medications used for neurological disorders + mental health and well-being | NURS112

while alzheimer’s disease is incurable, what are some type of medications that are use to manage symptoms?

1. cholinesterase inhibitors

2. NMDa receptor antagonist

what do acetylcholinesterase (AChE) inhibitors bind to? what is it main affect on acetylcholines on cholinergic neurons

acetylcholinesterase enzyme; inhibit acetylcholine to prevent break down of acetylcholine which increases acetylcholine availability; AChE enhance transmission of cholinergic neurons

what is the normal function of acetylcholinesterase?

it break down acetylcholine

what is the therapeutic benefits of AChE inhibitors in Alzheimer’s disease?

they improve symptoms and slow their progression by increasing acetylcholine levels in the brain, which helps support memory and cognition.

• they delay worsening symptoms (memory loss, confusion, thinking ability)

• they work by preventing the breakdown of acetylcholine, a key neurotransmitter for learning and memory

• this helps remaining neurons communicate better, even as the disease progresses

what is the MOA, indications, interactions, contraindications, and side effects of donepezil (Aricept)?

cholinesterase inhibitor

1. MOA: reversible inhibition of AChE (causes a prolonged and exaggerated cholinergic effects which enhances cognitive functions)

2. indications: mild to moderate Alzheimer’s disease, atropine (medications used to treat bradycardia) overdose

3. interactions: anticholinergic agents, antipsychotics, tricyclic antidepressants, parasympathomimetics, NSAIDs, beta blockers, and digoxin

4. contraindications: peptic ulcer disease (since an increased in Acetylcholine would stimulate gastric acid secretion since it stimulate rest and digest), active GIB (increases risk for bleeding), urinary or intestinal obstruction (since increased acetylcholine increases smooth muscle contraction during rest and digest, which if there is a blockage, it can worsen it), cardiac conduction disorders (since Acetylcholine slows the heart rate by suppressing the SA and AV nodes)

5. side effects: nausea, vomiting, diarrhea, abdominal pain, increased salivation, symptomatic bradycardia, HA, bronchoconstriction (since the body is resting)

what is glutamate’s role in the brain?

it is the primary excitatory neurotransmitter → crucial for fast synaptic transmission

what receptor does glutamate bind to for learning and memory? what happens when glutamate binds to the receptor? what happens when glutamate leave the receptors?

NMDA receptor; when glutamate binds to the NMDA receptors, calcium enter the neuron, producing an excitatory effect; when glutamate leaves the NMDA receptor, magnseium blocks the receptor, stopping calcium entry

why is calcium entry into neurons so important?

it is essential for learning and memory formation

why is the NMDA receptor response normally short-lived?

because glutamate quickly detaches, allowing magnesium to block the channel

what is the role of NMDA receptor antagonist?

they block excessive stimulation, protecting neurons from damage because when the receptors are overstimulated, excess calcium enters, causing excitotoxicity

what are the two NMDA receptor antagonist?

1. memantine

2. ketamine

what is the MOA indications, interactions, contraindications, and side effects of memantine (Namenda)?

NMDA receptor antagonist

1. MOA: binds to the NMDA receptor to regulate the influx of calcium, which improve cogitions skills, slows the progression by preventing neuronal damage

2. indications: moderate to severe dementia

3. interactions: acetazolamide, sodium bicarbonate

4. contraindications: renal and hepatic impairment (because the drugs is metabolized by the liver and clear by the kidney)

5. side effects: diarrhea, constipation, dizziness, HA, confusion, pancreatitis, hepatitis

what are the general nursing considerations for Alzeimher’s disease medications?

