Drug Therapy for Central Nervous System Problems PDF

9 Drug Therapy for Central Nervous System Problems LEARNING OUTCOMES 1. List the names, actions, possible side effects, and adverse effects of drugs for Parkinson's disease. 2. Explain what to teach patients and families about drugs for Parkinson's disease. 3. List the names, actions, possible side...

9 Drug Therapy for Central Nervous System Problems LEARNING OUTCOMES 1. List the names, actions, possible side effects, and adverse effects of drugs for Parkinson's disease. 2. Explain what to teach patients and families about drugs for Parkinson's disease. 3. List the names, actions, possible side effects, and adverse effects of drugs for Alzheimer's disease. 4. Explain what to teach patients and families about drugs for Alzheimer's disease. 5. List the names, actions, possible side effects, and adverse effects of drugs for epilepsy and other seizure problems. 6. Explain what to teach patients and families about drugs for epilepsy and other seizure problems. 7. List the names, actions, possible side effects, and adverse effects of drugs for multiple sclerosis. 8. Explain what to teach patients and families about drugs for multiple sclerosis. KEY TERMS antiepileptic drugs (AEDs) (ĂN-tī-ĕ-pĭ-LĔP-tĭk, p. 170) Drugs that reduce or prevent seizures. biological response modifier (BRM) (bī-ĕ-LŎ-jĭ-kăl rĭ-SPŎN(t)s MŎ-dĭ-fīr, p. 179) Drug that modifies the patient's immune response to abnormal triggers for immunity and inflammation. catechol-O-methyltransferase (COMT) inhibitor (KĂ-tĕ-kŏl-ō-MĔTH-ĭl-TRAN(t)sfĕr-ās, p. 161) Drug that suppresses the activity of the COMT enzyme so that both naturally occurring dopamine and dopamine agonist drugs remain active in the body longer, helping to restore the acetylcholine–dopamine balance in the brain. cholinesterase inhibitor (kō-lĕ-NĔS-tĕ-rās ĭn-HĬ-bă-tĕr, p. 167) Drug that delays memory loss by binding to the enzyme acetylcholinesterase and slowing its action, which allows any acetylcholine produced to remain functional longer. delirium (dĭ-LĬR-ē-ĕm, p. 163) A distressed state of mind that causes irrational beliefs characterized by illusions and paranoia. 296 dopamine agonist (DŌ-pĕ-mēn Ă-gă-nĭst, p. 161) Drug that has the same chemical structure of natural dopamine and is used to increase the levels of dopamine in the brain and restore balance between acetylcholine and dopamine action. dyskinesia (dĭs-kĕ-NĒ-zh(ē-)ă, p. 163) An abnormality and distortion in performing voluntary movements. It results in jerky motions and looks much like uncoordinated dance movements. dystonia (dĭs-TŌ-nē-ă, p. 164) Abnormal involuntary movements such as chewing, grinding of the teeth, protrusion of the tongue, opening and closing the mouth, head bobbing, or jerky, constant movements of the feet or hands. monoamine oxidase type B (MAO-B) inhibitor (mă-nō-ă-MĒN ŎK-să-dās, p. 161) Drug that suppresses the action of MAO-B, which allows dopamine levels to increase and reduce the symptoms of Parkinson's disease. neurotransmitter (nyūr-ō-trănz-MĬ-tĕr, p. 159) Chemical that is released from the end of one nerve, crosses a space (cleft), and then binds to receptors on the beginning of the next nerve in the line (or a skeletal muscle) to transmit the electrical signal from one nerve to the next. N-methyl-D-aspartate (NMDA) blocker (p. 166) Drug that slows the progression of Alzheimer disease by blocking the entrance of calcium into neurons, which reduces or slows neuronal damage. phenytoins (fĕ-NĬ-tĕ-wĕn, p. 170) Antiepileptic drugs that reduce or prevent seizures by binding to sodium channels on nerve membranes in the brain and making them less active, which prevents the spread of neuron excitation. Central Nervous System Functions The central nervous system (CNS) is the brain and the spinal cord (Fig. 9.1). The nerves coming from the spinal cord are part of the peripheral nervous system (PNS) and are controlled by the brain. The PNS nerves serve as a relay between the brain and the body by connecting the CNS to the organs, limbs, muscles, blood vessels, and glands. The CNS has many critical structures and actions that work together to ensure continued normal whole-body functioning. The brain monitors and regulates the coordination of body systems and activities, including movement, endocrine secretions, and the intellectual functions of thinking/decision making. It monitors body conditions by receiving sensory information from elsewhere in the body and by receiving sensory information from the environment from vision, hearing, smell, taste, spacial awareness, and touch. The brain interprets this information and then determines how the body should respond. For example, did you know that we do not actually see with our eyes? We “see” with our brain. The nerve endings (rods and cones) in the retina detect light and shape, then send these nerve signals as messages through the optic nerve to the brain. The brain translates the light image signals into what we “see” or think we see (perceive). Perception of vision is how optical illusions work. Magicians create illusions by taking advantage of how our brain interprets stimuli. 297 FIG. 9.1 Central nervous system. C, Cervical; L, lumbar; T, thoracic. Many problems can occur inside or outside of the CNS that can affect brain function. This chapter focuses on drug therapy for CNS problems that mainly affect physical function. These problems include Parkinson's disease (PD), Alzheimer's disease (AD), epilepsy, and multiple sclerosis (MS). Drug therapy for problems that primarily affect behavior and mental health is presented in Chapter 10. Movement is an important body motor function involving the brain, spinal cord, nerves, muscles, and bones. For example, your decision to move your arm deliberately first starts when you think about it, which excites nerve cells (neurons) in this part of the brain. This excitation is turned into an electrical signal that has to get to your arm muscles to actually move the arm in the direction you planned. Getting the signal from your brain to your arm muscles involves a relay of signals through a line of connected specific nerves. There is a space, or cleft, at each connection (Fig. 9.2). Electrical signals from neurons in the thinking area of your brain are sent (conducted) to the ends of these nerves, where the signal causes the release of neurotransmitters. 