WorksheetsPrinciples of NS Pharmacology 102925
Total questions: 101
Worksheet time: 51mins
The main functional cells of the nervous system are:
Erythrocytes
Neurons
Chondrocytes
Osteoclasts
Which glial cell forms myelin in the CNS?
Schwann cell
Oligodendrocyte
Astrocyte
Microglia
Primary immune cells of the CNS are:
Astrocytes
Microglia
Ependymal cells
Satellite cells
The BBB restricts passage mainly via:
Fenestrated capillaries
Tight junctions of endothelial cells
Lymphatic drainage
Loose basement membrane
A typical resting neuronal membrane potential is about:
+30 mV
0 mV
–70 mV
–10 mV
Depolarization of a neuron is primarily due to:
Cl– influx
Na+ influx
K+ efflux
Ca2+ efflux
Repolarization during an action potential is mainly caused by:
Na+ influx
K+ efflux
Ca2+ influx
Cl– efflux
Absolute refractory period occurs because:
K+ channels are closed
Na+ channels are inactivated
Ca2+ channels are open
Cl– channels are blocked
Saltatory conduction occurs in:
Unmyelinated axons
Dendrites only
Myelinated axons at nodes of Ranvier
Cell bodies
The PNS myelinating cell is the:
Oligodendrocyte
Schwann cell
Astrocyte
Microglia
Which ion triggers neurotransmitter vesicle fusion?
Na+
K+
Ca2+
Cl–
Electrical synapses primarily use:
Chemical transmitters
Gap junctions
Second messengers
Receptors
The BBB permits easiest entry of:
Large polar molecules
Charged peptides
Lipophilic small molecules
Plasma proteins
Gray matter is rich in:
Myelinated axons
Neuronal cell bodies and synapses
Collagen
CSF
A demyelinating disease of the CNS that impairs conduction is:
Guillain–Barré syndrome
Multiple sclerosis
Myasthenia gravis
Lambert–Eaton syndrome
The principal excitatory neurotransmitter in the CNS is:
GABA
Glycine
Glutamate
Acetylcholine
The main inhibitory transmitter in the brain is:
Dopamine
GABA
Glutamate
Serotonin
Dopamine is synthesized from:
Tryptophan
Tyrosine
Choline
Histidine
Serotonin (5-HT) is synthesized from:
Tyrosine
Tryptophan
Glutamine
Phenylalanine
Termination of catecholamine action mainly involves:
Diffusion only
Reuptake by transporters
Hydrolysis by AChE
Binding to albumin
MAO and COMT are enzymes that:
Synthesize serotonin
Degrade catecholamines
Synthesize acetylcholine
Degrade GABA
22. VMAT loads monoamines into:
A) Synaptic cleft
B) Vesicles
C) Mitochondria
D) Nucleus
Glycine is an important inhibitory transmitter mainly in the:
Cortex
Spinal cord and brainstem
Hippocampus
Cerebellar cortex only
Acetylcholine is degraded by:
MAO
COMT
Acetylcholinesterase
Tyrosine hydroxylase
Which transmitter is a gas and diffuses freely across membranes?
NO
NE
ACh
GABA
Neuropeptide transmitters are typically:
Synthesized at terminals
Stored in small clear vesicles
Degraded by peptidases after release
Recycled by high-affinity transporters
Co-transmission implies:
A) A neuron releases only one transmitter
B) Same vesicle always carries two transmitters
C) Neuron can release classical transmitter plus a peptide
D) Only peptides are released
SSRIs primarily increase synaptic levels of:
NE
DA
5-HT
ACh
Levodopa increases brain dopamine because it:
Inhibits MAO-B
Directly activates D2 receptors
Crosses BBB and is converted by AADC
Blocks DAT
Donepezil’s therapeutic effect is via inhibition of:
COMT
AChE
MAO-A
GABA-T
Ionotropic receptors are:
Enzymes
Ligand-gated ion channels
GPCRs
Nuclear receptors
Metabotropic receptors signal via:
Direct ion flux
GPCR second messengers
Voltage sensors
Pumps
NMDA receptor requires glutamate and:
GABA
Glycine/D-serine co-agonist
ACh
NE
At resting potentials, NMDA channels are blocked by:
Na+
Ca2+
Mg2+
Cl–
AMPA receptors primarily conduct:
Cl–
Na+ (and some Ca2+)
K+ only
HCO3–
Nicotinic receptors are:
GPCRs
Tyrosine kinases
Ligand-gated cation channels
Voltage-gated channels
Muscarinic receptors are:
Ionotropic
GPCRs
Nuclear receptors
Transporters
D1-like dopamine receptors couple to:
Gi → ↓cAMP
Gq → ↑IP3
Gs → ↑cAMP
Go → ↓Ca2+
5-HT1A typically couples to:
Gs
Gi
Gq
G12/13
β1-adrenoceptors primarily signal via:
Gs → ↑cAMP
Gi → ↓cAMP
Gq → ↑IP3/DAG
Ion channel opening directly
Receptor desensitization after prolonged agonist exposure often involves:
Channel opening
β-arrestin and internalization
Increased gene transcription
Enhanced G protein coupling
Allosteric modulators bind:
Orthosteric site
Active ion pore
Distinct site altering response
DNA
Benzodiazepines act at which receptor class?