1. administration: (1) take ER capsules whole and (2) allow oral disintegrating tablets to dissolve completely and follow with water

2. fall precautions: the medications can cause dizziness and stimulatory effect on GI/GU systems

3. GI upset is temporary

4. take donepezil AT BEDTIME

what is Parkinson’s disease?

a progressive neurologic disorder, caused by destruction of dopamine-secreting neuronswhy

why is dopamine important in Parkinson’s disease?

dopamine is essential for movement control and is needed to produce norepinephrine

why is doapmine important in Parkinson’s disease?

dopamine is essential for movement control and is needed to produce norepinephrine

what are the four key motor symptoms of Parkinson’s disease?

• Tremor

• Rigidity

• Bradykinesia (slow movement)

• Postural instability

👉 (Think: “TRAP” — super testable)

what symptoms are caused by loss of norepinephrine in Parkinson’s disease?

• Mood changes (depression, anxiety)

• Cognitive changes

• Perceptual disturbances

why is anticholinergic not often used for Parkinson’s diseasr

mainly due to the side effects

what is the MOA, indications, interactions, contraindications, and adverse effects of benztropine (Cogentin)?

anticholinergic used for Parkinson’s disease

1. MOA: directly inhibit parasympathetic nervous system → specifically the work of acetylcholine which help reduce stiffness, tremor due to overactivation of the cholinergic system which results in excessive muscle contractions

2. indications: adjunct therapy for PD, control of extrapyramidal syndrome (not tardive dyskinesia) → the medication improve balance between dopamine and ACh levels, it can reduce resting tremors, rigidity, and bradycardia

3. interaction: antihistamines, tricyclic antidepressants, cholinergic agonists, alcohol

4. contraindications: less than 3 years old, hypersens

5. adverse effects: anhidrosis, hyperthermia. heat stroke, constipation, urinary retention

what are the key nursing implications and patient teaching for anticholinergics in Parkinson’s

• monitor: urinary retention, constipation/ileus, photophobia

• interventions: dark room for light sensitivity, bladder scans PRN

• teach:

  • increase fluids & fiber

  • avoid alcohol/sedatives

  • wear sunglasses

  • change positions slowly (orthostatic hypotension)

  • do not stop abruptly

what are dopaminergic drugs and what do they do?

dopaminergics are medications that increase dopamine activity in the brain by either replacing dopamine (levodopa) or mimicking it (dopamine agonists) → they help improve motor symptoms like tremor, rigidity, and bradykinesia in Parkinson’s disease.

what is the MOA, indications, interactions, contraindications, and adverse effects of carbidopa/levodopa (Sinmet, Parcopa, Rytary)?

dopaminergics for PD

1. MOA: taken up by dopaminergic nerve terminals to convert into dopamine for use by neurons

2. indications: reduces symptoms of PD by increasing dopamine synthesis → reduces rigidity, tremors

3. interactionsL MAOIs, antihypertensives, iron, dopamine receptor antagonists, high protein

4. contraindicationsL narrow angle glaucoma

5. adverse effects: nausea, vomitting, dysrhythmias, “wearing of,” “on-off,” dyskinesia, psychosis, brown urine and sweat, increased impulsivity, melanoma, development

what are the general nursing implications for dopaminergics for Parkinson’s disease?

• monitor:

  • Depression/SI → dopamine changes can affect mood

  • Drowsiness/sleep attacks → can cause sudden sleep → safety risk

  • Impulse behaviors (gambling, sex, spending) → ↑ dopamine = poor impulse control

  • Melanoma → dopamine related to melanin production

  • Dyskinesias (face/mouth movements) → too much dopamine

• teach:

  • Take meds consistently → maintains stable dopamine levels

  • No immediate effect → takes time to build up

  • Do NOT stop abruptly → can cause severe symptom rebound

  • Report abnormal movements/behaviors → signs of excess dopamine

  • Skin checks → early melanoma detection

  • Avoid driving if sleepy → prevent accidents from sleep attacks

  • Eat high-iron foods → supports overall health (but note: iron can affect levodopa absorption if taken together)

which medication is the first-line treatment of mild to moderate PD? what are the different type of dopamine agonists?

