new study guide exam 3

CNS pharmacology — What neurotransmitter mainly produces neuronal inhibition?

GABA; it reduces neuronal excitability.

CNS pharmacology — What neurotransmitter is the major CNS excitatory transmitter?

Glutamate.

CNS pharmacology — What is the blood-brain barrier?

A selective barrier limiting drug entry from blood into the brain.

CNS pharmacology — What does CNS tolerance mean?

A diminished response to the same dose with prolonged exposure.

CNS pharmacology — What is physical dependence?

Abrupt drug cessation can trigger a withdrawal syndrome.

CNS pharmacology — Is physical dependence the same as addiction?

No. Addiction involves compulsive use despite harm; dependence can occur with prescribed therapy.

CNS pharmacology — Why combine two CNS depressants cautiously?

Additive sedation can impair breathing, alertness, and coordination.

CNS pharmacology — What priority assessments matter with CNS depressants?

Airway, respiratory rate/depth, level of consciousness, and fall risk.

CNS pharmacology — How can older adults respond to sedating CNS medications?

Greater risk of confusion, sedation, and falls; start cautiously.

CNS pharmacology — How do dopaminergic and anticholinergic drugs differ?

Dopaminergic drugs increase dopamine activity; anticholinergics reduce acetylcholine signaling.

Parkinson disease — What causes the characteristic motor symptoms?

Loss of dopamine-producing neurons in the substantia nigra reduces striatal dopamine.

Parkinson disease — Why does dopamine loss disturb movement?

Striatal acetylcholine activity becomes relatively unopposed.

Parkinson disease — What are the four classic motor findings?

Resting tremor, rigidity, bradykinesia, and postural instability.

Parkinson disease — What is bradykinesia?

Abnormally slow movement and difficulty initiating movement.

Parkinson disease — What two broad medication approaches treat motor symptoms?

Increase dopamine effects or reduce central cholinergic activity.

Parkinson disease — Do symptomatic drugs cure Parkinson disease?

No; they improve symptoms without reliably stopping neurodegeneration.

Parkinson disease — What nonpharmacologic measures support function?

Exercise, physical/occupational therapy, nutrition, and fall prevention.

Parkinson disease — What is an OFF period?

Return of motor symptoms when dopaminergic benefit wears off.

Parkinson disease — Which medicines can prolong levodopa benefit?

COMT inhibitors, MAO-B inhibitors, or dopamine agonists.

Levodopa/carbidopa — Drug class?

Dopamine precursor plus peripheral dopa-decarboxylase inhibitor.

Levodopa/carbidopa — Primary indication?

Symptomatic treatment of Parkinson motor dysfunction.

Levodopa/carbidopa — Why administer levodopa rather than dopamine?

Levodopa crosses the blood-brain barrier; dopamine does not effectively cross.

Levodopa/carbidopa — How does levodopa act?

It is converted to dopamine in the brain, replacing deficient dopamine signaling.

Levodopa/carbidopa — How does carbidopa help?

It reduces peripheral levodopa conversion, increasing brain delivery and reducing nausea.

Levodopa/carbidopa — Does carbidopa cross the blood-brain barrier?

No; its principal effect is peripheral enzyme inhibition.

Levodopa/carbidopa — Common side effects?

Nausea, dizziness, and orthostatic hypotension.

Levodopa/carbidopa — Major long-term motor complication?

Dyskinesias: involuntary abnormal movements.

Levodopa/carbidopa — Important psychiatric adverse effects?

Hallucinations, confusion, and sometimes psychosis.

Levodopa/carbidopa — What is end-of-dose wearing off?

Motor benefit declines before the next scheduled levodopa dose.

Levodopa/carbidopa — What are on-off fluctuations?

Sudden changes between good mobility and poor mobility during therapy.

Levodopa/carbidopa — What dietary issue affects absorption?

High-protein meals may compete with levodopa absorption; follow individualized dosing advice.

Levodopa/carbidopa — What should nursing staff assess?

Gait, mobility, orthostatic BP, falls, hallucinations, and dyskinesias.

Levodopa/carbidopa — Why avoid abruptly stopping therapy?

