1. Which of the following best describes the term "tolerance" in pharmacology?
A) The development of a withdrawal syndrome when a drug is stopped abruptly after prolonged use
B) The compulsive seeking and use of a drug despite harmful consequences, driven by dysregulation of dopaminergic reward pathways
C) An allergic reaction that develops after repeated exposure to a drug, mediated by IgE antibody formation
D) A progressive reduction in drug effect with repeated administration, requiring dose escalation to maintain the same therapeutic response
E) The pharmacokinetic process by which a drug induces its own metabolism, reducing plasma concentrations over time
ANSWER: D
Rationale:
Tolerance is defined as a reduction in drug effect following repeated administration, such that a higher dose is required to produce the same effect that was originally achieved at a lower dose. It is a pharmacodynamic or pharmacokinetic adaptation, not a behavioral or immunological phenomenon.
Option A: Option A describes physical dependence, which is a distinct concept -- the presence of a withdrawal syndrome on discontinuation does not define tolerance; a patient can be tolerant without being physically dependent and vice versa.
Option B: Option B describes addiction, a neurobiological disease characterized by compulsive drug use despite harm; addiction involves dysregulation of reward pathways and is distinct from the pharmacological definition of tolerance.
Option C: Option C describes drug allergy, an immunological phenomenon mediated by IgE or other immune mechanisms; this is unrelated to tolerance.
Option E: Option E describes pharmacokinetic autoinduction -- a mechanism that can contribute to pharmacokinetic tolerance -- but the definition of tolerance itself encompasses the reduced drug effect, not the specific mechanism by which it occurs.
2. A patient on long-term beta-blocker therapy for hypertension stops the medication abruptly. Three days later he presents with chest pain, palpitations, and a heart rate of 118 bpm. Which receptor-level adaptation best explains this withdrawal syndrome?
A) Upregulation -- chronic beta-receptor blockade caused compensatory increase in beta-receptor density and sensitivity; abrupt withdrawal exposes this upregulated receptor population to normal catecholamine levels, producing exaggerated sympathetic responses including tachycardia, hypertension, and potentially angina or myocardial infarction
B) Downregulation -- the beta-blockers caused a reduction in beta-receptor density during treatment, and the now-depleted receptor population cannot respond adequately to catecholamines, producing a paradoxical reflex tachycardia through baroreceptor-mediated mechanisms
C) Desensitization -- the beta-receptors became desensitized to catecholamines during treatment through GRK (G protein-coupled receptor kinase) phosphorylation, and the sudden removal of beta-blocker unmasks receptor hypersensitivity that was concealed during drug therapy
D) Tachyphylaxis -- a single high dose of propranolol depleted norepinephrine from sympathetic nerve terminals during initiation of therapy; abrupt withdrawal allows norepinephrine reaccumulation to supranormal levels, overwhelming the beta-receptor system
E) Inverse agonism -- beta-blockers reduced constitutive beta-receptor activity below baseline during treatment; abrupt withdrawal allows constitutive activity to rebound above baseline, producing tachycardia and hypertension through receptor-autonomous signaling
ANSWER: A
Rationale:
Chronic beta-receptor blockade removes agonist stimulation from beta-adrenergic receptors. In response to this sustained lack of stimulation, the receptor system undergoes upregulation -- an increase in receptor number and sensitivity as a homeostatic compensatory response. The patient is clinically stable on the drug because the upregulated receptors are still blocked. When the beta-blocker is stopped abruptly, the upregulated, hypersensitive receptor population is suddenly exposed to normal circulating catecholamine levels -- but it responds as if those levels were supraphysiological, producing exaggerated sympathetic effects: tachycardia, hypertension, and in patients with coronary artery disease, potentially angina or myocardial infarction. This is why beta-blockers must be tapered gradually, particularly in patients with ischemic heart disease.
Option B: Option B is incorrect -- downregulation (reduction in receptor density) occurs with chronic agonist exposure, not antagonist exposure; beta-blockers produce the opposite adaptation.
Option C: Option C is incorrect -- desensitization through GRK phosphorylation is produced by agonist activation, not by blockade; the mechanism described does not explain beta-blocker withdrawal syndrome.
Option D: Option D is incorrect -- tachyphylaxis refers to rapid tolerance after a few doses and does not involve norepinephrine depletion by beta-blockers; this mechanism has no pharmacological basis.
