mechanism of action Flashcards
Nitrous -
C: INORGANIC INHALATIONAL AGENT
MOA: MEYER-OVERTON THEORY; TARGET PROTEINS ARE THE SITE OF ACTION; ANESTHESIA OCCURS WHEN INHALATION MOLECULES DISSOLVE IN LIPID CELL MEMBRANE
HALOTHANE
C: HALOGENATED ALKALINE DERIVATIVE WITH BROMIDE SUBSTITUTION (SWEET, PUNGENT)
MOA: MEYER OVERTON THEORY, TARGET PROTEINS ARE THE SITE OF ACTION; ANESTHESIA OCCURS WHEN INHALATION MOLECULES DISSOLVE IN LIPID CELL MEMBRANE
ENFLURANE
C: HALOGENATED METHYL ETHYL ETHER (SWEET, ISOMER OF ISOFLURANE)
MOA: MEYER OVERTON THEORY, TARGET PROTEINS AT THE SITE OF ACTION, ANESTHESIA OCCURS WHEN INHALATION MOLECULES DISSOLVE IN LIPID CELL MEMBRANE
ISOFLURANE
C: HALOGENATED METHYL ETHYL ETHER (ISOMER OF ENFLURANE, PUNGENT - IRRITATING TO AIRWAYS)
MOA: MEYER OVERTON THEORY; TARGET PROTEINS AT THE SITE OF ACTION, ANESTHESIA OCCURS WHEN INHALATION MOLECULES DISSOLVE IN LIPID CELL MEMBRANE
DESFLURANE
C: FLUORINATED METHYL ETHYL ETHER (PUNGENT-PEDS DONT LIKE, FAST ON/OFF, TEC 6)
MOA: MEYER OVERTON THEORY, TARGET PROTEINS AT THE SITE OF ACTION, ANESHTESIA OCCURS WHEN INHALATION MOLECULES DISSOLVE IN LIPID CELL MEMBRANES
SEVOFLURANE
C: FLUORINATED METHYL ISOPROPYL ETHER (IDEAL FOR PEDS, SWEET, EXPENSIVE)
MOA: MEYER OVERTON THEORY, TARGET PROTEINS ARE THE SITE OF ACTION, ANESTHESIA OCCURS WHEN INHALATION MOLECULES DISSOLVE IN LIPID CELL MEMBRANES
Procaine
C: ESTER LA
MOA: BLOCKS NA CHANNELS IN NERVE CELL MEMBRANE WHILE IN CLOSED INACTIVE STATE, PREVENTS DEPOLARIZATION AND IMPULSE TRANSMISSION
TETRACANE
C: ESTER LA
MOA: BLOCKS NA CHANNELS IN NERVE CELL MEMBRANE WHILE IN CLOSED INACTIVE STATE, PREVENTS DEPOLARIZATION AND IMPUSE TRANSMISSION
BUPIVICAINE
C: AMIDE LA
MOA: BLOCKS NA CHANNELS IN NERVE CELL MEMBRANE WHILE IN CLOSE INACTIVE STATE, PREVENTS DEPOLARIZATION AND IMPULSE TRANSMISSION
LIDOCAINE:
C: AMIDE LA
MOA: BLOCKS NA CHANNELS IN NERVE CELL MEMBRANE WHILE IN CLOSE INACTIVE STATE AND PREVENTS DEPOLARIZATION AND IMPULSE TRANSMISSION
ETIDOCAINE
C: AMIDE LA
MOA: BLOCKS NA CHANNELS IN NERVE CELL MEMBRANE WHILE IN THE CLOSED INACTIVE STATE, PREVENTS DEPOLARIZATION ADN IMPULSE TRANSMISSION
MEPIVICAINE
C: AMIDE LA
MOA: BLOCKS NA CHANNELS IN NERVE CELL MEMBRANE WHILE IN THE CLOSED INACTIVE STATE, PREVENTS DEPOLARIZATION AND IMPULSE TRANSMISSION
CHLOROPROCAINE
C: ESTER LA
MOA: BLOCKS NA CHANNELS IN NERVE CELL MEMBRANE WHILE IN CLOSED INACTIVE STATE, PREVENTS DEPOLARIZATION AND IMPULSE TRANSMISSION
COCAINE:
C: ESTER LA
MOA: BLOCKS NA CHANNELS IN THE NERVE CELL MEMBRANE WHILE IN TEH CLOSED INACTIVE STATE
Diazepam (Valium) PROTOTYPE
C: BENZODIAZEPINE
MOA: BIND TO GABA RECEPTORS AT GAMMA SITES (A1: SEDATION, A2: ANXIETY); INCREASES THE GABA-A RECEPTORS AFFINITY FOR GABA; NO ANALGESIA
DOSE: 0.2MG/KG IV