Risk of severe rigidity and a dangerous hyperthermia syndrome.

Levodopa/carbidopa — Which urine/sweat change may occur?

Harmless darkening or discoloration of urine and sweat.

Levodopa/carbidopa — What major contraindication appears in the study guide?

Narrow-angle glaucoma; assess with prescriber for individual risk.

Dopamine agonists — Name three nonergot examples.

Pramipexole, ropinirole, and rotigotine.

Dopamine agonists — How do they work?

Directly stimulate dopamine receptors without conversion to dopamine.

Dopamine agonists — When are they used?

Early Parkinson disease or as adjuncts to levodopa in advanced disease.

Dopamine agonists — How effective are they compared with levodopa?

Usually less potent motor benefit, but may help reduce OFF time.

Dopamine agonists — Common adverse effects?

Nausea, dizziness, somnolence, and orthostatic hypotension.

Dopamine agonists — What nighttime/alertness hazard is high yield?

Sudden sleep attacks or marked daytime somnolence.

Dopamine agonists — Which psychiatric side effects should be monitored?

Hallucinations and confusion.

Dopamine agonists — What unusual behavioral effects should be assessed?

Impulse-control problems such as gambling, shopping, or hypersexuality.

Dopamine agonists — Why counsel about standing slowly?

Orthostatic hypotension can cause syncope and falls.

Dopamine agonists — Which drug is delivered by transdermal patch?

Rotigotine.

Dopamine agonists — Which agent treats sudden OFF episodes?

Apomorphine is a rapid-acting rescue dopamine agonist.

COMT inhibitors — Name the two examples emphasized in slides.

Entacapone and tolcapone.

COMT inhibitors — What is their mechanism?

Inhibit catechol-O-methyltransferase, reducing levodopa breakdown.

COMT inhibitors — Why are they prescribed with levodopa?

To prolong levodopa availability and decrease wearing-off periods.

COMT inhibitors — Are they effective as Parkinson monotherapy?

No; they have no meaningful independent antiparkinson effect.

COMT inhibitors — What are common adverse effects?

Diarrhea, nausea, orthostatic hypotension, and levodopa-related dyskinesias.

COMT inhibitors — Which harmless discoloration can entacapone cause?

Yellow-orange or brownish urine.

COMT inhibitors — What is the major danger of tolcapone?

Potentially fatal hepatotoxicity; liver monitoring is essential.

COMT inhibitors — Why may levodopa dosing need adjustment?

COMT inhibition increases levodopa exposure and dyskinesias.

COMT inhibitors — What combination product contains all three agents?

Carbidopa/levodopa/entacapone (Stalevo).

MAO-B inhibitors for Parkinson disease — Which two examples appear in lecture?

Selegiline and rasagiline.

MAO-B inhibitors for Parkinson disease — What is their mechanism?

Inhibit MAO-B-mediated breakdown of dopamine in the brain.

MAO-B inhibitors for Parkinson disease — When can they be used?

Mild early symptoms or as adjuncts to decrease levodopa wearing off.

MAO-B inhibitors for Parkinson disease — What interaction must be checked?

Other serotonergic or sympathomimetic medicines due to serious interaction potential.

MAO-B inhibitors for Parkinson disease — Do these drugs conclusively halt disease progression?

No established clinically proven neuroprotection.

Anticholinergics for Parkinson disease — Which drug is shown as an example?

Benztropine.

Anticholinergics for Parkinson disease — What is its mechanism?

Blocks central muscarinic receptors to counter relative cholinergic excess.

Anticholinergics for Parkinson disease — Which Parkinson symptom may improve especially?

Tremor, more than bradykinesia or postural instability.

Anticholinergics for Parkinson disease — What adverse effects are characteristic?

Dry mouth, blurred vision, constipation, urinary retention, and confusion.

Anticholinergics for Parkinson disease — Why are they often avoided in older patients?

They may worsen cognition, delirium, glaucoma, and urinary retention.

Alzheimer disease — What are two characteristic brain pathologies?

Amyloid plaques and neurofibrillary tau tangles.

Alzheimer disease — What area is affected early, impairing memory?