Option E: Option E is incorrect -- while some beta-blockers do have inverse agonist properties, the primary mechanism of withdrawal syndrome is receptor upregulation from chronic blockade, not rebound from suppressed constitutive activity.
3. Which of the following drugs is correctly paired with the type of tolerance it characteristically produces?
A) Carbamazepine -- pharmacodynamic tolerance -- it downregulates its own sodium channel targets, requiring dose escalation to maintain seizure control
B) Morphine -- pharmacokinetic tolerance -- it induces hepatic cytochrome P450 2D6 (CYP2D6), accelerating its own glucuronidation and reducing plasma concentrations over time
C) Rifampicin -- pharmacokinetic tolerance -- it is a potent inducer of CYP enzymes including cytochrome P450 3A4 (CYP3A4), accelerating its own metabolism and that of co-administered drugs, reducing plasma concentrations with continued use
D) Nitroglycerin -- pharmacokinetic tolerance -- it induces hepatic nitrate reductase enzymes, accelerating its own metabolism and requiring dose escalation
E) Salbutamol -- pharmacokinetic tolerance -- it induces beta-2 receptor gene transcription, increasing receptor density and amplifying its own bronchodilator effect over time
ANSWER: C
Rationale:
Rifampicin (rifampin) is one of the most potent CYP enzyme inducers in clinical use, particularly of CYP3A4, CYP2C9, and P-glycoprotein. With continued use, it accelerates its own metabolism (autoinduction) as well as the metabolism of numerous co-administered drugs including warfarin, oral contraceptives, antiretrovirals, and immunosuppressants. This produces pharmacokinetic tolerance -- the same dose achieves progressively lower plasma concentrations as enzyme induction develops over the first 1-2 weeks of therapy.
Option A: Option A is incorrect -- carbamazepine does produce autoinduction of CYP3A4 (pharmacokinetic tolerance) but the mechanism described (sodium channel downregulation) is not the established mechanism; the correct mechanism is pharmacokinetic, not pharmacodynamic sodium channel adaptation.
Option B: Option B is incorrect -- morphine does not induce CYP2D6; morphine's tolerance is primarily pharmacodynamic (receptor desensitization, downregulation) rather than pharmacokinetic; CYP2D6 is involved in morphine metabolism but morphine does not induce it.
Option D: Option D is incorrect -- nitroglycerin tolerance is pharmacodynamic, not pharmacokinetic; it results from depletion of sulfhydryl groups required for nitric oxide generation and oxidative stress in vascular smooth muscle, not from enzyme induction.
Option E: Option E is incorrect -- salbutamol tolerance involves pharmacodynamic beta-2 receptor downregulation, not upregulation; the mechanism described is inverted and pharmacokinetic autoinduction does not occur with salbutamol.
4. Nitroglycerin tolerance develops rapidly with continuous use. Which of the following correctly identifies the standard clinical strategy for preventing nitroglycerin tolerance in patients using transdermal patches?
A) Increasing the nitroglycerin dose progressively throughout the day to compensate for the developing tolerance, using a dose-escalation protocol
B) Co-administering a phosphodiesterase inhibitor to amplify the cyclic guanosine monophosphate (cGMP) signal and compensate for the reduced nitric oxide bioavailability that underlies tolerance
C) Rotating between different nitrate formulations (nitroglycerin, isosorbide mononitrate, isosorbide dinitrate) on a weekly basis, as cross-tolerance between nitrate formulations is incomplete
D) Using continuous nitroglycerin infusion rather than intermittent dosing, as the steady plasma concentration produced by infusion avoids the peak-trough fluctuations that trigger tolerance development
E) Providing a nitrate-free interval of 8-12 hours daily, typically overnight, to allow recovery of the sulfhydryl groups and mitochondrial aldehyde dehydrogenase activity required for nitric oxide generation from nitroglycerin
ANSWER: E
Rationale:
Nitroglycerin tolerance develops through depletion of tissue sulfhydryl groups and impairment of mitochondrial aldehyde dehydrogenase-2 (ALDH2), the enzyme responsible for bioactivating nitroglycerin to nitric oxide in vascular smooth muscle. Continuous nitrate exposure also generates reactive oxygen species that further impair nitric oxide signaling. The established clinical solution is a nitrate-free interval of 8-12 hours -- typically overnight, when anginal symptoms are less frequent -- which allows sulfhydryl group recovery and ALDH2 activity to restore, preventing tolerance from becoming clinically significant. Transdermal patches are removed at bedtime and reapplied in the morning for this reason.
