THE PRACTICE TEST
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- 96
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- Multiple choice
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pharmacotherapeutics pharmacodynamics pharmacokinetics pharmacy
side effect adverse effect drug allergy contraindication
toxic effect antagonism idiosyncrasy side effect
generic name over-the-counter name trade name chemical name
duration of action onset of action ceiling effect maximal response
poison OTC drug prescription drug controlled substance
posology toxicology pharmacodynamics pharmacotherapeutics
trade nonproprietary nonprescription brand
idiosyncrasy drug allergy teratogenicity carcinogenicity
ED50 maximal response ceiling effect onset of action
inhalation transdermal intramuscular sublingual
ionized positively charged water soluble lipid soluble
kidney blood vessels liver heart
B C D X
first-pass metabolism enzyme induction enzyme inhibition enterohepatic cycling
drug ionization water solubility positively charged drug negatively charged drug
weight age genetic variation placebo effect
Category A Category B Category C Category D
suicide substrates. orphan drugs. protein drugs. competitive antagonists.
idiosyncrasy. tachyphylaxis. heterologous desensitization. refractoriness.
tachyphylaxis. inactivation. desensitization. downregulation.
a physiologic antagonist. a competitive receptor antagonist. a noncompetitive receptor antagonist. a partial agonist.
increased heart rate bronchodilation vasoconstriction contraction of urinary bladder
vasodilation vasoconstriction cardiac stimulation cardiac depression
alpha-1 receptors alpha-2 receptors beta-1 receptors beta-2 receptors
alpha-1 receptors alpha-2 receptors beta-1 receptors beta-2 receptors
alpha-blocker nonselective beta-blocker selective beta-1 blocker adrenergic neuronal blocker
increased release of NE from adrenergic nerve ending alpha-1 receptor blocker beta-1 receptor blocker formation of a false transmitter in adrenergic nerve ending
norepinephrine phenylephrine pseudoephedrine epinephrine
decreasing heart rate decreasing force of myocardial contraction vasoconstriction of skeletal muscle blood vessels lowering of blood pressure
bronchodilation vasoconstriction relaxation of uterus increased heart rate
alpha-1 nicotinic-neural (Nn) nicotinic-muscle (Nm) muscarinic
increased heart rate increased gastrointestinal motility decreased urination pupillary dilation
direct-acting cholinergic drug reversible acetylcholinesterase inhibitor irreversible acetylcholinesterase inhibitor anticholinergic drug
slow pulse rate increased urination diarrhea sweating
bronchodilation increased heart rate increased gastrointestinal activity decreased respiratory secretions
scopolamine bethanechol neostigmine physostigmine
respiratory paralysis urinary retention increased heart rate bronchodilation
neostigmine tolterodine physostigmine bethanechol
the mechanism of action is the same as represented by dantrolene all of these drugs depolarize the muscle fiber before blockade occurs calcium ions are released from the storage sites there are two groups in this class: either depolarizing agents or nondepolarizing agents
stimulation of the actin and myosin muscle fibrils directly liver damage because the drug is metabolized only by the liver peripheral neuromuscular receptor blockade after stimulating the Nm receptors longer duration of action than vecuronium
include dantrolene and cisatracurium inhibit or reduce activity within the spinal cord (intraneuronal), interrupting the central stimulus to muscle contraction can only be given parenterally cause systemic release of histamine, leading to hypotension
the diaphragm is a skeletal muscle succinylcholine stimulates the respiratory centers in the brain like dantrolene, all muscle relaxants inhibit the action of norepinephrine at the neuromuscular junction relaxation of the muscles in the lower extremities pulls blood away from the lungs
neomycin corticosteroids general anesthetics like isoflurane alcohol
blockage of conduction in the spinal cord inhibiting nerve transmission blockage of the Nm receptors decreasing ACH in the neuromuscular junction
reduce muscle tear decrease body temperature potentiate vasodilators increase muscle tone
difficulty swallowing (dysphagia) skeletal muscle weakness decreased respiration bronchospasm
a drop in cytosolic Ca2+. a drop in cytosolic K+. a rise in cytosolic Ca2+. a drop in cytosolic Mg2+.
hemicholinium. acetylcholine. edrophonium. succinylcholine.
it is a nonpolar compound that penetrates the CNS more easily than neostigmine. it has a shorter half-life than neostigmine, making it more useful for emergency treatment. it has a longer half-life than neostigmine, better matching the half-life of atropine. it is eliminated via the kidneys, and dosage is not critical with compromised liver function.