dopamine agonists - mimic the role of dopamine in the brain (compared to dopaminergics, which are actual dopamine)

1. ergot = nonselective, so more cardiovascular side effects

2. non-ergot = selective for dopamine receptors

what is the MOA, indications, interactions, contraindications, and adverse effects of pramipexole?

dopamine agonists to treat PD

1. MOA: selectively binds to dopamine receptors to activate dopamine secretion

2. indications: monotherap in early-stage PD, combined with levodopa in late-stage PD → the monotherapy significantly improve motor performance; combo reduces motor fluctations and fewer dyskinesias

3. interactions: antipsychotic, dopamine antagonists, serotonin receptors antagonists, estrogen, medications that prolong QT

4. contraindications: pregnancy, breastfeeding

5. adverse effects: N, V, constipation, hallucinations (excess dopamine can overstimulate CNS), hyperhydrosis (dopamine affect autonomic regulation), sleep attacks, impulse control disorders, orthostatic hypotension (dopamine causes vasodilation and decrease sympathetic tone), bradycardia, dyskinesias (too much dopamine can lead to excess movement signaling)

what is MAO-B?

MAO-B is an enzyme that breaks down dopamine in the brain

what is the common ending for dopaminergics?

-dopa

what is the common ending for MAO-B?

-iline

what is the MOA, indications, interactions, contraindications, and adverse effects of selegiline (Eldepryl)?

Monoamine Oxidase-B inhibitors (MAO-Bs) - prevent the break down of dopamine in the brain

1. MOA: selectively and irreversibly inhibits MAO-B, an enzyme that metabolizes doapmine in the brain

2. indications: adjunct therapy for PD with carbidopa/levidopa helps decrease fluctuations in motor control

3. interactions: morphone, merepidine, tramadol, SSRIs, TCAs, sympathominetics

4. contraindications: cautious use in patients with melanoma, hepatic impairment, or severe psychotic disorder

5. adverse effects: insomnia, HA, dizziness, depression, melanoma, hallucinations, QT prolongations, impulse control, serotonin syndrome

what are centrally acting muscle relaxants and what do they treat in multiple sclerosis? what are one example?

they act on the CNS (brain/spinal cord) to treat spasticity and nerve pain; no direct effect on skeletal muscle; baclofen (lioresal)

how are centrally acting muscle relaxants administered?

orally or intrathecally (into the spinal cord)

what are peripherally acting muscle relaxants and how do they work? what is one example?

they are the muscle relaxants that act directly on muscle fibers, not the brain of which they prevent muscle contration to reduce spasticity; dantrolene sodium (Dantrium)

what is a major side effects that the nurse should watch out for for peripherally acting muscle relaxants?

muscle weakness (impaired strength)

what is the MOA, indications, interactions, contraindications, and adverse effects of baclofen (lioresal)?

centrally acting muscle relaxants

1. MOA: reduces nerve impulse transmission from the spinal cord to the skeletal muscle and inhibits GABA receptors located on the spinal cord

2. indications: reversible muscle spasticity associated with multiple sclerosis and spinal cord injuries → suppress hyperactive reflexes involving in regulating muscle movement

3. interactions: CNS depressants, alcohol, anticholinergic

4. contraindications: hypersensitivity

5. adverse effects: drowsiness, fatigue, confusion, HA, insomnia, N, V, constipation, urinary retention, hypotension, arrythmias

what is the MOA, indications, interactions, contraindications, and adverse effects of dantrolene sodium (Ryanodex, Dantrium)?

peripherally acting muscle relaxants

1. MOA: acts directly on excitation-contractions mechanism in skeletal muscle and inhibits the release of calcium to prevent muscle contractions

2. indications: chronic spasticity, malignant hyperthermia after anesthesia, neuroleptic malignant syndrome → reduce muscle spasticity

3. interactions: CNS depressants, estrogen, CCBs, other muscle relaxants

4. contraindications: hypersensitivity, known liver disease

5. adverse effects: hepatotoxicity, muscular weakness, diarrhea, vomitting, abdominal pain, photosensitivity

what are the general nursing considerations for muscle relaxants?

