Pharm Unit 5

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Created by:

annay1120  on April 26, 2011

Subjects:

central nervous system drugs

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Pharm Unit 5

amitripytyline
Elavil®
tricyclic antidepressant (TCA)

MOA: block the reuptake of NE and 5HT into the neuronal nerve endings

SE: sedation; anticholinergic effects (dry mouth, constipation, urinary retention, blurred vision, rapid HR); increased CNS activity (restlessness, tremors, convulsions, mania)
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amitripytyline
Elavil®
tricyclic antidepressant (TCA)

MOA: block the reuptake of NE and 5HT into the neuronal nerve endings

SE: sedation; anticholinergic effects (dry mouth, constipation, urinary retention, blurred vision, rapid HR); increased CNS activity (restlessness, tremors, convulsions, mania)
imipramine
Tofranil®
tricyclic antidepressant (TCA)

MOA: block the reuptake of NE and 5HT into the neuronal nerve endings

SE: sedation; anticholinergic effects (dry mouth, constipation, urinary retention, blurred vision, rapid HR); increased CNS activity (restlessness, tremors, convulsions, mania)
isocarboxazid
Marplan®
monoamine oxidase inhibitor (MAOI)
antidepressant

MOA: block MAO; increase NE and 5HT

avoid foods that contain tyramine (wine, beer, aged cheese) - it can cause massive release of NE and cause a stroke or HTN
tranylcypromise
Parnate®
monoamine oxidase inhibitor (MAOI)
antidepressant

MOA: block MAO; increase NE and 5HT

avoid foods that contain tyramine (wine, beer, aged cheese) - it can cause massive release of NE and cause a stroke or HTN
fluoxetine
Prozac®
selective serotonin reuptake inhibitor (SSRI)
antidepressant

MOA: block reuptake of 5HT; increase 5HT in the brain
sertaline
Zoloft®
selective serotonin reuptake inhibitor (SSRI)
antidepressant

MOA: block reuptake of 5HT; increase 5HT in the brain
escitalopram
Lexapro®
selective serotonin reuptake inhibitor (SSRI)
antidepressant

MOA: block reuptake of 5HT; increase 5HT in the brain
venlafaxine
Effexor®
miscellaneous antidepressant

MOA: SSRI (blocks reuptake of 5HT; increase 5HT in the brain)
duloxetine
Cymbalta®
miscellaneous antidepressant

MOA: affect 5HT, NE, DA
mirtazapine
Remeron®
miscellaneous antidepressant

MOA: affect 5HT, NE, DA
lithium carbonate
Lithium®
antimanic/bipolar

MOA: salt; decrease excitability of nerve tissues; decrease release of NE and DA at nerve ending; increase reuptake of NE and DA (less free NT to produce effects)

SE: tremors, NVD, tinnitus, low BP, loss of equilibrium, nephritis, arrhythmias
chlorpromazine
Thorazine®
typical antipsychotic

MOA: block DA receptor; prevent DA from binding to receptor

SE: sedation; anticholinergic effects (dry mouth, constipation, visual disturbances); neurological effects (dystonic reactions, akathisia, parkinsonism, tardive dyskinesia)
haloperidol
Haldol®
typical antipsychotic

MOA: block DA receptor; prevent DA from binding to receptor

SE: sedation; anticholinergic effects (dry mouth, constipation, visual disturbances); neurological effects (dystonic reactions, akathisia, parkinsonism, tardive dyskinesia)
olanzapine
Zyprexa®
atypical antipsychotic

MOA: DA agonist; 5HT antagonist

no extraparameter side effects

works on + and - symptoms
levodopa + carbidopa
Sinemet®
dopaminergic
antiparkinson

MOA: increase effects of DA; DA agonist
diphenhydramine
Benadryl®
antihistamine
antiparkinson

MOA: anticholinergic effects against ACh; antiparkinson action (increase DA and decrease ACh)
benztropine
Cogentin®
anticholinergic
antiparkinson

MOA: block ACh, decrease cholinergic activity (reduces tremors, muscle rigidity)
amantadine
Symmetrel®
antiviral
antiparkinson

MOA: increase activity of DA in basal ganglia
selegeline
Eldepryl®
DA conserver/MAO-B inhibitor
antiparkinson

MOA: inhibit metabolism of DA in brain
alprazolam
Xanax®
short-acting benzodiazepine
antianxiety; sedative/hypnotic

MOA: increase inhibitory action of GABA; decrease excitability of specific areas of the brain and spinal cord (decrease activities of the reticular formation, limbic system, cerebral cortex/medulla, spinal cord)

SE: drowsiness, dizziness, physical/psychological dependence, memory loss (long-term use)
*less side effects are produced, does not interfere with REM sleep (mental restoration)
lorazepam
Ativan®
short-acting benzodiazepine
antianxiety; antiepileptic

