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Pharmacology for Nurses

10.4 Alzheimer’s Drugs

Pharmacology for Nurses10.4 Alzheimer’s Drugs

Learning Outcomes

By the end of this section, you should be able to:

  • 10.4.1 Identify the characteristics of drugs used to treat Alzheimer’s disease.
  • 10.4.2 Explain the indications, actions, adverse reactions, and interactions of drugs used to treat Alzheimer’s disease.
  • 10.4.3 Describe nursing implications of drugs used to treat Alzheimer’s disease.
  • 10.4.4 Explain the client education related to drugs used to treat Alzheimer’s disease.

AChE Inhibitors

AChE inhibitors bind to and interfere with the enzyme AChE. This enzyme is responsible for the destruction of ACh. By inhibiting this enzyme, more internally released ACh is available for use within cholinergic synapses. The result is enhanced transmission by central cholinergic neurons that have not yet been destroyed. Elevated ACh levels in the cortex can slow the neuronal degradation that occurs in this disease. Treatment with AChE inhibitors does not stop the progression of AD but reduces how quickly neurons are destroyed.


Donepezil, a centrally acting reversible cholinesterase inhibitor, is used primarily for treatment of mild to severe forms of AD. Centrally acting agents readily cross the blood–brain barrier. Donepezil increases ACh in the brain by preventing its breakdown. Drug absorption is unaffected by food. Peak effects occur in 3–8 hours. Metabolism occurs in the liver, resulting in the production of several pharmacologically active metabolites. Excretion is through the kidneys. An important pharmacokinetic note is that donepezil is highly protein bound (96%); therefore, it has a prolonged half-life of 70 hours. This means that it takes an estimated 15 days for the drug to reach steady state.

Safety Alert

Similarly Named Drugs

Do not confuse Aricept (AChE inhibitor) with Aciphex (proton pump inhibitor).

(Source: Institute for Safe Medication Practices [ISMP], 2023)


Galantamine is only used in those with mild to moderate AD. The drug is prepared by extraction from daffodil bulbs. Like donepezil, this drug is a reversible inhibitor of AChE. GI effects are greater than with donepezil but less than with oral rivastigmine (see the next section). Adverse effects are the same as for donepezil with the addition of potential life-threatening skin reactions, such as Stevens–Johnson syndrome. Clients and caregivers should stop the drug and report any signs of a skin rash to their health care provider. As with the other AChE inhibitors, benefits of the drug are modest and short-term. The drug is available in IR and ER tablets as well as an oral solution. Its half-life is 7 hours.


Rivastigmine is FDA-approved for those with mild to severe AD because it enhances cholinergic function. The manner in which it does so is not fully known. It is believed to increase the ACh concentration by reversible inhibition of its hydrolysis by cholinesterase. Additionally, rivastigmine is used in the management of mild to moderate dementia due to Parkinson’s disease. The drug is available in capsules, oral solution, and a transdermal patch. Peripheral cholinergic effects, such as nausea, vomiting, diarrhea, and anorexia, occur more frequently with this drug. Blood levels are lower when using the transdermal route; therefore, the intensity of adverse effects is decreased. The liver does not metabolize this agent, so there are no significant drug–drug interactions.

Clinical Tip

Rivastigmine and Weight

Rivastigmine blood levels vary with weight; careful titration and monitoring should be performed in clients with low or high body weights.

Client Teaching Guidelines

The client using a rivastigmine transdermal patch should:

  • Apply the patch every 24 hours to clean, dry, hairless, and intact healthy skin in a place where clothes will not rub against it.
  • Avoid skin areas where cream, lotion, or powder has recently been applied.
  • Press down firmly for 30 seconds when applying the patch until the edges stick well.
  • Use the upper or lower back as the site of application to prevent inadvertent removal. If sites on the back are not accessible, apply the patch to the upper arm or chest.
  • Only wear one patch at a time. (They should remove the previous day’s patch before applying a new patch). If a patch falls off or a dose is missed, they should apply a new patch immediately.
  • Place used patches in the previously saved pouch and discard in the trash, away from pets or children.
  • Wash hands with soap and water after removing the patch; avoid touching the eyes until hands are washed. In case of contact with eyes after handling the patch, rinse immediately with water.

