Neurology Lecture Notes Flashcards
Parkinson's disease: overview, pathophysiology, and symptoms
Parkinson's disease (PD) is a progressive neurological disorder of the CNS with dopaminergic neuron impairment or death in the brain, leading to imbalanced neurotransmission.
Two key abnormal factors:
Low dopamine: slows movement, causes bradykinesia, poor motor control, and overall slowed movement.
Excess acetylcholine: contributes to rigidity and stiff muscles.
Common motor symptoms: tremor (often at rest), rigidity, bradykinesia, shuffling gait, poor motor coordination, postural changes, drooling, masked facies (reduced facial expression).
Non-motor features and functional impact: difficulty with activities of daily living (ADLs) such as walking, bathing, feeding; speech changes; emotional masking (reduced facial expression).
Video observation (described): predominantly left-sided rest tremor involving hands and feet; tremor most prominent at rest and improves somewhat with action; gait and speech changes observed.
Therapeutic goal in PD: restore balance by increasing dopamine and decreasing acetylcholine to improve motor function and ADLs.
Conceptual model: treat PD by “the opposite” of the disease mechanism — increase dopamine, decrease acetylcholine.
Pharmacologic strategies in PD: classes and rationale
Dopaminergic medications (increase dopamine activity in brain)
Anticholinergic medications (decrease acetylcholine activity to rebalance the dopamine–acetylcholine ratio)
Enzyme inhibitors to prevent dopamine breakdown (MAO inhibitors, COMT inhibitors) to increase synaptic dopamine
Dopaminergic agonists vs. medications that increase endogenous dopamine synthesis
Overall goal: relieve dyskinesias, bradykinesia, resting tremor, and rigidity to improve ADLs
Levodopa/carbidopa: cornerstone of therapy
Levodopa (precursor to dopamine) converted to dopamine in the brain and increases brain dopamine levels.
Carbidopa: peripheral decarboxylase inhibitor; prevents peripheral breakdown of levodopa, allowing more to reach the brain and reducing peripheral side effects.
Dosing concept: combination therapy leverages the brain-centrally active dopamine and peripheral protection; over time, wearing-off phenomena can occur as the dose cycle ends and effects wane.
Important dosing considerations:
Do not rely on high protein meals to optimize absorption; avoid meals high in protein around dosing because protein competes with levodopa for intestinal absorption.
Vitamin B6 (pyridoxine)-containing foods can reduce levodopa effectiveness by increasing peripheral decarboxylation; avoid foods high in B6 while on levodopa therapy.
Tyramine-containing foods and MAO inhibitors interactions (see MAO inhibitors) can complicate therapy; diet considerations apply especially with MAO-B inhibitors.
Wearing-off: loss of medication effect before next dose; can occur randomly and even at high doses; requires monitoring and plan B strategies.
Common adverse effects: nausea, vomiting, drowsiness; dyskinesias (exaggerated or involuntary movements), hypotension, tachycardia, hallucinations, and discoloration of sweat and urine.
Practical nursing/education points:
Take with food to reduce nausea.
Monitor for hypotension, dizziness, and syncope; instruct patients to rise slowly when ambulating.
Monitor for neuropsychiatric side effects (hallucinations, confusion).
Screen for dyskinesias and adjust therapy as needed; monitor for wearing-off and on-off phenomena.
Safety: assess driving ability and risk of falls during fluctuating motor control.
Important interactions and related drugs:
MAO inhibitors (MAO-B selective like selegiline) inhibit dopamine breakdown, augmenting effect but require dietary and drug interaction caution (tyramine-containing foods can precipitate hypertensive crises with non-selective MAO inhibitors).
Other dopaminergic agents (see below) can be used in combination or as monotherapy depending on disease stage and tolerability.
Notable drug combination example: Levodopa + Carbidopa formulation; conceptually: Levodopa provides dopamine precursor, Carbidopa protects it from peripheral metabolism.
Other dopaminergic medications and strategies
Dopamine agonists (mimic dopamine at receptors):
Examples: pramipexole, ropinirole. Can be used as monotherapy or in combination with levodopa/carbidopa.
Mechanism: directly stimulate dopamine receptors in the brain.
Often used earlier in disease or to reduce levodopa requirements.
Side effects: similar dopaminergic effects (nausea, dizziness, somnolence, confusion), impulse control issues, and orthostatic hypotension.
Amantadine (antiviral with anti-Parkinsonian effects)
Mechanism: increases dopamine release and/or inhibits reuptake; modest symptomatic benefit, often used early or adjunctively.
Side effects: CNS effects (dizziness, confusion, restlessness), dry mouth, urinary retention; anticholinergic-type effects in some patients.