298 FIG. 9.2 Continuation of nerve signals by neurotransmitters. (From Fulcher EM, Fulcher RM, Soto CD: Pharmacology, ed 3, St. Louis, 2012, Saunders.) Neurotransmitters are chemicals that are released from the end of one nerve, cross a space (cleft), and then bind to receptors on the beginning of the next nerve in the line. This action transmits the signal that was started in your brain to the next nerve in the line. When the last nerve in the line gets to your arm muscles, the neurotransmitter binds to receptors on your arm muscles to trigger the muscle contractions needed to make your arm move. Neurotransmitters can be excitatory or inhibitory. Excitatory neurotransmitters include acetylcholine (ACh), epinephrine, and norepinephrine. When the excitatory neurotransmitter ACh is released from the end of a nerve in response to thinking about moving your arm, it ensures this “action” signal gets transmitted to the next nerve in the line. At the point where the last nerve in the line is stimulated, the ACh it releases binds to receptors on the arm's skeletal muscles so they contract and move your arm as you intended. Other neurotransmitters are inhibitory. Inhibitory neurotransmitters include dopamine, some types of serotonin, and GABA (gamma-aminobutyric acid). Smooth movement requires input from both an excitatory neurotransmitter (ACh) and an inhibitory neurotransmitter (dopamine). These inputs are balanced in such a way that when you decide to move your arm, you can control the direction of movement, the degree of movement, and the strength of the movement. After all, you do not need the same strength of arm movement to rub your eye gently as you do to throw a baseball 60 feet. Without dopamine modifying your arm muscle contractions, your arm movement would be fast, jerky, and wild. Think of how much hot coffee you would spill moving a cup to your mouth if dopamine were not modifying this arm movement. Some problems that occur within the CNS, such as PD, are a result of an imbalance of excitatory and inhibitory neurotransmitters. Others problems, such as epilepsy, result from conditions within the brain that allow neurons to become excited when the excitation is not needed. Still others, such as AD and MS, result from degenerative changes that occur within nerves or within the support cells of the brain. 299 Drugs for Parkinson's Disease PD is a CNS disorder in which there is not enough dopamine present to modify excitatory signals to skeletal muscles. Dopamine is an inhibitory neurotransmitter that is mostly produced deep in the midbrain area known as the substantia nigra part of the basal ganglia. When this brain area slows or stops production of dopamine, the balance between excitatory motor nerve signals and inhibitory motor nerve signals is reduced, causing mostly excitatory input (Fig. 9.3). Movements become hard to control and jerky, and some muscles are rigid because they fail to relax sufficiently. When the arms and legs move they “catch” at certain points in a “stop and go” fashion known as cogwheel rigidity. The neurologic problems also cause facial features to become “masklike” (Fig. 9.4). The gait becomes slow and shuffling with short steps. The risk for falls greatly increases. Other common symptoms of PD include tremors, stooped posture, difficulty stopping motion once it has started, difficulty chewing and swallowing, and drooling. FIG. 9.3 The neurotransmitter abnormality in Parkinson's disease. (From Lilley LL, Rainforth Collins S, Snyder J: Pharmacology and the nursing process, ed 8, St. Louis, 2017, Elsevier.) 300 FIG. 9.4 The masklike facial expression of a patient with Parkinson disease. (From Perkin D: Mosby's color atlas and test of neurology, London, 1998, Mosby-Wolfe.) Depression, hallucinations, anxiety, and delusions are frequent complications of PD. Delusions and hallucinations can result from the changes in the brain that PD causes or they can occur from the adverse effects of PD drugs themselves. The PD drugs increase the dopamine levels to improve the motor symptoms, but unfortunately at the same time, increasing the dopamine supply can cause hallucinations and delusions. Symptoms of PD worsen over time until finally the patient requires total care. See Box 9.1 for the motor and nonmotor symptoms of PD. Box 9.1 Symptoms of Parkinson's Disease Motor Symptoms Nonmotor Symptoms Slow movements (bradykinesia) Decreased arm swing when walking Difficulty rising from a chair or turning in bed Absence of facial expressions Instability when standing up Freezing in place and having a rigid stance Stooped, shuffling gait Tremors Constipation Diminished sense of smell Depression, anxiety, and irritability Problems with focused attention and planning Slowing of thought, language and memory difficulties Personality changes, dementia Hallucinations and delusions Sleep disturbances Urinary frequency PD is the most common neurodegenerative disease, second to AD. The exact cause of PD is unknown but is thought to be caused from a combination of factors that include genetic, protective, and environmental reasons. The incidence of PD increases with age, but it can occur before the age of 50 years. The disease strikes more men than women. The diagnosis of PD takes quite a while because there is no specific test for the disease. Diagnosis is made after all other neurologic disease 301 processes have been ruled out. By the time the diagnosis of PD is made, most of the person's dopamine has been depleted. Bookmark This! Clinical trials and research into PD are ongoing and changing the face of the disease. Check out the Michael J Fox website: https://www.michaeljfox.org Although drug therapy does not cure PD, it can delay the worsening of symptoms and allow patients to remain independent longer. Drug therapy for PD includes the drug classes of dopamine and dopamine agonists, catechol-O-methyltransferase (COMT) inhibitors, and monoamine oxidase type B (MAO-B) inhibitors. The common drugs in these classes are listed in Table 9.1. Table 9.1 Examples of Common Drugs Used to Manage Parkinson's Disease Dopamine and dopamine agonists: These drugs have the same chemical structure of natural dopamine and improve Parkinson symptoms by increasing the levels of dopamine in the brain to restore balance between acetylcholine and dopamine action. DRUG/ADULT DOSAGE RANGE NURSING IMPLICATIONS carbidopa/levodopa (Rytary, Sinemet) • Carbidopa/levodopa tablets come in different dosages and are increased Rytary (23.75 mg carbidopa/95 mg levodopa) orally initially three frequently from three times daily to up to five times daily according to times per day and increase to a maximum daily dose of 612.5 improvement of symptoms. Tablets also come in extended-release form. mg/2450 mg Extended-release tablets are scored. Sinemet (25 mg carbidopa/100 mg levodopa) orally three times a • Do not crush or chew whole or half tablets; they must be swallowed intact. day and increase dosage to a total of 200 mg/2000 mg/day • Extended-release forms of the drugs that are not scored should not be halved, pramipexole (Mirapex, Mirapex ER) initially, 0.125 mg orally three crushed, or chewed to retain the slow-release effect. times per day; dose is increased by 0.125–0.25 mg/dose every 5–7 • Give with 6–8 ounces of water at least 30–60 minutes before eating to maximize days to a maximum dosage of 1.5 mg orally three times per day absorption. Give with nonprotein snack to avoid nausea. (4.5 mg/day) • Do not give with high-protein foods because they decrease absorption. ropinirole (Requip, Requip XL) initially, 0.25 mg orally three times • Instruct patients to get up slowly to avoid postural hypotension with all per day for the first week; gradually titrate at weekly intervals to a dopamine agonists. maximum of 24 mg/day • Monitor blood glucose levels closely in diabetic patients to avoid hypoglycemia rotigotine (Neupro) apply transdermal patch at an initial dose of 2 caused by increased sympathetic tone. mg/24 hours to a maximum of 8 mg/24 hours • Closely monitor patients with a history of cardiac disease for hypotension and increasing dysrhythmias. • Monitor liver function studies because these drugs are metabolized in the liver and monitor complete blood counts because this drug can increase the risk for GI bleeding. • Notify the healthcare provider for any behavioral changes, hallucinations, or delusions. • Monitor for worsening dyskinesia and/or dystonia reactions and notify the healthcare provider if they