11.2 Anti-Parkinsonian Drugs

Adverse Effects and Contraindications

This drug classification can cause numerous adverse effects, which is why it is not used as commonly as it was in the past. Anhidrosis can occur from the decreased secretion from sweat glands. This can be dangerous because the body is unable to release heat, which can lead to hyperthermia or heat stroke. Dry mouth, due to the decrease in salivation, can become very severe, resulting in difficulty with swallowing or speaking. This increases the client’s risk for choking and/or aspiration pneumonia. Dry mouth can also cause dental caries, halitosis (bad breath), gum problems, and oral infections. A slight reduction in dosage may control nausea and still give sufficient relief of symptoms (DailyMed, Benztropine Mesylate, 2021; Parkinson’s Foundation, 2023a).

Clients with mental disorders may experience an intensification of mental symptoms. In such cases, anti-Parkinsonian drugs can precipitate a toxic psychosis characterized by confusion, memory impairment, visual hallucinations, delusions, and nervousness. Clients with mental disorders should be kept under careful observation.

Blockade of cholinergic receptors in the eye may precipitate or aggravate glaucoma because it increases the aqueous humor in the anterior chamber by disrupting the exit of the fluid. In addition, these drugs cause mydriasis (pupil dilation) by blocking muscarinic receptors on the ciliary muscle and sphincter of the iris; paralysis of the iris sphincter results, preventing pupil constriction. The eye is unable to adapt to bright light, which causes photophobia, or intolerance to light (DailyMed, Benztropine Mesylate, 2021; Parkinson’s Foundation, 2023a).

Blocking cardiac muscarinic receptors will eliminate parasympathetic nervous system influence on the heart. Anticholinergics cause an increase in heart rate, which can cause dysrhythmias in a client with preexisting tachycardia or a co-existing condition, such as hyperthyroidism. Urinary retention can occur due to the blockade of muscarinic receptors of the urinary tract. This relaxes the detrusor muscle, which reduces pressure within the bladder and increases the tone of the urinary internal sphincter, placing the client at risk for urinary tract infections. Also, muscarinic antagonists block receptors in the intestine, decreasing the tone and motility of the intestinal smooth muscle. This can result in constipation or paralytic ileus. Furthermore, because anticholinergics block muscarinic receptors in the bronchi, they can promote bronchial dilation. This is a benefit for those who have asthma; however, these drugs also cause drying and thickening of bronchial secretions, which can lead to mucus plugging. Clients with asthma must be closely monitored (Capriotti, 2020).

If a client has any type of intestinal or urinary obstruction, like benign prostatic hypertrophy, these medications should be avoided because they will worsen the condition. Those with a diagnosis of myasthenia gravis should avoid anticholinergics because they could further reduce ACh’s ability to send signals, which could worsen symptoms or trigger a crisis.

Antihistamines, first-generation antipsychotics, and tricyclic antidepressants should not be used concurrently with anticholinergics because these agents also possess antimuscarinic properties. The combination of multiple anticholinergic drugs can worsen the adverse effects mentioned previously. The use of alcohol can increase the risk of psychosis. Cholinergic agents, such as bethanechol used for urinary retention, can negate the effects of the anticholinergic agents because these drugs stimulate the parasympathetic nervous system by mimicking the action of ACh.

Table 11.2 is a drug prototype table for anticholinergics featuring benztropine mesylate. It lists drug class, mechanism of action, adult dosage, indications, therapeutic effects, drug and food interactions, adverse effects, and contraindications.