MIDAZOLAM (VERSED)
C: BENZOIAZEPINE
MOA: BIND TO GABA RECEPTORS AT GAMMA SITES ( A1: SEDATION, A2: ANXIETY); INCREASES THE GABA-A RECEPTORS AFFINITY FOR GABA, NO ANALGESIA
DOSE: 1-2.5MG IV SEDATION (MAX 5 MG)
PREMED: 0.5MG/KG PO (MAX 20MG PEDS)
LORAZEPAM (ATIVAN)
C: BENZODIAZEPINE
MOA: BIND TO GABA RECEPTORS AT GAMMA SITES (A1: SEDATION, A2: ANXIETY)
INCREASES THE GABA-A AFFINITY FOR GABA, NO ANALGESIA
DOSE: 1-4 MG IV
ATRACURIUM - tracurium
C: NMB- INTERMEDIATE ACTING BISQUATERNARY BENZYLLISOQUINOLINE
MOA: INHIBITS ACH AT POST-JUNCTIONAL NICOTINIC RECEPTORS PREVENTING DEPOLARIZATION OF MUSCLE CELL MEMBRANE AND INHIBIT MUSCULAR CONTRACTION
CISATRACURIUM - NIMBEX
C: NMB: INTERMEDIATE ACTING BENZYLLISOQUINOLINE
MOA: INHIBITS ACH AT POST JUNCTIONAL NICOTINIC CELL MEMBRANE PREVENTING DEPOLARIZATION F MUSCLE CELL MEMBRANE AND INHIBIT MUSCULAR CONTRACTION
ROCURONIUM - ZEMURON
C: NMB - SHORT/INTERMEDIATE ACTING STEROID TYPE
MOA: INHIBITS ACH AT POSTJUNCTIONAL NICOTINIC CELL MEMBRANE PREVENT DEPOLARIZATION OF MUSCLE CELL MEMBRANE AND MUSCLE CONTRACTION
VECURONIUM - NORCURON
C: NMB - INTERMEDIATE ACTING STEROID TYPE
MOA: INHIBITS ACH AT POST JUNCTIONAL NICOTINIC CELL MEMBRANE PREVENTING DEPOLARIZATION OF MUSCLE CELL MEMBRANE AND INHIBIT MUSCULAR CONTRACTION
PANCURONIUM - PAVULON
C: NMB - LONG ACTING STEROID TYPE
MOA: INHIBITS ACH AT POST JUNCTIONAL NICOTINIC CELL MEMBRANE PREVENTING DEPOLARIZATION OF MUSCLE CELL MEMBRANE AND INHIBITS MUSCULAR CONTRACTION
DOXACURIUM - NEUROMAX
C: NMB - LONG ACTING BENZYLISOQUINOLINE
MOA: INHIBITS ACH AT POST JUNCTIONAL NICOTINIC CELL MEMBRANE PREVENTING DEPOLARIZATION OF MUSCLE CELL MEMBRANE AND INHIBITS MUSCULAR CONTRACTION
SUCCS
BINDS TO ALPHA SUBUNITS OF ACH NICOTINIC RECEPTORS AND MIMICS ACH AND DEPOLARIZES POST JUNCTIONAL MEMBRANE, CAUSES FASCIULATIONS FOLLOWED BY FLACCID PARALYSIS, TERMINATES BY DIFFUSION AWAY FROM NMJ
MORPHINE
C: NATURAL ORGANIC OPIOID
MOA: ACTIVATES MU, KAPPA, AND DELTA RECEPTORS ON THE PERIPHERAL ENDS OF THE PRIMARY AFFERENT NEURONS TO DECREASE TRANSMISSION AND INHIBIT RELEASE FROM NEUROTRANSMITTERS
DOSE: 2.5-15 MG IV PRE/POST OP
MEPEREDINE (DEMEROL)
C: PHENYL PIPERDINE SYNTHETIC OPIOID AGONIST (USEFUL IN OB, POST OP PAIN, DECREASES SHIVERING AT A DOSE OF 12.5 MG IV, NO HISTAMINE RELEASE)
MOA: ACTIVATES MU AND KAPPA RECEPTORS ON THE PERIPHERAL ENDS OF THE PRIMARY AFFERENT NEURONS TO DECREASE TRANSMISSION AND INHIBIT RELEASE FROM NEUROTRANSMITTERS
DOSE: 5 MG IV Q5 MIN,
12.5 MG IV: SHIVERING
FENTANYL
C: PHENYL PIPERDINE SYNTHETIC OPIOID AGONIST (BLUNTS DVL)
MOA: ACTIVATES THE MU RECEPTORS OF THE BRAIN STEM AND PERIPHERAL ENDS OF THE PRIMARY AFFERENT NEURON TO DECREASE TRANSMISSION AND INHIBIT RELEASE FROM NEUROTRANSMITTERS