opioid analgesics produce little or no respiration depression with long-term use of analgesic doses opioid antagonists include endorphins all drugs in the opioid analgesic group are controlled substances, Schedule III in low doses, opioids produce nausea and vomiting
hyperventilation and deep breathing bronchospasms spasmogenic activity in the ureters and sphincter muscle relaxation of the skeletal muscles controlling posture (spasmolytic)
induction of Monitored Anesthesia Care and treatment of chronic severe pain routine treatment of migraine unmonitored treatment of chronic severe pain analgesia for patients with paralytic ileus
endorphin is an abbreviation from the terms meaning inside the organ endogenous opioid receptors include mu, alpha-2 adrenergic, and delta receptors agonism means the drug occupies the receptor and causes a response opioid agonism means the drug occupies the receptor and stimulates the release of endorphins
heroin codeine methadone acetaminophen
reversal of respiratory depression from barbiturates use only for the relief of acute pain cough suppression alone or in combination with other analgesics over-the-counter tolerance develops to the analgesic response
can be used for relief of cancer pain has many formulations (lozenge, film) because it is used routinely in dental surgery induces neuropathic pain primarily works on peripheral nerve endings rather than higher centers
unmyelinated myelinated A-delta CTZ C fibers
poppy opium chemical synthesis alkaloids
constipation polyuria convulsions mydriasis
fewer receptors are available to produce a response increased pain by the patient requires greater doses of medication the body reacts to removal of the opioid analgesic histamine release causes hypotension
producing complementary effects using a few drugs avoids unnecessary intense (deep) CNS depression with one anesthetic to achieve the same effect the concentration of volatile anesthetic in the alveoli is balanced against the amount of anesthetic in the blood less monitoring of anesthesia is required fewer patients experience emergence delirium
it is a potent analgesic at all doses it slowly brings the patient to the stage of surgical anesthesia it is a complete anesthetic with a quick onset of action and recovery period uncomplicated by nausea and vomiting it is administered by special vaporizer to avoid mask delivery
ketamine causes chloride ions to flow out of the nerve cell by binding to GABA propofol binds to the GABA A receptor and enhances hyperpolarization of the neuron barbiturates and propofol act on the receptor and directly on the chloride channel potent anesthetics enhance GABA A receptor function
hepatic metabolism and renal excretion excretion through the lungs and sweating accumulation in fat tissue and redistribution increased salivation and bile production
local anesthesia Monitored Anesthesia Care general anesthesia balanced anesthesia
intravenous dissociative anesthesia oral topical
analgesics antiarrhythmics antianxiety, short-acting CNS depressants like midazolam anticholinergics
increase NREM stage 2 sleep increase REM sleep increase NREM stage 4 sleep cause REM rebound
risk of drug dependency disruption of normal stages of sleep suppression of REM sleep all of these statements are true
zolpidem binds to the GABAB receptor benzodiazepines increase chloride channel opening barbiturates block the GABA receptor ramelteon is a melatonin antagonist
forms active metabolites may cause next-day residual effects increases chloride ion influx all of these statements are true
is classified as a benzodiazepine has a half-life of 1-2 hours increases total sleep time is used as an antianxiety agent
increase levels of norepinephrine increase levels of serotonin decrease levels of norepinephrine decrease levels of serotonin
antihistaminic anticholinergic sedation all of the above
monoamine oxidase inhibitors selective serotonin reuptake inhibitors psychomotor stimulants lithium
increase norepinephrine increase acetylcholine increase serotonin increase norepinephrine and serotonin only
MAOI TCA SSRI SNRI
cardiac arrhythmias convulsions postural hypotension all of these
paroxetine—SSRI amitriptyline—TCA methylphenidate—MAOI this is targets dop transporter duloxetine—SNRI
nortriptyline (TCA) tranylcypromine (MAOI) venlafaxine (SNRI) fluoxetine (SSRI)
spinal cord limbic system reticular formation basal ganglia
stimulation of DA receptors stimulation of serotonin receptors blockage of serotonin receptors blockade of dopamine receptors
clozapine alprazolam (benzodiazepine) haloperidol chlorpromazine
cerebral cortex reticular formation spinal cord all of these
excess levels of acetylcholine treatment with some antipsychotic drugs decreased levels of dopamine drug administration after a high-protein meal
amantadine benztropine ropinirole entacapone (COMT)
tolcapone selegiline rasagiline all of these
rigidity bradykinesia tremor dystonia
carbidopa and entacapone entacapone carbidopa selegiline
ropinirole entacapone pramipexole tolcapone
muscular rigidity increased sweating salivary drooling movement disturbances
amantadine levodopa bromocriptine procyclidine
converted to dopamine in the substantia nigra neurons increases level of dopamine in the brain peripheral metabolism to DA inhibited by carbidopa all of these
MAO-B inhibitor dopamine receptor agonist COMT inhibitor anticholinergic drug
muscarinic-M1 receptor. muscarinic-M2 receptor. muscarinic-M3 receptor. muscarinic-M4 receptor.
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