Week 7 Exam: NR566 / NR 566 (Latest 2026 / 2027) Advanced Pharmacology for Care of the Family | Questions & Answers | Grade A | 100% Correct – Chamberlain

Week 7 Exam: NR566 / NR 566 (Latest 2026 / 2027) Advanced Pharmacology for Care of the Family | Questions & Answers | Grade A | 100% Correct – Chamberlain Question : What is the function of the blood-brain barrier? Answer It impedes the entry of drugs into the brain. Question : What types of agents can cross the blood-brain barrier? Answer Passage across the barrier is limited to lipid-soluble agents and to drugs that cross by way of specific transport systems. Question : Which types of drugs cannot cross the blood-brain barrier? Answer Protein-bound drugs and highly ionized drugs Question : What is one advantage of the blood-brain barrier? Answer It protects the brain from injury by potentially toxic substances. Question : How is the blood-brain barrier developed at birth? Answer It is not fully developed at birth. Question : How does food affect the absorption of levodopa? Answer Food delays absorption by slowing gastric emptying. Question : What is the effect of high-protein foods on levodopa? Answer High-protein foods reduce therapeutic effects by competing with levodopa for intestinal absorption and transport across the blood-brain barrier. Question : How can nausea and vomiting from levodopa be reduced? Answer Taking levodopa with low-fat, low-protein foods such as fruits and vegetables Question : Should levodopa be taken with meals? Answer Administration with meals should be avoided if possible, as it can reduce therapeutic effects by decreasing levodopa absorption. Question : What can a high-protein meal trigger in patients taking levodopa? Answer A high-protein meal could trigger an abrupt loss of effect, known as an off episode. Question : How should protein consumption be managed throughout the day for levodopa patients? Answer Patients should be advised to spread their protein consumption evenly throughout the day. Question : What is the effect of high-fat foods on levodopa absorption? Answer High-fat foods can decrease absorption, delaying peak effects by several hours. Question : When should levodopa be taken for optimal absorption? Answer Patients should take levodopa on an empty stomach, if tolerated. Question : What is the mechanism of action of Levodopa in Parkinson's Disease? Answer It reduces symptoms by increasing dopamine synthesis in the striatum. Question : How does Levodopa enter the brain? Answer It enters the brain through an active transport system that carries it across the blood-brain barrier. Question : What happens to Levodopa after it enters the brain? Answer It is taken up into the remaining dopaminergic nerve terminals in the striatum. Question : What is Levodopa converted into in the brain? Answer dopamine, its active form. Question : What is the role of dopamine in the treatment of Parkinson's Disease? Answer It helps restore a proper balance between dopamine and acetylcholine. Question : What enzyme catalyzes the conversion of Levodopa to dopamine? Answer decarboxylase. Question : What are the steps leading to the alteration of central nervous system function by Levodopa? Answer 1. Transported across the blood-brain barrier; 2. Taken up by dopaminergic nerve terminals in the striatum; 3. Converted into dopamine; 4. Released into the synaptic space; 5. Bound to dopamine receptors on striatal GABAergic neurons. Question : What effect does dopamine binding have on striatal GABAergic neurons? Answer It causes them to fire at a slower rate. Question : What is the initial treatment for patients with mild symptoms of Parkinson's Disease? Answer Treatment can begin with an MAO-B inhibitor. Question : What should be the initial treatment for patients with more severe symptoms of Parkinson's Disease? Answer Treatment should begin with either levodopa (combined with carbidopa) or a dopamine agonist. Question : Which treatment is more effective for Parkinson's Disease: levodopa or dopamine agonists? Answer Levodopa is more effective than dopamine agonists. Question : What is a risk associated with long-term use of levodopa in Parkinson's Disease treatment? Answer Long-term use carries a higher risk for disabling dyskinesias. Question : When is levodopa preferred in the treatment of Parkinson's Disease? Answer If improving motor function is the primary objective. Question : When should a dopamine agonist be preferred in the treatment of Parkinson's Disease? Answer If drug-induced dyskinesias are a primary concern. Question : What are the adverse effects of Carbidopa? Answer It has no adverse effects of its own. Question : What can occur when levodopa is combined