• monitor mental status → CNS depression/sedation

• assess muscle strength before & after → risk of excess weakness

• check baseline LFTs → risk of hepatotoxicity (esp. dantrolene)

• use nonpharmacologic measures (stretching, positioning)

• taper medication → avoid withdrawal/rebound spasticity

what the MOA, indications, interactions, contraindications, and adverse effects of gabapentin (Neurontin)

gamma-aminobutyric acid structural analogs

1. MOA: increases GABA availability to bind to receptors that decrease the release of neurotransmitters responsible for pain and seizures like glutamate and norepinephrine

2. Indications: focal seizures → stabilizes overactive neurons → prevents abnormal electrical activity; neuropathic pain → damaged nerves fire excessively → gabapentin reduces pain signal transmission; restless leg syndrome (RLS) → abnormal nerve activity in legs → calms nerve excitability

3. Interactions: opioids, antiepileptics, antacids

4. Contraindications: hypersensitivity

5. Adverse: SI, depression, Stevens-Johnson syndrome, anaphylaxis, angioedema, withdrawal symptoms/seizures

what is the MOA, indications, therapeutic effects, interactions, contrainications, and adverse effects of phenytoin (Dilantin)?

hydantoins - anticonvulsants/antiepileptic

1. MOA: decreases abnormal electrical activity in the brain by blocking the channels responsible for creating action potentials

2. indications: tonic-clonic and psychomotor seizure treatment; prevent and treat seizures that occur during neurosurgery → reduced seizure activity

3. interactions: antineoplastic medications, NMBs, warfarin, CCB, antacids

4. contraindications: hypersensitivity, hepatotoxicity, bradycardia or heart blocks; use cautiously in patients with SI and pregnancy

5. adverse: nystagmus, ataxia, slurred speech, decreased coordination, somnolence, mental confusion

what is the MOA, indications, therapeutic effects, interactions, contrainications, and adverse effects of phenobarbital?

barbiturates - anticonvulsant/antiepileptic

1. MOA: inhibits the central nervous system by enhancing GABA to slow down the brain

2. indication: seizures, sedation

3. therapeutic effects: reduces seizures and enhances sleep

4. interactions: anticoagulants, corticosteroids, other anticonvulsants, MAOIs, estrogen, hormones

5. contraindications: hypersensitivity, hepatic failure, respiratory disease; use cautiously in patients with history of substance use disorder

6. adverse effects: CNS depression, respiratory depression, N, V, HA

what is the MOA, indications, therapeutic effects, interactions, contrainications, and adverse effects of carbamazepine (Tegretol)?

dibenzoazepine - anticonvulsant/antiepileptic

• MOA: inhibits the central nervous system by enhancing GABA to slow down the brain

• Indication: seizures, sedation

• therapeutic Effects: reduces seizures, promotes sedation

• interactions: none

• contraindications: hypersensitivity, bone marrow suppression, TCAs, MAOIs; use cautiously in patients with hyponatremia and SIADH

• adverse effects: photosensitivity, edema, dyspnea, urinary retention, drowsiness, HA, fatigue, bone marrow depression

what is the MOA, indications, therapeutic effects, interactions, contrainications, and adverse effects of valproic acid (Depakote)?

