mechanism of action Flashcards

(55 cards)

1
Q

Nitrous -

A

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

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2
Q

HALOTHANE

A

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

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3
Q

ENFLURANE

A

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

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4
Q

ISOFLURANE

A

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

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5
Q

DESFLURANE

A

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

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6
Q

SEVOFLURANE

A

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

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7
Q

Procaine

A

C: ESTER LA
MOA: BLOCKS NA CHANNELS IN NERVE CELL MEMBRANE WHILE IN CLOSED INACTIVE STATE, PREVENTS DEPOLARIZATION AND IMPULSE TRANSMISSION

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8
Q

TETRACANE

A

C: ESTER LA
MOA: BLOCKS NA CHANNELS IN NERVE CELL MEMBRANE WHILE IN CLOSED INACTIVE STATE, PREVENTS DEPOLARIZATION AND IMPUSE TRANSMISSION

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9
Q

BUPIVICAINE

A

C: AMIDE LA
MOA: BLOCKS NA CHANNELS IN NERVE CELL MEMBRANE WHILE IN CLOSE INACTIVE STATE, PREVENTS DEPOLARIZATION AND IMPULSE TRANSMISSION

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10
Q

LIDOCAINE:

A

C: AMIDE LA
MOA: BLOCKS NA CHANNELS IN NERVE CELL MEMBRANE WHILE IN CLOSE INACTIVE STATE AND PREVENTS DEPOLARIZATION AND IMPULSE TRANSMISSION

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11
Q

ETIDOCAINE

A

C: AMIDE LA
MOA: BLOCKS NA CHANNELS IN NERVE CELL MEMBRANE WHILE IN THE CLOSED INACTIVE STATE, PREVENTS DEPOLARIZATION ADN IMPULSE TRANSMISSION

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12
Q

MEPIVICAINE

A

C: AMIDE LA
MOA: BLOCKS NA CHANNELS IN NERVE CELL MEMBRANE WHILE IN THE CLOSED INACTIVE STATE, PREVENTS DEPOLARIZATION AND IMPULSE TRANSMISSION

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13
Q

CHLOROPROCAINE

A

C: ESTER LA
MOA: BLOCKS NA CHANNELS IN NERVE CELL MEMBRANE WHILE IN CLOSED INACTIVE STATE, PREVENTS DEPOLARIZATION AND IMPULSE TRANSMISSION

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14
Q

COCAINE:

A

C: ESTER LA
MOA: BLOCKS NA CHANNELS IN THE NERVE CELL MEMBRANE WHILE IN TEH CLOSED INACTIVE STATE

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15
Q

Diazepam (Valium) PROTOTYPE

A

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

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16
Q

MIDAZOLAM (VERSED)

A

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)

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17
Q

LORAZEPAM (ATIVAN)

A

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

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18
Q

ATRACURIUM - tracurium

A

C: NMB- INTERMEDIATE ACTING BISQUATERNARY BENZYLLISOQUINOLINE
MOA: INHIBITS ACH AT POST-JUNCTIONAL NICOTINIC RECEPTORS PREVENTING DEPOLARIZATION OF MUSCLE CELL MEMBRANE AND INHIBIT MUSCULAR CONTRACTION

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19
Q

CISATRACURIUM - NIMBEX

A

C: NMB: INTERMEDIATE ACTING BENZYLLISOQUINOLINE
MOA: INHIBITS ACH AT POST JUNCTIONAL NICOTINIC CELL MEMBRANE PREVENTING DEPOLARIZATION F MUSCLE CELL MEMBRANE AND INHIBIT MUSCULAR CONTRACTION

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20
Q

ROCURONIUM - ZEMURON

A

C: NMB - SHORT/INTERMEDIATE ACTING STEROID TYPE
MOA: INHIBITS ACH AT POSTJUNCTIONAL NICOTINIC CELL MEMBRANE PREVENT DEPOLARIZATION OF MUSCLE CELL MEMBRANE AND MUSCLE CONTRACTION

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21
Q

VECURONIUM - NORCURON

A

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

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22
Q

PANCURONIUM - PAVULON

A

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

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23
Q

DOXACURIUM - NEUROMAX

A

C: NMB - LONG ACTING BENZYLISOQUINOLINE
MOA: INHIBITS ACH AT POST JUNCTIONAL NICOTINIC CELL MEMBRANE PREVENTING DEPOLARIZATION OF MUSCLE CELL MEMBRANE AND INHIBITS MUSCULAR CONTRACTION

24
Q

SUCCS

A

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

25
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
26
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
27
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
28
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
29
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
30
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
31
butorphanol
opioid agonist-antagonist nasal spray for migranes moa: agonist at kappa (weak antagonist at mu) dose: 0.01-0.04 mg/kg
32
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)
33
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
34
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)
35
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
36
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
37
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
38
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
39
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:
40
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
41
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
42
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
43
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
44
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
45
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
46
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
47
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
48
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
49
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
50
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
51
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
52
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
53
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
54
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
55
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