Option A: Option A is incorrect -- progressive dose escalation does not prevent tolerance; it merely overcomes it temporarily while worsening the underlying mechanism and increasing adverse effects such as headache and hypotension.
Option B: Option B is incorrect -- co-administering a phosphodiesterase inhibitor (e.g., sildenafil) with nitroglycerin is contraindicated due to risk of severe hypotension; this is not a clinical strategy for tolerance prevention.
Option C: Option C is incorrect -- cross-tolerance between nitrate formulations is complete, not incomplete; all organic nitrates share the same mechanism and rotating between them does not prevent tolerance.
Option D: Option D is incorrect -- continuous infusion produces continuous nitrate exposure, which is precisely the condition that causes tolerance; intermittent dosing with nitrate-free intervals is the correct approach, the opposite of what this option states.
5. Physical dependence is best defined as which of the following?
A) A neurobiological disease characterized by compulsive drug seeking and use despite harmful consequences, involving dysregulation of the dopaminergic reward system
B) A pharmacodynamic state defined by the presence of a withdrawal syndrome upon drug discontinuation, reflecting receptor-level adaptations that developed during chronic drug exposure
C) A psychological state of craving and preoccupation with drug use that develops in individuals with a genetic predisposition to addictive behavior
D) A pharmacokinetic state in which the body has become so efficient at eliminating a drug that therapeutic plasma concentrations can no longer be maintained at standard doses
E) A receptor-level state in which drug-receptor binding affinity has permanently decreased through prolonged receptor occupancy, requiring permanently higher doses for any pharmacological effect
ANSWER: B
Rationale:
Physical dependence is defined pharmacologically as the state in which abrupt drug discontinuation or administration of an antagonist produces a characteristic withdrawal syndrome. It reflects the receptor-level adaptations -- downregulation, desensitization, compensatory upregulation of opposing systems -- that developed during chronic drug exposure. These adaptations maintain homeostasis in the presence of the drug; when the drug is removed, the adaptations are unmasked and produce the withdrawal syndrome. Physical dependence can develop with many drug classes including opioids, benzodiazepines, beta-blockers, corticosteroids, and antidepressants. Importantly, physical dependence does not equal addiction -- a patient can be physically dependent on a drug (e.g., corticosteroids for autoimmune disease) without any addictive behavior.
Option A: Option A describes addiction (substance use disorder), a distinct neurobiological condition involving compulsive use and loss of control; the defining feature is behavioral, not the presence of withdrawal.
Option C: Option C describes psychological craving, which may accompany addiction but is not the pharmacological definition of physical dependence.
Option D: Option D describes a pharmacokinetic phenomenon -- accelerated drug elimination -- which relates to pharmacokinetic tolerance, not physical dependence.
Option E: Option E is incorrect -- drug-receptor binding affinity does not permanently decrease through prolonged occupancy; tolerance involves functional adaptations in receptor signaling, not permanent loss of binding affinity.
6. Which of the following correctly describes tachyphylaxis?
A) Rapid tolerance developing after just one or a few doses, often due to depletion of a mediator or vesicular neurotransmitter stores, receptor internalization, or rapid post-receptor desensitization -- in contrast to the slower tolerance that develops over weeks of continuous exposure
B) Slow, progressive tolerance developing over weeks to months of continuous drug exposure, driven by receptor downregulation and post-receptor signaling changes
C) The phenomenon in which tolerance to one drug in a class confers tolerance to all other drugs in the same class through shared receptor mechanisms
D) An accelerated rate of drug metabolism developing within 24-48 hours of first exposure, due to rapid transcriptional upregulation of hepatic CYP enzymes
E) The paradoxical increase in drug sensitivity that occurs after a period of drug abstinence, explaining why recently abstinent individuals are at higher risk of overdose
ANSWER: A
Rationale:
Tachyphylaxis refers to rapid tolerance -- a marked reduction in response occurring after just one or a few doses, sometimes within a single dosing interval. It is distinguished from the slower tolerance that develops over days to weeks of repeated exposure. The mechanisms underlying tachyphylaxis include depletion of vesicular neurotransmitter stores (as seen with indirect-acting sympathomimetics such as ephedrine and amphetamine), rapid receptor internalization driven by agonist-induced GRK phosphorylation and beta-arrestin recruitment, and rapid post-receptor desensitization of downstream signaling. Classic examples include ephedrine (depletion of norepinephrine vesicular stores with repeated doses) and nitrates (though nitrate tolerance can develop both rapidly and with sustained use).