Monoamine oxidase B (MAO-B) inhibitors
Example: Selegiline (and other MAO-B inhibitors not named in transcript).
Mechanism: inhibit MAO-B enzyme, reducing dopamine breakdown and increasing dopaminergic activity.
Practical notes: can cause insomnia if given late in the day; educate about interactions and dietary restrictions related to tyramine-containing foods (less pronounced with selective MAO-B inhibitors, but still relevant in some regimens).
Catechol-O-methyltransferase (COMT) inhibitors (enzyme that breaks down dopamine)
Rationale: block degradation of levodopa, prolonging its effect and increasing brain dopamine availability.
Examples (in general): entacapone, tolcapone. These drugs are typically added to levodopa/carbidopa therapy when wearing-off is problematic.
Anticholinergic medications for PD
Example: benztropine (cogentin).
Role: reduce acetylcholine activity to rebalance dopamine–acetylcholine, mitigating tremor and rigidity.
Side effects: classic anticholinergic dry effects (dry mouth, blurred vision, urinary retention, constipation, decreased sweating); CNS depression/drowsiness; confusion or memory issues, particularly in older adults.
Contraindications: glaucoma, urinary obstruction (prostatic hypertrophy), myasthenia gravis; caution in elderly.
Summary of PD medication strategy
Goal: increase dopamine, decrease acetylcholine to restore motor function and ADLs.
Common therapy sequences: Levodopa/Carbidopa as cornerstone therapy; introduce dopamine agonists or MAO-B inhibitors to optimize control and possibly reduce Levodopa dose; add COMT inhibitors for wearing-off; add anticholinergics for tremor/rigidity in select patients.
Non-pharmacologic and lifestyle considerations in PD care
Nutritional considerations:
Avoid high-protein meals around levodopa dosing to maximize absorption.
Avoid or limit pyridoxine (Vitamin B6) rich foods when taking levodopa, as B6 can reduce levodopa effectiveness.
Common B6-containing foods include whole grains, some greens, bananas, etc. Specific dietary guidance should be tailored.
Monitoring and safety
Monitor for wearing-off, dyskinesias, orthostatic hypotension, and psychiatric effects.
Educate family/caregivers to communicate changes in symptoms and to report new or worsened motor or cognitive symptoms.
Education on adverse effects and when to seek care
Recognize signs of possible adverse effects (extreme drowsiness, confusion, hallucinations, fainting, severe dyskinesias, uncontrolled movements) and contact healthcare provider.
Instruct patients about gradual changes and potential need for dose adjustments.
Seizures and antiepileptic drugs (AEDs)
Epilepsy basics
Epilepsy is defined by two or more seizures occurring within a period; seizures involve abnormal electrical activity in the brain.
Triggers can include fever, head trauma, infections, tumors, stroke; some cases are idiopathic. Some patients receive AEDs for prevention after events like stroke.
Sudden discontinuation of AEDs can precipitate seizures; medications are often continued long-term with gradual taper when appropriate.
Common AED categories and representative drugs
Hydantoins: Phenytoin (Dilantin)
Mechanism: stabilize nerve membranes by blocking sodium influx; reduces neuronal excitability.
Pharmacokinetics: well absorbed through GI tract; hepatic metabolism; therapeutic serum level: .
Toxicity signs: nystagmus, ataxia, double vision, sedation, cognitive changes; seizures may worsen if levels become toxic.
Additional adverse effects: gingival hyperplasia; skin rash (potential allergy); pretreatment oral hygiene recommended; cardiac arrhythmias or hypotension risk; decreased vitamin D metabolism (bone health risk); potential vitamin K interactions in infants; pregnancy risk (category D); not advisable in pregnancy; avoid abrupt withdrawal; dose adjustments needed in hepatic/renal impairment.
Monitoring: regular blood level checks, liver and kidney function tests; monitor for bone health (calcium/vitamin D).
Carbamazepine (Tegretol)
Class: anticonvulsant, mood stabilizer.
Key risk: hematologic suppression (leukopenia, anemia, thrombocytopenia) increasing infection and bleeding risk; hepatic enzyme induction (drug interactions common).
Other notes: CNS side effects; potential suppression of pregnancy contraception effectiveness; not ideal for breastfeeding.
Valproic acid (valproate)
Broad-spectrum AED; reduces electrical activity; used for various seizure types and some bipolar disorder cases.
Major risks: hepatotoxicity, thrombocytopenia, pancreatitis; teratogenic risk; monitor liver function tests; risk of pancreatitis and bleeding due to low platelets.
