NGR 6460 Pharmacology Exam 1 Questions With Complete
Solutions
Methohexital (Bervital) dose, onset, duration, Vd, half-life
Dose = 0.5-1mg/kg
Onset = 30 - 60 seconds
Duration = < 5 minutes
VD 2.2 L/kg
Half-life 3.9 hours
Propofol chemical name, MOA, dose, onset, duration, protein
binding, Vd, metabolization, half-life
2, 6 diisopropylphenol
The mechanism by which propofol induces a state of general
anesthesia may involve facilitation of inhibitory
neurotransmission mediated by GABA
Intubating dose 1 to 2.5 mg/kg
98% protein binding
High volume of distribution: 2-10L/kg, rapid redistribution
Metabolized to inactive metabolites by liver, lungs, and kidneys
Elimination half-life 4 to 7 hours
Etomidate (Amidate) class, MOA, onset, duration, Vd, protein
binding, half-life, metabolism, elimination, and dose
,General Anesthetic/ Imidazole derivative
MOA: Potentiates GABA A mediated chloride channels that
result in hyperpolarization
Onset- Rapid
Duration- 3-8 minutes (100 seconds of unconsciousness per 0.1
mg/kg administered)
Vd- 2.5-4.5 L/kg
Protein binding-77%
Elimination half life- 2.9 to 5.3 hours
Metabolism- Primarily in the liver to inactive compounds
Elimination- Urine (78%), Bile (22%). <3% excreted unchanged
in urine
Induction- 0.1-0.3 mg/kg IV
Etomidate adrenocortical effects
Causes adrenocortical suppression: Produces inhibition of 11β-
hydroxylase, the enzyme necessary for conversion of cholesterol
to cortisol
Lasts 4-8 hours after induction dose
Ketamine class, MOA, onset, dosage, VD, half-life
phencyclidine derivative that produces dissociative anesthesia
state.
Noncompetitive N-methyl-D-aspartate (NMDA) antagonist that
causes a selective depressant effect on the medial thalamic
nuclei.
, Responsible for blocking the afferent signals to the thalamus and
cortex, resulting in dissociative anesthesia with analgesic effects
IV onset: 30 seconds-5 min
IM onset: 5-15 min
PO onset: 10-20 min
Induction dosages:
-2 to 4 mg/kg IV
-4 to 6 mg/kg IM
-10mg/kg Orally
VD 1.5 to 3.2 L/kg (highly lipid soluble)
Elimination half-life 1 to 2 hours in children, 2.5 to 3 hours in
adults
Dexmedetomidine (Precedex) onset, DOA, Vd, elimination half-
life, metabolism, excretion, and protein binding
Onset of action w/ a loading dose: 10-20 min
Duration of action after infusion stopped: 10-30 min
Vd: 118L/kg
Elimination half life: 2 hrs
Metabolism: in the liver
Excretion: Urine and bile
Protein binding: 94% to albumin and glycoprotein
Dexmedetomidine (Precedex) MOA and dosing
Alpha-2 agonist, binding in the locus coeruleus causes sedation
Loading Dose: 1mcg/kg over 10 min
Maintenance Infusion: 0.2-0.7 mcg/kg/hr
Solutions
Methohexital (Bervital) dose, onset, duration, Vd, half-life
Dose = 0.5-1mg/kg
Onset = 30 - 60 seconds
Duration = < 5 minutes
VD 2.2 L/kg
Half-life 3.9 hours
Propofol chemical name, MOA, dose, onset, duration, protein
binding, Vd, metabolization, half-life
2, 6 diisopropylphenol
The mechanism by which propofol induces a state of general
anesthesia may involve facilitation of inhibitory
neurotransmission mediated by GABA
Intubating dose 1 to 2.5 mg/kg
98% protein binding
High volume of distribution: 2-10L/kg, rapid redistribution
Metabolized to inactive metabolites by liver, lungs, and kidneys
Elimination half-life 4 to 7 hours
Etomidate (Amidate) class, MOA, onset, duration, Vd, protein
binding, half-life, metabolism, elimination, and dose
,General Anesthetic/ Imidazole derivative
MOA: Potentiates GABA A mediated chloride channels that
result in hyperpolarization
Onset- Rapid
Duration- 3-8 minutes (100 seconds of unconsciousness per 0.1
mg/kg administered)
Vd- 2.5-4.5 L/kg
Protein binding-77%
Elimination half life- 2.9 to 5.3 hours
Metabolism- Primarily in the liver to inactive compounds
Elimination- Urine (78%), Bile (22%). <3% excreted unchanged
in urine
Induction- 0.1-0.3 mg/kg IV
Etomidate adrenocortical effects
Causes adrenocortical suppression: Produces inhibition of 11β-
hydroxylase, the enzyme necessary for conversion of cholesterol
to cortisol
Lasts 4-8 hours after induction dose
Ketamine class, MOA, onset, dosage, VD, half-life
phencyclidine derivative that produces dissociative anesthesia
state.
Noncompetitive N-methyl-D-aspartate (NMDA) antagonist that
causes a selective depressant effect on the medial thalamic
nuclei.
, Responsible for blocking the afferent signals to the thalamus and
cortex, resulting in dissociative anesthesia with analgesic effects
IV onset: 30 seconds-5 min
IM onset: 5-15 min
PO onset: 10-20 min
Induction dosages:
-2 to 4 mg/kg IV
-4 to 6 mg/kg IM
-10mg/kg Orally
VD 1.5 to 3.2 L/kg (highly lipid soluble)
Elimination half-life 1 to 2 hours in children, 2.5 to 3 hours in
adults
Dexmedetomidine (Precedex) onset, DOA, Vd, elimination half-
life, metabolism, excretion, and protein binding
Onset of action w/ a loading dose: 10-20 min
Duration of action after infusion stopped: 10-30 min
Vd: 118L/kg
Elimination half life: 2 hrs
Metabolism: in the liver
Excretion: Urine and bile
Protein binding: 94% to albumin and glycoprotein
Dexmedetomidine (Precedex) MOA and dosing
Alpha-2 agonist, binding in the locus coeruleus causes sedation
Loading Dose: 1mcg/kg over 10 min
Maintenance Infusion: 0.2-0.7 mcg/kg/hr