Option B: Option B describes the slower form of tolerance -- pharmacodynamic tolerance developing over weeks -- which is distinct from tachyphylaxis by its time course.
Option C: Option C describes cross-tolerance, a separate phenomenon in which tolerance to one drug extends to pharmacologically related drugs sharing the same receptor.
Option D: Option D describes pharmacokinetic autoinduction, which typically develops over days to weeks of enzyme induction, not 24-48 hours, and is not a form of tachyphylaxis.
Option E: Option E describes tolerance reversal during abstinence, which is the opposite of tachyphylaxis -- it represents increased sensitivity, not decreased sensitivity.
7. Benzodiazepine withdrawal can be life-threatening. Which of the following correctly identifies the primary mechanism responsible for the CNS hyperexcitability seen during benzodiazepine withdrawal?
A) Upregulation of mu-opioid receptors during chronic benzodiazepine use; abrupt withdrawal exposes the upregulated opioid receptor population to endogenous opioids, producing paradoxical CNS excitation through disinhibition of dopaminergic pathways
B) Upregulation of adenosine receptors during chronic benzodiazepine use; abrupt withdrawal produces excessive adenosine-mediated inhibition that paradoxically triggers compensatory seizure activity in cortical neurons
C) Depletion of endogenous GABA stores by chronic benzodiazepine use; abrupt withdrawal leaves synapses without inhibitory neurotransmitter, producing unopposed excitatory activity
D) Downregulation of GABA-A receptors combined with upregulation of NMDA receptors during chronic benzodiazepine use; abrupt withdrawal removes GABAergic enhancement while the upregulated excitatory glutamatergic system remains active, producing net CNS hyperexcitability that can cause seizures and delirium
E) Upregulation of glycine receptors in the spinal cord during chronic benzodiazepine use; abrupt withdrawal produces excessive spinal inhibition that reflexively drives supraspinal excitation through disinhibitory circuits
ANSWER: D
Rationale:
Chronic benzodiazepine use enhances GABA-A receptor activity continuously. In response, the CNS undergoes homeostatic adaptations in the opposite direction: GABA-A receptors are downregulated -- reduced in number, altered in subunit composition, and less sensitive to both GABA and benzodiazepines. Simultaneously, NMDA glutamate receptors are upregulated and sensitized as a compensatory response to the sustained GABAergic inhibition. The system reaches a new equilibrium in which both GABAergic tone (enhanced by drug) and glutamatergic tone (upregulated compensatorily) are elevated. When the benzodiazepine is abruptly removed, the GABAergic enhancement disappears immediately, but the upregulated NMDA system remains. The result is net CNS hyperexcitability -- anxiety, tremor, insomnia, and in severe cases, generalized seizures and delirium tremens equivalent, which can be fatal.
Option A: Option A is incorrect -- mu-opioid receptor upregulation is not the mechanism of benzodiazepine withdrawal; opioid receptors are not significantly altered by chronic benzodiazepine exposure.
Option B: Option B is incorrect -- adenosine receptor changes are not the established mechanism of benzodiazepine withdrawal syndrome; the excitatory-inhibitory imbalance involving GABA-A and NMDA receptors is the primary mechanism.
Option C: Option C is incorrect -- benzodiazepines do not deplete GABA stores; GABA synthesis is not impaired by benzodiazepine use, and the withdrawal syndrome reflects receptor adaptation rather than neurotransmitter depletion.
Option E: Option E is incorrect -- glycine receptor upregulation in the spinal cord is not an established mechanism of benzodiazepine withdrawal; glycine is a spinal inhibitory transmitter and its upregulation would not drive supraspinal excitation through the mechanism described.
8. A patient on chronic high-dose opioid therapy for cancer pain undergoes opioid rotation from morphine to hydromorphone. The equianalgesic dose calculated from standard conversion tables is reduced by 25-50% when initiating hydromorphone. Which of the following best explains why this dose reduction is applied?