occur because this can indicate a need for dosage change. • Skin reactions are common with the use of the rotigotine (Neupro) patch. Do not apply the patch in the same place for 14 days and, after removing the patch, gently clean the skin with mild soap and water. COMT inhibitors: These drugs reduce the symptoms of Parkinson's disease by suppressing the activity of the COMT enzyme so that both naturally occurring dopamine and dopamine agonist drugs remain active in the body longer, helping to restore the acetylcholine–dopamine balance in the brain. DRUG/ADULT DOSAGE RANGE NURSING IMPLICATIONS entacapone (Comtan) 200 mg orally given with each • Give entacapone with every dose of carbidopa/levodopa to enhance drug effect. levodopa/carbidopa dose up to a maximum of 1600 mg/day • Give the first dose of tolcapone with the first dose of carbidopa/levodopa and tolcapone (Tasmar) initially, 100 mg orally three times daily with subsequent doses 6–12 hours later. the first dose given with carbidopa/levodopa; maximum dose is • Review liver function studies and monitor for liver failure in patients who are 600 mg/day taking tolcapone. • Report signs of liver failure, such as abdominal pain, jaundice, and dark urine with nausea and vomiting, to the healthcare provider. • Remind patients that these drugs may cause a nondangerous side effect of turning the urine to orange-brown. • These drugs enhance the effect of dopamine, so symptoms of worsening dyskinesia or psychosis may occur. Notify the healthcare provider if these changes occur. • These drugs cannot be given with nonselective MAO inhibitors because of the increased cardiovascular risk. • Anticipate that the dose of carbidopa/levodopa may be decreased as these drugs take effect. Selective MAO-B inhibitors: MAO-B breaks down dopamine in the brain and elsewhere in the body. These inhibitors allow existing dopamine to remain active in the brain longer. DRUG/ADULT DOSAGE RANGE NURSING IMPLICATIONS rasagiline (Azilect) 0.5–1 g orally once daily • Give these drugs at the same time every day. Once-a-day doses can be taken at safinamide (Xadago) 50–100 mg orally once daily nighttime because they can cause drowsiness. 302 selegiline (Eldepryl, Emsam, Zelapar) 5 mg tablet orally twice daily • Teach patients to avoid foods and beverages that contain large amounts of tyramine when using all of these drugs and for 2 weeks after therapy is stopped. • Monitor vital signs, particularly blood pressure. • Teach patients and families to report severe headache, palpitations, nausea, and vomiting to the healthcare provider immediately because these are signs of a hypertensive crisis. • These drugs enhance the effect of dopamine, so symptoms of worsening dyskinesia or psychosis may occur. Teach patients and families to notify the healthcare provider if these changes occur. • Anticipate that the healthcare provider may decrease the dosage of carbidopa/levodopa as these drugs take effect. COMT, Catechol-O-methyltransferase; MAO-B, monoamine oxidase type B. At one time, the main drug category to manage PD was the anticholinergic drugs. These drugs attempted to balance the decreased dopamine levels by reducing the amount of ACh present. However, this action did not address the main problem of PD (lack of dopamine) and induced many side effects and adverse reactions. As a result, the anticholinergic drugs are not the most common therapy for PD. Memory Jogger The three classes of drugs to manage PD are: • dopamine agonists • COMT inhibitors • MAO-B inhibitors Dopamine Agonists Action and Uses Dopamine agonists are drugs that have the same chemical structure as natural dopamine and are given to increase the levels of dopamine in the brain to restore balance between ACh and dopamine action. The therapeutic effect of these drugs helps reduce muscle tremors and rigidity and improve mobility, muscular coordination, and performance. Dopamine agonists can be used alone or, as symptoms progress, can be used in combination. The National Parkinson Foundation recommends that carbidopa/levodopa (Sinemet, Rytary) be used as a first-line treatment for patients with PD who are older than 70 years and the newer dopamine agonists, such as pramipexole (Mirapex, Mirapex ER), ropinirole (Requip, Requip XL), and rotigotine (Neupro), be used as first-line treatment in patients between the ages of 50 and 70 years. All patients will eventually require levodopa because dopamine is what is deficient in PD. Levodopa is synthesized in the brain and converted to natural dopamine. For this reason, levodopa is the most important drug used to manage the symptoms of PD. Carbidopa is usually given in combination with levodopa because it enhances the levodopa so lower doses of levodopa can be used, thus preventing the nausea and vomiting that accompanies the continual increasing of the levodopa dose to control disease symptoms. Levodopa (Larodopa) is rarely given alone for this reason. “Wearing off” is an issue of the drug losing its effectiveness that can occur after levodopa is used for several years. Levodopa peaks in about 1 hour and wears off in 4 or 5 hours. This wearing-off effect causes rapid swings of symptoms. 303 Symptoms improve when dopamine is present and worsen as the dopamine wears off. This can also be called an “on/off effect.” The extended-release form of carbidopa/levodopa and the longer half-lives of dopamine agonists help to prevent this effect. Carbidopa/levodopa is also available as an intestinal infusion pump (Duopa). The pump is inserted directly into the small intestines via a small feeding tube and can deliver 16 continuous hours of carbidopa and levodopa to reduce motor symptoms. Expected Side Effects/Adverse Reactions The most common side effects of carbidopa/levodopa and all dopamine agonists include both postural and general hypotension, headache, GI disturbances, insomnia, dream abnormalities, impulse control, and confusion. The most common adverse reaction to carbidopa/levodopa (Rytary, Sinemet) is dyskinesia or involuntary muscle movements that look like uncoordinated dance movements. Dyskinesia is common in patients on long-term carbidopa/levodopa therapy (longer than 3 years). The effect of dyskinesia is minimized with the use of pramipexole (Mirapex, Mirapex ER), ropinirole (Requip, Requip XL), rotigotine (Neupro), and other dopamine agonists. Dopamine agonists can also cause delirium, psychosis, and hallucinations. If these problems occur, the healthcare provider will need to determine whether the symptoms are related to the advancing disease process, depression, or the PD drug response. Do Not Confuse Risperidone is an antipsychotic sometimes used to combat psychosis in PD. Ropinirole is used to treat symptoms of PD (stiffness, tremors, muscle spasms, and poor muscle control). Carbidopa/levodopa dosages may be decreased as COMT inhibitors and MAO-B inhibitors are added to the drug regimen. This could precipitate neuroleptic malignant syndrome, with symptoms of agitation, coma, muscle rigidity, tremors, high fever, and an unstable blood pressure. Also, keep in mind that as COMT inhibitors and MAO-B inhibitors are added to the regimen of dopamine agonists, there will be an increase in available dopamine that can increase the adverse effects of the dopamine agonists until dosages of the dopamine agonists are adjusted by the healthcare provider. When dopamine agonists are taken with protein, either as a meal or a