DOSE: 25-100 MCG : PREMED
1-2 MCG/KG ANALGESIA
12.5-100 MCG/KG INTRA OP
0.1-0.5 MCG/KG/MIN INFUSION
SUFENTANYL
C: PHENYL PIPERDINE SYNTHETIC OPIOID AGONIST (GOOD FOR CARDIAC SURGERY)
MOA: ACTIVATES THE MU RECEPTORS ON THE PERIPHERAL ENDS OF THE PRIMARY AFFERENT NEURONS TO DECREASE TRANSMISSION AND INHIBIT RELEASE FORM NEUROTRANSMITTERS.
DOSE: 0.1-1 MCG/KG BOLUS
1-2 MCG/KG MINOR
2-8 MCG/KG MODERATE
8-50 MCG/KG SOLE ANESTHETIC
ALFENTANYL
C: TETRAZOLE FENTANYL DERIVATIVE, SYNTHETIC OPIOID AGONIST
MOA: activates the mu receptors on the peripheral ends of the primary afferent neuron thereby decreasing transmission and inhibiting release from neurotransmitters
dose 0.5-0.1 mcg/kg/min
Nalbuphine
c: opioid agonist - antagonist
moa: works at the kappa and sigma receptors to antagonize opioid induced resp depression while maintaining analgesia
dose: 0.1-0.3 mg/kg
butorphanol
opioid agonist-antagonist
nasal spray for migranes
moa: agonist at kappa (weak antagonist at mu)
dose: 0.01-0.04 mg/kg
NARCAN/NALOXONE
N ALKYL DERIVATIVE OF OXYMORPHONE; PURE NONSELECTIVE OPIOID ANTAGONIST; BLOCKS RECEPTOR SITES AND REVERSES REPIRATORY DEPRESSION/ANALGESIA/SEDATION
MOA: INHIBITOR AT MU, KAPPA, DELTA AND BLOCSK THE RECEPTOR SITES AND REVERSES RESPIRATORY DEPRESSION AND ANALGESIA
DOSE: 0.1-2 MG IV Q3MIN (START WITH LOWEST DOSE)
PRECEDEX
C: ALPHA 2 AGONIST (INHIBITS NE RELEASE)
MOA: ACTIVATION OF ALPHA 2 RECEPTORS = HYPNOSIS, SEDATION, ANXIOLYSIS, AND ANALGESIA, decreases thermoregulation so it masks shivering
DOSE: 1 mcg/kg bolus over 10 minutes
0.2-1 mcg/kg/hr infusion
KETAMINE
C: NON BARBITUATE INDUCTION AGENT
MOA: NMDA RECEPTOR BLOCKADE INHIBITING NA/CA IONS AND EXCITATORY GLUTAMATE; ANALGESIA AND SUB ANESTHETIC DOSES; DISSOCIATIVE EFFECT
DOSE: 0.5-2 MG/KG IV INDUCTION (>2MG DELIRIUM)
ETOMIDATE
C: NON BARBITUATE INDUCTION AGENT
MOA: MIMICS INHIBITORY GABA AND GABA-A RECEPTOR. INCREASING CHLORIDE CONDUCTANCE AND HYPERPOLARIZES POST SYNAPTIC MEMBRANE PRODUCING HYPNOSIS
DOSE: 0.3MG/KG
PROPOFOL
C: NON BARBITUATE INDUCTION AGENT; 2,6 DI-ISO PROPHENOL
MOA: DISCOURAGES DISSOCIATION OF GABA FROM GABA-A RECEPTORS. INCREASED CHLORIDE CONDUCTANCE AND HYPERPOLARIZES POST SYNAPTIC MEMBRANE PRODUCING HYPNOSIS, INHIBITS GLUTAMATE ACTION AT NMDA RECEPTOR
DOSE: 1-2.5 MG/KG IV. N/V 10 MG
GA: 100-300 MCG/KG/MIN
SEDATION 25-100 MCG/KG/MIN
ATROPINE
C: TERTIARY AMINE: ANTICHOLINERGIC: CROSSES BBB
MOA: INHIBITS EFFECTS OF ACH AT MUSCARNIC RECEPTORS AND DECREASE PNS ACTIVITY;
USES: INCREASES HR BY ACTING ON MU2 AT SA NODE
DOSE: 0.01 MG/KG REVERSAL (EDROPHONIUM)
BRADYCARDIA 0.4-1 MG
1 MG Q3MIN FOR ASYSTOLE/BRADYCARDIA
GLYCOPYROLATE
C: SYNTHETIC QUARTENARY AMMONIUM, ANTICHOLINERGIC, DOES NOT CROSS BBB
