general anesthetics

How does levetiracetam (Keppra) work?

Acts on SV2A synaptic vesicle protein → ↓ excitatory neurotransmitter release.

Major advantage of levetiracetam?

No drug-drug interactions and fewer major side effects.

How does lamotrigine (Lamictal) work?

Blocks voltage-gated Na⁺ channels → ↓ excitatory synaptic activity.

Advantage of lamotrigine?

Can be combined with multiple other antiseizure medications.

What is topiramate used for?

Broad-spectrum antiseizure medication + migraine prevention; multiple mechanisms.

What is divalproex?

Combination of valproate + valproic acid with less GI effects than original drug; mechanism unclear in chart.

How does gabapentin (Neurontin) work?

Blocks voltage-gated Ca²⁺ channels → ↓ excitatory synaptic activity.

What are additional uses of gabapentin?

Neuropathic pain + spasticity.

How do diazepam and lorazepam act as antiseizure medications?

Increase inhibitory synaptic activity through GABA-A receptors.

When are benzodiazepines particularly useful for seizures?

Acute status epilepticus.

What additional uses does diazepam have?

Spasticity + anxiety.

Common antiseizure medication adverse effects?

N/V, sedation, ataxia, rash, hyponatremia, weight changes, teratogenicity, osteoporosis.

Major PT considerations with antiseizure medications?

Pregnancy, withdrawal, sedation/ataxia, long half-lives, rash; light/sound can worsen seizures in some patients.

A patient taking an antiseizure medication develops ataxia and sedation. What is the major PT concern?

Increased balance/fall risk and impaired safe mobility.

What is spasticity?

Exaggerated muscle stretch reflex from hyperexcitability of alpha motor neurons at spinal cord.

How does diazepam reduce spasticity?

GABA-A receptor agonist at spinal cord → ↓ muscle tone.

Major disadvantage of diazepam for spasticity?

Sedation at effective doses + dependence risk.

How does baclofen work?

GABA-B receptor agonist at spinal cord.

Major baclofen withdrawal concern?

Rebound spasticity if not tapered.

How does tizanidine (Zanaflex) work?

α2 adrenergic agonist acting at spinal cord.

When is tizanidine used in the chart?

Spasticity after spinal cord injury.

Major tizanidine adverse effects?

Drowsiness + hypotension.

How does gabapentin reduce spasticity?

Blocks voltage-gated Ca²⁺ channels → ↓ excitatory synaptic activity/lower motor neuron activity.

Major gabapentin adverse effects?

Sedation, fatigue, ataxia.

How does botulinum toxin (Botox) reduce spasticity?

Inhibits ACh at NMJ → ↓ muscle hyperexcitability.

Major systemic risk of botulinum toxin?

Widespread paralysis.

A patient receives botulinum toxin for focal spasticity. Why does muscle tone decrease?

↓ ACh release at NMJ → ↓ muscle activation.

Spasticity vs muscle spasm?

Spasticity = CNS/UMN-related exaggerated stretch reflex; spasm = local response after peripheral MSK injury/inflammation.

How does cyclobenzaprine (Flexeril) work?

Centrally inhibits stretch reflex at spinal cord → treats acute muscle spasm.

Major cyclobenzaprine concerns?

Sedation, tolerance/dependence, risk of fatal overdose.

Why is cyclobenzaprine used judiciously?

It treats acute muscle spasm but carries CNS depression, tolerance/dependence, and overdose risk.

How does levodopa treat Parkinson disease?

Some crosses BBB → converted to dopamine in brain → improves bradykinesia.

Why is levodopa combined with carbidopa?

Carbidopa inhibits premature peripheral conversion of levodopa → more reaches brain.

What is levodopa + carbidopa called?

Sinemet.

Major levodopa adverse effects?

GI issues, orthostatic hypotension, arrhythmias, dyskinesia, behavioral changes, symptom fluctuations, diminishing response.

Why does PT treatment timing matter with levodopa?

Symptoms fluctuate with medication effects.

A patient with PD moves well shortly after medication but becomes increasingly bradykinetic before the next dose. What explains this?

Levodopa-related symptom fluctuations.

What is dopamine dysregulation syndrome associated with?

Levodopa.

What drugs interact with levodopa according to the chart?

Nonspecific MAO inhibitors + pyridoxine/vitamin B6.

How do ropinirole and pramipexole (Mirapex) work?

D2/D3 dopamine receptor agonists.

When are dopamine agonists used in Parkinson disease?

Mild or advanced PD; may be combined with levodopa.

How do dopamine agonist adverse effects compare with levodopa?

Similar but generally less pronounced.

What is selegiline?

Selective MAO-B inhibitor used for mild PD or inadequate response to levodopa.

Major selegiline concern?

Drug interactions including serotonin syndrome; long-term effectiveness unclear.

What is serotonin syndrome characterized by in the chart?

Autonomic dysfunction + neuromuscular dysfunction + altered mental status.

How does entacapone (Comtan) help Parkinson disease?

COMT inhibitor → prevents peripheral levodopa metabolism.

Why combine entacapone with levodopa/carbidopa?

Enhances levodopa effect, permits lower dose, reduces fluctuations.

What is Stalevo?

Combination therapy involving levodopa/carbidopa with entacapone.

What can initially occur when entacapone is added?

Increased levodopa side effects.

How do benztropine and trihexyphenidyl help Parkinson disease?

Block muscarinic ACh receptors in basal ganglia.