snack, the effectiveness of the drug is reduced. These drugs are best absorbed on an empty stomach. Drug Interactions Using antihypertensive agents with dopamine agonists can cause severe hypotension. Using older, nonselective MAO inhibitors like phenelzine (Nardil) along with dopamine agonists can precipitate a hypertensive crisis. Phenytoin (Dilantin) reduces the effectiveness of dopamine agonists. Multivitamins that contain iron decrease the effects of carbidopa/levodopa. Vitamin B6 increases the metabolism 304 of levodopa (Larodopa) without carbidopa. Metoclopramide (Reglan) can reduce the effectiveness of the dopamine agonists because metoclopramide is a dopamine antagonist and prevents the dopamine from combining with the dopamine receptors. Using dopamine agonists with sedatives will worsen drowsiness and can increase the risk for confusion, hallucinations, and delusions, especially in those persons already suffering from mental illnesses. Nursing Implications and Patient Teaching Assessment. Dopamine agonists frequently cause postural hypotension, so take a full set of vital signs, including orthostatic blood pressure readings (supine, sitting, and standing). Assessment of the patient's motor skills and functional ability for walking and eating is important to establish a baseline, as well as to ensure safety from falls and aspiration. Ask whether patients have had melanoma or closed-angle glaucoma. These conditions are contraindicated for dopamine agonist therapy because the drugs can worsen them. Closely monitor blood glucose levels because the sympathetic effects of levodopa can cause hypoglycemia. Observe for symptoms such as headache, anxiety, shakiness, weakness, and irritability that can indicate low blood glucose. Check blood urea nitrogen (BUN) and creatinine levels before starting pramipexole (Mirapex) to rule out renal impairment because 90% of the drug is excreted by the kidneys. Monitor liver enzymes before and at intervals during treatment because other drugs used in the treatment of PD are metabolized by the liver. Planning and implementation. Dopamine agonists are recommended to be given 30 to 60 minutes before meals, not only for better absorption but also to have maximum effect so the patient has less difficulty chewing and swallowing, which lessens the risk for aspiration. Never crush the extended-release tablets. When using rotigotine (Neupro) transdermal patches, apply at the same time every day and rotate application sites. Do not apply to the same site more than once every 14 days to avoid a skin reaction. Dopamine agonists should be withdrawn slowly, because these drugs have a long half-life. When withdrawing one preparation and beginning a new preparation, the new drug is started in small doses and the old drug is withdrawn gradually. These agents are usually started at the lowest dose possible, and the dose is increased gradually until the maximum therapeutic effect has been obtained. Dopamine agonists are available in patches, tablets, sustained-release capsules, syrups, and elixirs. They are generally well absorbed from the GI tract. Peak blood levels of carbidopa/levodopa (Sinemet), one of the main treatment drugs, is achieved in 1 to 6 hours, depending on the route of administration and the formulation of the drug given. Sustained-release capsules reach peak plasma blood levels in 8 to 12 hours. Sustained-release capsules are not recommended for initial therapy because they do not allow enough flexibility in dosage regulation. Evaluation. Tell the patient and family the following: 305 • Take care when using drugs for sleep, pain, to relax muscles, and to control bladder function along with your drugs for PD because the combination can lead to confusion, hallucinations, and other symptoms. • Change positions slowly from lying down to standing up because low blood pressure can occur and cause you to fall. • Contact your healthcare provider as soon as possible if you develop hallucinations or delusions. Long-term use of dopamine agonists may lead to akinesia (loss of movement), tardive dyskinesia (abnormal and involuntary movements, especially of the lower face), and dystonia (impairment of muscle tone). The dosage is likely to be reduced to the minimum effective level to reverse these effects, and very slow and careful changes in dosages are made as necessary to avoid overmedication. Monitor all patients closely for behavior changes because these drugs can exacerbate depression and psychosis. Report abnormal involuntary movement such as chewing, grinding of the teeth, protrusion of the tongue, repeated opening and closing of the mouth, head bobbing, or jerky, constant movements of the feet or hands because this can indicate dystonia, which can be related to either progression of the disease itself or the wearing off of dopamine. If these appear, alert the healthcare provider because the drug dosage may need to be adjusted. Patient and family teaching. Tell the patient and family the following: • Clinical improvements are cumulative (get better over time) and may take 2 to 3 weeks. Therefore continue to take the drug even if you see no changes at first. • If possible, take the drug on an empty stomach 30 to 60 minutes before a meal or snack so the drug is absorbed well and can help you chew and swallow better. • If the drug causes nausea, you can take it with some crackers or other carbohydrates. Do not take the drug with food containing protein because this can reduce the drug's effectiveness. • Avoid taking levodopa (Larodopa) with vitamin B6 (pyridoxine) because the vitamin accelerates the inactivation of the drug. This is not a problem if you are 306 taking levodopa/carbidopa (Sinemet). • Contact your healthcare provider immediately if symptoms suddenly become worse, if you have intermittent winking or muscle twitching, or if abdominal pain, constipation, distention, or urinary problems occur. • Take care when using drugs for sleep, pain, to relax muscles, and to control bladder function along with your drugs for PD because the combination can lead to confusion, hallucinations, and other symptoms. • Change positions slowly from lying down to standing up because low blood pressure can occur and cause you to fall. • Contact your healthcare provider as soon as possible if you develop hallucinations or delusions. Catechol-O-Methyltransferase Inhibitors Action and Uses Catechol-O-methyltransferase (COMT) is an enzyme that breaks down (metabolizes) naturally occurring catecholamine-based neurotransmitters, including dopamine. It also breaks down dopamine agonist drugs. Catechol-O-methyltransferase (COMT) inhibitors are drugs that suppress the activity of the COMT enzyme so that both naturally occurring dopamine and dopamine agonist drugs remain active in the body longer, helping to restore the ACh–dopamine balance in the brain. Levodopa is the main dopamine agonist drug used in PD. COMT is given with levodopa to allow blood levels of levodopa to stay high enough to enter the brain, where it is converted to dopamine. Entacapone (Comtan) and tolcapone (Tasmar) are two COMT inhibitors that are currently used for PD. Expected Side Effects/Adverse Reactions Both of these drugs can potentiate the dopaminergic adverse effects of levodopa and can cause dyskinesia and hypotension. The most common expected effects are GI upset and discoloration of the urine (brownish orange color). Both drugs are metabolized by the