• MOA: blocks sodium, potassium, and ion channels to decrease brain activity

• indication: seizures, bipolar disorder

• therapeutic Effects: reduces seizures activity and bipolar symptoms of mania

• interactions:  a lot - carbmazepine, clonazepam, diazepam, phenobarbitol, phenytoin, warfarin

• contraindications: hypersensitivity, hepatic insufficiency, bone marrow depression, pregnancy

• adverse effects: HA, somnolence, dizziness, thrombocytopenia, tinnitus, emotional lability

what is the MOA, indications, therapeutic effects, interactions, contrainications, and adverse effects of levetiracetam (Keppra)?

anticonvulsant/antiepileptic

• MOA: binds to a protein in the brain that inhibits neurotransmitter release, which reduces the probability of excitatory neurotransmitter release

• indication: seizures

• therapeutic effects: reduces seizures activity; causes sedation

• interactions:  baclofen, melatonin, opioids, trazodone

• contraindications: hypersensitivity

• adverse effects: somnolence, fatigue, rash, coordination problems, emotional lability, HA

what is the common ending of tricyclic antidepressants (TCAs)? how do they work?

-ptyline, -pramine

• block acetylcholine receptors and prevent reuptake of norepinephrine and serotonin

what is the MOA, indication, therapeutic effects, interactions, contraindications, and adverse effects of amitriptyline (Elavil)?

tricyclic antidepressants (TCAs)

1. MOA: block acetylcholine receptors and prevent reuptake of norepinephrine and serotonin

2. indications: major depressive disorder, primary insomnia, anxiety, chronic pain

3. therapeutic effects: increases effects of norepinephrine, serotonin, and dopamine

4. interaction: anticholinergics, phenothiazines, haloperidol, MAOIs, CCBs, BBs, digoxin, CNS depressants, antihistamine

what are the common must-known side effects of SSRIs?

the four S’s

1. (S)erotonin syndrome - potentially life-threatening drug reaction caused by excessive serotonin accumulation in the body, usually within 2-24 hours of starting or increasing medication (causing mental status changes like agitation/confusion, autonomic hyperactivie like fever, high heart rate, sweating)

2. (S)uicidal thoughts

3. (S)exual dysfunction

4. (S)tomach upset

how so SSRIs work?

inhibit the uptake of serotonin to allow it to accumulate in the synaptic cleft → it have little effect on other neurotransmitter

what is the MOA, indication, therapeutic effects, interactions, contraindications, and adverse effects of fluoxetine (Prozac)? (very likely to be on th quiz!)

SSRIs

• MOA: blocks serotonin reuptake

• indication: OCD, panic disorders, PMDD, bulimia, bipolar depression, treatment-resistant depression

• interactions:  MAOIs, warfarin, aspirin, NSAIDs

• contraindications: < 8 years old

• adverse: N, HA, insomnia, sexual dysfunction, weight gain, SI

what are the side effects and therefore nursing consideration of fluoxetine? (very likely to be on the quiz! I think!)

FLUOXETINE as a mnemonics

1. (F)atigue

2. (L)oss of libido and weight loss

3. (U)pset stomach

4. (O)verstimulation (insomnia, anxiety)

5. (X)erostomia (dry mouth)

6. (E)motional changes (mood swings)

7. (T)remor

8. (I)ncreased risk of bleeding

9. (N)ausea

10. (E)levated serotonin

nursing interventions:

1. monitor for increased suicide risks (epsecially in the first few weeks)

2. educating on the 1-4 week delays in therapeutic effects

3. manage side effects like insomnia and GI distress

what is the main difference between SSRIs and SNRIs

SNRIs have the addition of also blocking norepinephrine

when SNRIs should be discontinue?

FINISH mnemonics

1. (F)lu-like symptoms

2. (I)nsomnia

3. (N)ausea

4. (I)mbalance

5. (S)ensory disturbances

6. (H)yperarousal

what are the nursing interventions for serotonin norepinephrine reuptake inhibitors (SNRIs)?