Nursing Implications

The nurse should do the following for clients who are taking anticholinergics:

• Assess for decreased rigidity and tremor.
• Monitor client’s ability to engage in self-care tasks and walk independently.
• Assess for an increase in heart rate and/or blood pressure.
• Monitor for any signs of respiratory distress or moist, nonproductive cough.
• Assess level of consciousness and orientation.
• Darken room for photophobia due to mydriasis (dilated pupils).
• Ensure the client is receiving proper oral hygiene.
• Encourage frequent sips of water to prevent dehydration.
• Assess for difficulty with swallowing—if needed, request consult with occupational therapy.
• Assess for speech impairments—if needed, request consult for speech pathologist.
• Monitor intake and output for reduction of urine output and positive net balance.
• Perform a bladder scan to assess for residual volume of urine due to urinary retention.
• Assess for signs and symptoms of paralytic ileus, such as constipation, abdominal pain, diminished bowel sounds, and abdominal distention.
• Assess for muscle weakness.
• Provide frequent rest periods during the day to avoid aggravating the tremors and rigidity.
• Provide client teaching regarding the drug and when to call the health care provider. See below for client teaching guidelines.

Levodopa

Levodopa was introduced in the 1960s and has been a cornerstone of PD treatment for many years (Ovallath & Sulthana, 2017). Levodopa is a metabolic precursor of dopamine and is inactive until it undergoes conversion to its active state. This drug has proven to be extremely beneficial in the early stages of PD. Unfortunately, over time, the number of neurons decreases, and fewer cells are capable of converting the levodopa to dopamine. Motor fluctuations then develop, and the client experiences the relief of symptoms only when the drug is present.

The purpose of this drug is to replenish the brain’s reduced supply of dopamine by increasing dopamine synthesis. Levodopa is absorbed in the blood from the small intestine and travels through the circulation to the brain. Once it crosses the blood–brain barrier, it binds to dopamine receptors on GABA neurons, helping to restore the balance between neurotransmitters (Parkinson’s Foundation, 2023b).

Levodopa is not used as a monotherapy; given alone, it is not beneficial. It should be administered with carbidopa (discussed later in this chapter). Without the combination, a large majority of levodopa gets decarboxylated in the periphery—causing systemic effects such as nausea and vomiting, dysrhythmias, and hypotension—and resulting in less levodopa crossing the blood–brain barrier. The drug combination increases the amount available to cross the blood–brain barrier.

Inbrija is an inhaled levodopa powder that is a dopamine precursor commonly used for early morning or sudden “off” episodes. These episodes are seen when levodopa’s effects wear off before the next dose is due. The inhalation route enables a low but quicker acting boost of dopamine. Inbrija is not intended to replace a client’s maintenance medications but is given concurrently with levodopa/carbidopa. The drug comes in a capsule and must be administered through the appropriate inhaler device. Inhalation-specific contraindications include asthma, chronic obstructive pulmonary disease, or other long-term underlying lung disease (DailyMed, Inbrija, 2023).

Carbidopa/Levodopa

Carbidopa is a dopamine decarboxylase inhibitor; combined with levodopa, levodopa’s effects are enhanced. The drug inhibits decarboxylation of levodopa in the intestines and peripheral tissues. Therefore, less levodopa is converted into dopamine within the periphery, and more is available to cross the blood–brain barrier. This is beneficial, not only to increase the amount of dopamine that reaches the brain, but also to diminish the adverse effects dopamine causes when circulating in the periphery. Combining levodopa with carbidopa allows the dosage of levodopa to be reduced by 75%. Carbidopa has no pharmacological effects on its own and is unable to cross the blood–brain barrier. This drug combination stops the motor symptoms early in the disease process but has no effect on the disease itself.

Therapeutic effects may not be seen for weeks or months. This drug should be taken on an empty stomach, typically 30 minutes before a meal. Food can significantly decrease absorption, especially a large amount of protein. Carbidopa decreases nausea and vomiting and the cardiovascular response by reducing the amount of dopamine in the periphery (DailyMed, Sinemet, 2022). Levodopa comes in multiple forms and is administered via several routes, including oral (immediate-release, control-release, and extended-release) tablets, intestinal gel, and inhalation.