liver, but tolcapone (Tasmar) has a higher risk for causing severe liver failure, so it is not used unless other measures have failed. Tolcapone is not used in persons with existing hepatic disease. Liver function studies must be closely monitored every 6 months if tolcapone (Tasmar) is used. Drug Interactions Neither entacapone nor tolcapone should be taken with other MAO inhibitors like 307 phenelzine (Nardil) because they reduce catecholamine metabolism and can cause cardiovascular problems such as severe hypertension, tachycardia, and dysrhythmias. Likewise, any direct catecholamine drugs like epinephrine or methyldopa may increase heart rates, cause dysrhythmias, and cause severely high blood pressures. The MAO-B inhibitors selegiline (Eldepryl, Zelapar) and rasagiline (Azilect) used in PD are considered safe to take with COMT inhibitor drugs because they are selective in blocking the breakdown of dopamine and not other catecholamines, so the adverse cardiac effects are avoided. Nursing Implications and Patient Teaching Assessment. The patient may experience orthostatic hypotension because COMT inhibitor drugs potentiate the action of carbidopa/levodopa. Take a full set of vital signs and orthostatic blood pressures, and remind patients to rise slowly to avoid falls. In addition, monitor for indications of dyskinesia and hyperkinesia, and notify the healthcare provider if they occur. Planning and implementation. Entacapone is given with every dose of carbidopa/levodopa; tolcapone is given with the first dose of carbidopa/levodopa, with subsequent doses being given 6 to 12 hours later. If tolcapone is used, monitor patients for liver failure and review liver function studies. Evaluation. Evaluate patients for akinesia, dystonia, and tardive dyskinesia as discussed earlier because these drugs are given with carbidopa/levodopa and increase the response of dopamine agonists. Also monitor patients for depression and psychosis. Patient and family teaching. Tell the patient and family the following: • Take entacapone with each levodopa/carbidopa dose for best effect. • The first dose of tolcapone is given with levodopa/carbidopa, and subsequent doses are given about 6 and 12 hours later. • Notify your healthcare provider if you develop jaundice, abdominal pain, or swelling because these symptoms may indicate liver failure. This is especially important if taking tolcapone. • Notify your healthcare provider if you have worsening depression, delirium, or hallucinations. 308 • Do not suddenly stop taking either of these drugs because they must be tapered off slowly to avoid a worsening condition. • Your urine may have a brownish orange discoloration that is an expected side effect and is not dangerous. • Rise slowly from a sitting or lying position to prevent faintness, dizziness, and falls caused by an unexpected drop in blood pressure. Monoamine Oxidase Type B Inhibitors Action and Uses MAO is an enzyme made in many body areas that breaks down (metabolizes) many substances. MAO-A breaks down many neurotransmitters, including epinephrine, norepinephrine, serotonin, and dopamine. MAO-B is more specific for breaking down dopamine and serotonin. MAO-B inhibitors suppress the action of MAO-B, which allows dopamine levels to increase and reduce the symptoms of PD. It is sometimes used to help treat depression because this drug category also reduces the breakdown of serotonin. These drugs have fewer side effects than MAO-A inhibitors, which are nonselective. Three MAO-B inhibitor drugs—selegiline (Eldepryl, Zelapar), rasagiline (Azilect), and safinamide (Xadago)—are used in combination with carbidopa/levodopa. They are usually used early in the disease as monotherapy or in addition to dopamine agonist drugs. Adding MAO-B inhibitors to the drug regimen can allow the dose of levodopa to be decreased, thus lessening the side effects of higher levodopa levels. Expected Side Effects/Adverse Reactions The usual side effects of MAO-B inhibitors are dry mouth, nausea, constipation, and light-headedness. Confusion and hallucinations can occur, especially in older adults. An adverse effect of severe hypertension can occur if MAO-B inhibitors are used in high doses, but they are unlikely to occur at lower doses. Tyramine-rich foods need to be avoided when taking any MAO inhibitor because these foods can cause a severe hypertensive crisis. See Box 9.2 for a partial list of foods to avoid when taking MAO inhibitors. Also, photosensitivity can occur and increase the risk for sunburn. These drugs cause drowsiness. Box 9.2 Foods That Contain Tyramine • Cured or smoked meats, fish, and cheeses (e.g., salami, anchovies) • Avocados, bananas, figs, and raisins 309 • Beer and red wine • Sauerkraut • Sour cream • Soy sauce or soy-containing foods like miso soup • Yeast extract found in some breads, canned foods, and snacks • Yogurt • Pickled herring Drug Interactions MAO-B inhibitors have interactions with some opiate drugs used for pain, such as meperidine, tramadol, and methadone, and can cause a hypertensive crisis. They should not be used with droperidol or cyclobenzaprine. Taking MAO-B inhibitors with tricyclic antidepressants, such as amitriptyline, or selective serotonin reuptake inhibitors, such as fluoxetine, or other MAO inhibitors can cause hyperthermia, tremors, seizures, or delirium. Drugs that stimulate the sympathetic (fight-or-flight) nervous system, such as amphetamines, phenylephrine (decongestant), and dextromethorphan (cough medicine), can cause a hypertensive crisis. Ginseng, ephedra, ma huang, and St. John's wort can also cause a hypertensive crisis and should be avoided with MOA inhibitors. Nursing Implications and Patient Teaching Assessment. Monitor vital signs, especially during dose increases. Alert the healthcare provider for any changes, especially in blood pressure and pulse, because orthostatic hypotension, hypertension, or tachycardia with new dysrhythmias may indicate adverse reactions to these drugs. Monitor all patients closely for behavior changes because these drugs can cause hallucinations, delusions, depression, or confusion. Patient and family teaching. Tell the patient and family the following: • These drugs can take several weeks to begin working. • Do not exceed the prescribed drug dose because doing so can cause dangerously high blood pressure. • Avoid foods that contain tyramine, such as beer, red wine, aged cheese, smoked meat, cheese, fish, soy, pickled herring, among others. • Report symptoms of very high blood pressure, such as a severe headache, irregular pulse, or nausea and vomiting to your healthcare provider immediately. 