Hippocampus.

Alzheimer disease — Which neurotransmitter is depleted?

Acetylcholine from loss of cholinergic neurons.

Alzheimer disease — What are typical early manifestations?

Short-term memory loss, disorientation, and difficulty with routine tasks.

Alzheimer disease — What can occur in advanced disease?

Dependence for basic care, speech loss, incontinence, and weight loss.

Alzheimer disease — What is sundowning?

Late-day worsening agitation, confusion, or wandering.

Alzheimer disease — Which two drug strategies are emphasized?

Acetylcholinesterase inhibition and NMDA receptor antagonism.

Alzheimer disease — Do approved symptomatic agents cure Alzheimer disease?

No; they may temporarily improve or stabilize symptoms.

Alzheimer disease — What non-drug interventions help?

Routines, safety measures, caregiver support, and environmental modification.

Cholinesterase inhibitors for Alzheimer disease — Which three examples appear in the lecture?

Donepezil, rivastigmine, and galantamine.

Cholinesterase inhibitors for Alzheimer disease — What is their mechanism?

Inhibit acetylcholinesterase, increasing available acetylcholine.

Cholinesterase inhibitors for Alzheimer disease — What are common gastrointestinal effects?

Nausea, vomiting, diarrhea, and appetite/weight loss.

Cholinesterase inhibitors for Alzheimer disease — Which cardiovascular adverse effect is dangerous?

Bradycardia or syncope, potentially causing falls.

Cholinesterase inhibitors for Alzheimer disease — What respiratory condition requires caution?

Asthma or obstructive lung disease due to potential bronchoconstriction.

Cholinesterase inhibitors for Alzheimer disease — Which medicines can reduce benefit?

Anticholinergics such as some antihistamines or tricyclic antidepressants.

Cholinesterase inhibitors for Alzheimer disease — What does the nurse monitor?

Pulse, weight, syncope/falls, GI symptoms, and cognitive/ADL response.

Cholinesterase inhibitors for Alzheimer disease — What should patients understand about treatment?

Take consistently; benefit is symptomatic, not curative.

Donepezil — What is its indication?

Mild, moderate, or severe Alzheimer dementia.

Donepezil — What adverse effects require prompt assessment?

Slow pulse, fainting, severe dizziness, or unexplained weight loss.

Donepezil — What drug class?

Reversible acetylcholinesterase inhibitor.

Rivastigmine — What adverse effects are emphasized?

Nausea, vomiting, diarrhea, loss of appetite, and significant weight loss.

Rivastigmine — Which conditions warrant caution?

Bradycardia, peptic ulcer disease, urinary obstruction, and lung disease.

Rivastigmine — What dosage form may improve GI tolerability?

Transdermal patch (when prescribed), with appropriate site rotation.

Galantamine — For which disease stage is it generally used?

Mild to moderate Alzheimer dementia.

Galantamine — What are major monitoring concerns?

Weight loss, bradycardia, syncope, and cholinergic GI effects.

Memantine — What drug class?

NMDA glutamate receptor antagonist.

Memantine — Indication?

Moderate to severe Alzheimer dementia.

Memantine — How does it work?

Reduces pathologic glutamate-mediated excitotoxicity at NMDA receptors.

Memantine — Common adverse effects?

Dizziness, headache, confusion, and constipation.

Memantine — How does tolerability compare with cholinesterase inhibitors?

Usually causes fewer cholinergic gastrointestinal effects.

Multiple sclerosis — What is its underlying pathophysiology?

Immune-mediated CNS demyelination disrupts nerve conduction.

Multiple sclerosis — What type of disease activity do disease-modifying therapies target?

Relapses and inflammatory lesion activity; many also slow disability progression.

Multiple sclerosis — Name common symptom areas.

Vision, motor strength, sensation, balance, bowel/bladder, and fatigue.

Multiple sclerosis — How do disease-modifying and symptomatic drugs differ?

Disease modifiers reduce inflammatory activity; symptomatic drugs treat specific impairments.

Multiple sclerosis — What non-drug therapies help spasticity and mobility?

Physical therapy, stretching, exercise, and assistive devices.