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MCPHS PHARMACOLOGY I FINAL EXAM QUESTIONS AND ANSWERS WITH COMPLETE SOLUTIONS VERIFIED LATEST UPDATE 2024/2025 $10.49
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MCPHS PHARMACOLOGY I FINAL EXAM QUESTIONS AND ANSWERS WITH COMPLETE SOLUTIONS VERIFIED LATEST UPDATE 2024/2025
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MCPHS PHARMACOLOGY I FINAL EXAM QUESTIONS AND ANSWERS WITH COMPLETE SOLUTIONS VERIFIED LATEST UPDATE 2024/2025 Drug An exogenous chemical administered to alter biological/physiological process to cure/treat/prevent disease/illness Dissociation Constant (Kd) The smaller the numerical value the g...

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MCPHS PHARMACOLOGY I FINAL EXAM QUESTIONS

AND ANSWERS WITH COMPLETE SOLUTIONS VERIFIED

LATEST UPDATE 2024/2025

Drug


An exogenous chemical administered to alter biological/physiological process to cure/treat/prevent

disease/illness


Dissociation Constant (Kd)


The smaller the numerical value the greater the affinity a drug has for a given receptor/drug target


Transporters


Moves substances into a cell


Pumps


Moves substances out of a cell


Ion-Channels (and the two different types)


Selective transmembrane proteins with 2 types of gating mechanisms: Ligand-Gated OR Voltage-Gated


Intracellular Ion at resting membrane potential


K+

,Extracellular Ions at resting membrane potential


Na+/Ca++/Cl-


4 Main types of receptors


1. Ion-Channels

2. G-Protein Coupled Receptors (GPCR's)

3. Nuclear Hormone Receptor (NOT on cell surface but rather inside cell and response usually involves

DNA transcription

4. Receptor Tyrosine Kinase (Phosphorylation of Tyrosine amino acid)


GPCR's (3 types, subunits, effectors and second messengers)


Gs and Gq = Stimulatory whereas Gi = inhibitory

Alpha, Beta, Gamma subunits, Alpha dissociates after receptor activation to affect adenylyl cyclase (will

increase cAMP) or phospholipase C which is an enzyme that degrades phospholipid into DAG (activates

protein kinase C) and IP3 (open Ca++ ligand gated channel to increase Ca++ influx causing smooth

muscle contraction)


4 types of "Agonists" to form stable receptor-complex conformation


1. Full Agonist (selective exclusively for active receptor)

2. Partial Agonist (mostly selective for active receptors)

3. Neutral Agonist (Similar affinity for active/inactive receptor conformations) "Clinical Antagonist"

4. Inverse Agonist (Selective exclusively for inactive receptor) "Clinical Antagonist"


Graded Response dose response curve


Numerical value outcomes --> HR/BP/etc

,Quantal Response dose response curve


Yes/No outcomes --> Did pt fall asleep/get pregnant?


Explain dose response curve


Emax --> Max effect of a drug (where graph plateaus) (measure of efficacy/response)

ED50 --> Dose required for 50% of max response (measure of potency)

X-Axis(mg of drug) --> measure of a drugs potency (ED50) (Ex: If 2 drugs get to 100%, they are equally

effective)

Y-Axis (% response) --> measure of a drugs efficacy (Emax) (Ex: If 2 drugs have same ED50, they're

equally potent)


Additive Effect


Coadministration of two active agents will produce a response equal to the sum of each drug if given

separately


Synergistic Effect


Coadministration of two active drugs yield a greater response than if each drug was given individually


Potentiation


Coadministration of 1 active and 1 inactive drug yields an increased effect than the active drug alone


Competitive Antagonist


-A drug that competes with agonist for REVERSIBLE binding at the receptor active site.

-DOES NOT change the Emax (effectiveness of drug)

-DOES SHIFT ED50 to the RIGHT (appear less potent)


Noncompetitive Antagonist

, -IRREVERSIBLY bound to receptor

-DOES NOT change the ED50

-DOES REDUCE Emax ( appear less effectiveness)


Affinity


How well a ligand binds to a protein/receptor. Positive correlation between affinity and potency


Selectivity


How well a drug binds to its intended target. Ideally should have greater affinity for target receptor than

other receptors


Side effect


ANY effect other than the therapeutic effect regardless if it was beneficial or detrimental


Adverse effect (and 2 types)


a side effect that is harmful

1. Mechanism based: activation of the same receptor target elsewhere in the body (ex: Albuterol

stimulates Beta receptor in lung = bronchodilation, but it can also stimulate Beta receptor in heart which

increases HR)

2. Off-Target: Result of drug binding to something (receptor) other than intended target (ex: Diazoxide is

a direct vasodilator that can open K+ channels in pancreas to induce the release of insulin)


Toxic effect


Extension of pharmacological effect due to high dosing of a drug


Hypersensitivity/allergic effects


Invokes an immune response

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