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44 Cards in this Set

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what are the narcotic agonists?
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)
what are the Narcotic partial agonists?
NalbuPHINE
Butorphanol
BupreNORPHINE
("B-Blocks Narcotics)
PE of narcotic analgesics?
-sedation
-dose-dep resp depression
-cough suppression
-truncal ridigity
how induce withdrawal in narcotic-dependent person?
give them a narcotic antagonist
Sx of Narcotic toxicity
triad:
1. depressed resp
2. pinpoint pupils
3. coma
narcotic antagonists
naloxone (IV)--works faster
*reverse excessive resp/CNS depression d/t narcotics
naltrexone (po)--longer acting
actions of Mu opiate receptor:
*Mu1:
~supraspinal analgesia
~euphoria
~miosis

*Mu2
~spinal analgesia
~resp depression
~physical dependence
~constipation

ligands:
-morphine
-synethetic opioids
-endorphins
actions of Kappa opiate receptor
: spinal analgesia, supraspinal analgesia, miosis, sedation
actions of delta opiate receptor
spinal analgesia, modulates Mu receptor activity
where does a narcotic bind?
wherever there is an opiate receptor
aspirin: MOA, Tx, SE?
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
proprionic acid: Tx, SE?
=Ibuprofen

Tx:
-low-mod intensity pain
-antipyresis (reduce ELEVATED body temp)

S/E: nasal polyps
non-narcotic analgesic to Tx high intensity pain?
ketorolac

(but lots S/E)
ketorolac: Tx and SE?
Tx: high-intensity pain
S/E: lots of S/e!!

-bronchospasm
-gastric ulcers
-inhibit platelet agg
acetaminophen: MOA, TX, SE?
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
COX1?
-Constitutive & expressed in most tissues
-Regulates kidney fxn (PG influences Na/H2O balance)
-Provides gastric cytoprotection (gastric acid production & release
COX2?
*COX II:
-Inducible: activated by cellular mediators that are released due to tissue damage
-Responsible, in part, for inflamm response
Tx Park?
-levodopa
-levodopa+carbidopa
-benztropine
-bromocriptine
-pramipexole
-pergolide
-selegiline
-entacapone
-amantadine
Tx drug-induced Park in pts on antipsychotics?
Benztropine
Benztropine: MOA, PE, Tx?
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
what Park Rx gives u insomnia and hallucinations?
-how Tx it?
-Levodopa
-use clozapine to elim insomnia and hallucinations
precursor of DA?
-levodopa
-levo+carbi
levodopa+carbidopa-PE, Tx?
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
what are the DA receptor agonists?
-PE?
-bromocriptine
-pramipexole
-pergolide

PE: *Stimulates DA receptors directly: use if Nigralstriatal neurons are gone
Tx Neuroleptic Malignant Syndrome
bromocriptine + dantrolene
selegiline: MOA, PE?
MOA:
*MAOI-type B (thus blocks breadown of DA in CNS)

PE:
incr DA levels,
neuroprotective
what do you use if Nigralstriatal neurons are gone?
-bromocriptine
-pramipexole
-pergolide

PE: *Stimulates DA receptors directly
entacapone: MOA, PE?
Tx: Park

MOA: *Catechol-O-methyltransferase Inhibitor (COMI)

mneum: "COMI" sounds like "Capone"-- "COMI CAPONE"

PE: *Elev DA levels
*neuroprotective
Amantadine: MOA, PE?
Tx: mild Park

MOA: antiviral

PE: may stim DA release
Tx Tourettes
haloperidol (DA antagonist)
haloperidol: MOA, Tx?
MOA: DA antagonist
Tx: Tourettes
DOC for generalized tonic clonic seizures (Grand Mal)
phenytoin
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)
botulinum toxin
*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
Vecuronium
*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
use for brief surgical procedures?
succinylcholine
(SkM relaxant)
cisatracurium
*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
succinylcholine
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)
Diazepam, site of action, etc?
=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
Tx: *Flexor spasms & sk muscle rigidity assoc w/ MS & spinal cord injury
Baclofen?
Baclofen
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
Dantrolene--site of action, etc?
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
*Prophylaxis for anesthetic induced malignant hyperthermia (Neuroleptic Malignant Syndrome,
how work?
Dantrolene

relaxes hypertonic (already contracted) muscle
Tx: Spasticity assoc w/ UMN lesion
dantrolene