A) Hydromorphone has lower oral bioavailability than morphine, so the equianalgesic dose calculated from conversion tables systematically overestimates the dose needed when switching to hydromorphone by the oral route
B) Hydromorphone has a narrower therapeutic index than morphine, and the dose reduction is a fixed safety margin applied to all opioid rotations regardless of the mechanism
C) Incomplete cross-tolerance -- the receptor adaptations produced by chronic morphine exposure are partially, but not fully, shared with hydromorphone; the patient has less tolerance to hydromorphone than to morphine, so the full equianalgesic dose would produce greater-than-expected effect and risk of toxicity
D) The dose reduction compensates for the pharmacokinetic interaction between morphine's active metabolite morphine-6-glucuronide and hydromorphone, which compete for renal elimination and raise hydromorphone plasma concentrations
E) Hydromorphone is a partial agonist at the mu-opioid receptor, meaning its intrinsic efficacy ceiling effect limits its analgesic potential, and the dose reduction reflects the lower maximum effect achievable with a partial agonist
ANSWER: C
Rationale:
Cross-tolerance refers to the phenomenon in which tolerance developed to one drug in a class confers some degree of tolerance to other drugs sharing the same receptor. In opioid rotation, the patient has developed substantial tolerance to morphine through chronic mu-opioid receptor adaptation. When switching to hydromorphone, which also acts at mu-opioid receptors, one might expect the patient's tolerance to transfer completely -- and the full equianalgesic dose to be required. However, cross-tolerance between opioids is incomplete: the receptor adaptations produced by one opioid are not fully shared with another, because different opioids differ in their GRK phosphorylation patterns, beta-arrestin recruitment, and receptor conformational changes. The patient therefore has less tolerance to hydromorphone than to morphine, meaning the full equianalgesic dose would produce a greater effect than anticipated, with risk of respiratory depression. Standard practice applies a 25-50% reduction from the calculated equianalgesic dose and titrates upward as needed.
Option A: Option A is incorrect -- while hydromorphone does have variable oral bioavailability, the primary reason for dose reduction in opioid rotation is incomplete cross-tolerance, not bioavailability differences.
Option B: Option B is incorrect -- the dose reduction in opioid rotation is not a fixed safety margin unrelated to mechanism; incomplete cross-tolerance is the specific pharmacological rationale.
Option D: Option D is incorrect -- morphine-6-glucuronide does not pharmacokinetically interact with hydromorphone through competitive renal elimination in a clinically significant way; this is not the basis for the dose reduction.
Option E: Option E is incorrect -- hydromorphone is a full agonist at mu-opioid receptors, not a partial agonist; it produces analgesia equivalent to or greater than morphine on a per-milligram basis.
9. Which of the following correctly distinguishes pharmacodynamic tolerance from pharmacokinetic tolerance?
A) Pharmacodynamic tolerance occurs only with opioids, while pharmacokinetic tolerance occurs only with anticonvulsants and antimicrobials that induce hepatic enzymes
B) Pharmacodynamic tolerance always develops faster than pharmacokinetic tolerance because receptor desensitization occurs within hours, while enzyme induction requires days to weeks
C) Pharmacokinetic tolerance is always reversible when the drug is stopped, while pharmacodynamic tolerance produces permanent receptor changes that persist indefinitely after drug discontinuation
D) Pharmacodynamic tolerance and pharmacokinetic tolerance always develop simultaneously and cannot be distinguished clinically because both produce the same pattern of dose escalation
E) Pharmacodynamic tolerance involves reduced drug effect at the same plasma concentration, due to receptor-level adaptations such as downregulation or desensitization; pharmacokinetic tolerance involves reduced plasma concentration at the same dose, due to accelerated drug metabolism through enzyme induction or increased renal clearance
ANSWER: E
Rationale:
The distinction between pharmacodynamic and pharmacokinetic tolerance is fundamental. Pharmacodynamic tolerance occurs at the receptor or post-receptor level -- the same plasma concentration of drug produces a smaller effect than before, because the receptor system has adapted through downregulation, desensitization, uncoupling from G proteins, or post-receptor signaling changes. Plasma concentrations may be unchanged, but the pharmacodynamic response is diminished. Pharmacokinetic tolerance occurs because the drug itself is eliminated more rapidly -- typically through induction of metabolizing enzymes (most commonly CYP isoforms) or transporter upregulation -- so that the same dose produces lower plasma concentrations than it did initially. The pharmacodynamic response to a given plasma concentration is unchanged; it is the concentration itself that has fallen. Both types can coexist, as with chronic opioid use.