DUOPA is the intestinal gel form of carbidopa/levidopa delivered through a surgically implanted tube in the small intestine. This drug is used for clients who have advanced disease and have difficulty swallowing. The overall goal of this delivery method is to increase “on” time episodes. The maximum recommended daily dose of DUOPA is 2000 mg administered over 16 hours (Parkinson’s Foundation, 2023b). Distinct contraindications for this route include complications from the insertion of the intestinal tube or incision site inflammation (DailyMed, DUOPA, 2022).

Table 11.3 lists common dopaminergics and typical routes and dosing for adult clients.

Adverse Effects and Contraindications

Nausea and vomiting are common symptoms that usually disappear after a few months on levodopa/carbidopa. The symptoms are usually caused by activation of dopamine receptors in the chemoreceptor trigger zone, which contains receptors that detect emetic agents in the blood and relay that information to the vomiting center. This is reduced with carbidopa. Carbidopa can be given as a single drug (Lodosyn). If added to levodopa/carbidopa, the extra carbidopa can reduce levodopa-induced nausea and vomiting. It also allows smaller doses of levodopa to be used while promoting a faster response.

Conversion of levodopa to dopamine in the periphery can produce excessive activation of beta-adrenergic receptors in the heart. Dysrhythmias can result, especially in clients with heart disease. Clients with preexisting coronary artery disease may take propranolol to counteract cardiac dysrhythmias.

“Wearing off” develops near the end of the dosing interval, indicating drug levels have declined to a subtherapeutic value. This can be minimized in three ways: (1) shortening the dosing interval, (2) giving a drug that prolongs levodopa’s plasma half-life (MAO-B inhibitors or COMT inhibitors), or (3) giving a direct-acting dopamine agonist. “On-off” episodes occur any time during the dosing interval, even if drug levels are high. These episodes may last from minutes to hours. Over time, off periods usually increase in both intensity and frequency. One reason these episodes occur in PD is because the gastrointestinal (GI) motility decreases, delaying absorption of levodopa and altering serum levels.

About 80% of clients treated with levodopa will experience drug-induced dyskinesias during the advanced stages of the disease, and 30% will develop it after only 3 years of levodopa treatment (Kwon et al., 2022). Some of these are just bothersome (head bobbing tics, grimacing), whereas others can be disabling, such as ballismus—rapid, involuntary jerking or flinging of proximal muscle groups—or choreoathetosis—slow, involuntary, writhing movements. Levodopa exacerbates symptoms of psychosis, possibly through the buildup of central dopamine. Urine and sweat can become brownish because of the melanin produced from catecholamine oxidation.

This drug can cause clients to become impulsive. Clients may either begin to engage in or increase already existing gambling/sexual urges or uncontrolled spending. This is due to the increase of dopamine in the brain.

There have been reports of clients suddenly falling asleep without warning of feeling drowsy. Before these sleep attacks, the clients were engaged in performing activities of daily living, driving a vehicle, or conversing. If these occur, the drug should be discontinued. Importantly, the drug should not be stopped abruptly because it could lead to the reemergence of signs and symptoms of PD, sometimes worse than the initial manifestations. It could also lead to confusion, muscle rigidity, autonomic instability, and hyperpyrexia, which resembles neuroleptic malignant syndrome (NMS).

Narrow-angle glaucoma is a contraindication as levodopa can worsen the condition due to the potential of further increase of intraocular pressure.

Epidemiological studies have shown that clients with PD have a higher risk (two- to approximately six-fold) of developing melanoma than the general population. It is unknown whether this is due to PD itself or the drugs used in the treatment of PD. Clients and providers are advised to monitor for melanomas frequently and on a regular basis when using carbidopa and levodopa for any indication. Ideally, periodic skin examinations should be performed by appropriately qualified individuals (e.g., dermatologists).

