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44 Cards in this Set
- Front
- Back
what are the narcotic agonists?
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MorPHINE, Methadone, & Fentanol are Mu agonists
(Mu agonists="Morphine Met Me Finally") -Kappa agonists=MorPHINE, NalbuPHINE, Butorphanol "Kappas have big BUTTS" (BUTT=BUTorphanol, butt=NALgas in Spanish (NALbuPHINE) |
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what are the Narcotic partial agonists?
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NalbuPHINE
Butorphanol BupreNORPHINE ("B-Blocks Narcotics) |
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PE of narcotic analgesics?
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-sedation
-dose-dep resp depression -cough suppression -truncal ridigity |
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how induce withdrawal in narcotic-dependent person?
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give them a narcotic antagonist
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Sx of Narcotic toxicity
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triad:
1. depressed resp 2. pinpoint pupils 3. coma |
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narcotic antagonists
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naloxone (IV)--works faster
*reverse excessive resp/CNS depression d/t narcotics naltrexone (po)--longer acting |
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actions of Mu opiate receptor:
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*Mu1:
~supraspinal analgesia ~euphoria ~miosis *Mu2 ~spinal analgesia ~resp depression ~physical dependence ~constipation ligands: -morphine -synethetic opioids -endorphins |
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actions of Kappa opiate receptor
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: spinal analgesia, supraspinal analgesia, miosis, sedation
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actions of delta opiate receptor
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spinal analgesia, modulates Mu receptor activity
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where does a narcotic bind?
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wherever there is an opiate receptor
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aspirin: MOA, Tx, SE?
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MOA: *Inhibit prostaglandin synthesis (PG mediate pain) via inhibition of prostaglandin synthetase (COX I & II) at both Central & Peripheral sites
Tx: -low-mod intensity pain -antipyresis (reduce ELEVATED body temp) -decr platelet agg by IRREV inhibiting COX1 S/E: -gastric irritation -ppl w/renal dz ight get interstitial nephritis -hypersensitivity==>nasal polyps, bronchospasm, hypotension -Severe ASA toxicity: marked hyperventilation from incr CO2 & direct stim of medullary resp center -->paradoxical ↑temp |
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proprionic acid: Tx, SE?
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=Ibuprofen
Tx: -low-mod intensity pain -antipyresis (reduce ELEVATED body temp) S/E: nasal polyps |
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non-narcotic analgesic to Tx high intensity pain?
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ketorolac
(but lots S/E) |
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ketorolac: Tx and SE?
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Tx: high-intensity pain
S/E: lots of S/e!! -bronchospasm -gastric ulcers -inhibit platelet agg |
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acetaminophen: MOA, TX, SE?
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MOA: Inhibit PG synthesis via weak inhibition of COX I & II at central sites
Tx: *Low to moderate intensity pain *Antipyresis (reduction of ELEVATED body temp) *NOT AN Anti-inflammatory: high [peroxides] found at inflammatory site inactivates acetaminophen SE: *Renal Tubular Necrosis: long term abuse of acetaminophen & aspirin combos |
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COX1?
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-Constitutive & expressed in most tissues
-Regulates kidney fxn (PG influences Na/H2O balance) -Provides gastric cytoprotection (gastric acid production & release |
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COX2?
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*COX II:
-Inducible: activated by cellular mediators that are released due to tissue damage -Responsible, in part, for inflamm response |
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Tx Park?
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-levodopa
-levodopa+carbidopa -benztropine -bromocriptine -pramipexole -pergolide -selegiline -entacapone -amantadine |
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Tx drug-induced Park in pts on antipsychotics?
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Benztropine
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Benztropine: MOA, PE, Tx?
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MOA: Ach antagonist
PE: balance Ach/DA systems by reducing Ach dominance Tx: *Mild to mod Park *In combo w/ levodopa/carbodopa severe Park *Drug induced Park in pts on antipsychotics *Most beneficial effect on tremor & rigidity, little or no effect on bradykinesia |
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what Park Rx gives u insomnia and hallucinations?
-how Tx it? |
-Levodopa
-use clozapine to elim insomnia and hallucinations |
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precursor of DA?
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-levodopa
-levo+carbi |
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levodopa+carbidopa-PE, Tx?
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PE: *Carbidopa is a peripheral DOPA decarboxylase inhibitor that does not cross BBB & will block peripheral conversion (outside CNS) of L to DA (thus more L goes to CNS, so ↑ effect)
Tx: *Benefits of C: -Dose of L can be greatly effective does reached quickly -N/V are elim -cardiac S/E -Vit B6 antagonization of Levodopa avoided (vit-B6 co-enzyme for decarboxylase) Note: *No obvious pharm effects in pts w other neurological d/o or in normal individuals |
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what are the DA receptor agonists?
-PE? |
-bromocriptine
-pramipexole -pergolide PE: *Stimulates DA receptors directly: use if Nigralstriatal neurons are gone |
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Tx Neuroleptic Malignant Syndrome
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bromocriptine + dantrolene
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selegiline: MOA, PE?
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MOA:
*MAOI-type B (thus blocks breadown of DA in CNS) PE: incr DA levels, neuroprotective |
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what do you use if Nigralstriatal neurons are gone?
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-bromocriptine
-pramipexole -pergolide PE: *Stimulates DA receptors directly |
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entacapone: MOA, PE?
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Tx: Park
MOA: *Catechol-O-methyltransferase Inhibitor (COMI) mneum: "COMI" sounds like "Capone"-- "COMI CAPONE" PE: *Elev DA levels *neuroprotective |
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Amantadine: MOA, PE?