The client using a rivastigmine transdermal patch should not:

  • Use the patch if the pouch seal is broken or the patch is cut, damaged, or altered in any way.
  • Apply to skin that is red, irritated, or cut.
  • Use the same site for a period of 14 days.

Table 10.5 lists common AChE inhibitors and typical routes and dosing for adult clients.

Drug Routes and Dosage Ranges
Mild to moderate AD:
Tablet, oral disintegrating tablet, or solution: Initial dose: 5 mg daily at bedtime. Clients should be on 5 mg daily for 4–6 weeks before dose is increased to 10 mg daily.
Moderate to severe AD:
Tablet, oral disintegrating tablet, or solution: Initial dose: 10 mg orally daily. A dose of 23 mg daily can be administered once clients have been on a dose of 10 mg daily for at least 3 months.
Donepezil transdermal
5–10 mg, administered on a weekly basis.
Tablets and solution: Initial dose: 8 mg orally daily in the morning; increase to 16 mg daily after a minimum of 4 weeks on 8 mg daily. Dose may be increased to 24 mg daily after a minimum of 4 weeks taking 16 mg daily.
Capsules and solution: Initial dose: 1.5 mg orally twice daily; after at least 2 weeks and if well tolerated, dose can be increased. Maximum dose: 6 mg twice daily (12 mg daily).
Transdermal patch: Initial dose: 4.6 mg daily. Increase dose only after a minimum of 4 weeks at the previous dose, but only if the previous dose has been tolerated. For mild to moderate AD, continue the effective dose of 9.5 mg daily for as long as therapeutic benefit persists. Maximum dose: 13.3 mg daily. For clients with severe AD, 13.3 mg daily is the effective dose.
Table 10.5 Drug Emphasis Table: Acetylcholinesterase Inhibitors (source:

Adverse Effects and Contraindications

Many of the adverse effects caused by AChE inhibitors relate to the stimulation of the PSNS. GI effects are the most common, including nausea, vomiting, diarrhea, abdominal pain, increased salivation, and anorexia. These drugs can cause cardiac-suppressive effects, which can result in symptomatic bradycardia, heart block, and even cardiac arrest. They stimulate the contraction of the bladder muscle and relax the internal sphincter, which causes a sense of urinary urgency for the client. CNS cholinergic effects include miosis, blurred far vision, and difficulty seeing in dim light. Other CNS effects of headaches, dizziness, drowsiness, and possible seizures can also occur. AChE inhibitor drugs can also impair breathing in those with pulmonary disorders, such as asthma and chronic obstructive pulmonary disease (COPD), due to bronchoconstriction and increased bronchial secretions. Frequent monitoring of the breathing pattern is required. Clients with cardiac conduction disorders should be monitored carefully due to the suppressive effects on cardiac impulses.

Contraindications include peptic ulcer disease because these drugs increase the secretion of hydrochloric acid in the stomach, which can worsen the ulcer and potentially cause perforation and/or bleeding. Because of the stimulatory effect on the bladder and bowel, anyone with a bladder or bowel obstruction (mechanical or neurologic) should avoid taking these drugs to reduce the risk of rupture.

Any drugs with anticholinergic effects—such as first-generation histamine-1 receptor antagonists (H1RAs), conventional antipsychotics, and tricyclic antidepressants (TCAs)—should not be used concurrently because they will reduce or block therapeutic effects of cholinergic agonists. Other parasympathomimetics can cause a synergistic effect if used concurrently. Frequent intake of nonsteroidal anti-inflammatory drugs (NSAIDs) or glucocorticoids (steroids) can increase the risk of peptic ulcer disease. Clients taking drugs such as beta blockers (propranolol/metoprolol) or digoxin should be especially careful of significant bradycardia because they both cause negative chronotropic effects.

