NURS 200- FINAL EXAM STUDY GUIDE Questions with Correct
Answers (Grade A+)
Question 1: Antipsycotics adverse effects in general
Answer: two kinds: second ones - phenothiazines and phenothiazine-like drugs produce less AE in relation
to extrapyramidal effects extrapyramidal effects (acute dystoniasevere muscle spasms, akathisiainability to
rest or relax, Parkinsonismtremor, loss of fine motor skills, tardive dyskinesiainvoluntary unusual tongue
and face movements) anticholingergic, sexual dysfunction, sedation, orthostatic hypotension, weight gain,
Question 2: Action of antidepressants
Answer: inhibit/slowing neuronal reuptake of serotonin = increase in serotonin levels AND/OR blocking
the enzymatic breakdown of norepinephrine - increased sensitivity of post-synaptic - takes 4-6 weeks -
restoring normal NT balance in specific brain regions - based on individual needs and if they respond well
Question 3: Lorazepam (Ativan)- action and adverse effects
Answer: MOA: binds/potentiating the effects of GABA (an inhibitory neurotransmitter), causing inhibition
of post synaptic neurons in thalamus, hypothalamus, limbic system - for anxiety, status epileptics, seizures,
pre anaesthetic med AE: drowsiness, sedation, ataxia, blurred vision, disorientation, anterograde amnesia
(IV)
Question 4: Lithium toxicity -causes
Answer: S/S of toxicity: diarrhea, vomiting, tremor, drowsiness, muscle weakness, ataxia - diruetics
increase risk of toxicity (SODIUM LOSS)- body replaces lithium as salt - NSAIDS, thiazide diuretics - long
term therapy can produce serious toxicity, kidney impairment, dysrhythmias, circulatory collapse,
leukocytosis
Question 5: Phenytoin (Dilantin) IV
Answer: for partial and tonic clonic seizures (NOT ABSENCE) MOA: blocs Na+ influx = neurons are kept
in absolute refractory for a longer time = less frequent action potentials - desensitizing sodium channels in
CNS that are responsible for neuronal responsivity AE: drowsiness, bradycardia, agranulocytosis, rashes,
weight loss, hypotension, gingivitis, ataxia, lethargy, alter vit K, vent. fib., headache, nystagmus, ataxia,
confusion, insomnia SE: agranulocytosis and aplastic anemia - no CNS depression or the abuse potential
signs of phenytoin toxicity: - coma, confusion, fever, nystagmus, lethargy, loud BP, nausea, sleepiness,
slow or slurred speech, staggering gait, swollen gums, tremor, unsteadiness, vomiting narrow therapeutic
index 40-80 for IV mix with saline ONLY and max rate is 50 mg/minute - no other meds or dextrose as
emboli will form
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, Question 6: (IV) diazepam (Valium)
Answer: BENZODIAZEPINES - short term control due to dependency TE: anxiety, alcohol withdrawal,
sedation, seizure, muscle spasm, status epileptic (longer than 5 minutes) MOA: binds to GABA
receptor-chloride channels in brain, reducing neuronal discharges and suppressing neuronal activity in the
limbic system, calming without strong sedation - effects are immediate when given IV and last 20 minutes
AE: drowsiness, fatigue, dizziness, vertigo, ataxia, laryngeal spasms, urinary retention, menstrual
irregularities - IV watch for hypotension, muscular weakness, tachycardia, and respiratory depression
Question 7: Phenobarbital
Answer: Luminal - barbiturate TE: status epilepticus, seizures, sedation, insomnia (NOT ABSENCE
SEIZURE)- long acting - increase a pts sensitivity to pain MOA: increase activity of GABA receptor,
decrease excitability of post-synaptic neurons and increasing seizure threshold - never really given IM AE:
drowsiness, sedation, excitation (child), difficulty focusing, confusion, depression, headache, N&V, vit.
