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Block IV drugs

PCL and lecture drugs

QuestionAnswer
nafcillin class penicillin-derived antibiotic
nafcillin MOA inhibits 3rd and final stage of bacterial cell wall synthesis- they prevent the cross linkining of bacterial cell wall by binding to penicillin binding proteins (PBPs) causing bacterial cell lysis and death
ampicillin class penicillin-derived antibiotic
ampicillin MOA inhibits 3rd and final stage of bacterial cell wall synthesis- they prevent the cross linkining of bacterial cell wall by binding to penicillin binding proteins (PBPs) causing bacterial cell lysis and death
ceftriaxone sodium class cephalosporin
ceftriaxone sodium MOA inhibits 3rd and final stage of bacterial cell wall synthesis- they prevent the cross linkining of bacterial cell wall by binding to penicillin binding proteins (PBPs) causing bacterial cell lysis and death
gentamicin class aminoglycoside
gentamicin MOA interferes with bacterial protein synthesis by binding to 30S ribosomal subunit
edrophonium chloride class short acting cholinesterase inhibitor
edrophonium chloride MOA competes with ACh for it's binding site on AChE, interfering with ACh enzymatic destruction, potentiating the action of ACh on it's receptors
pyridostigmine class intermediate acting cholinesterase inhibitor
pyridostigmine MOA competes with ACh for it's binding site on AChE, interfering with ACh enzymatic destruction, potentiating the action of ACh on it's receptors
azathioprine class immunosuppressive
azathioprine MOA suppresses hypersensitivities of the cell-mediated type and causes variable alterations in Ab production
prednisone, methylprednisone corticosteriods
prednisone, methylprednisone MOA binds to the cytoplasmic cortisol receptor; the hormone-receptor complex enters the nucleus and acts as a TF to alter gene transciption; also inhibits phospholipase A2 to have anti-inflammatory effects
mycophenolate mofetil class immunosuppressive
mycophenolate mofetil MOA inhibitor of inosine monophosphate dehydrogenase (IMPDH), which inhibits the de novo synthesis of guanosine nucleotides; has cytostatic effects on lymphocytes
carbamzepine class neurologic agent and TCA
carbamzepine MOA inhibit serotonin and NE uptake, modulate Na+ and K+ channels, block NDMA (glutamate R) and adenosine receptors, and inhibit TNF-alpha
amitriptyline class TCA
amitripyline MOA potentiates the actions of NE and serotonin by blocking their uptake by transporter on the presynaptic membrane; stimulates 5-HT descending pathways
propoxyphene class opiod analgesic
propoxyphene MOA weak opioid agonist, binding primarily to mu opiod receptors, producing analgesia and other CNS effects
buspirone class anxiolytic
buspirone MOA partial 5-HT1A receptor agonist
alprazolam class anxiolytic, sedative, hypnotic
alprazolam MOA facilitates GABA-mediated inhibition of neuronal activity in the CNS
sertraline class SSRI antidepressant
sertraline MOA inhibition of serotonin uptake at the neuronal membrane
gabapentin class anticonvulsant- neurologic agent
gabapentin MOA GABA analog; interacts with cortical neurons at auxillary subunits of voltage-gated Ca++ channels
tramadol class analgesic
tramadol MOA central opiate receptor agonist; inhibits NE and serotonin reuptake in the CNS
duloxetine class antidepressant
duloxetine MOA inhibits the reuptake of NE and serotonin
pregabalin class Ca++ channel blocker; analgesic, neurologic agent
pregabalin MOA GABA analog; binds to the alpha-2-delta subunit of voltage-gated Ca++ channels in the CNS to reduce neuronal Ca++ currents to reduce pain
metoclopramide class prokinetic agent, antiemetic
metoclopramide MOA 5-HT4 agonist; D2 antagonist
tegaserod maleate class prokinetic agent
tegaserod maleate MOA selective 5-HT4 partial agonist
Beta-1a interferon class biologic response agent, neurologic agent
Beta-1a interferon MOA increases the levels of 2,5-oligo-adenylate synthetase, which degrades viral RNA
Baclofen class skeletal muscle relaxant
baclofen MOA GABA-B agonist: depresses output from the spinal cord
mitoxantrone class anti-neoplastic agent
mitoxantrone MOA inhibits DNA and RNA synthesis and topoisomerase II to have cytocidal effects
rituximab class anti-neoplastic agent, biologic response modifier
rituximab MOA monoclonal Ab that binds to the CD20; causes cell lysis and inhibits Ab release
fluconazole class antifungal
fluconazole MOA inhibits fungal cytochrome P-450 C-14 alpha demethylation, resulting in disruption of packing of acyl chains of phospholipids and inhibiting fungal growth
acyclovir class antiviral
acyclovir MOA as acyclovir triphosphate, it stops replication of viral DNA in 3 ways
doxycycline class tetracycline antibiotic
doxycycline MOA binds to the 30S ribosomal subunit, preventing protein translation
carbidopa-levodopa class antiparkinsonian agent
carbidopa-levodopa MOA Levodopa: converted to dopamine; C: inhibits DOPA decarboxylase in periphery
pramipexole class antiparkinsonian agent; dopaminergic
pramipexole MOA dopamine receptor agonist
enalapril maleate class ACE inhibitor
enalapril maleate MOA by inhibition of angiotensin converting enzyme, it stops the conversion of angiotensin I to angiotensin II, decreasing vasopressor activity and aldosterone secretion
selegiline class antiparkinsonian agent, MAOI
selegiline MOA Antagonist of MAO-B, the main MAO in the brain, which metabolizes dopamine. It may also block presynaptic dopamine uptake and decreases free radical production
prazosin class sympatholytic and antihypertensive agent
prazosin MOA Selective alpha-1 antagonist
ASA class analgesic, platelet inhibitor, anti-inflammatory agent
ASA MOA irreversibly inhibits COX via acetylation of ser residues and the production of thromboxanes and prostaglandins
ibuprofen, sulindac, ketolorac class NSAID
ibuprofen (reversible), sulindac (pro-drug), ketolorac MOA NSAIDs: competitively inhibit both COX-1 and COX-2, decreasing PG synthesis. Is anti-inflam, anti-platelet, and anti-pyretic. Actions primarily peripheral- CNS involvement only in overdose (tinnitus, MA, thirst).