Table 10.6 is a drug prototype table for AChE inhibitors featuring donepezil. It lists drug class, mechanism of action, adult dosage, indications, therapeutic effects, drug and food interactions, adverse effects, and contraindications.

Drug Class
Acetylcholinesterase inhibitor

Mechanism of Action
Causes reversible inhibition of AChE
Drug Dosage
Mild to moderate AD:
Tablet, oral disintegrating tablet, or solution: Initial dose: 5 mg daily at bedtime. Clients should be on 5 mg daily for 4–6 weeks before dose is increased to 10 mg daily.
Moderate to severe AD:
Tablet, oral disintegrating tablet, or solution: Initial dose: 10 mg orally daily. A dose of 23 mg daily can be administered once clients have been on a dose of 10 mg daily for at least 3 months.
Mild to severe Alzheimer’s disease
To treat overdoses of atropine and other centrally acting anticholinergic drugs

Therapeutic Effects
Enhances cognitive function (memory, thought, reasoning)
Drug Interactions
Anticholinergic agents
First-generation H1RAs
Conventional antipsychotics
Tricyclic antidepressants (TCAs)
Beta blockers

Food Interactions
No significant interactions
Adverse Effects
Abdominal pain
Muscle cramps
Symptomatic bradycardia
AV block
Active peptic ulcer disease
Active GI bleeding
Urinary or intestinal obstruction

History of peptic ulcer disease
Cardiac conduction disorders
Table 10.6 Drug Prototype Table: Donepezil (source:

NMDA Receptor Antagonist

Glutamate is the primary excitatory amino acid in the CNS. When glutamate binds to the NMDA receptors, it displaces magnesium from the receptor channel and causes calcium to enter neurons, producing an excitatory effect. The brief period of calcium entry creates a signal in the learning and memory process. Glutamate will then quickly dissociate from the receptor, which permits magnesium to block the channel again. This prevents further calcium influx. If there is a pathological situation, glutamate will slowly but steadily leak from the presynaptic neuron, which prevents magnesium from reblocking the channel and allows calcium to continue entering the neuron. Too much neuronal calcium is toxic, causing neurodegeneration. In addition, excessive calcium overpowers the signal and impairs the memory and learning process.


Memantine (Namenda, Namenda XR) is indicated for clients with moderate to severe dementia of the Alzheimer’s type. This drug has been shown to exhibit neuroprotective action (slows the neurotoxicity). Memantine is an antagonist of the NMDA receptor subtype of the glutamate receptor. The drug blocks the influx of calcium when extracellular glutamate is low but permits calcium influx when extracellular glutamate is high. When the glutamate level is low, memantine can occupy the NMDA receptor channel. During this time, the level of intracellular calcium can normalize because no further calcium entry is permitted. During an action potential, a burst of glutamate is released, displacing memantine. This causes a short period of calcium influx. Because intracellular calcium is low, normal signaling of memory and learning can occur. When glutamate moves away from the receptor, memantine reblocks the channel, which stops further calcium entry.

Memantine ER has a terminal half-life of 60–80 hours; therefore, it can be prescribed once a day. In contrast, the immediate-release form is administered at 10 mg twice daily. A target dose of 5 mg twice daily is recommended in clients with severe renal impairment. This drug is predominately excreted unchanged in the urine. The drug is available in capsule form and administered orally. Any condition or drug that raises urinary pH to 8 or more can reduce drug elimination by 80% (see drug interactions and caution in Table 10.7), which will result in the accumulation of memantine within the plasma and increase the risk of adverse effects. If a client takes too much memantine, acidifying the urine with K-Phos Neutral or ascorbic acid, for example, will help promote elimination of the drug.

Table 10.7 is a drug prototype table for NMDA receptor antagonists featuring memantine ER. It lists drug class, mechanism of action, adult dosage, indications, therapeutic effects, drug and food interactions, adverse effects, and contraindications.