First-generation antipsychotics block receptors for dopamine in the striatum, diminishing the therapeutic effects of levodopa. This may augment Parkinsonian symptoms. Low doses of atypical antipsychotics are sometimes used to treat levodopa-induced psychotic symptoms. Nonselective monoamine oxidase inhibitors (MAOIs) can result in a hypertensive crisis if administered to a client taking levodopa. Nonselective MAOIs should be withdrawn at least 2 weeks before starting levodopa. Dopamine receptor antagonists, such as phenothiazines, risperidone, or metoclopramide, should be avoided because they will decrease the effects due to their dopamine receptor antagonistic properties.

If levodopa is administered alone, pyridoxine (B₆) will decrease its effects (greater than 200 mg daily) because it enhances decarboxylase and increases peripheral breakdown of levodopa. If given in combination with carbide, this is not a concern. Other antihypertensives can exacerbate orthostatic hypotension. Iron salts can form chelates with levodopa and reduce its bioavailability. Because amino acids compete with levodopa for intestinal absorption and for transport across the blood–brain barrier, high-protein foods will reduce levodopa’s therapeutic effects.

Table 11.4 is a drug prototype table of dopaminergics featuring oral carbidopa/levodopa. It lists drug class, mechanism of action, adult dosage, indications, therapeutic effects, drug and food interactions, adverse effects, and contraindications.

Nursing Implications

The nurse should do the following for clients who are taking dopaminergics:

• Encourage slow position changes to minimize postural hypotension.
• Assess neurological status, such as orientation, grip strength, gait, reflexes, tremors, or spasticity.
• Inform client that hallucinations and other psychotic behavior can occur, and these will be treated appropriately.
• Evaluate therapeutic effects—decrease in drooling, tremors, bradykinesia, or rigidity and increase in facial expressions.
• Space activities evenly throughout the day for adequate rest periods.
• Monitor serum liver enzymes, hemoglobin/hematocrit, bilirubin, blood urea nitrogen (BUN), Coombs tests, and elevated serum glucose periodically throughout treatment.
• Monitor for involuntary movements of the tongue, mouth, and face.
• Provide demonstration on proper technique of using the inhalation form and have client return demonstrate.
• Look for signs of increased depression or suicidal ideations.
• Specifically ask the client about feeling drowsy or sleepy while performing certain activities.
• Advise clients to exercise caution while driving, operating machinery, or working at heights.
• Ask about new or increased gambling urges, sexual urges, or uncontrolled spending.
• Monitor for melanomas frequently by performing a thorough skin assessment.
• Explain to client that the color of the urine may become brownish orange, but this is harmless.
• Provide dietary counseling about high-protein foods and to evenly space their intake throughout the day.
• Provide client teaching regarding the drug and when to call the health care provider. See below for client teaching guidelines.

Adverse Effects and Contraindications

Nonergot derivatives are known to produce unusual effects, such as compulsive gambling, hypersexuality, overspending, and overeating. These behaviors are dose related and will reverse when the drug is discontinued. Providers should screen for compulsive and addictive behaviors before starting medication. Also, clients may not be aware of this behavior, so they should be specifically asked about it. Another unusual effect is these medications can make one quickly fall asleep while performing daily activities. Often the person will not feel drowsy before falling asleep. This creates an elevated risk of injury and/or accidents.

Hyperhidrosis (excessive sweating unrelated to heat or exercise) is caused by the dysregulation of the autonomic nervous system, which could be related to PD or the dopamine agonist. Hyperhidrosis can result in dehydration and electrolyte loss. Older adults and clients with a history of psychiatric disorders are more sensitive and at increased risk of experiencing confusion and hallucinations. Dyskinesias are seen more frequently in the aforementioned dopamine agonists when combined with levodopa. Clinical studies have revealed this drug class has teratogenic effects and should be avoided in pregnancy and breastfeeding (DailyMed, Pramipexole Dihydrochloride, 2023).

Cardiovascular disease may occur due to severe hypotension and impaired perfusion. Orthostatic hypotension occurs due to a dopamine-mediated blunting of the noradrenergic response to standing and subsequent decrease in peripheral vascular resistance. Valvular heart disease occurs due to activation of serotonin receptors on the heart valves.