NMDA receptor orthosteric site
GABA_A allosteric site
GABA_B GPCR
AMPA receptor
Ketamine is an antagonist at:
AMPA
NMDA
GABA_A
5-HT3
Clozapine mainly targets:
D2 only
5-HT2A and D2 (multireceptor)
NMDA
α4β2 nAChR
Vesicle docking is mediated by:
SNARE proteins
Na+/K+ pump
Tubulin
Dynein
Ca2+ sensor for vesicle fusion is primarily:
Synaptophysin
Synaptotagmin
Dynamin
Clathrin
Endocytosis of vesicles after release requires:
Clathrin and dynamin
SNAREs
NMDA receptors
Na+ channels
A reuptake inhibitor increases transmitter by:
Enhancing degradation
Blocking transporter
Blocking synthesis
Activating autoreceptors
Autoreceptors typically:
Enhance release
Inhibit further release
Degrade transmitter
Open voltage-gated Na+ channels
EPSPs are usually mediated by:
Cl− influx
Na+/Ca2+ influx
K+ efflux only
Pump activity
IPSPs often involve:
Na+ influx
Ca2+ influx
Cl− influx or K+ efflux
HCO3− influx exclusively
Desensitization reduces response to:
Antagonists
Agonists after sustained exposure
Placebo
Inverse agonists only
Potency is best reflected by:
E_max
EC50/ED50
Hill slope
Therapeutic index only
Efficacy is:
Maximal effect (E_max) a drug can produce
Concentration to produce 50% effect
Binding affinity alone
Slope of dose–response
Competitive antagonism shifts the dose–response curve:
Left, ↓E_max
Right, same E_max
Down, ↓E_max
Left, same E_max
Irreversible antagonists typically:
Reduce E_max
Shift right only
Increase potency
Have no effect
Cocaine increases synaptic monoamines by blocking:
MAO
Vesicular transport
Reuptake transporters (DAT/NET/SERT)
COMT
Botulinum toxin impairs release by cleaving:
Voltage-gated Ca2+ channels
SNARE proteins
GABA_A subunits
DAT
Reserpine depletes monoamines by inhibiting:
VMAT
MAO
COMT
Tyrosine hydroxylase
Benzodiazepines enhance:
GABA_B currents
GABA_A receptor Cl− channel opening frequency
NMDA currents
AMPA currents
Barbiturates mainly:
Block DAT
Prolong GABA_A channel open time
Antagonize NMDA
Activate 5-HT3
Methylxanthines (e.g., caffeine) primarily:
Inhibit AChE
Antagonize adenosine receptors
Block Na+ channels
Enhance GABA
Amphetamines increase synaptic monoamines by:
Blocking MAO only
Reversing transporters and releasing vesicular stores
Inhibiting AChE
Blocking NMDA
General anesthetics typically:
Increase CNS excitability
Enhance inhibitory or reduce excitatory transmission
Block all GPCRs
Only block Na+ channels
Sedative vs hypnotic distinction is primarily by:
Mechanism
Dose producing calming vs sleep
Route of administration
Half-life
Physical dependence risk increases with:
Short half-life and rapid CNS entry
Long half-life
Poor oral absorption
Peripheral action
Overdose with benzodiazepines is most dangerous when combined with:
Antihistamines
Opioids/alcohol
SSRIs
Antacids
Tolerance to barbiturates includes:
Enzyme induction and receptor adaptation
Only receptor upregulation
Only enzyme inhibition
No tolerance
Which is a wake-promoting agent targeting DAT/NET modestly?
