When allergies are the cause of eye inflammation, ophthalmic allergy drugs are commonly prescribed to treat the underlying cause. These allergy drugs contain antihistamines and mast cell stabilizers. Ophthalmic Atropine is used before eye examinations to dilate (open) the pupil. It is also used to relieve pain caused by swelling and inflammation of the eye. Ocular sensations that include burning, stinging, blurred vision are common adverse effects reported. CAUTION: Ocular corticosteroids can mask infections, delay healing, and are contraindicated in persons with untreated ocular infections. Corticosteroids can worsen glaucoma by reducing the outflow of aqueous humor and increasing IOP. Increased ocular pessure Decongestants: Eye inflammation typically presents with redness due to vascular congestion of the conjunctiva. Ophthalmic decongestants such as phenylephrine, naphazoline, and tetrahydrozoline stimulate alpha-adrenergic receptors in the arterioles of the conjunctiva, vasoconstricting (narrowing) the blood vessels and thereby decreasing congestion. Many ocular decongestants are available without prescription. If these are absorbed in significant amounts, their sympathetic nervous system effects may pose problems for patients with increased IOP and hypertension. CAUTION: Ocular decongestants are contraindicated in patients with angle-closure glaucoma because