1
ADVANCED PHARMACOLOGY PROCTORED
EXAM ACTUAL QUESTIONS AND CORRECT
ANSWERS ALREADY GRADED A+
GUARANTEED PASS
Efficacy
Efficacy is the relationship between receptor occupancy and the ability to initiate a
response at the molecular, cellular, tissue or system level. In other words, efficacy
refers to how well an action is took after the drug is bound to a receptor
Affinity
Affinity is how well a drug can bind to a receptor (Fast/strong binding = higher
affinity)
Explain the therapeutic window
therapeutic window is the amount of a medication between the amount that gives
an effect (effective dose) and the amount that gives more adverse effects than
desired effects
Duration of action
duration of action of a drug is the length of time that particular drug is effective
Explain bioavailability
drug's bioavailability can be defined as the proportion of the drug that reaches its
site of action
6 rights to medication administration
RIGHT CLIENT
RIGHT MEDICATION
RIGHT DOSAGE
, 2
RIGHT ROUTE
RIGHT TIME
RIGHT DOCUMENTATION
Potency
potency is a measure of drug activity expressed in terms of the amount required to
produce an effect of given intensity
(more morphine is needed to give the same effects as fentanyl)
Benzodiazepine MOA
Act on GABA which is a major inhibitory NTM in the CNS; Effects are produced
by interacting with a protein complex with in the neuronal membrane GABA
which has a high 'affinity' for benzo's specifically;
Benzodiazepine uses/indications
Similar actions however different doses/concentrations/combinations produce
different actions thus have different uses
Anxiety/panic disorders
skeletal muscle relaxation
seizures
sedation for procedures (due to relaxation and amnesic properties)
Benzodiazepines adverse effects
Most derived through CNS actions; Ataxia, dizziness, drowsiness/sedation, blurred
vision, hypnosis, weakness, fatigue
More severe: hypersensitivity, mental depression, hypotension, paradoxical
stimulation, rebound seizures
Benzo pharmacokinetics
Widely distributed throughout the body
accumulate in lipid rich areas (CNS and adipose tissue)
the more lipophilic the agent the faster it is absorbed
, 3
Onset 30 min- 1 hr lasting 4-6 hours, peak at 1-2 hours
IV Admin: onset 1-5 min, peak immediately, last 15-20 min
metabolized by the liver and excreted in urine
Beta blocker (BB) MOA
Interrupts the nerve impulses across the neurons by antagonizing the receptors with
in the cardiac cells resulting in blockade of the beta 1 receptors';
-B1 blockade results in reduction of heart rate (chronotropic), rate of conduction
through the AV node (dromotropic), and force of contraction (inotropic)
This in turn decreases the oxygen demand on the myocytes, reduction in BP from
the reduced HR and inotropic actions
Hypoglycemia can occur with beta blockade because β2-adrenoceptors normally
stimulate glycogen breakdown (glycogenolysis) in the liver and pancreatic release
of the hormone glucagon, which work together to increase plasma glucose
Beta blocker Therapeutic uses
Useful in angina, HTN, cardiac dysrhythmias, MI, HF, Hyperthyroidism,
migraines, pheochromocytoma, Glaucoma
In angina/MI: reduction of oxygen demand
HTN: B1 blockade as well as suppressed renin release via B1 blockade in the
kidneys shows a marked decrease in PVR which results in improved stroke volume
Beta Blocker Adverse effects
B1 blockade: bradycardia resulting in reduced CO and precipitating HF, AV heart
block, Rebound cardiac Excitability
B2 effects incl: bronchoconstriction, and Inhibition of glycogenolysis resulting in
hypoglycemia
Beta blocker Pharacokinetics
Highly lipid soluble
, 4
Absorption usually rapid/complete
50% 1st pass metabolism
peak concentrations approx. 1.5-2 hours, onset about 4-5 hrs
liver metabolized, renal excretion as a metabolite
Beta blocker interactions
Calcium channel blockers: Negative Ino/dromo/chronotropic effects
anti-arrhythmics: may enhance their effects leading to unwated outcomes
Nitrates: may potentiate hypotensive effects
MAO inhibitors: may increase reduction of sympathetic activity thus the inability
to respond to Fight/flight mechanism resulting in reduced BP/HR overall
Digitalis: Can potentiate suppressed AV conduction
Calcium Channel Blockers (CCB) MOA
inhibition of calcium movement in smooth and cardiac muscle tissue by selectively
antagonizing calcium influx movment across the cellular membrane responsible for
smooth/cardiac muscle conduction velocity: produces relaxation of coronary
smooth muscles, dilation of coronary arteries; reduced dromotropic effects of the
sa/av node and reduced automaticity
Effects peripherally result in vasodilation through smooth muscle relaxation
Different agents have different effects on different receptors within the
transmembrane calcium channels
Non specific effects in blood coagulation by inhibiting platelet aggregation in the
clotting cascade
CCB indications
Hypertension, angina, dysrhythmias
CCB Adverse effects
Peripheral edema, flushing, palpitations, headache