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Tx: mild Park
MOA: antiviral PE: may stim DA release |
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Tx Tourettes
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haloperidol (DA antagonist)
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haloperidol: MOA, Tx?
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MOA: DA antagonist
Tx: Tourettes |
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DOC for generalized tonic clonic seizures (Grand Mal)
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phenytoin
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NMJ blocking Agents (NMBA);
where do they work? |
1. Botulinum toxin (pre-synaptic at NMJ)
2. Cisatracurium (post-syn at NMJ) 3. Succinylcholine (post-syn at NMJ) |
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botulinum toxin
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*pre-syn at NMJ
MOA: *Cleaves presynaptic proteins which are involved in exocytosis of synaptic vesicles containing ACh *Blocks vesicular release of ACh Tx: *Reduce muscle contractures & decr myofascial pn |
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Vecuronium
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*SkM relaxant
*post-syn at NMJ (like succinylcholine) MOA: *competitive full antagonist of ACh to postjunctional receptor (antagonist=affinity for receptor but no instrinsic activity; muscle will still respond to direct electrical stim) *Blockade can be overcome by incr ACh in synapse *incr acetylcholinesterase inhibitors reverse the block *May also block prejunc Na channels PE: *Duration of effect reflects diffusion from active site followed by hepatic metabolism and renal clearance *Adjuvant in surgical anesthesia to reflex movement and to relax skeletal muscle to gain access to surgical sites *Drug Interactions: -Inhalational anesthetic agents augment NM blockade in dose dependent fashion -Antibiotics esp aminoglycosides can augment blockade -Cholinesterase inhibitors antagonize blockade |
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use for brief surgical procedures?
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succinylcholine
(SkM relaxant) |
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cisatracurium
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*SkM relaxant
*Cisatracurium is metabolized by Hofmann elimination (base-catalyzed hydrolysis) *post-syn at NMJ MOA: *competitive full antagonist of ACh to postjunctional receptor (antagonist=affinity for receptor but no instrinsic activity; muscle will still respond to direct electrical stim) *Blockade can be overcome by incr ACh in synapse *incr acetylcholinesterase inhibitors reverse the block *May also block prejunc Na channels PE: *Duration of effect reflects diffusion from active site followed by hepatic metabolism and renal clearance *Adjuvant in surgical anesthesia to reflex movement and to relax skeletal muscle to gain access to surgical sites *Drug Interactions: -Inhalational anesthetic agents augment NM blockade in dose dependent fashion -Antibiotics esp aminoglycosides can augment blockade -Cholinesterase inhibitors antagonize blockade |
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succinylcholine
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MOA:
*Depolarizing (Non-Competitive) Blocking Agent *Not degraded by esterases as quickly as ACh so it stays on receptor & neuron remains depol: -Phase 1 (Depolarize) = initial blockade w/ depol & is potentiated by acetylcholinesterase inhibition *noncompetitive -Phase 2 (Densensitize): continued occupation of receptor produces desensitization & membrane repol ==>as long as S occupies receptor, membrane can’t be depol again by ACh ==>charac of competitive blockade ==>can be reversed by acetylcholinesterase inhibitors (thus, competitive) PE: *Rapidly hydrolyzed by plasma cholinesterases such that only a small amt reaches the NMJ *Diffusion-->brief duration of action SE: -cardiac dysrhythmias - incr intraocular pressure -myoglobinuria -MG pts are resistent to effects (b/c MG pts have defective post-jxn receptors, so S can’t bind well to it) *pts w/ burn injuries or trauma (esp CNS) respond w/ marked hyperkalemia to S (due to inc in receptors over injured site) -Any agent that lowers serum K should be used w/ caution since dosage requirements for Succinylcholine may increase (Jeff: with Succinylcholine, need enough K in the cytoplasm because of the Na-K pump; in order for Na to rush into the cell (during action potential), lots of K must rush out of the cell (causing hyperkalemia); if not enough K in cytoplasm, less Na can rush into the cell; thus need more S) |
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Diazepam, site of action, etc?
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=Valium
*site of action=Spinal Interneurons (polysynaptic reflexes) MOA: incr GABA mediated inhibitory synaptic transmission PE: *Depress activity of spinal & supraspinal interneurons in motor reflex pathways Tx: decr Motor reflexes (spasticity) resulting from sprains, arthritis, myositis, & fibrositis |
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Tx: *Flexor spasms & sk muscle rigidity assoc w/ MS & spinal cord injury
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Baclofen?
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Baclofen
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SkM relaxant
*site of action=Spinal Interneurons (polysynaptic reflexes) MOA: incr GABA mediated inhibitory synaptic transmission PE: *Depress activity of spinal & supraspinal interneurons in motor reflex pathways Tx: *Flexor spasms & sk muscle rigidity assoc w/ MS & spinal cord injury SE: -mental confusion *Sudden withdrawal of therapy can lead to auditory & visual hallucinations |
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Dantrolene--site of action, etc?
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site of action=SkM contractile process (b/c that's where the SR is)
MOA: *Direct effect on excitation-contraction coupling mech of sk muscle *decr Ca release from SR ==>permits relaxation of hypertonic sk muscle Tx: *Prophylaxis for anesthetic induced malignant hyperthermia (Neuroleptic Malignant Syndrome) relaxes hypertonic (already contracted) muscle *Spasticity assoc w/ UMN lesion *Sk muscle relaxation in pts w/ Strokes, MS, Postenephalitic athetosis & Dystonia |
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*Prophylaxis for anesthetic induced malignant hyperthermia (Neuroleptic Malignant Syndrome,
how work? |
Dantrolene
relaxes hypertonic (already contracted) muscle |
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Tx: Spasticity assoc w/ UMN lesion
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dantrolene
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