310 • Very low blood pressure is possible, as well as dizziness, light-headedness, and fainting, so slowly rise from a sitting or lying position. • Do not take over-the-counter drugs or herbs without checking with the pharmacist or your healthcare provider. • These drugs cause drowsiness, so avoid driving or using dangerous machinery until you know how the drug affects you. • Wear sunscreen, sunglasses and protective clothing when outside because this drug increases the risk for serious sunburn, even if you have dark skin. Drugs for Alzheimer's Disease AD is a common form of dementia. Dementia is the progressive loss of brain function. There are many causes and types of dementia, and AD is one that can be helped initially with drug therapy. In AD there is a familial tendency or genetic predisposition to develop problems within and around brain neurons that affect their function. The protein beta amyloid builds up and forms deposits in the brain. The nerves themselves also become tangled and form nonfunctional meshes within the brain. The excitatory neurotransmitter ACh is decreased in the brain, which results in more difficulty with memory and learning. In addition, blood flow throughout the brain decreases. Over time, these changes reduce the size of the brain and all aspects of brain function (Fig. 9.5). Unfortunately no single test can be used to diagnose AD, and drug therapy does not cure the problem. Drugs provide only temporary improvement in symptoms and include cholinesterase inhibitors and Nmethyl-D-aspartate (NMDA) blockers. Research in the area of AD is ongoing, and help for family and professional caregivers is available. 311 FIG. 9.5 Cross sections of a normal brain and a brain affected by Alzheimer's disease. Neurons die in areas of the brain that are important to memory and language. (From Workman ML, LaCharity LA: Understanding pharmacology, ed 2, St. Louis, 2016, Elsevier.) The symptoms of early AD involve memory issues and can be mistaken for normal aging. The disease is progressive and memory problems become increasingly more challenging, such as getting confused regarding times and places or forgetting how to get home. Changes in mood, judgment, and personality eventually occur. Box 9.3 lists the 10 warning signs of AD. Box 9.3 Ten Warning Signs of Alzheimer's Disease 1. Memory loss that disrupts daily life 2. Challenges in planning or solving problems 3. Difficulty completing familiar tasks at home, at work, or at leisure 4. Confusion with time or place 5. Trouble understanding visual images and spatial relationships 6. New problems with words in speaking or writing 7. Misplacing things and losing the ability to retrace steps 8. Decreased or poor judgment 9. Withdrawal from work or social activities 10. Changes in mood and personality More than 5 million persons suffer from AD. Risk factors include older age (65), a family history, and having the APOE-e4 gene. Diagnosis is made based on symptoms, family interviews, physical examination, and neurologic and cognitive examinations. As previously mentioned, the drugs available for AD may simply offer a temporary improvement in symptoms. The effectiveness of the drugs is different from person to person, and the length of time that the drug is therapeutic is limited as well. Table 9.2 lists examples of the common names, adult dosages, and 312 nursing implications for these drugs. Table 9.2 Examples of Common Drugs for Management of Alzheimer's Disease Cholinesterase inhibitors: work to delay memory loss in Alzheimer's disease by binding to the enzyme acetylcholinesterase and slowing its action, which allows any acetylcholine produced to remain functional longer DRUG/ADULT DOSAGE RANGE NURSING IMPLICATIONS donepezil (Aricept) 5–10 mg orally once daily • Give donepezil (Aricept) once a day in the evening. rivastigmine (Exelon) 1.5–3 mg orally twice daily; 4.6/24 • If using the disintegrating tablet, place the tablet on the tongue before swallowing. hours to 9.5/24 hours transdermal patch • Teach patients and families to measure and give the oral solution with a syringe. galantamine (Razadyne) 4–8 mg orally twice daily; • Rivastigmine (Exelon) must be given with food. extended-release tablets 8–16 mg orally once daily • If using the transdermal rivastigmine (Exelon) patch: • Apply once daily to clean, dry, hairless, intact healthy skin to the upper or lower back to avoid removal by the patient. • Do not use on areas with recent application of lotions, creams, or powder. • Rotate application sites daily. Do not apply to the same site more than once every 14 days. • May be used while bathing or showering. • Apply patch at about the same time every day. • Always remove the old patch before applying a new patch. • Give galantamine (Razadyne) twice-a-day oral dosage with food and the once-a-day oral dosage in the morning with food. • If using the liquid oral form of galantamine (Razadyne), measure the ordered dosage from the enclosed pipette into 3–4 ounces of a nonalcoholic drink. • Monitor weekly weights because these drugs may cause weight loss. • Monitor laboratory work as ordered to ensure safety from adverse effects. NMDA blockers: work to slow the progression of Alzheimer's disease by blocking the entrance of calcium into neurons, which reduces or slows neuronal damage DRUG/ADULT DOSAGE RANGE NURSING IMPLICATIONS memantine (Namenda, Namenda XR) 5–10 mg orally twice • Extended release can be opened and contents sprinkled on applesauce before daily; extended-release capsules 7–28 mg orally once daily swallowing. Do not divide the contents of the capsules because this will result in unequal dosing. • If the oral solution of the drug is used, do not mix it with other liquids. Use a syringe or dropper to measure and give directly in the mouth. • Monitor the patient's neurologic function, serum creatinine levels, blood urea nitrogen, and liver function studies and notify the healthcare provider for changes from baseline. • Weigh the patient weekly because this drug can cause weight loss. Bookmark This! The Alzheimer's Foundation of America provides care and services to individuals living with AD and to their families and caregivers: https://alzfdn.org. Cholinesterase Inhibitors Action and Uses Drug therapy attempts to increase ACh levels because the excitatory neurotransmitter ACh is reduced in the brain of patients with AD. Acetylcholinesterase is an enzyme that specifically breaks down ACh. Cholinesterase inhibitors are drugs that bind to acetylcholinesterase and slow its action, which allows any ACh produced to remain functional longer. This action appears to delay memory loss and improve the patient's ability to perform his or her activities of daily living. Unfortunately, the drug is useful only temporarily. As the disease progresses, fewer intact neurons are available to make ACh. When this occurs, the drug is no longer effective. Currently, three cholinesterase inhibitors are being used in the treatment of AD: donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne). Table 9.2 lists examples of the common names, adult dosages, and nursing implications for these drugs. 