Which Parkinson symptoms respond most to antimuscarinics?

Tremor + rigidity.

Why are antimuscarinics limited in PD?

Less effective alone, do not treat all symptoms, and cause CNS/peripheral effects especially in older adults/cognitive impairment.

A patient with PD has primarily tremor and rigidity. Which drug class may specifically help these symptoms?

Antimuscarinics such as benztropine or trihexyphenidyl.

What medications are used to treat MS in the chart?

Immunosuppressants, interferon-β, monoclonal antibodies such as alemtuzumab + antispasticity drugs for symptoms.

What is the overall drug-treatment goal for ALS?

Improve survival time + slow disease progression.

How do barbiturates such as phenobarbital work?

Promote GABA-induced CNS inhibition.

What are barbiturates used for?

Occasionally sleep; more often general anesthesia or antiseizure treatment.

Major barbiturate disadvantages?

Low therapeutic index, tolerance, dependence/abuse, fatal overdose risk.

How do benzodiazepines such as flurazepam work?

Promote GABA-induced CNS inhibition.

Why are benzodiazepines generally safer than barbiturates?

Lower chance of lethal overdose.

Major benzodiazepine concerns with chronic use?

Residual CNS depression, tolerance, physical dependence.

How does zolpidem (Ambien) differ from benzodiazepines?

Similar action but more specific for α1 subunit → hypnotic effects.

Advantages of zolpidem in the chart?

Effective for sleep with fewer side effects and less dependence risk.

What determines how quickly sedative-hypnotics enter CNS?

Lipid solubility.

What pregnancy/lactation concern applies to sedative-hypnotics?

All cross placenta and are present in breast milk.

How are barbiturates generally metabolized?

Slowly; long half-life and many active metabolites.

How are second-generation hypnotics generally metabolized?

Rapidly to inactive metabolites.

What are the dose-dependent effects of sedative-hypnotics?

Sedation/anxiolysis → hypnosis → anesthesia; also antiseizure effects.

How do sedative-hypnotics affect respiratory/CV function?

Depress respiratory drive + cardiac muscle contraction.

Major sleep-related adverse effects of sedative-hypnotics?

Daytime sedation, rebound insomnia, reservoir effect.

What happens when sedative-hypnotics are combined with other CNS depressants?

Additive CNS depression.

A patient arrives for morning PT extremely drowsy after taking a hypnotic the night before. What may explain this?

Residual CNS depression/reservoir effect.

How does fluoxetine (Prozac) work?

SSRI → inhibits serotonin reuptake.

What conditions can SSRIs treat?

MDD, GAD, PTSD, OCD, panic disorder, PMDD, bulimia.

Major SSRI adverse effects?

Sexual dysfunction, weight gain, serotonin syndrome, discontinuation syndrome.

What can SSRI discontinuation syndrome cause?

Dizziness + paresthesia, particularly with short half-life/no active metabolite.

How does venlafaxine (Effexor) work?

SNRI → blocks serotonin + NE reuptake.

What conditions can SNRIs treat?

MDD, GAD, neuropathies, fibromyalgia, stress IC, menopausal vasomotor symptoms.

How does bupropion (Wellbutrin) work?

↓ dopamine + NE reuptake → ↑ availability.

What is bupropion used for?

Major depression + smoking cessation.

How do TCAs such as imipramine work?

Block serotonin + NE reuptake.

What are TCAs used for?

Treatment-resistant depression, neuropathic pain, UI, insomnia.

Major TCA adverse effects?

Sedation, orthostatic hypotension, cardiac toxicity, weight gain, dry mouth, constipation, tachycardia/arrhythmias, urinary retention, N/V, drowsiness.

Why is TCA overdose particularly concerning?

Significant toxicity/cardiac effects.

A patient taking a TCA becomes dizzy when standing during PT. What medication effect should you suspect?

Orthostatic hypotension.

How do MAOIs such as phenelzine work?

Inhibit MAO-A + MAO-B.

What are MAOIs used for?

Treatment-resistant depression; low-dose selegiline can treat PD.

Major MAOI concerns?

Food/medication interactions, serotonin syndrome, discontinuation syndrome, sexual dysfunction, weight gain, orthostatic hypotension.

What medication is used for acute and chronic management of bipolar disorder?

Lithium.

Major lithium adverse effects?

Headache, hand tremor, dizziness, fatigue.

Why is lithium toxicity a major concern?

Low therapeutic index.

Signs of lithium toxicity?

Ataxia, slurred speech, tremors, confusion, seizures.

A patient taking lithium develops new ataxia, slurred speech, and confusion. What should you suspect?

Lithium toxicity.

What medications may be used across bipolar disorder phases?

Antiseizure meds, antipsychotics for mania, antidepressants for depressive episodes.

What is haloperidol (Haldol)?

First-generation antipsychotic used to reduce hallucinations/delusions and manage agitation/disruptive behavior.

What is risperidone (Risperdal)?

Second-generation antipsychotic.

Major antipsychotic adverse effects?

Weight gain, extrapyramidal symptoms, orthostatic hypotension, arrhythmias, drowsiness, lower seizure threshold.

What movement disorder can occur with long-term first-generation antipsychotic use?

Tardive dyskinesia.

What rare serious syndrome can occur with antipsychotics?

Neuroleptic malignant syndrome.

A patient on long-term haloperidol develops involuntary repetitive movements. What medication complication should you suspect?

Tardive dyskinesia.