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MDA Drugs
| Drug | Indication | Mechanism |
|---|---|---|
| Desflurane | General Anesthetic | Halogenated volatile (inhaled) Agent |
| Nitrous Oxide | General Anesthetic | Non-Halogenated volatile (inhaled) agent |
| Propofol | General Anesthetic | Binds alcohol site on GABA-A (enhance inhibitory effect of GABA) |
| Thiopental | General Anesthetic | Binds barbiturate site on GABA-A (enhance inhibitory effect of GABA) |
| Midazolam | General Anesthetic | Binds benzodiazepine site on GABA-A (enhance inhibitory effect of GABA) |
| Ketamine | General Anesthetic | Binds the PCP site on Glutamate (inhibits excitatory effect) |
| Lidocaine | Local Anesthetic | Block voltage-gated NA+ channels ------blocks pain signals from unmyelinated C fibers & myelinated Aδ fibers |
| Triazolam | Sedative-hypnotic | Non-selective GABA-A receptor potentiator acting through BDZ binding site (binds to α1 & α2) |
| Zaleplon | Sedative-hypnotic | Selective GABA-A receptor potentiators having action at BDZ site α1 protein subunit (BZ1 or ω receptor)-------lack antianxiety action, have low tolerance, withdrawal properties) |
| Secobarbital | Sedative-hypnotic | Potentiate GABA-A receptors by binding barbiturate site (no co-agonist needed) |
| Chloral Hydrate | Sedative-hypnotic | Agents potentiate GABA-A receptors by binding alcohol site |
| Hydroxyzine | Sedative-hypnotic | Block histamine-1 (H-1) receptors in CNS------often used for motion sickness |
| Ramelteon | Sedative-hypnotic | Agonist MT1 and MT2 receptors in suprachiasmic nucleus (SCN)-------no CNS depression, SCN controls normal sleep-wake cycle |
| Diazepam | Anti-anxiety | Non-selective GABA-A receptor potentiator acting through BDZ binding site |
| Oxcarbazepine | Anti-convulsant | Inhibit voltage-gated sodium channels (bind in inactivated channel state & inhibit reactivation)------reduces sustained high-frequency firing of action potentials, which occurs during seizures |
| Clonazepam | Anti-convulsant | Binds Benzodiazepine site on GABA-A (enhance inhibitory effect of GABA) - direct GABA-A stimulant |
| Phenobarbital | Anti-convulsant | Binds barbiturate site on GABA-A (enhance inhibitory effect of GABA) - direct GABA-A stimulation |
| Tigabine | Anti-convulsant | Indirectly stimulates GABA-A receptors (reduce metabolism of GABA) - increase GABA present |
| Vigabatrin | Anti-convulsant | Indirectly stimulates GABA-A receptors (reduce metabolism of GABA) - increase GABA present |
| Gabapentin | Anti-convulsant | Inhibit voltage-gated calcium channel (bind to α2δ-1 protein subunit, target T-type & P/Q-type------inhibit Ca+ influx into cells |
| Ethosuximide | Anti-convulsant | Block T-type Ca2+ channels located in thalamic neurons (associated with absence seizures) |
| Levetiracetam | Anti-convulsant | Blocks N-type Ca++ channels, site of action is synaptic vesicle protein SV2A & inhibits NT release |
| Despiramine | Antidepressant | Selective NE reuptake inhibitor (NRI) -- inhibits NET |
| Paroxetine | Antidepressant | Selective serotonin reuptake inhibitor (SSRI) -- inhibits SERT |
| Venlafaxine | Antidepressant | Nonselective amine reuptake inhibitor (SNRI) -- block NET & SERT, block reuptake of serotonin & NE |
| Tranylcypromine | Antidepressant | Monoamine Oxidase Inhibitor (MAOI) ------MAO breaks down NE, E, DA, Seretonin |
| Mirtazapine | Antidepressant | α2 adrenergic antagonists-----initial inhibits autoreceptors, so don't need to wait for down regulation --> faster onset |
| Buspirone | Antidepressant | 5-HT1A/D receptor agonist, direct seretonin agonist------stimulates & in long term down regulates autoreceptors |
| Bupropion | Antidepressant | DA reuptake inhibitors -------act like autoreceptors --> decrease NT synthesis and release, followed by desensitization & increase in NT --> remodeling |
| Trazadone | Antidepressant | 5-HT2/1C antagonist (post synaptic receptor), not understood------down-regulation of receptor |
| Levodopa | Parkinson's Disease | Restoration of DA in DA neurons |
| Carbidopa | Parkinson's Disease | DOPA Decarboxylase (AAD) inhibitors-------blocks L-DOPA going to Dopamine in periphery (does not cross BBB) |
| Entacopone | Parkinson's Disease | COMT inhibitor------Blocks L-DOPA going to 3-O-MD in periphery (does not cross BBB) |
| Ropinirole | Parkinson's Disease | Direct acting DA agonist |