1. monitor for serotonin syndrome

2. manage increased blood pressure/heart rate

3. providing education on the 1-4 weeks lag time for therapeutic effects

what is the MOA, indication, therapeutic effects, interactions, contraindications, and adverse effects of bupropion (Wellbutrin)?

norepinephrine dopamine reuptake inhibitor (NDRI)

1. MOA: inhibits reuptake of dopamine, norepinephrine, and serotonin

2. indications: depression, SAD, smoking cessation

3. interactions: sertraline, fluoxetine, paroxetine, MAOIs used within 14 days

4. contraindications: hypersensitivity, seizures, conditions that may lower the seizure threshold

5. adverse effects: seizures, activation of mania, insomnia, tachycardia, hypertension, dry mouth, HA, N, V, constipation, anorexia/weight loss, photosensitivity

what is the third-line (not commonly used) medication used for treating depression and what is its main concerns?

MAO inhibitors

1. Monoamine oxidase inhibitors

2. can cause severe hypertension (e.g., phenelzine [Nardil], selegiline [Emsam])

what is the MOA, indication, therapeutic effects, interactions, contraindications, and adverse effects of phenelzine (Nardil)?

• MOA: binds to MAO-A enzyme

• indication: major depression

• interactions:  increases and enhances the effect of norepinephrine, dopamine, and serotonin

• contraindications: severe hepatic impairment, pheochromocytoma, CHF, hypersensitivity

• adverse: hypertensive crisis, dysrhythmias, CNS stimulation, hepatotoxicity, orthostatic dysfunction, sexual dysfunction, dizziness

what are the priority nursing implications for antidepressants?

1. check mood and anxiety frequently

2. monitor for seizure activity

3. provide education on:

• Medications can take up to 2 weeks to start seeing effects and 4*6 weeks for full therapeutic effects

• High probability of sexual dysfunction

• Notify provider if increased depression or SI

• Assess for signs of bleeding

• Do not eat foods high in tyramine if taking an MAOI

• Be in direct sunlight without appropriate clothing and sunscreen

why are first-generation antipsychotics called neuroleptics?

because they cause the patient to have an increased risk of producing EPS, pseudoparkinsonism, dystonia, akathisia, and tardive dyskinesia

most antipsychotics are which type of medications?

dopamine receptor antagonists

• help with thought organization

• first generation = typical

• second generation = atypical

true or false: antipsychotic medication therapy will be life-long to prevent relapse

true!

what is the MOA, indication, therapeutic effects, interactions, contraindications, and adverse effects of haloperidol (Haldol)

• MOA: dopamine-2 receptor blockers, which prevent dopaminergic stimulation of neurons

• Indication: schizophrenia, treatment of psychotic symptoms, acute agitation (particularly when caused by psychosis or delirium)

• interactions:  CNS depressants, antiarrhythmic medications that prolong QT, kava kava, alcohol

• contraindications: Parkinson’s disease, dementia, cardiac arrhythmias, liver damage, CAD, CVD

• adverse effects: PR and QT prolongation, anticholinergic effects, sexual dysfunction, hypotension, arrhythmias, tardive dyskinesia, impaired mobility, slurred speech, drowsiness, sedation, impaired speech, and mental processes

what is the MOA, indication, therapeutic effects, interactions, contraindications, and adverse effects of lithium (Eskalith, Lithobid)

• MOA: exact unknown

• indication: treatment of active manic episodes, maintenance therapy to prevent or diminish the frequency and intensity of future manic episodes

• interactions:  diuretics, serotonergic agents, NMBs, carbamazepine, theophylline, sodium, fluids

• contraindications: renal failure, cardiovascular insufficiency, Addison’s disease, untreated hypothyroidism, children < 12, pregnancy and breastfeeding

• adverse: nephrotoxicity, neurotoxicity, thyroid toxicity (goiter), weight gain, metallic taste, hand taste, polyuria, polydipsia, N, V, D, edema, weight gain, muscular weakness

what i the therapeutic index of lithium

0.6-1.2 mEq/L

what is the priority nursing intervention for lithium?

1. monitor for lithium toxicity due to its narrow therapeutic index of 0.6-1.2 mEq/L)

2. regularly check for dehydration or low sodium as they increases lithium reabsorption, causing toxic levels

3. administer with food or milk to reduce GI discomfort