Antipsychotics or dopamine antagonists will cancel the dopamine agonist effects. Higher doses of estrogens reduce clearance of the drug. Starting or stopping hormone replacement therapy may require adjustment of dosage. Because significant hypotension and loss of consciousness has occurred with these drugs when taken with serotonin receptor antagonists, this combination should be avoided.

Although apomorphine is a morphine derivative, this drug does not cause analgesia, euphoria, or respiratory depression. The most common adverse reactions specific to this drug are excessive yawning, injection-site reactions, rhinorrhea, and cardiac issues. It is important to monitor cardiac status due to the associated risk for hypotension and dose-related prolongation of the QT interval. There have been reports of chest pain, myocardial infarction, dysrhythmias, and cardiac arrest. Furthermore, this drug has the potential to exacerbate coronary and cerebral ischemia in clients with known disease. Any client with an allergy to sulfites should not receive apomorphine (DailyMed, Apomorphine Hydrochloride, 2022).

Table 11.6 is a drug prototype table of dopamine agonists featuring pramipexole. It lists drug class, mechanism of action, adult dosage, indications, therapeutic effects, drug and food interactions, adverse effects, and contraindications.

Nursing Implications

The nurse should do the following for clients who are taking dopamine agonists:

• Measure blood pressure and heart rate in the supine and standing positions before and after dosing.
• Emphasize to the client/caregiver to maintain safety precautions because falling asleep can suddenly occur without feeling drowsy.
• Monitor for peripheral edema and perfusion.
• Ask about compulsive and uncontrollable behaviors.
• Assess for any involuntary movements, especially with the upper and lower extremities.
• Teach client ways to cope with the excessive sweating they may experience.
• Provide clients education about high-fiber foods to reduce risk of constipation.
• Monitor routine electrocardiogram (ECG, EKG) for prolongation of QT interval when receiving apomorphine.
• Evaluate electrolytes periodically if individual has hyperhidrosis.
• Instruct client about the correct way to administer the subcutaneous apomorphine.
• Provide client teaching regarding the drug and when to call the health care provider. See below for client teaching guidelines.

Adverse Effects and Contraindications

Because selegiline hydrochloride causes insomnia, taking it late in the day could disrupt sleep. Severe hypertension is a possibility if administered in high doses because the drug becomes nonselective and can then inhibit both MAO-A and MAO-B. At doses less than or equal to 10 mg/day, the drug is selective for MAO-B. It does not affect MAO-A, which metabolizes tyramine, norepinephrine, epinephrine, and serotonin, unless given above the recommended dose. This subtype can cause excessive stimulation of the sympathetic nervous system (SNS), causing severe hypertension and possibly stroke. This crisis can be triggered by taking sympathomimetic drugs and by ingesting foods containing tyramine. High levels of tyramine are found in foods that are aged, cured, or fermented (DailyMed, Selegiline Hydrochloride, 2023).

Several opioids should not be used concurrently with this drug classification. Combining MAO-B inhibitors with morphine can increase the opioid adverse reactions. Sympathomimetics, including over-the-counter medications containing dextromethorphan, should also be avoided due to increased risk of exaggerating psychotic symptoms. Serotonin syndrome is a life-threatening condition characterized by delirium, extreme agitation, tachycardia, labile blood pressure, rigidity, and hyperthermia. Several medications, including meperidine, tramadol, and selective serotonin reuptake inhibitors (SSRIs), can increase the risk of serotonin syndrome and should be avoided. SSRIs should be stopped 2–5 weeks before the initiation of selegiline. The tapering of the SSRIs is dependent on that particular drug’s half-life. Severe CNS toxicity characterized by hyperpyrexia, seizures, changes in behavioral status, agitation, muscle rigidity, and death have been reported with combining tricyclic antidepressants (TCAs) and nonselective MAOIs (DailyMed, Selegiline Hydrochloride, 2023).