MOA: INHIBITS EFFECTS OF ACH AT MUSCARNIC RECEPTORS AND DECREASES PNS ACTIVITY
USES: REDUCE THE VOLUME OF SECRETIONS SUCH AS SALIVARY AND GASTIC, INCREASES HR, USED WITH REVERSALS
DOSE: 0.01-0.02 MG/KG IV with neostigmine
0.1-0.2 antisialogogue and bradycardia
SCOPALAMINE
C: TERTIARY AMINE: CROSSES THE BBB, ANTICHOLINERGIC
MOA: INHIBITS THE EFFECTS OF ACH AT MUSCARNIC RECEPTORS AND DECREASES PNS ACTIVITY
USES: MOTION SICKNESS, PONV, ANTISIALOGOUE
DOSE: 0.2-0.6 MG IV q4-6 hours
scopalamine patch:
PYRIDOSTIGMINE
C: COMPETITIVE ANTICHOLINESTERASE INHIBITOR, QUARTENARY AMINE - NO CROSS BBB
MOA: reversibly binds to acetylcholinesterase, inhibiting its action and increasing the concentration of acetylcholine at the motor end plate
DOSE: 0.2 MG/KG IV
WITH GLYCO 0.01 MG/KG IV
ORAL FOR MG
EDROPHONIUM
C: COMPETITIVE ANTICHOLINESTERASE INHIBITOR, QUARTENARY AMINE - NO CROSS BBB
MOA: REVERSIBILY BINDS TO ACHE, INHIBITING ITS ACTION AND INCREASING THE CONCENTRATION OF ACH AT THE MOTOR END PLATE
DOSE: 0.5-1 MG/KG
WITH ATROPINE 0.01 MG/KG IV
NEOSTIGMINE
C: COMPETITIVE ANTICHOLINESTERASE INHIBITOR - QUARTENARY AMINE - NO CROSS BBB
MOA: Irreversibly binds to and inhibits AChE, thereby increasing the concentration of acetylcholine (ACh) in the synaptic cleft
DOSE: 0.05-0.07 MG/KG IV
WITH GLYCO 0.01 MG/KG IV
PHYSOSTIGMINE
C: TERTIARY AMINE- CROSSES BBB,
useful for atropine TOX, MG, GLAUCOMA
MOA: reversible competitive inhibitor of acetylcholinesterase by forming a carbamyl ester complex at the esteratic site of the enzyme WHICH decreases acetylcholine metabolism and increases acetylcholine levels at the synaptic level.
DOSE: 15-60 MCH/KG IV Q1-2 HRS
EPINEPHRINE
C: ENDOGENOUS CATECHOLAMINE, NONSELECTIVE ADRENERGIC AGONIST
MOA: ACTS ON G PROTEINS TO INCREASE CAMP, DIRECT STIMULATE OF ALPHA AND BETA RECEPTORS (BETA>ALPHA)
LOW DOSES = B2 STIMULATION (BRONCHODILATION, VASODILATION)
INCREASED DOSES OF EPI = ALPHA EFFECT PREDOMINATES (VASOCONSTRICTION AND INCREASED SYSTOLIC PRESSURES)
DOSES:
ACLS: 1 MG Q3 MIN FOR ARREST
B2: 1-2 MCG/MIN iv
B1: 4-5 MCG/MIN IV
Single IV Dose Hypotension = 2-8mcg/KG IV
Continuous infusion 1-20mcg/min
1-2mcg/min = B2
4-5 mcg/min = B1
10-20mcg/min= alpha and beta effects
NOREPINEPHRINE
C: DIRECT ACTING ENDOGENOUS CATECHOLAMINE AND ADRENERGIC AGONIST
MOA: ACTS ON G PROTEINS TO INCREASE CAMP, INFLUX OF CALCIUM CAUSING AGONIST ACTIVITY AND INCREASE CONTRACTILITY, ALPHA AND B1 >B2, POTENT VASOCONSTRICTOR
DOSE: 4-16 MCG/MIN
DOPAMINE
C: ENDOGENOUS CATECHOLAMINE, Sympathomimetic amine and adrenergic agonist
MOA: extracted from L-dopa in the catecholamine synthesis of tyrosine. binds to the dopaminergic, β and α receptors Which cause vasodilatation and ↑ levels of cAMP by stimulating adenylyl cyclase in vascular smooth muscle.