celecoxib, rofecoxib, valdecoxib class NSAID
celcoxib, rofecoxib, valdecoxib MOA more selectively inhibits COX-2 to have anti-inflammatory, analgesic, and anti-pyretic effects
acetaminophen class non-opioid analgesic
acetaminophen MOA Works in the CNS to increase pain threshold and reduce fever Does NOT inhibit COX and is NOT anti-inflammatory
morphine, hydromorphine, meperidine, fentanyl, methadone, codeine, hydrocodone, propoxyphene MOA full opiate agonists; cause hyperpolarization, inhibition of cell firing, presynaptic inhibition of NT release, and may cause excitation by dysinhibition. Inhibit adenylate cyclase, decreasing cAMP and also activate MAPKs and PLC
pentazocine, nalbuphine, butorphanol MOA mixed opiate agonists/antagonists; block delta, kappa, and mu receptors, but still have some analgesic effects following opiate MOA
naloxone, naltrexone MOA opioid receptor antagonists; bind to and block the actions of opiates at mu and delta opioid receptors
dextromethorphan, levopropoxyphene MOA centrally active antitussive agents. Dextromorphan can block NDMA receptors and reverse tolerance to opioids.
phenylephrine class selective alpha 1 receptor agonist
prazosin, terazosin, doxazosin, tamsulosin class selective alpha 1 antagonist
clonidine, dexmedetomidine class alpha-2 receptor agonist
yohimbine, atipamezole class selective alpha 2 antagonist
dobutamine class B-1 receptor agonist
metoprolol, atenolol class B-1 receptor antagonist
terbutaline, albuterol class B-2 agonist
direct acting sympathomimetics action act on adrenergic receptors
indirect-acting sympathomimetic actions enhance catecholamine levels at the receptor
amphetamine class indirect acting sympathomimetic
amphetamine MOA enhances catecholamine levels at receptors; releases NE in the absence of an AP by entering the nerve terminal via uptake 1
ephendrine class direct acting sympathomimetic
ephendrine MOA synthetic analog of Epi and NE, directly activating the receptors of these catecholamines
bromocreptine MOA postsynaptic dopamine receptor agonist; used after activity of DOPA decarboxylase is reduced
amantadine MOA inhibits the penetration of A2 influenza virus into cells. In PD, may inhibit the uptake of dopamine intor synaptosomes and may cause dopamine release because it has an indirect amphetamine-like effect
trihexyphenidyl, benztropine MOA anticholinergic: inhibit cholinergic receptors to decrease cholinergic hyperactivity
ropinirole MOA non-ergoline dopamine receptor agonist
cabergoline MOA ergoline structure D-2 receptor agonist
tolcapone, entacapone MOA COMT inhibitors; inhibit COMT synthesis of 3-O-methyl-dopa, prolonging the plasma half life of L-dopa
clopidogrel class platelet inhibitor
clopidogrel MOA selectively and irreversibly inhibits ADP induced platelet aggregation and subsequently prevents the binding of fibrinogen to platelets, preventing platelet aggregation
atorvastatin class HMG-CoA reductase inhibitor
atorvastatin MOA selective and competitive inhibitor of the rate-limiting enzyme in the cholesterol synthesis pathway
phenytoin sodium class anti-convulsant
phenytoin sodium MOA limits the spread of seizure activity and seizure propagation by slowing rate of recovery of Na+ channels from inactivation, thereby decreasing neuron excitability
aspirin MOA salicylate; COX inhibitor
carbamazapine class anti-convulsant
carbamazapine MOA blocks voltage-gated Na+ channels, inhibiting sustained repetitive firing
doxazosin class alpha blocker; sympatholytic
doxazosin MOA Competitively inhibits alpha-1 adrenergic receptors in the sympathetic nervous system leading to peripheral vasodilation, decreased peripheral vascular resistance, and lowered blood pressure
Rivastigmine class cholinesterase inhibitor
Rivastigmine MOA Selective inhibitor of brain ACh-esterase. Preferential inhibition of G-1 isoforms of ACh-esterase (higher concentrations in the hippocampus and cortex). "Pseudo-irreversible" actions due to its long binding time and short dissociation from ACh-esterase
endogenous opioids pro-opiomelanocortin (POMC), enkephalins, dynorphans
Created by: jmullally
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