with carbidopa? Answer Abnormal movements and psychiatric disturbances can occur sooner and can be more intense than with levodopa alone. Question : What are some common adverse effects of levodopa? Answer Nausea and vomiting, dyskinesias, postural hypotension, and psychosis. Question : What CNS effects can levodopa cause? Answer Anxiety, agitation, memory and cognitive impairment, insomnia, and nightmares. What behavioral changes can result from impulse control problems associated with levodopa? Answer Promiscuity, gambling, binge eating, or alcohol abuse. What harmless effect can levodopa have on bodily fluids? Answer Levodopa may darken sweat and urine. What are the two groups of dopamine agonists used in Parkinson's Disease? Derivatives of ergot and nonergot derivatives. Name four nonergot derivative dopamine agonists. Pramipexole, ropinirole, rotigotine, and apomorphine. How selective are nonergot derivative dopamine agonists? They are highly selective for dopamine receptors. Name two ergot derivative dopamine agonists. Bromocriptine and cabergoline. How selective are ergot derivative dopamine agonists? They are less selective. What is a serious adverse effect of Tolcapone? Liver failure. What effect can Tolcapone have on levodopa-related effects? It can intensify levodopa-related effects, especially dyskinesias. What are some common side effects of Tolcapone? Diarrhea, hematuria, and yellow-orange discoloration of the urine. What symptoms can occur with abrupt withdrawal of Tolcapone? Symptoms resembling neuroleptic malignant syndrome (fever, muscular rigidity, altered consciousness). What potential effects have been observed in rats given large doses of Tolcapone? Renal tubular necrosis and tumors of the kidneys and uterus. Parkinson Disease Side Effects of Dopamine Agonists hallucinations, daytime sleepiness, and postural hypotension What is the mechanism of action of Parkinson Disease dopamine agonists? They activate dopamine receptors and cause mild blockage of serotonergic and α-adrenergic receptors. Why are nonergot derivatives of dopamine agonists preferred over ergot derivatives? Nonergot derivatives cause fewer side effects than ergot derivatives. Which dopamine receptors does Pramipexole bind to selectively? It binds selectively to dopamine-2 (D2) and dopamine-3 (D3) receptors. What underlies the therapeutic effects of Pramipexole? Binding to D2 receptors underlies the therapeutic effects of Pramipexole. What is the therapeutic goal of Levodopa combinations in Parkinson's Disease? To maintain or improve the patient's ability to carry out activities of daily living. What should patients be evaluated for when using Levodopa combinations? Improvements in activities of daily living. What symptoms should be monitored for reductions in patients using Levodopa combinations? Bradykinesia, postural instability, tremor, and rigidity. What are the two types of motor fluctuations associated with long-term treatment of Parkinson's Disease? 'Off' times and drug-induced dyskinesias. What are 'off' times in Parkinson's Disease treatment? Loss of symptom relief. Which types of drugs can reduce 'off' times in Parkinson's Disease? Dopamine agonists, COMT inhibitors, and MAO-B inhibitors. Which COMT inhibitor has the strongest evidence of efficacy for reducing 'off' times? Entacapone. Which MAO-B inhibitor has the strongest evidence of efficacy for reducing 'off' times? Rasagiline. What are the first-choice drugs for patients with mild or moderate Parkinson's disease symptoms? Dopamine agonists How do dopamine agonists compare to levodopa in terms of effectiveness? They are less effective than levodopa. What is a key advantage of dopamine agonists over levodopa? They are not dependent on enzymatic conversion to become active. Do dopamine agonists compete with dietary proteins for uptake? No What is a potential risk associated with levodopa that dopamine agonists avoid? They are not converted to potentially toxic metabolites. What is the incidence of response failures when using dopamine agonists long term? They have a lower incidence of response failures. Why are younger patients preferred for dopamine agonist treatment? They tolerate the side effects better than older patients. What is the primary mechanism of action of Lamotrigine? Blocking sodium channels What is a secondary mechanism of action of Lamotrigine? Blocking calcium channels What neurotransmitter's release is decreased by Lamotrigine? Glutamate What type of medication is Lamotrigine? Antiseizure medication Lamotrigine Black Box Warning It may cause serious skin reactions such as SJS and TEN. Fatalities have been reported. What is the mechanism of action (MOA) of Ethosuximide? It