Table 11.8 is a drug prototype table of MAO-B inhibitors featuring selegiline hydrochloride. It lists drug class, mechanism of action, adult dosage, indications, therapeutic effects, drug and food interactions, adverse effects, and contraindications.

Nursing Implications

The nurse should do the following for clients who are taking MAO-B inhibitors:

• Perform a skin assessment to monitor for melanomas.
• Assess cardiac monitoring periodically for prolonged QT interval and episodes of angina.
• Evaluate therapeutic effectiveness of PD clinical manifestations.
• Assess mood for depression, impulsivity, and psychotic behavior.
• Monitor liver function tests routinely for elevations in liver enzymes.
• Periodically monitor clients for visual changes.
• Provide client teaching regarding the drug and when to call the health care provider. See below for client teaching guidelines.

Adverse Effects and Contraindications

Most of the adverse effects of these drugs result from the increased dopamine levels. These can be managed by decreasing the levodopa dose. GI and urinary adverse reactions are the most common manifestations of the COMT inhibitors themselves. Notably, only 10% of the dose is excreted in the urine; the remaining 90% is through biliary excretion. If there is biliary obstruction, these drugs may not get eliminated adequately and will accumulate.

There are reports of clients suddenly falling asleep without warning of feeling drowsy. If this occurs, the COMT inhibitors should be discontinued because these sleep attacks can recur.

Because these drugs increase dopamine (pleasure neurotransmitter) in the brain, they can cause intense urges to gamble, engage in sex, or spend money uncontrollably. In these cases, it may be necessary to reduce the dose or stop it altogether. Diarrhea can be experienced and is thought to be caused by drug-induced microscopic colitis. Diarrhea can lead to associated weight loss, dehydration, and electrolyte imbalance. If this occurs, the drug should be discontinued.

Dyskinesia occurs because entacapone potentiates the dopaminergic side effect of levodopa and may either cause or worsen preexisting dyskinesia.

Entacapone can increase levels of methyldopa, dobutamine, and isoproterenol because they are metabolized by the COMT enzyme. The accumulation of these drugs results in tachycardia, elevated blood pressure, and possible arrhythmias. Nonselective MAOIs should not be used concurrently. COMT and MAO are two major enzyme systems involved in metabolizing catecholamines. Combining a COMT inhibitor with a nonselective MAOI could lead to the inhibition of most of the pathways responsible for normal catecholamine metabolism. This leads to accumulation of catecholamines and sympathomimetic responses. Entacapone is a chelator of iron (DailyMed, Entacapone, 2022).

This class is contraindicated in clients with a history of psychotic disorder who are at risk of experiencing exacerbation of symptoms. Also, certain medications used to treat psychosis may exacerbate the symptoms of PD and decrease the effectiveness of the COMT inhibitor. This drug classification should not be stopped abruptly because it could lead to the reemergence of signs and symptoms of PD, which are sometimes worse than the initial manifestations. It could also lead to confusion, muscle rigidity, hyperpyrexia, and autonomic instability that resembles NMS.

Table 11.10 is a drug prototype table of COMT inhibitors featuring entacapone. It lists drug class, mechanism of action, adult dosage, indications, therapeutic effects, drug and food interactions, adverse effects, and contraindications.

Nursing Implications

The nurse should do the following for clients who are taking COMT inhibitors:

• Monitor liver enzymes at baseline and throughout therapy as recommended.
• Monitor blood pressure with position changes due to the risk of orthostatic hypotension.
• Encourage and educate the client to be compliant with the required lab testing to identify liver disease early.
• Routinely assess level of consciousness and orientation.
• Educate the client to monitor temperature periodically due to the risk of NMS.
• Specifically ask the client about feeling drowsy or sleepy while performing certain activities.
• Advise clients to exercise caution while driving, operating machinery, or working at heights.
• Ask about new or increased gambling urges, sexual urges, or uncontrolled spending.
• Monitor for melanomas frequently by performing a thorough skin assessment.
• Inform client that hallucinations and other psychotic behavior can occur.
• Explain to client that the color of the urine may become brownish orange, but this is harmless.
• Provide client teaching regarding the drug and when to call the health care provider. See below for client teaching guidelines.