LOW DOSES: INCREASES RENAL BF 0.5-2mcg/kg/min
MEDIUM DOSES: INCREASE CO 2-10mcg/kg/min
LARGE DOES: INCREASE BP, CO >10mcg/kg/min
Drug of choice for treatment of shock, especially in sepsis
DOBUTAMINE
C: sympathomimetic synthetic catecholamine - b1 selective agonist
moa: derived from beta-phenylethyalmine, synthetic an along of isoprotenerol which is made from dopamine, acts on b1, g proteins to increase camp. influx of calcium causes increase contractility and co. also works on beta 1 and alpha 1 receptors. useful in CHF pts
dose: 2-10 mcg/kg/min
b1: 5mcg/kg/min
vasopressin
c: exogenous antidiuretic peptide and vasopresor
moa: used for diabetes insidious, hemorrhage, shock, acls. acts on renal tubules to retain water and constrict the efferent arteriole. increase vwf and factor 8
dose: 40 U push: cardiac arrest
20 U iv - esophageal varices
0.04 u/min sepsis
isopreteronol
c: Selective beta agonist synthetic catecholamine,
beta 1 > beta 2
used for hb, bb od, bradycardia
moa: Produces beta1 > beta 2 effects by stimulating G protein coupled receptors, which activate cAMP to produce pharmacologic effects (increased inotropy and increased chronotropy)
dose: 0.5-10 mcg/min
ephedrine
c. synthetic non catecholamine, direct and indirect adrenergic receptors
moa: Stimulates alpha and beta (adrenergic) receptors by direct and indirect actions. Indirect affects alpha and beta by stimulating NE release. Directly acts on B1 and increases contractility. Greater venous constriction than arteriolar constriction
dose: 5-25 mg IV
phenylephrine
synthetic nn catecholamine, direct acting, selective alpha 1
moa: direct stimulation of alpha 1 receptors, vents> arterial constriction. increasing BP and decreasing HR
DOSE: 50-200 mcg iv
ampicillin
c: beta lactum, 2nd generation, broad spectrum,
moa: bactericidal, inhibits bacterial cell wall synthesis
pharmaco: 90% renal unchanged
e1/2t=~2 hr
pb= 20%
s/e: analphylaxis, rash, gi upset, SLE,
ci: increased sensitivity to pcn, rapid infusions = sz.
dose: 2g iv q30 min preop
cefazolin
c: beta lactum, 1st generation, broad spectrum
moa: bactericidal, inhibits bacterial cell wall synthesis
pharm: excreted: 90% unchanged in urine.
pb: 80%
e1/2t: 2 hours
s/e analaphaszis, rash, gi upset, cross sensitivity to PCN,
c/i: decreased dose in renal failure, hypersensitivity
dose: 1-2 g iv 30 min preop
gentamycin
c: antimicrobial aminoglycide broad spectrum
moa: inhibit bacterial cell wall synthesis
pharm: extensive renal secretion urine unchanged
e1/2t: 2 hours
s/e: neuro/oto.nephro toxic
ci: decreased doses in renal pts, caustion in MG
dose: 60-120 mg iv
clindamycin
c: narrow spectrum, lincosamide, antimicromia, tx pcn resistant staph and bacteriocides
moa: bacteriostatic, inhibits bacterial protein synthesis
pharm: liver metabolism active metabolites in bile feces and urine excerteion
s/s: pseudomembranous colitis, neutropenia
contra: increases sensitivity to pseduomembranous colitis. , liver disase, cross placenta
dose: 600 mg iv