ADVANCED PHARMACOLOGY PROCTORED
EXAM ACTUAL QUESTIONS AND CORRECT
ANSWERS ALREADY GRADED A+
GUARANTEED PASS
Efficacy
Efficacy is the relationship between receptor occupancy and the ability to initiate a
response at the molecular, cellular, tissue or system level. In other words, efficacy
refers to how well an action is took after the drug is bound to a receptor
Affinity
Affinity is how well a drug can bind to a receptor (Fast/strong binding = higher
affinity)
Explain the therapeutic window
therapeutic window is the amount of a medication between the amount that gives
an effect (effective dose) and the amount that gives more adverse effects than
desired effects
Duration of action
duration of action of a drug is the length of time that particular drug is effective
Explain bioavailability
drug's bioavailability can be defined as the proportion of the drug that reaches its
site of action
6 rights to medication administration
RIGHT CLIENT
RIGHT MEDICATION
RIGHT DOSAGE
, 2
RIGHT ROUTE
RIGHT TIME
RIGHT DOCUMENTATION
Potency
potency is a measure of drug activity expressed in terms of the amount required to
produce an effect of given intensity
(more morphine is needed to give the same effects as fentanyl)
Benzodiazepine MOA
Act on GABA which is a major inhibitory NTM in the CNS; Effects are produced
by interacting with a protein complex with in the neuronal membrane GABA
which has a high 'affinity' for benzo's specifically;
Benzodiazepine uses/indications
Similar actions however different doses/concentrations/combinations produce
different actions thus have different uses
Anxiety/panic disorders
skeletal muscle relaxation
seizures
sedation for procedures (due to relaxation and amnesic properties)
Benzodiazepines adverse effects
Most derived through CNS actions; Ataxia, dizziness, drowsiness/sedation, blurred
vision, hypnosis, weakness, fatigue
More severe: hypersensitivity, mental depression, hypotension, paradoxical
stimulation, rebound seizures
Benzo pharmacokinetics
Widely distributed throughout the body
accumulate in lipid rich areas (CNS and adipose tissue)
the more lipophilic the agent the faster it is absorbed
, 3
Onset 30 min- 1 hr lasting 4-6 hours, peak at 1-2 hours
IV Admin: onset 1-5 min, peak immediately, last 15-20 min
metabolized by the liver and excreted in urine
Beta blocker (BB) MOA
Interrupts the nerve impulses across the neurons by antagonizing the receptors with
in the cardiac cells resulting in blockade of the beta 1 receptors';
-B1 blockade results in reduction of heart rate (chronotropic), rate of conduction
through the AV node (dromotropic), and force of contraction (inotropic)
This in turn decreases the oxygen demand on the myocytes, reduction in BP from
the reduced HR and inotropic actions
Hypoglycemia can occur with beta blockade because β2-adrenoceptors normally
stimulate glycogen breakdown (glycogenolysis) in the liver and pancreatic release
of the hormone glucagon, which work together to increase plasma glucose
Beta blocker Therapeutic uses
Useful in angina, HTN, cardiac dysrhythmias, MI, HF, Hyperthyroidism,
migraines, pheochromocytoma, Glaucoma
In angina/MI: reduction of oxygen demand
HTN: B1 blockade as well as suppressed renin release via B1 blockade in the
kidneys shows a marked decrease in PVR which results in improved stroke volume
Beta Blocker Adverse effects
B1 blockade: bradycardia resulting in reduced CO and precipitating HF, AV heart
block, Rebound cardiac Excitability
B2 effects incl: bronchoconstriction, and Inhibition of glycogenolysis resulting in
hypoglycemia
Beta blocker Pharacokinetics
Highly lipid soluble
, 4
Absorption usually rapid/complete
50% 1st pass metabolism
peak concentrations approx. 1.5-2 hours, onset about 4-5 hrs
liver metabolized, renal excretion as a metabolite
Beta blocker interactions
Calcium channel blockers: Negative Ino/dromo/chronotropic effects
anti-arrhythmics: may enhance their effects leading to unwated outcomes
Nitrates: may potentiate hypotensive effects
MAO inhibitors: may increase reduction of sympathetic activity thus the inability
to respond to Fight/flight mechanism resulting in reduced BP/HR overall
Digitalis: Can potentiate suppressed AV conduction
Calcium Channel Blockers (CCB) MOA
inhibition of calcium movement in smooth and cardiac muscle tissue by selectively
antagonizing calcium influx movment across the cellular membrane responsible for
smooth/cardiac muscle conduction velocity: produces relaxation of coronary
smooth muscles, dilation of coronary arteries; reduced dromotropic effects of the
sa/av node and reduced automaticity
Effects peripherally result in vasodilation through smooth muscle relaxation
Different agents have different effects on different receptors within the
transmembrane calcium channels
Non specific effects in blood coagulation by inhibiting platelet aggregation in the
clotting cascade
CCB indications
Hypertension, angina, dysrhythmias
CCB Adverse effects
Peripheral edema, flushing, palpitations, headache