MOA for anxiety: increase inhibitory action of GABA; decrease excitability of specific areas of the brain and spinal cord (decrease activities of the reticular formation, limbic system, cerebral cortex/medulla, spinal cord)
MOA for epilepsy: prevent occurrence of seizures by decreasing the excitability of brain cells

SE: drowsiness, dizziness, physical/psychological dependence, memory loss (long-term use)
midazolam
Versed®
short-acting benzodiazepine
antianxiety; sedative/hyponotic

MOA: increase inhibitory action of GABA; decrease excitability of specific areas of the brain and spinal cord (decrease activities of the reticular formation, limbic system, cerebral cortex/medulla, spinal cord)

SE: drowsiness, dizziness, physical/psychological dependence, memory loss (long-term use)
*less side effects produced, does not interfere with REM sleep (mental restoration)
chlordiazepoxide
Librium®
long-acting benzodiazepine
antianxiety

MOA: increase inhibitory action of GABA; decrease excitability of specific areas of the brain and spinal cord (decrease activities of the reticular formation, limbic system, cerebral cortex/medulla, spinal cord)

SE: drowsiness, dizziness, physical/psychological dependence, memory loss (long-term use)
clonazepam
Klonopin®
long-acting benzodiazepine
antianxiety

MOA: increase inhibitory action of GABA; decrease excitability of specific areas of the brain and spinal cord (decrease activities of the reticular formation, limbic system, cerebral cortex/medulla, spinal cord)

SE: drowsiness, dizziness, physical/psychological dependence, memory loss (long-term use)
diazepam
Valium®
long-acting benzodiazepine
antianxiety; antiepileptic
drug of choice for grand mal/tonic-clonic seizures

MOA for anxiety: increase inhibitory action of GABA; decrease excitability of specific areas of the brain and spinal cord (decrease activities of the reticular formation, limbic system, cerebral cortex/medulla, spinal cord)
MOA for epilepsy: prevent occurrence of seizures by decreasing the excitability of brain cells

SE: drowsiness, dizziness, physical/psychological dependence, memory loss (long-term use)
buspirone
Buspar®
azapirone - nonbenzodiazepine
antianxiety

MOA: bind to 5HT; reduce levels of 5HT and level of anxiety

Advantages: no abuse potential, no alcohol effect, anticonvulant/skeletal muscle relaxant, no sedation

Disadvantages: slow onset, needs to be taken continuously, full therapeutic effect in 3-4 weeks
meperidine
Demerol®
narcotic/opioid analgesic agonist

MOA: react on opioid receptors; mimic analgesic peptides like endorphins

SE: decreased mental alertness, mood change, GI upset, HA, hypoventilation (CO₂ retention), spasmogenic activity, increase histamine release (bronchoconstriction), orthostatic hypotension, miosis (pupil constriction)
fentanyl
Sublimaze®
narcotic/opioid analgesic agonist

MOA: react on opioid receptors; mimic analgesic peptides like endorphins

SE: decreased mental alertness, mood change, GI upset, HA, hypoventilation (CO₂ retention), spasmogenic activity, increase histamine release (bronchoconstriction), orthostatic hypotension, miosis (pupil constriction)
morphine sulfate
Morphine®, MS Contin®
narcotic/opioid analgesic agonist

MOA: react on opioid receptors; mimic analgesic peptides like endorphins

SE: decreased mental alertness, mood change, GI upset, HA, hypoventilation (CO₂ retention), spasmogenic activity, increase histamine release (bronchoconstriction), orthostatic hypotension, miosis (pupil constriction)
codeine sulfate
Codeine®
narcotic/opioid analgesic agonist

MOA: react on opioid receptors; mimic analgesic peptides like endorphins

SE: decreased mental alertness, mood change, GI upset, HA, hypoventilation (CO₂ retention), spasmogenic activity, increase histamine release (bronchoconstriction), orthostatic hypotension, miosis (pupil constriction)
hydromorphone
Dilaudid®
narcotic/opioid analgesic agonist

MOA: react on opioid receptors; mimic analgesic peptides like endorphins

SE: decreased mental alertness, mood change, GI upset, HA, hypoventilation (CO₂ retention), spasmogenic activity, increase histamine release (bronchoconstriction), orthostatic hypotension, miosis (pupil constriction)
methadone
Dolophine®, Methadose®
narcotic/opioid analgesic agonist

MOA: react on opioid receptors; mimic analgesic peptides like endorphins

SE: decreased mental alertness, mood change, GI upset, HA, hypoventilation (CO₂ retention), spasmogenic activity, increase histamine release (bronchoconstriction), orthostatic hypotension, miosis (pupil constriction)
oxycodone
Oxycontin®
narcotic/opioid analgesic agonist

MOA: react on opioid receptors; mimic analgesic peptides like endorphins

SE: decreased mental alertness, mood change, GI upset, HA, hypoventilation (CO₂ retention), spasmogenic activity, increase histamine release (bronchoconstriction), orthostatic hypotension, miosis (pupil constriction)
naloxone
Narcan®
pure narcotic/opioid antagonist
drug of choice for antagonist