Amantadine

Amantadine (Gocovri) is a second-line therapy because it is not as effective as other anti-Parkinsonian drugs. Although multiple drugs fit this classification, amantadine is the most used in PD. This drug falls into two drug classifications: antiviral and anti-Parkinsonian agent. Onset of action usually occurs within 48 hours, and it has a half-life of 10–25 hours. Because the medication is excreted unchanged in the kidneys, it may accumulate within the plasma of older adults and those with renal insufficiency. The dose should be reduced in those with renal impairment and in clients who are 65 years of age or older. This is one reason it is a second-line therapy, because older adults are more likely to have PD (DailyMed, Amantadine, 2023).

Adverse Effects and Contraindications

Suicidal attempts, some of which have been fatal, have been reported. The practitioner must sufficiently assess suicide risk factors and suicidal ideations before medication is prescribed. Other psychiatric manifestations caused by this drug include delirium, hypertonia, delusions, hallucinations, anxiety, euphoria, paranoia, manic reaction, and tremors. This drug can cause clients to engage in compulsive behavior and to lack impulse control. In some clients, reduction of dose or discontinuing the drug can stop these urges. Other clients may need additional help with psychotherapy. CNS stimulants can exacerbate the mental and psychiatric manifestations.

Amantadine can cause elevated levels of creatinine phosphate kinase (CPK), serum myoglobin, BUN, serum creatinine, alkaline phosphatase, low-density lipoprotein (LDL), and liver enzymes. Clients who take amantadine for more than 1 month often develop livedo reticularis, which is characterized by purple mottling of the skin. This condition is benign and gradually subsides after the drug is discontinued (DailyMed, Amantadine, 2023).

Abrupt discontinuation may precipitate agitation, slurred speech, depression, stupor, delirium, delusions, and hallucinations. In addition, several cases of NMS have occurred upon discontinuing the medication. This is a life-threatening condition and immediate treatment is necessary. Clinical manifestations of this includes high fever, muscle rigidity, involuntary movements, altered consciousness, tachycardia, tachypnea, and changes in blood pressure.

The drug can exacerbate symptoms in clients with heart failure. The seizure threshold is lowered by this drug; therefore, those with seizure disorders are more apt to have frequent seizures if their medications are not adjusted.

Angle-closure glaucoma is a contraindication due to the mydriasis and further narrowing of the angle between the cornea and iris. This can worsen the glaucoma.

Table 11.11 is a drug prototype table of dopamine antagonists featuring amantadine. It lists drug class, mechanism of action, adult dosage, indications, therapeutic effects, drug and food interactions, adverse effects, and contraindications.

Nursing Implications

The nurse should do the following for clients who are taking dopamine antagonists:

• Ask about suicidal ideations, plan, and accessibility of their plan.
• Measure temperature for increases because client is at risk for infection due to reduction in white blood cell count, or it can indicate NMS.
• Monitor for an increase in respirations and heart rate as these are related to NMS.
• Assess for decreases in blood pressure upon position changes.
• Obtain a periodic ECG to monitor the QT interval.
• Assess for any seizure activity because the drug can decrease the seizure threshold.
• Perform a skin examination to monitor for melanomas.
• Specifically ask client about new or increased gambling urges, sexual urges, and uncontrolled spending.
• Monitor intake and output for a positive net result due to risk of urinary retention.
• Assess for peripheral edema, shortness of breath, and increased blood pressure.
• Provide client teaching regarding the drug and when to call the health care provider. See below for client teaching guidelines.