313 Expected Side Effects/Adverse Reactions Expected side effects of cholinesterase inhibitors are mild diarrhea, especially when starting treatment. Drowsiness, headache, loss of appetite, GI discomfort, as well joint pain and muscle cramping, can occur. Adverse effects include hallucinations, dysrhythmias, GI bleeding, infection, and difficulty urinating or incontinence. These drugs increase ACh concentrations, so they are considered to be cholinergic agonists and can have adverse effects on other body systems that cause symptoms of overstimulation of the parasympathetic nervous system (rest and digest). Box 9.4 lists these adverse effects. Box 9.4 Common Adverse Effects of Cholinergic Agonists and Cholinesterase Inhibitors Cardiac: slow heart rate, low blood pressure, heart blocks, fainting CNS: convulsions, headaches, seizures, sweating GI: increased secretions, increased salivation, abdominal cramps, vomiting, diarrhea Respiratory: increased secretions and bronchospasm Urinary: urinary incontinence Drug Interactions Cholinesterase inhibitors should not be given with other drugs that can prolong the QT interval on the ECG because this can cause a fatal dysrhythmia known as torsade de pointes, a form of ventricular tachycardia. Dextromethorphan found in over-thecounter cough medication, quinidine, and fluconazole are three such drugs. Consult a drug reference or pharmacist to determine whether these drugs interact with any other drug(s) the patient is taking. Anticholinergic drugs decrease the effectiveness of cholinesterase inhibitors, and taking the drug with other cholinesterase inhibitors such as edrophonium (Tensilon) increases the risk for adverse effects. Nursing Implications and Patient Teaching Assessment. Obtain a baseline weight and reassess at weekly intervals because these drugs can cause a loss of appetite. Observe for signs and symptoms that may indicate a GI bleed, such as dark, tarry stools and decreasing hemoglobin and hematocrit levels. Monitor blood test levels and report abnormal baseline liver function studies and BUN/creatinine levels to the healthcare provider because abnormalities can affect the metabolism of the drugs. Assess the urinary patterns and reassess for any changes that can indicate side effects of the drugs. Before a patient starts a cholinesterase inhibitor, assess him or her using an Alzheimer's Disease Assessment Scale so that an objective evaluation can be made when evaluating for symptom improvement. The assessment tools evaluate cognition, functional capacity, behavior, general 314 health, and quality of life. By using these tools, you can better gauge how and if the drug is actually helping the patient. Assess for swallowing difficulties so that the proper drug formulation can be given (liquid, sublingual tablets). Planning and implementation. Monitor patients who have asthma carefully for worsening of symptoms. Check vital signs, especially heart rate, and look for adverse signs and symptoms indicating parasympathetic stimulation, as indicated in Box 9.3. Evaluation. Monitor for improvement using an Alzheimer's Disease Assessment Scale. Monitor for any changes in vital signs and/or adverse reactions. Patient and family teaching. Tell the patient and family the following: • It may take several weeks for the drugs to have a therapeutic effect. • These drugs will not cure AD. • If difficulty breathing, fainting, or GI bleeding occurs, notify your healthcare provider immediately. • Notify your healthcare provider if expected side effects are causing increased discomfort or if new symptoms develop. • Use the bathroom every 2 hours to avoid urinary incontinence because these drugs increase urination. • Take donepezil (Aricept) at bedtime. • Take galantamine (Razadyne) and rivastigmine (Exelon) at the same time twice a day with food to avoid GI upset. • Your risk for falls is increased because these drugs can cause dizziness and weakness. • Keep all follow-up appointments so that the effects of these drugs can be evaluated. Bookmark This! A list of cognitive assessment and family informational tools can be found on the Alzheimer's Association website: http://www.alz.org/health-care- 315 professionals/cognitive-tests-patient-assessment.asp. N-Methyl-D-Aspartate Blockers Action and Uses There are NMDA receptors in the brain. When activated, these receptors allow more calcium into the brain neurons, which appears to be important in memory and learning. However, too much calcium damages neurons. It is thought that excess calcium is one mechanism that causes neuronal “tangles” to form in the brains of patients with AD. NMDA blockers are drugs that block the entrance of calcium into neurons, which reduces or slows the neuronal damage in AD. Memantine (Namenda, Ebixa) is used with the drugs donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne) to increase the effects of these cholinergic agonists. Expected Side Effects/Adverse Reactions The expected side effects of memantine are headaches, dizziness, and constipation. Adverse side effects include hallucinations, worsening confusion, depression, somnolence, shortness of breath, incontinence, and weight loss. This drug can also cause hypertension in certain individuals. Drug Interactions Drugs that increase the urine pH (alkaline) or are also excreted by the kidneys can interfere with the renal excretion of memantine and cause an increase in expected and adverse side effects. Carbonic anhydrase inhibitors like acetazolamide, which are used in the treatment of glaucoma and high-altitude sickness, quinidine, and dextromethorphan are such examples. Nursing Implications and Patient Teaching Assessment. Memantine is eliminated primarily by the kidney and should be used with caution in patients with kidney disease, people with risk for renal impairment due to age, and those taking other drugs that also have a risk for renal impairment. Baseline creatinine and BUN, as well as liver enzymes, should be measured. Urinary tract infections can increase the levels of memantine by increasing the pH. If the patient has symptoms of a urinary tract infection, obtain a urinalysis and consult with the healthcare provider before starting drug therapy. Monitor the respiratory rate and vital signs, especially the blood pressure in patients with heart disease. Report symptoms such as ataxia, dizziness, and other adverse reactions to the healthcare provider. Patient and family teaching. Tell the patient and family the following: • Take or give memantine at the same time every day. • The extended-release capsule can be opened and all of 316 the contents can be sprinkled on applesauce if swallowing is difficult. • If using the liquid form of the drug, do not mix it with other liquids to avoid interactions. • Report problems with vision, skin rash, shortness of breath, agitation or restlessness, confusion, dizziness, incontinence, and weight loss to your healthcare provider. • Avoid driving or engaging in hazardous activities until you know how the drug affects you. • Report symptoms of a urinary tract infection (acute changes in mental status, frequency in urination, pain or discomfort during urination, or concentrated and badsmelling urine) to your healthcare provider. Drugs for Epilepsy Epilepsy is a common type of chronic seizure disorder in which neurons of the brain become hyperexcitable and trigger electrical signals when they are not needed. The unnecessary signals cause rapid and repeated refiring of nerves in the brain, leading to seizures. Seizures are the body's total responses to those inappropriate brain signals. When these signals reach the skeletal muscles, a convulsion may occur, which is the sudden contraction of many muscle groups without the person's conscious control. A convulsion is the part of a seizure that is seen as the motor response to these brain signals. Other parts of seizure activity include changes in or loss of consciousness; a variety of sensory changes in vision, hearing, touch, smell, and taste; and autonomic symptoms such as facial flushing, incontinence, nausea, and drooling. Symptoms of seizures vary with the area of the brain affected and the type of seizure experienced. Seizures are classified first as partial or generalized. Each classification has subtypes based on symptoms, how long an episode lasts, whether convulsions occur, how widespread the response is, and the degree of change in consciousness. Box 9.5 lists the classifications of seizures. Box 9.5 Classification of Major Seizures Types TYPE SYMPTOMS PARTIAL SEIZURES