| Rasagiline | Parkinson's Disease | MAO-B inhibitors ------MAO-B found in substantia nigra in mitochondria |
| Trihexyphenidyl | Parkinson's Disease | Block muscarinic receptors (M2) in basal ganglia in striatum ------blocks ACh, has CNS activity |
| Amantadine | Parkinson's Disease | Noncompetitive inhibitor of glutamate NMDA receptors (PCP site)-------only weak inhibitors tolerated, lessen & prevents dyskinesias |
| Istradefylline | Parkinson's Disease | Blockade of Adenosine-2A receptors------Side effects outweigh effectiveness |
| CoQ10 | Parkinson's Disease | Antioxidant & mitochondrial enhancer, block free radicals causing lipid peroxidation & cell damage------helps slow progression of PD |
| Creatinine | Parkinson's Disease | Increases Mitochondrial function (PD Prevention) |
| Haloperidol | Antipsychotic | Strong inhibition (high affinity) of D2 receptors (typical antipsychotics)-----Cause EPS (extrapyramidal symptoms, Parkinson's-like), treat positive symptoms (hallucinations/delusions) |
| Clozapine | Antipsychotic | Mild inhibition (low affinity) of D2 receptors (atypical antipsychotics)------Do not cause EPS effects, also treat negative effects (social withdrawal, apathy) & positive effects (hallucinations/delusions) |
| Thioridazine | Antipsychotic | Strong inhibition of D2 receptors + high antimuscarinic activity------have low EPS effects, have other problems |
| Lithium | Bipolar Disorder | Inhibit dephosphorylation of inosine-phosphate to inosine------decreasing synthesis of PIP2 --> decrease in DAG & IP3, blocks NT release |
| Methylphenidate | CNS Stimulant | Indirect acting DA/NE agonist act on CNS (block reuptake or cause release [or both] of DA &/or NE)------treat ADHD, narcolepsy, |
| Sibutramine | CNS Stimulant | Indirect acting 5-HT agonist acting in CNS (blocks 5-HT reuptake,blocks seretonin reuptake)------used more for appetite suppression, also some action at inhibiting reuptake of NE & DA |
| Atomoxetine | CNS Stimulant | Selective NE reuptake inhibitor(NRI)----Approved for ADHD, less abusive effects |
| Modafinil | CNS Stimulant | Agonist at hypocretin/orexin receptors (decrease DA reuptake --> increase serotonin)------used for narcolepsy, weak effect, mechanism unsure, good for wakefulness |
| Rimonabant | CNS Stimulant | Inhibitor of CB1 receptor (inhibits type-1 cannabinoid receptors------used for weight loss |
| Orlistate | CNS Stimulant | Inhibits gastric & pancreatic lipase ------used for weight loss, reduces dietary fat absorption, not absorbed and has no systemic effects |
| Caffeine | CNS Stimulant | Inhibitor of purine (P1) adenosine (A1 & A2) receptor --> increase nerve firing-------action of adenosine is inhibitory to nerve firing causing general CNS depression, A2 receptors more important |
| Morphine | Opiod Analgesic | Mu opiod receptor agonist in CNS and Spinal Cord |
| Tramadol | Opiod Analgesic | Mu opiod receptor agonist plus serotonin reuptake inhibitor------Synergistic effect |
| Tapentadol | Opiod Analgesic | Mu opiod receptor agonist plus NE reuptake inhibitor------Synergistic effect, low addiction |
| Buprenorphine | Opiod Analgesic | Partial mu opiod receptor agonist -------may also be useful in treating or preventing drug abuse, has long duration of action, has higher affinity & lower efficacy |
| Butorphanol | Opiod Analgesic | Kappa receptor agonist & mu receptor antagonist or weak partial agonist---------non-addicting analgesic, due to mu antagonism - can lead to immediate withdrawal symptoms if substitute for mu agonist |
| Loperamide | Opiod Analgesic | Mu agonist acting preferentially on gut------anti-diarrheal agents, not addicting because not cross BBB, very lipophilic (can't be IV) |
| Codeine | Opiod Analgesic | Agents that suppress cough reflex--------probably not true opiod effect since non-analgesic (+) isomer of morphine |
| Naloxone | Opiod Analgesic | (Pure) antagonist to opiod receptor-------treat opiod overdose & may be used to treat or prevent drug addiction |
| Alvimopan | Opiod Analgesic | selective inhibition of peripheral mu opiod receptor ------useful for antagonist to opiod induced constipation, selective localized antagonism |
| Capsaicin | Opiod Analgesic | Releases Substance P from neuronal stores & desensitize nociceptive nerve terminal receptors-------hot substance in peppers, can deplete store of Substance P (tolerance) |
| Sumatriptan | Migraines | Selective 5-HT1B/1D agonist---------1B is more pre-synaptic, 1D is more post-synaptic |