Lamotrigine (Lamictal, Lenictal)
Mood stabilizer and AED; generally well tolerated but can cause skin rash; risk of serious rash including Stevens–Johnson-like reactions; monitor for rash; dose adjustments needed.
Gabapentin (Neurontin)
AED with widespread use for neuropathic pain; mechanism not fully understood but acts on GABA-related pathways and reduces neuronal excitability.
Side effects: edema, weight gain, mood changes; dizziness, fatigue; may interact with alcohol; renal dosing adjustments may be needed.
Pregabalin (Lyrica)
Similar to gabapentin; faster absorption; controlled substance (C-5 in many jurisdictions).
Indications: neuropathic pain, anxiety, seizures adjunctively; side effects similar to gabapentin; monitor for edema, weight gain, CNS effects.
Levetiracetam (Keppra)
Broad-spectrum AED; IV option; binds SV2A to modulate neurotransmitter release and reduce excessive neuronal firing.
Side effects: CNS effects (dizziness, weakness, agitation); potential for allergic reactions including angioedema; hepatotoxicity possible; monitor for mood changes and suicidality; usually well tolerated.
Other agents mentioned briefly
Lenictal (lamotrigine) already covered; Keppra (levetiracetam) highlighted; Gabapentin and Pregabalin covered.
Clinical considerations for AED management
Therapeutic monitoring and dose adjustments based on clinical response and drug levels (especially phenytoin, carbamazepine).
Avoid abrupt discontinuation of any AED due to risk of withdrawal seizures; taper under supervision.
CNS depression is a common theme across AEDs and is a safety consideration for driving and operating machinery; assess patient status.
Pregnancy considerations: several AEDs have teratogenic potential; counsel regarding pregnancy planning and alternative strategies if applicable.
Special monitoring: blood dyscrasias with carbamazepine; liver function with valproic acid; blood level monitoring for phenytoin; liver/kidney function for several AEDs.
Practical patient education and safety
Driving and activities requiring alertness may be impaired; evaluate on an individual basis.
Take all AEDs as prescribed; do not stop abruptly; inform about possible withdrawal symptoms and the need for tapering.
Alerts and safety reminders: carry medical alert information if taking AEDs; recognize signs of an impending seizure and when to seek help.
Lipid and diet considerations: most AEDs interact with other drugs; inform healthcare provider about all medications and supplements.
Anxiolytics, hypnotics, and sleep-related medications
Benzodiazepines (anxiolytics and sedatives)
Role: reduce anxiety, provide sedation, and can be used as pre-procedure medication to induce relaxation.
Mechanism: potentiate GABA activity in the reticular activating system, leading to sedation and anxiolysis; in higher doses can induce hypnosis/sleep.
Pharmacokinetics and safety: absorbed well from GI tract; peak ~30 minutes; cross placenta; excreted in urine; caution in pregnancy and breastfeeding (unclear safety). In older adults, lower dosing is preferred due to increased sensitivity and fall risk.
Overdose reversal: flumazenil is the antidote for benzodiazepine overdose (note: transcript mentions Narcan in a delayed example, but naloxone (Narcan) reverses opioids, not benzodiazepines).
Contraindications and cautions: do not use with respiratory depression or glaucoma; avoid in concomitant alcohol use; avoid in pregnancy/breastfeeding when possible; elderly require conservative dosing.
Side effects and risks: CNS depression, confusion, dizziness, amnesia, dependence and withdrawal potential; tolerance can develop.
Common suffix cue for inhalation/normally prescribed anxiolytics: many end with -zolam (e.g., diazepam) or -pam (e.g., lorazepam).
Non-benzodiazepine sleep medications (Z-drugs)
Includes zolpidem (Ambien), zaleplon (Sonata), eszopiclone (Lunesta).
Mechanism: enhance GABA activity at GABA-A receptors but are not benzodiazepines; primarily for short-term treatment of insomnia.
Highlights: faster onset of sleep; risk of next-day sedation, dizziness, and cognitive effects; primarily for short-term use.
Important safety notes: avoid alcohol; elderly patients at higher risk of falls and confusion; do not drive after taking; pregnancy and breastfeeding considerations apply undefined safety.
Dosing and administration nuances: zolpidem may be taken with food to slow absorption and reduce morning sedation; avoid abrupt changes in sleep schedule.
Acute sedation and anesthesia context
Benzodiazepines and non-benzodiazepine sedatives may be used for preoperative anxiety or procedural sedation, with monitoring for respiratory depression.
Neuromuscular blocking agents and perioperative paralysis
Purpose and context
Used to facilitate anesthesia during surgery, intubation, and certain procedures by inducing skeletal muscle paralysis while the patient remains unconscious under anesthesia.