Drug Class
NMDA receptor antagonist

Mechanism of Action
Binds to the NMDA receptor to prevent the central channel from opening, which regulates the influx of calcium and slows intracellular calcium accumulation
Drug Dosage
Starting dose: 7 mg daily; maximum maintenance dose: 28 mg daily.
The dose is increased weekly by 7 mg daily until maximum dose is reached. 
Moderate to severe dementia of the Alzheimer’s type

Therapeutic Effects
Improves memory and reduces dementia
Slows the rate of clinical progression of AD
Drug Interactions
Carbonic anhydrase inhibitors
Sodium bicarbonate
Thiazide diuretics

Food Interactions
No significant interactions
Adverse Effects
Stevens–Johnson syndrome

Severe renal impairment
Severe hepatic impairment
Conditions that raise urine pH can cause a decreased drug elimination of memantine
Table 10.7 Drug Prototype Table: Memantine (source:

Safety Alert

Similarly Named Drugs

Do not confuse memantine (NMDA receptor antagonist) with methadone (full opioid agonist).

(Source: ISMP, 2023)

AChE Inhibitor/NMDA Receptor Antagonist

This is a fixed combination dose of a cholinesterase inhibitor and an NMDA receptor antagonist (Namzaric). The agent combines donepezil and memantine. Combining these drugs can be beneficial because each drug has a different mechanism of action. The cholinesterase inhibitors address the cholinergic defect, and the NMDA receptor antagonist reduces the abnormally high levels of glutamate. Essentially, the two agents confer independent benefits, and they act synergistically to enhance each other’s effects.

This is an extended-release oral agent that is administered to clients with moderate to severe AD. The combination form is for those who are stabilized on 10 mg of donepezil daily but not taking memantine. Initial dose of memantine ER is 7 mg combined with donepezil 10 mg daily at bedtime. The dose can be increased weekly with a maintenance dose of memantine ER 28 mg and donepezil 10 mg daily. The nurse must monitor the client’s mental status and ability to perform activities of daily living (DailyMed, Namzaric, 2019).

Nursing Implications

The nurse should do the following for clients receiving medications for AD:

  • Emphasize that treatment is not a cure and will not reverse signs or symptoms and usually will only produce modest benefits.
  • Obtain baseline data, such as orientation, mood/affect, and ability to carry out activities of daily living.
  • Assess client’s presence of bowel sounds, urine output, muscle strength, and mental status.
  • Assess blood pressure, heart rate, electrocardiogram, respiratory status, and changes in urine and bowel elimination.
  • Evaluate the client’s ability to swallow with ease and speech pattern.
  • Administer antiemetics to reduce nausea and vomiting.
  • Monitor client’s therapeutic response to the drug, such as improved memory and mood stabilization.
  • Monitor renal and liver function periodically because this can alter the metabolism and elimination of the drugs.
  • Ensure that caregivers are provided additional resources to help cope with the disease of their loved one.
  • Provide client teaching regarding the drug and when to call the health care provider. See below for client teaching guidelines.

Client Teaching Guidelines

The client taking a drug for AD should:

  • Take ER capsules whole.
  • When taking an oral disintegrating tablet, allow medication to dissolve completely on the tongue and follow with water.
  • Prevent possible falls due to dizziness (remove clutter and rugs, have adequate lighting, use walking devices, etc.).
  • Ensure they have ready access to restroom/commode due to the stimulatory effect on the GI and GU systems.
  • Take medication with food to decrease gastric irritation.
  • Understand GI upset is usually temporary and will subside over time.
  • Contact their health care provider immediately if there is any difficulty with swallowing, speaking, breathing, or increased memory loss or agitation occurs.
  • Report severe nausea, vomiting, diarrhea, anorexia, weight loss, dehydration, or signs of GI bleeding.
  • Take donepezil at bedtime.
  • Know how to manage and cope with emotional outbursts.
  • Assess for any skin rashes and notify the health care provider instantly if observed.

The client taking a drug for AD should not:

  • Chew, break, or crush ER capsules.
  • Rise or change positions quickly due to possible orthostatic hypotension.
  • Stop drugs abruptly because symptoms will quickly reoccur.
  • If a dose of medication is missed, do not double up on the next dose—take the next dose as scheduled.

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