suppresses neurons in the thalamus that are responsible for generating absence seizures. What specific calcium currents does Ethosuximide inhibit? It inhibits low-threshold calcium currents, known as T currents. Does Ethosuximide block sodium channels? No Does Ethosuximide enhance GABA-mediated neuronal inhibition? No What are common central nervous system side effects of phenytoin at therapeutic levels? Sedation and mild CNS effects. What can occur at plasma levels of phenytoin above 20 µg/mL? Toxicity. What is a common eye-related side effect of excessive phenytoin dosage? Nystagmus. What are other manifestations of excessive phenytoin dosage? Sedation, ataxia, diplopia, and cognitive impairment. What is gingival hyperplasia? Excessive growth of gum tissue. What type of rash can be a side effect of phenytoin? Morbilliform rash. What severe reactions can a morbilliform rash from phenytoin progress to? Stevens-Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN). What genetic mutation is associated with an increased risk of developing SJS or TEN from Phenytoin? HLA-B*1502 In which population is the HLA-B*1502 mutation most commonly found? People of Asian descent What is Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)? A potentially fatal reaction characterized by skin eruptions, lymphadenopathy, fever, and multi organ involvement. What is required if a patient experiences hypersensitivity symptoms while on Phenytoin? Discontinuation of the drug. What is the effect of phenytoin on hepatic enzymes? Phenytoin induces hepatic enzymes. What happens when phenytoin is administered in doses slightly greater than therapeutic effects? The liver's capacity to metabolize phenytoin is overwhelmed, causing plasma levels to rise dramatically. What is used to determine phenytoin dosage? Serum drug levels, trough levels, and assessments of seizure control. How do therapeutic doses of phenytoin compare to doses that saturate hepatic enzymes? Therapeutic doses are only slightly smaller than the doses needed to saturate the hepatic enzymes. What is the FDA-approved use of Gabapentin in epilepsy? Adjunctive therapy of partial seizures. What do the AAN/AES guidelines recommend for Gabapentin in epilepsy? Monotherapy of partial seizures. What is the common name for the form of gabapentin approved for epilepsy? Neurontin. Does gabapentin have significant drug interactions? No Does food affect the absorption of gabapentin? No, food does not affect the absorption of gabapentin. What happens to the percentage of gabapentin absorbed as the dosage increases? The percentage absorbed gets smaller as the dosage increases. Why does the percentage of gabapentin absorbed decrease at high doses? At high doses, the intestinal transport system for uptake of the drug becomes saturated. What are the most common side effects of Gabapentin? Somnolence, dizziness, ataxia, fatigue, nystagmus, and peripheral edema. Do the side effects of Gabapentin diminish over time? Yes, they often diminish with continued drug use. Pregabalin Indications neuropathic pain associated with diabetic neuropathy, postherpetic neuralgia, adjunctive therapy of partial seizures, and fibromyalgia What symptoms should patients inform their prescriber about when taking Topiramate? Hyperventilation, fatigue, and anorexia. What symptoms of glaucoma should patients on Topiramate be aware of? Ocular pain, unusual redness, sudden worsening or blurring of vision. What metabolic condition can Topiramate cause? Metabolic acidosis. What should be monitored before and during the treatment course of Topiramate? Suicidality. Is Carbamazepine teratogenic? Yes What genetic variant is associated with increased risk of skin reactions to Carbamazepine? The risk for a reaction is strongly associated with the HLA-B*1502 variant. How does Carbamazepine affect oral contraceptives and warfarin? It accelerates the inactivation of oral contraceptives and warfarin. What effect do phenytoin and phenobarbital have on Carbamazepine metabolism? Phenytoin and phenobarbital can further accelerate the metabolism of Carbamazepine, decreasing its effects. How does grapefruit juice affect Carbamazepine levels? Grapefruit juice can increase peak and trough levels of by 40%. What should patients taking Carbamazepine avoid? Patients should avoid grapefruit juice. What is the mechanism of action (MOA) of Ezogabine? It activates voltage-gated potassium channels in the neuronal membrane. What effect does Ezogabine have on potassium efflux? It facilitates potassium efflux. How does Ezogabine affect neuronal firing and seizure activity? It reduces repetitive neuronal firing and related seizure activity. Absence Seizures traditional Treatment