Modafinil
Diazepam
Propofol
Phenobarbital
Flumazenil is a/an:
Benzodiazepine agonist
Benzodiazepine antagonist
Barbiturate antagonist
Opioid antagonist
Propofol’s major CNS action is:
NMDA antagonism
GABA_A potentiation
Na+ channel block
5-HT1A agonism
Methylphenidate primarily:
Inhibits MAO-B
Blocks DAT/NET reuptake
Blocks SERT only
Activates α2 autoreceptors
Z-drugs (zolpidem) preferentially act at:
GABA_B
GABA_A α1 subunit sites
NMDA
H1 receptors
The stimulant with greatest risk of psychosis at high doses:
Caffeine
Modafinil
Amphetamines
Melatonin
Parkinson’s disease involves loss of neurons in the:
Locus coeruleus
Substantia nigra pars compacta
Raphe nuclei
Amygdala
Levodopa is combined with carbidopa to:
Increase central conversion and reduce peripheral side effects
Inhibit COMT centrally
Block MAO-B
Reduce tolerance
Alzheimer’s hallmark pathology includes:
Lewy bodies
β-amyloid plaques and tau tangles
Pick bodies
Tuberous sclerosis
Epileptic discharges reflect:
Hypopolarization
Abnormal synchronized neuronal firing
Decreased excitability
Purely glial dysfunction
First-line therapy for absence seizures targets:
Na+ channels
T-type Ca2+ channels
NMDA receptors
GABA_B only
Major depression is associated with:
Excess monoamines
Deficits/dysregulation in monoaminergic signaling
Schizophrenia positive symptoms relate to:
Reduced glutamate
Excess mesolimbic dopamine activity
Low serotonin
Low NE
Neuropathic pain responds best to:
NSAIDs only
Anticonvulsants/SNRIs/TCAs
Acetaminophen only
Placebo
Levodopa long-term use commonly causes:
Nephrotoxicity
Dyskinesias and motor fluctuations
Agranulocytosis
Severe rash
Valproate’s broad antiepileptic effect involves:
Only Na+ channel block
Na+ channel block + ↑GABA + T-type effects
Only GABA-A agonism
Only NMDA block
SSRIs treat depression by:
Inhibiting 5-HT reuptake
Blocking MAO-A
Blocking NMDA
Activating D2 receptors
Atypical antipsychotics reduce EPS risk largely due to:
Pure D2 blockade
5-HT2A antagonism with moderate D2 block
NMDA agonism
GABA_B agonism
Triptans relieve migraine via:
D2 agonism
5-HT1B/1D agonism causing cranial vasoconstriction and ↓neuropeptide release
H1 antagonism
β2 agonism
For acute status epilepticus first choice is:
Ethosuximide
Lorazepam/diazepam
Lamotrigine
Levetiracetam only
Cholinesterase inhibitors in AD most improve:
Motor symptoms
Cognitive/behavioral symptoms modestly
Disease progression halt
Hallucinations only
Sympathetic postganglionic transmitter to most organs is:
ACh
NE
Dopamine
Serotonin
Parasympathetic postganglionic transmitter is:
NE
ACh
DA
5-HT
Heart rate increase is mediated primarily by:
M2 activation
β1 activation
α1 activation
M3 activation
Bronchoconstriction is mediated by:
β2
α1
M3
D1
Mydriasis (radial muscle) is via:
M3
β2
α1
M2
Bladder detrusor contraction uses:
β3
M3
α1
D2
β2 stimulation in bronchi causes:
Constriction
Dilation
Secretion
Edema
α2 autoreceptor activation generally:
Increases NE release
Decreases NE release
No effect
Increases ACh release
Cholinesterase inhibitors will:
Decrease secretions
Increase parasympathetic tone
Cause mydriasis
Tachycardia always
Atropine blocks:
Nicotinic receptors
Muscarinic receptors
α receptors
β receptors
Phenylephrine primarily stimulates
β1
β2
M3
α1