MOA: attach to opioid receptors, no pharmalogical effect on its own
butorphanol
Stadol®
partial narcotic/opioid antagonist

MOA: attach to opioid receptors, may produce mild respiratory depression
nalbuphine
Nubain®
partial narcotic/opioid antagonist

MOA: attach to opioid receptors, may produce mild respiratory depression
aspirin (ASA)
Anacin®, Bufferin®, Bayer®
nonnarcotic/nonopioid analgesic
salicylate

MOA: block prostaglandin stimulation of CNS; vasodilation; increased sweating; loss of heat from body; inhibit synthesis of prostaglandin; inhibit aggregation of platelets
ibuprofen
Motrin®, Advil®
nonnarcotic/nonopioid analgesic
non-steroidal anti-inflammatory drug (NSAID)

MOA: treats inflammatory action by inhibiting the pathway of prostaglandin synthesis

Uses: antipyretic (fever), analgesia (pain)

SE: disrupts stomach lining, makes it more acidic
naproxen
Anaprox®, Naprosyn®
nonnarcotic/nonopioid analgesic
non-steroidal anti-inflammatory drug (NSAID)

MOA: treats inflammatory action by inhibiting the pathway of prostaglandin synthesis

Uses: antipyretic (fever), analgesia (pain)

SE: disrupts stomach lining, makes it more acidic
ketorolac tromethamine
Toradol®
nonnarcotic/nonopioid analgesic
nonsteroid anti-inflammatory drug (NSAID)

MOA: treats inflammatory action by inhibiting the pathway of prostaglandin synthesis

Uses: antipyretic (fever), analgesia (pain)

SE: disrupts stomach lining, makes it more acidic
sulindac
Clinoril®
nonnarcotic/nonopioid analgesic
non-steroidal anti-inflammatory drug (NSAID)

MOA: treats inflammatory action by inhibiting the pathway of prostaglandin synthesis

Uses: antipyretic (fever), analgesia (pain)

SE: disrupts stomach lining, makes it more acidic
celecoxib
Celebrex®
nonnarcotic/nonopioid analgesic
COX-2 selective inhibitor

MOA: treats inflammatory action by inhibiting the pathway of prostaglandin synthesis

Uses: antipyretic (fever), analgesia (pain)

No effect on stomach lining --> no GI upset
acetaminophen (APAP)
Tylenol®
nonnarcotic/nonopioid analgesic
antipyretic/analgesic

MOA: acts on heat regulation center; inhibit prostaglandin synthesis in CNS

SE: hepatotoxicity; do not take with alcohol
acetylcysteine antidote for Tylenol® toxicity
APAP + codeine
Tylenol® with Codeine®
combination analgesic

to get more effect and pain control
hydrocodone + APAP
Vicodin®
combination analgesic

to get more effect and pain control
colchicine
Colcrys®
anti-gout

MOA: alters ability of phagocytes to attack uric acid crystals

SE: NVD
allopurinol
Zyloprim®
anti-gout
prophylactic therapy for long-term hypouricemic

MOA: inhibit enzyme needed to produce uric acid

can be used if patient has renal failure

SE: fever. rash
benzocaine
Solarcaine®
local anesthetic
ester

MOA: decrease Na⁺-influx; interferes with conduction
lidocaine
Xylocaine®
local anesthetic
amine

MOA: decrease Na⁺-influx; interferes with conduction
nitrous oxide general anesthetic

MOA: increase GABA
phenobarbital
Luminal®
barbiturate
antiepileptic; sedative-hypnotic

MOA: increase inhibitory effects of GABA (depress brain cell activity)

SE: sedation, dizziness, rash, NV

treatments should not be abruptly stopped, must gradually reduce doses
phenytoin
Dilantin®
hydantoin
antiepileptic

MOA: decrease Na⁺ levels inside nerve cells, decreasing hyperexcitability

SE: little sedation effects, dizziness, throbocytopenia, anemia, arrhythmias, lupus, visual disturbances, gingival hyperlasia
carbamazepine
Tegretol®
miscellaneous antiepileptic

MOA: block Na⁺ ion channels, decrease amount of Na⁺ inside nerve cells, inhibit rapid firing neurons
ethosuximide
Zarontin®
miscellaneous antiepileptic

MOA: affects ions not entirely understood
secobarbital
Seconal®
barbiturate
sedative-hypnotic

MOA: increase GABA
chloral hydrate
Noctec®
nonbarbiturate
sedative-hypnotic

MOA: increase GABA; pediatric sedation, similar to alcohol
zolpidem
Ambien®
nonbenzodiazepine
sedative-hypnotic

MOA: increase GABA (acts on it)
eszopiclone
Lunesta®
nonbenzodiazepine
sedative-hypnotic

MOA: increase GABA (enhances it)

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