Selection Ethosuximide and Valproic acid Absence Seizures Newer Treatment Selection Lamotrigine What is the mechanism of action of cholinesterase inhibitors in Alzheimer's Disease? They prevent the breakdown of acetylcholine by acetylcholinesterase (AChE), increasing the availability of acetylcholine at cholinergic synapses. What effect do cholinesterase inhibitors have on central cholinergic neurons in Alzheimer's Disease? They enhance transmission by central cholinergic neurons that have not yet been destroyed. Do cholinesterase inhibitors cure Alzheimer's Disease? No Do cholinesterase inhibitors stop the progression of Alzheimer's Disease? No What are the cardiovascular effects of cholinesterase inhibitors in Alzheimer's Disease? Increased activation of cholinergic receptors in the heart can cause symptomatic bradycardia, leading to fainting, falls, fall-related fractures, and pacemaker placement. What should be done if a patient on cholinesterase inhibitors experiences bradycardia, fainting, or falls? Drug withdrawal may be indicated, especially if cognitive benefits are lacking. What should be assessed at each visit for a patient on cholinesterase inhibitors? Orientation, cognition, functional status, weight, and changes in respiratory, cardiovascular, or gastrointestinal status compared to baseline. What are cholinesterase inhibitors approved for? Mild to moderate symptoms of Alzheimer's disease. Which cholinesterase inhibitor is approved for severe symptoms of Alzheimer's disease? Donepezil. What is Sumatriptan used for? To abort an ongoing migraine attack. What can subsequent administration of oral Sumatriptan do after subQ Sumatriptan? Delay recurrence of a migraine attack but does not prevent it. In addition to migraine, what other condition is Sumatriptan approved for? Cluster headaches. What is the recommended limit for the use of abortive medications for headaches? 1 or 2 days a week What can frequent use of abortive medications lead to? Medication overuse headache (MOH) What are other names for medication overuse headache (MOH)? Drug-induced headache or drug-rebound headache What is the role of antiemetics in migraine therapy? Antiemetics are important adjuncts to migraine therapy by reducing nausea and vomiting. How do antiemetics improve patient comfort during migraine treatment? By reducing nausea and vomiting, antiemetics can make the patient more comfortable. What is one benefit of using antiemetics in migraine therapy? They permit therapy with oral antimigraine drugs. Which two antiemetics are most often used in migraine therapy? Metoclopramide (Reglan) and prochlorperazine (formerly Compazine). What is a contraindication for sumatriptan related to heart conditions? Sumatriptan is contraindicated for patients with a history of ischemic heart disease, myocardial infarction (MI), uncontrolled hypertension, or other heart disease. Is sumatriptan contraindicated during pregnancy? Yes Why should sumatriptan not be combined with SSRIs or SNRIs? Combining with SSRIs or SNRIs can lead to excessive serotonin receptor activation. What type of headaches can tricyclic antidepressants help prevent? Migraine and tension-type headaches What is the proposed mechanism of action for tricyclic antidepressants in migraine prevention? Inhibiting reuptake of serotonin How does pramipexole work as a dopamine agonist in the treatment of Parkinson’s disease? stimulates dopamine receptors D2 and D3 ↓ tremor, rigidity, and bradykinesia (MAO-B) inhibitor for patients with mild symptoms of Parkinson’s disease? ↓ breakdown of dopamine early-stage Parkinson’s mild side effects and neuroprotective Effects of increased dopamine in PD ↓ tremor, rigidity, and bradykinesia potential disadvantages of combining levodopa with carbidopa in the treatment of Parkinson’s disease? long-term use causes dyskinesias and on-off phenomena How does combining levodopa with carbidopa help with PD? More levodopa reaches the brain → better symptom control. Lower dose of levodopa needed. Fewer side effects How do dopamine agonists alleviate motor symptoms in Parkinson’s disease? directly stimulates dopamine receptors (bypassing synthesis) ↑ Dopamine ↑motor control ↓rigidity and bradykinesia. How does lamotrigine suppress seizures by binding to sodium channels? inhibition stabilizes and ↓ excitatory neurotransmitter release particularly glutamate=suppressing seizure activity How do tricyclic antidepressants like amitriptyline prevent migraines? ×reuptake of 5HT and NE (5HT and NE help regulate pain) ↑ 5HT and NE calm hyperexcitable neurons and ↓ sensitivity to pain Why are serotonin1B/1D receptor agonists (Triptans) recommended for patients with a known allergy to