Option A: Option A is incorrect -- pharmacodynamic tolerance occurs with many drug classes beyond opioids (benzodiazepines, nitrates, beta-agonists) and pharmacokinetic tolerance is not limited to anticonvulsants and antimicrobials.
Option B: Option B is incorrect -- the time course varies considerably by drug and mechanism; pharmacokinetic enzyme induction can begin within 24-48 hours for some inducers, while pharmacodynamic tolerance to some drugs (e.g., nitrates) can develop within hours.
Option C: Option C is incorrect -- both forms of tolerance are generally reversible after drug discontinuation; permanent receptor changes are not a defining feature of pharmacodynamic tolerance.
Option D: Option D is incorrect -- pharmacodynamic and pharmacokinetic tolerance are distinguishable clinically by measuring plasma drug concentrations: if tolerance develops with unchanged plasma levels, it is pharmacodynamic; if plasma levels have fallen, pharmacokinetic tolerance has occurred.
10. Clonidine is an alpha-2 adrenergic agonist used for hypertension, ADHD (attention-deficit/hyperactivity disorder), and opioid withdrawal. Which of the following correctly describes the withdrawal syndrome associated with abrupt clonidine discontinuation?
A) Abrupt clonidine withdrawal causes acute urinary retention and constipation through sudden loss of alpha-2 mediated parasympathetic enhancement in the urinary bladder and gastrointestinal tract
B) Abrupt clonidine withdrawal causes hypertensive rebound crisis within hours -- chronic alpha-2 agonism suppresses central sympathetic outflow, and abrupt discontinuation unmasks rebound sympathetic hyperactivity, producing severe hypertension, tachycardia, agitation, and diaphoresis
C) Abrupt clonidine withdrawal causes profound bradycardia and heart block because chronic alpha-2 stimulation upregulates cardiac conduction system receptors, and sudden removal of the agonist exposes these upregulated receptors to endogenous catecholamines that slow conduction
D) Abrupt clonidine withdrawal causes benzodiazepine-like seizures because alpha-2 receptors regulate GABA-A receptor sensitivity, and sudden loss of alpha-2 tone destabilizes GABAergic inhibition in cortical circuits
E) Abrupt clonidine withdrawal is safe in most patients because clonidine's alpha-2 selectivity means that withdrawal predominantly affects peripheral alpha-2 receptors on blood vessels rather than central sympathetic control circuits
ANSWER: B
Rationale:
Clonidine acts on presynaptic and postsynaptic alpha-2 adrenergic receptors in the brainstem, particularly the nucleus tractus solitarius and locus coeruleus, reducing central sympathetic outflow. This produces its antihypertensive effect. With chronic use, compensatory upregulation of adrenergic receptors and sensitization of central sympathetic circuits develops -- the system adapts to maintain adequate sympathetic tone in the face of continuous alpha-2 mediated suppression. If clonidine is stopped abruptly, the suppressive alpha-2 agonism disappears but the upregulated, sensitized sympathetic circuits remain, producing a rebound surge of sympathetic activity -- severe hypertension (sometimes exceeding pre-treatment levels), tachycardia, diaphoresis, and agitation within hours of the missed dose. This is clinically significant and can be dangerous, particularly in patients with coronary artery disease. Clonidine must always be tapered.
Option A: Option A is incorrect -- clonidine withdrawal does not cause urinary retention or constipation; its withdrawal syndrome is dominated by sympathetic hyperactivity, not parasympathetic effects.
Option C: Option C is incorrect -- clonidine withdrawal produces tachycardia, not bradycardia; the rebound sympathetic surge accelerates heart rate rather than slowing conduction.
Option D: Option D is incorrect -- alpha-2 receptors do not regulate GABA-A receptor sensitivity through an established mechanism; clonidine withdrawal does not produce benzodiazepine-like seizures as its primary manifestation.
Option E: Option E is incorrect -- clonidine's primary antihypertensive mechanism is central (brainstem alpha-2 receptors reducing sympathetic outflow), not peripheral; abrupt discontinuation of central sympathetic suppression is precisely what makes withdrawal dangerous.
ANSWER KEY: Q1=D Q2=A Q3=C Q4=E Q5=B Q6=A Q7=D Q8=C Q9=E Q10=B
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