deficiency, risk of dependency, overdose, laryngeal spasm - do not stop meds abruptly
Question 8: valproic acid (Depakene)
Answer: phenytoin-like drug TE: seizures (absence, and tonic clonic), bipolar mania, migraine prophylaxis
MOA: increase GABA, block Na+ influx = neurons are kept in absolute refractory for a longer time = less
frequent action potentials AE: headache, dizziness, N&V&D, abd pain, increased bleeding times, it is GI
irritant, sedation, visual disturbances, muscle weakness, rash, alopecia SE: bone marrow suppression,
photosensitivity, hepatotoxic, pancreatitis
Question 9: sumatriptan (Imitrex)-adverse effects
Answer: for treatment of migraine AE: tingling, flushing, dizziness, weakness, somnolence, chest pain, dry
mouth, N, constricts your intracranial vessels (decreased ICP), drowsiness, or warming sensation *caution if
MI or hx of angina
Question 10: Methadone
Answer: opoid agonist TE: long term pain treatment, detoxification (give during opioid withdrawal) MOA:
drug binds to opioid receptor (Mu 1 & 2, kappa, delta) in PNS and CNS = produces effects of analgesia and
cough suppression AE: decreased RR, flushing, hypotension, pupil constriction, dizziness, N&V,
constipation, drowsiness - needs a double sign now prevents drug withdrawal and reduces drug cravings
Question 11: NSAIDadverse effects
Answer: abdo pain, bleeding, N&V, decrease kidney function, diarrhea, N, ulcers, live toxicity, drowsiness,
tinnitus, bladder infection, HTN, GI system *high doses may produce salicylism*
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Answers (Grade A+)
Question 1: Antipsycotics adverse effects in general
Answer: two kinds: second ones - phenothiazines and phenothiazine-like drugs produce less AE in relation
to extrapyramidal effects extrapyramidal effects (acute dystoniasevere muscle spasms, akathisiainability to
rest or relax, Parkinsonismtremor, loss of fine motor skills, tardive dyskinesiainvoluntary unusual tongue
and face movements) anticholingergic, sexual dysfunction, sedation, orthostatic hypotension, weight gain,
Question 2: Action of antidepressants
Answer: inhibit/slowing neuronal reuptake of serotonin = increase in serotonin levels AND/OR blocking
the enzymatic breakdown of norepinephrine - increased sensitivity of post-synaptic - takes 4-6 weeks -
restoring normal NT balance in specific brain regions - based on individual needs and if they respond well
Question 3: Lorazepam (Ativan)- action and adverse effects
Answer: MOA: binds/potentiating the effects of GABA (an inhibitory neurotransmitter), causing inhibition
of post synaptic neurons in thalamus, hypothalamus, limbic system - for anxiety, status epileptics, seizures,
pre anaesthetic med AE: drowsiness, sedation, ataxia, blurred vision, disorientation, anterograde amnesia
(IV)
Question 4: Lithium toxicity -causes
Answer: S/S of toxicity: diarrhea, vomiting, tremor, drowsiness, muscle weakness, ataxia - diruetics
increase risk of toxicity (SODIUM LOSS)- body replaces lithium as salt - NSAIDS, thiazide diuretics - long
term therapy can produce serious toxicity, kidney impairment, dysrhythmias, circulatory collapse,
leukocytosis
Question 5: Phenytoin (Dilantin) IV
Answer: for partial and tonic clonic seizures (NOT ABSENCE) MOA: blocs Na+ influx = neurons are kept
in absolute refractory for a longer time = less frequent action potentials - desensitizing sodium channels in
CNS that are responsible for neuronal responsivity AE: drowsiness, bradycardia, agranulocytosis, rashes,
weight loss, hypotension, gingivitis, ataxia, lethargy, alter vit K, vent. fib., headache, nystagmus, ataxia,
confusion, insomnia SE: agranulocytosis and aplastic anemia - no CNS depression or the abuse potential
signs of phenytoin toxicity: - coma, confusion, fever, nystagmus, lethargy, loud BP, nausea, sleepiness,
slow or slurred speech, staggering gait, swollen gums, tremor, unsteadiness, vomiting narrow therapeutic
index 40-80 for IV mix with saline ONLY and max rate is 50 mg/minute - no other meds or dextrose as
emboli will form
Page 1
, Question 6: (IV) diazepam (Valium)
Answer: BENZODIAZEPINES - short term control due to dependency TE: anxiety, alcohol withdrawal,
sedation, seizure, muscle spasm, status epileptic (longer than 5 minutes) MOA: binds to GABA
receptor-chloride channels in brain, reducing neuronal discharges and suppressing neuronal activity in the
limbic system, calming without strong sedation - effects are immediate when given IV and last 20 minutes
AE: drowsiness, fatigue, dizziness, vertigo, ataxia, laryngeal spasms, urinary retention, menstrual
irregularities - IV watch for hypotension, muscular weakness, tachycardia, and respiratory depression
Question 7: Phenobarbital
Answer: Luminal - barbiturate TE: status epilepticus, seizures, sedation, insomnia (NOT ABSENCE
SEIZURE)- long acting - increase a pts sensitivity to pain MOA: increase activity of GABA receptor,
decrease excitability of post-synaptic neurons and increasing seizure threshold - never really given IM AE:
drowsiness, sedation, excitation (child), difficulty focusing, confusion, depression, headache, N&V, vit.
deficiency, risk of dependency, overdose, laryngeal spasm - do not stop meds abruptly
Question 8: valproic acid (Depakene)
Answer: phenytoin-like drug TE: seizures (absence, and tonic clonic), bipolar mania, migraine prophylaxis
MOA: increase GABA, block Na+ influx = neurons are kept in absolute refractory for a longer time = less
frequent action potentials AE: headache, dizziness, N&V&D, abd pain, increased bleeding times, it is GI
irritant, sedation, visual disturbances, muscle weakness, rash, alopecia SE: bone marrow suppression,
photosensitivity, hepatotoxic, pancreatitis
Question 9: sumatriptan (Imitrex)-adverse effects
Answer: for treatment of migraine AE: tingling, flushing, dizziness, weakness, somnolence, chest pain, dry
mouth, N, constricts your intracranial vessels (decreased ICP), drowsiness, or warming sensation *caution if
MI or hx of angina
Question 10: Methadone
Answer: opoid agonist TE: long term pain treatment, detoxification (give during opioid withdrawal) MOA:
drug binds to opioid receptor (Mu 1 & 2, kappa, delta) in PNS and CNS = produces effects of analgesia and
cough suppression AE: decreased RR, flushing, hypotension, pupil constriction, dizziness, N&V,
constipation, drowsiness - needs a double sign now prevents drug withdrawal and reduces drug cravings
Question 11: NSAIDadverse effects
Answer: abdo pain, bleeding, N&V, decrease kidney function, diarrhea, N, ulcers, live toxicity, drowsiness,
tinnitus, bladder infection, HTN, GI system *high doses may produce salicylism*
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