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Advanced Pharmacology Test Bank.

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Advanced Pharmacology Test Bank. latest 2024

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  • August 22, 2024
  • 44
  • 2024/2025
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  • advanced pharmacology
  • advanced pharmacology test bank

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Advanced Pharmacology

Study online at https://quizlet.com/_ffm3ks

Advanced Pharmacology Test Bank.
Latest 2024/2025
1. Explain Pharmacokinetics: The study of how drugs are moved through the body
and are encompassed in mechanisms of:
Absorption
Distribution
Metabolism
Excretion

Think Kinetic (movement)
2. Pharmacodynamics: study of the biochemical and physiologic effects of drugs on
the body

Think Dynamic (change)

majority of drugs either
(a) mimic or inhibit normal physiological/biochemical processes or inhibit patholog-ical
processes in animals or
(b) inhibit vital processes of endo- or ectoparasites and microbial organisms
3. Summarize the main drug actions: 1 - stimulating action through direct receptor
agonism and downstream effects
2 - depressing action through direct receptor agonism and downstream effects (ex.:
inverse agonist)
3- blocking/antagonizing action (as with silent antagonists), the drug binds the
receptor but does not activate it
4- stabilizing action, the drug seems to act neither as a stimulant or as a depressant 5-
exchanging/replacing substances or accumulating them to form a reserve (ex.: glycogen
storage)
4. Desired activity is achieved through what main mechanisms?: -Cellular membrane
disruption
-Chemical reaction with downstream effects
-Interaction with enzyme proteins
-Interaction with structural proteins
-Interaction with carrier proteins
-Interaction with ion channels
-Ligand binding to receptors: 1)Hormone receptors 2) Neuromodulator receptors





, Advanced Pharmacology

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3)Neurotransmitter receptors
5. 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
6. Duration of action: duration of action of a drug is the length of time that particular
drug is effective
7. Explain bioavailability: drug's bioavailability can be defined as the proportion of the
drug that reaches its site of action
8. 6 rights to medication administration: RIGHT CLIENT
RIGHT MEDICATION
RIGHT DOSAGE
RIGHT ROUTE
RIGHT TIME
RIGHT DOCUMENTATION
9. 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)
10. 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
11. Affinity: Affinity is how well a drug can bind to a receptor (Fast/strong binding =
higher affinity)
12. 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;

Inhibition of polysynaptic afferent pathways resulting in skeletal muscle relaxation; It
decreases the spread of seizure activity due to an increased pre-synaptic inhibition of the
CNS
13. 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)





, Advanced Pharmacology

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14. 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
15. 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
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
16. 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 ²2-adrenoceptors normally
stimulate glycogen breakdown (glycogenolysis) in the liver and pancreatic release of the
hormone glucagon, which work together to increase plasma glucose
17. 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
18. 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
19. Beta blocker Pharacokinetics: Highly lipid soluble
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





, Advanced Pharmacology

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20. 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
21. 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
22. CCB indications: Hypertension, angina, dysrhythmias
23. CCB Adverse effects: Peripheral edema, flushing, palpitations, headache
Pulmonary edema, rebound tachycardia, bradycardia, skin rash
24. CCB drug interactions: BB and other antiarrhythmics can potentiate their effects
increased concentrations of theophyliine and digoxin may occur
25. Non-depolarizing Neuromuscular Blocker MOA: Prevent Ach from activating
Nicotinic 'm' receptors on skeletal muscle, causing relaxation and flaccidity (does
not cause depolarization at the neuromuscular endplate)

Competes with Ach for biding with Nm receptors, blocking Ach thus preventing
stimulation causing the muscle to no longer be engaged and relax; effect lasts until there
is insufficient amount available to overtake the Ach

(muscles paralyze at different times: Levator muscles of the eyelids first, than limbs,
abdomen, and lastly the glottis diaphragm and intercostal)
26. Non-depolarizing Neuromuscular Blocker indications: To facilitate muscular
relaxation for general procedures requiring its purose such as to facilitate ETI,

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