NSAIDs? act directly on 5HT receptors constrict cranial blood vessels and × neuropeptide release Prevents need for NSAIDs What serious skin reactions are highlighted in the Black Box Warning for lamotrigine? SJS and TENs What is medication overuse headache (MOH), and how can it develop from excessive use of abortive medications? Overuse alters pain thresholds and perpetuates headache cycles. How do antiemetics improve comfort during a migraine attack? × D2 and 5HT receptors ↑ 5HT and D2 speeds up stomach emptying and ↓ vomiting reflex effected by vagal nerves Why is gabapentin well-suited for combined use with other antiseizure drugs? minimal drug interactions different MOA than others binds to alpha-2-delta of CA channels Why is gabapentin approved for adjunctive therapy of partial seizures in adults? targets Ca ↓ glutamate preventing partial seizures favorable safety profile How does the absorption of gabapentin change with increasing dosage? has saturable absorption transporter system gets overwhelmed at higher doses the more you take, the less your body can absorb How does gabapentin’s zero-order kinetics affect its dosing and efficacy? Doesn't follow zero-order elimination (where a fixed amount is eliminated per time regardless of concentration, like alcohol does). BUT does exhibit zero-order absorption low doses are absorbed efficiently As dose ↑, absorption plateaus, body can’t keep up. bioavailability drops with higher doses (remember: 60% at 300 mg → ~30% at 1200 mg). How does ezogabine facilitate potassium efflux to provide seizure control? Opens K channels Makes inside more negative Less like to fire What are the common side effects of gabapentin, and why is somnolence significant? somnolence, dizziness, and ataxia. Somnolence is significant because it may impair safety (e.g., driving) and limit adherence Why can lipid-soluble agents readily cross the blood-brain barrier? The endothelial cell membranes of the BBB are composed of lipid bilayers (phospholipids). Lipid-soluble (lipophilic) molecules can dissolve into this lipid bilayer and passively diffuse across the membrane. In contrast, water-soluble or highly ionized molecules cannot passively diffuse due to their inability to integrate into the lipid layer. How does ethosuximide block voltage-gated calcium channels to treat absence seizures? Block Ca channels from opening ↓ excitability ↓ activity between thalamus and cortex Interrupts cycle that generates absence seizures. Why is carbamazepine contraindicated in patients with depression and anxiety? worsen mood disorders and cause CNS depression interacts with antidepressants and ↓ their efficacy via CYP450 How does the blood-brain barrier restrict the passage of highly ionized drugs into the brain? Highly ionized (charged) drugs are hydrophilic (water loving) →cannot pass through the lipid membrane of BBB without transport mechanism Why are cholinesterase inhibitors approved for the treatment of Alzheimer’s disease? inhibit breakdown of ACH (critical for memory and cognition) ACH is deficient in Alzheimer's disease Why is monitoring cognitive and functional status important in patients on cholinesterase inhibitor therapy? they do not cure Alzheimer’s disease, monitoring helps determine if the patient is benefiting from therapy, tolerating side effects, and whether continued treatment is appropriate. (aim to slow cognitive decline by increasing ACH in the brain) Why is ethosuximide considered the most appropriate initial choice for treating absence seizures? first-line agent Blocks T-type Ca channels from opening high efficacy, and favorable side effect profile for absence seizures How do cholinesterase inhibitors enhance cholinergic neurotransmission in the brain? blocks AChE from breaking down ACH in the synaptic cleft How is the genetic mutation HLA-B*1502 associated with the risk of Stevens-Johnson syndrome in patients taking phenytoin? part of the human leukocyte antigen system Trigger T-cell–mediated hypersensitivity reaction, leading SJS/TEN How does phenytoin's induction of hepatic enzymes affect the efficacy of other drugs? CP450 accelerates metabolism of other drugs reducing concentration and decreasing therapeutic effect. Why is it important to monitor serum bicarbonate levels in patients on topiramate? Can cause carbonic anhydrase inhibitory activity which decreases bicarbonate ions in the kidneys causing metabolic acidosis (blood becomes too acidic) Topiramate uses Seizure, epilepsy and migraine prevention Why should sumatriptan be avoided in patients taking SSRIs like fluoxetine? Both increase serotonin levels- risk for SS Effects of increased ACH enhances neurotransmission in brain ↑ memory, attention, and learning