Non-depolarizing (quietly blocking) agents
Examples discussed: pancuronium (pan curonium), vecuronium.
Mechanism: block acetylcholine receptors at the neuromuscular junction, preventing depolarization and muscle contraction.
Clinical use: muscle relaxation for operative conditions; patient remains asleep under anesthesia.
Important safety notes: monitor cardiovascular and respiratory status closely; risk of respiratory arrest if ventilation is not managed.
Depolarizing (depolarizing) agent
Example discussed: succinylcholine.
Mechanism: initially depolarizes the receptor leading to transient fasciculations, followed by paralysis due to receptor blockade.
Characteristics: rapid onset; short duration, useful for rapid sequence intubation.
Side effects and risks: malignant hyperthermia (a life-threatening reaction with high fever and severe rigidity), hyperkalemia, bradycardia, bronchospasm; heightened concern in patients with neuromuscular conditions (e.g., myasthenia gravis) or asthma; significant risk with certain comorbidities.
Malignant hyperthermia: emergency management
Signs: severe muscle rigidity, hyperthermia.
Immediate actions: provide 100% oxygen, discontinue triggering agent, administer dantrolene (muscle relaxant) and implement cooling measures.
Monitoring: continuous vital signs and telemetry; ensure airway and ventilation support.
Contraindications and cautions for neuromuscular blockers
Not suitable for patients with asthma or myasthenia gravis (these conditions affect neuromuscular transmission and may worsen paralysis).
Caution in patients with significant hepatic or cardiac disease due to potential drug effects on heart rate and blood pressure; monitor closely for bradycardia and hypotension.
User notes and memory cues
The general principle: these drugs blunt acetylcholine signaling at the neuromuscular junction to prevent muscle contraction.
Anesthesiologists monitor patients closely; these agents are typically used in controlled surgical environments.
Practical nursing implications and test-preparation takeaways
PD-related nursing considerations
Recognize the signs of dyskinesia improvement with medication as a therapeutic success.
Watch for wearing-off and on-off phenomena; communicate changes promptly to the care team.
Educate patients about dietary interactions (protein and B6) with levodopa/carbidopa therapy.
Monitor for orthostatic hypotension and fall risk; implement safety measures for gait and mobility.
AED-related nursing considerations
Monitor for therapeutic levels where applicable (e.g., phenytoin at 10–20 μg/mL).
Watch for CNS side effects: dizziness, drowsiness, ataxia, confusion, and potential gait instability.
Monitor for hematologic toxicity with carbamazepine (leukopenia, anemia, thrombocytopenia) and for hepatic toxicity with valproic acid.
Screen for rash and potential Stevens–Johnson-like reactions with lamotrigine; stop the medication if a rash develops.
Avoid abrupt withdrawal of AEDs; plan gradual taper under clinician supervision.
Safety and patient education for anxiolytics/hypnotics
Advise against driving or operating machinery when taking benzodiazepines or Z-drugs until sedative effects are understood.
Emphasize the risk of dependence and withdrawal; taper rather than abrupt stopping.
Warn against combining with alcohol or other CNS depressants.
For benzodiazepine overdose (uncommon but serious): the recommended reversal agent is flumazenil (not always used in all settings; naloxone reverses opioid overdose).
Monitoring and follow-up priorities across therapies
Regular assessment of motor function, tremor, rigidity, bradykinesia, gait, and ADLs for PD.
Routine labs and monitoring for AED-associated adverse effects (LFTs for valproic acid, CBC for carbamazepine, etc.).
Ongoing patient and caregiver education about diet, adherence, and safety.
Quick reference: key numerical values and concepts
Levodopa-related dietary/interactions:
Avoid high-protein meals around dosing: protein competes with intestinal absorption of levodopa.
Avoid vitamin B6 (pyridoxine)-rich foods to prevent peripheral dopamine breakdown and reduce levodopa efficacy.
Phenytoin therapeutic level and toxicity threshold:
Therapeutic serum level:
Signs of toxicity: nystagmus, ataxia, double vision, sedation, confusion; gait instability.
MAO inhibitors (dietary cautions): tyramine-containing foods can precipitate hypertensive crises when combined with non-selective MAO inhibitors; selective MAO-B inhibitors have fewer dietary restrictions but caution still advised.
Anticholinergic dry effects (benztropine): dry mouth, blurred vision, urinary retention, constipation; decreased sweating; CNS effects (confusion, memory issues).
Malignant hyperthermia (neuromuscular blockers): emergency with severe hyperthermia and rigidity; treated with dantrolene and supportive measures.