Simple No loss of consciousness, isolated or discrete motor symptoms (e.g., twitching of one toe or foot), changes in one or more senses, one or more autonomic symptom (e.g., drooling, facial flushing, etc.), usually last 20 to 60 seconds Complex Consciousness altered or impaired and person does not respond to environmental stimulation, may have a fixed gaze stare and be 317 motionless, automatism (performance of repetitive motions such as head-turning from side to side, foot peddling motions), usually last 45 to 90 seconds Begins as a partial seizure with the patient retaining consciousness and then progresses to loss of consciousness Partial with secondary generalization GENERALIZED SEIZURES: ALL HAVE THE FEATURE OF LOSS OF CONSCIOUSNESS Absence (petit Consciousness loss is brief (10 to 30 seconds) without loss of posture, minimal or no change in motor activity mal) Tonic-clonic Often preceded by an aura or cry, whole-body convulsions starting with muscle rigidity followed by powerful contractions, posture (grand mal) lost, urinary incontinence, confusion after muscle responses are over, usually lasts less than 90 seconds Atonic Muscle tone loss in one or more muscle groups, usually lasts 10 to 60 seconds Myoclonic Brief (1 to 2 seconds) contraction of one (focal) or more muscle groups (can involve the whole body) Status Single seizure lasting 15 to 30 continuous minutes or a series of recurring seizures between which the patient does not regain epilepticus consciousness; may be convulsive, absence, myoclonic, or generalized convulsive (life-threatening) Febrile Tonic-clonic seizures induced by temperature elevation (usually in children), last 15 to 30 seconds A variety of problems can produce seizures. For example, high temperatures in infants and children, strokes, head trauma, brain tumor, meningitis, and poisoning (especially from excessive alcohol intake or drugs) may induce seizures. Epilepsy is one cause of chronic and recurring seizures. Although other types of epilepsy management exist, most often drug therapy is used. Antiepileptic drugs (AEDs) are drugs that reduce or prevent seizures. AEDs are divided into traditional and newer categories. Some drugs categorized as AEDs have additional uses for other problems and disorders. Traditional Antiepileptic Drugs The traditional AEDs include phenytoins, carbamazepine, ethosuximide, phenobarbital, and valproic acid. Although these drugs have different actions, side effects, adverse effects, and drug interactions, some nursing implications are the same for all of them. In addition, many of the points to teach patients and families about these drugs are the same. Box 9.6 describes these common nursing considerations for AEDs, and Box 9.7 describes general patient teaching points. Nursing considerations and patient teaching issues specific to any single drug type are listed with the individual drug categories in Table 9.3. Although these older drugs have more side effects and other issues than do some newer drugs, they are still used effectively today for most patients, often in combination with newer AEDs. Box 9.6 General Nursing Considerations for Antiepileptic Drugs Assessment • Before giving any AED, obtain a complete list of drugs that the patient is taking, including over-the-counter and herbal preparations, because these drugs interact with numerous drugs, herbals, and supplements. • Always consult a drug reference or pharmacist to determine possible interactions between AEDs and any other drug a patient is prescribed. • Check baseline vital signs, level of consciousness, and gait, all of which can change as a result of AEDs. 318 • Assess adolescents for recent changes in height and weight because these changes affect the dosage needed to prevent seizures. • Ask female patients of childbearing age if they are pregnant, planning to become pregnant, or breast-feeding because many of the AEDs have an increased risk for birth defects and/or enter breast milk and affect the infant. • Ask patients whether an aura occurs before any seizure. • Tell the patient to put on his or her call light if he or she feels that a seizure is about to occur. Planning and Implementation • Be sure to place the patient's bed in the lowest position and raise the side rails to prevent injury. • Remind the patient to call for help when getting out of bed and make sure that the call light is within easy reach because many AEDs cause dizziness. • Make sure that oxygen and suction equipment are in the patient's room and in good working order in case a seizure does occur. • Monitor the patient for seizure activity and be prepared to protect the patient from injury if one occurs. • Monitor regularly scheduled blood levels of the drug(s) to determine whether they are in the effective range or could cause adverse reactions. • Many AEDs increase the patient's suicidal ideation. Report to the healthcare provider immediately any patient statements or actions that indicate he or she may be considering self-harm. • AEDs work in the CNS and depress its activity to some degree. They should not be taken with alcohol or any other type of CNS depressant. • Suddenly stopping AED therapy can result in seizures. When changing drugs or discontinuing drugs, taper doses slowly to reduce the risk for seizures. Box 9.7 General Patient and Family Teaching Points for Antiepileptic Drugs • Teach patients about the importance of keeping follow-up appointments with the healthcare provider to monitor drug effectiveness and drug blood levels. • Instruct patients to take the drug exactly as prescribed and not to suddenly stop taking the drug, because seizures may occur. • Teach patients to take a missed dose as soon as it is remembered, but not to take a double dose. Teach patients to immediately report any new, worsening, or unusual symptoms to the healthcare provider. • Remind patients to avoid any over-the-counter drugs or supplements without checking with their healthcare provider to prevent possible interactions. 319 • Instruct patients to avoid alcoholic beverages or other drugs known to depress the CNS because severe CNS depression may occur. Also, for some patients, alcohol triggers seizure activity. • Remind patients to avoid driving, operating dangerous equipment, or doing anything that requires mental alertness until they know how the AED affects their level of consciousness and reflexes. • Tell patients and families that if signs of increasing depression are seen to notify the healthcare provider immediately because many of these drugs increase depression and suicidal ideation. Table 9.3 Examples of Common Traditional Antiepileptic Drugs DRUG/ADULT DOSAGE RANGE NURSING IMPLICATIONS phenytoin (Dilantin, Phenytek) • Dosages for different forms of phenytoin are not interchangeable because the drug Loading dose: 15–20 mg/kg orally or IV given in divided concentrations vary by type. doses throughout the day • Warn patients that gum hyperplasia is a side effect of this drug and that good oral Maintenance dose: 4–7 mg/kg per day orally divided into 2– hygiene is needed to prevent tooth loss from gum disease. 3 doses • Remind patients who take warfarin that closer monitoring is needed and the warfarin dose may need to be adjusted because phenytoin has mixed interactions on warfarin's effect. • Ask patients about all other drugs they take because phenytoin interacts with many, many other drugs. Check with a pharmacist and the pat