| Ergotamine | Migraines | Non-selective 5-HT1 agonist--------not orally effective, must be injected, has lots of side effects |
| Botulinum Toxin | Migraines | Block activation of cholinergic neurons-------stop propagation of migraine, can also be used as antispasmolytic for local effects at blocking ACh release & muscle spasms |
| Valproate | Migraines | Stop initiation of "migraine generator" by slowing general CNS excitability; prophylaxis |
| Dantrolene | Antispasmotics | Binds to ryanodine receptor (RYR-1) on sarcoplasmic reticulum & prevent release of Ca++--------Toxic, but effective; prevents excitation-contraction coupling of muscle fibers |
| Diazepam | Antispasmotics | Stimulate inhibitory effect of GABA-A receptors on pre-synaptic excitatory efferent neurons-------agents tend to be highly sedating due to effect on brain |
| Baclofen | Antispasmotics | GABA-B receptor agonist-------inhibits release of excitatory NTs in spinal cord by inhibitory action on neuron depolarization, less sedating |
| Tizanidine | Antispasmotics | Activation of α2-adrenergic receptors on dorsal horn efferent nerves |
| Chlorphenesin | Antispasmotics | Unknown, believed to : work through GABA-A receptors (by modulating enhancing action w/GABA) |
| Chlorzoxazone | Antispasmotics | Activate K+ channel currents (hyperpolarize neurons & inhibit general brain output) |
| Cyclobenzapine | Antispasmotics | Activate neurons in locus coeruleus --> increase release of NE & stimulate of α2-adrenergic receptor-------increase NE in ventral horn of spinal cord |
| Orphenadrine | Antispasmotics | Potent histamine-1 (H-1) receptor blocker & has strong CNS sedating effects--------also reported to be uncompetitive NMDA receptor antagonist |
| Riluzole | Neuroprotective | Inhibit glutamate neurotransmission (protect against excitotoxicity --> activation of NMDA receptors)--------interferes with Ca++ mediated release of glutamate, inhibits opening of AMPA & NMDA glutamate channels, prolongs life for 60 days |
| Memantine | Alzheimer's | Weak (low affinity) non-competitive inhibitor of NMDA glutamate receptor by binding PCP site-------may protect against all neurodegenerative diseases; blocks excessive opening of Ca++ channels, not normal function of NMDA receptor |
| Donepezil | Alzheimer's | Reversible inhibition of CNS acetylcholinesterase-------result in increase in CNS ACh --> mild memory enhancing effect, but doesn't slow progression of disease |
| Tetrabenazine | Huntington's | Depletes stores of all monoamine neurotransmitters--------Huntington's Disease = marked by loss of GABA cells & generally treated w/high doses of DA antagonist |
| Nicotine (Abused) | CNS Stimulant | Stimulates ACh nicotinic receptors-------results in activation of several neuronal nerve tracts, esp. DA neurons in VTA |
| Varenicline | Smoking Cessation | Nicotinic receptor partial agonist of α4β2 subtype |
| Cocaine (abused) | CNS Stimulant | Potent inhibitor of DA reuptake (DAT inhibitor) |
| Amphetamine (abused) | CNS Stimulant | DA reuptake inhibitor |
| γ-hydroxybutyric acid (abused) | CNS Depressant | GABA-B agonist-------AKA GHB, date rape drug, GABA converted by GABA-T to Succinic semialdehyde --> reduced to GHB |
| Heroin (Abused) | CNS Depressant | Mimic endogenous opiod peptides, especially at mu opiod receptors------Opiod, morphine is converted by acetic anhydrous to heroin (prodrug) --> diacetylates to increase lipophilicity & CNS penetration |
| THC (abused) | CNS Depressant | Mimic endogenous cannabinoids at CB1 receptors---------Cannabinoid, is primary active substance in marijuana, used legally in cancer pts, may lead to loss of memory, stimulate appetite |
| Inhalant (abused) | CNS Depressant | Action most related to mechanism of general anesthetics------cause brain and nerve cell toxicity, includes paints, gas, glues, solvents |
| Phencyclidine (PCP) (abused) | Hallucinogen | Strong (high affinity) noncompetive antagonist of NMDA receptors------Psychotomimetic |
| LSD (abused) | Hallucinogen | Agonist effect on 5-HT receptors (exact 5-HT subtype is unknown)-------Psychedelic agent |
| MDMA - ecstasy (abused) | Hallucinogen | Blockade of DA reuptake or DA release & direct or indirect stimulation of 5-HT receptors------Psychedelic agent, lead to euphoric effect, toxic to 5-HT neurons (degeneration) |
Created by:
mopfro
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