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Pharmacology : pharmacodynamics

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a complete pharmacology review for students who are preparing to sit for exams; it provides a recap on the basics of pharmacology, diving deep into pharmacodynamics

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Pharmacology
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Pharmacology

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Uploaded on
March 19, 2025
Number of pages
12
Written in
2024/2025
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Exam (elaborations)
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Pharmacology
pharmacodynamics
EXAM PREVIEW

Pharmacodynamics: Sample Questions, answers , and Explanations

1. What is pharmacodynamics? Answer: It is the study of how drugs affect the body. Explanation:
Pharmacodynamics focuses on the mechanisms of drug action, their effects at molecular and cellular
levels, and their relationship to therapeutic and toxic effects.



2. What are the main types of drug-receptor interactions? Answer: Agonists, antagonists, partial
agonists, and inverse agonists. Explanation: Agonists activate receptors to produce a response, while
antagonists block receptor activation. Partial agonists produce submaximal responses, and inverse
agonists decrease receptor activity below basal levels.



3. What is the difference between efficacy and potency? Answer: Efficacy is the maximum effect a
drug can produce, while potency is the drug's ability to produce an effect at a given concentration.
Explanation: A highly potent drug requires a lower dose to achieve the same effect, but its efficacy
depends on its ability to activate a receptor fully.



4. What is an EC50 value? Answer: The concentration of a drug that produces 50% of its maximum
effect. Explanation: EC50 reflects the potency of the drug; lower EC50 values indicate higher potency.



5. How do competitive and non-competitive antagonists differ? Answer: Competitive antagonists bind
reversibly to the same receptor site as the agonist, while non-competitive antagonists bind irreversibly
or to a different site. Explanation: Competitive antagonists can be overcome by increasing agonist
concentration, but non-competitive antagonists reduce the maximal response regardless of agonist
levels.



6. What is a therapeutic index, and why is it important? Answer: It is the ratio of a drug's toxic dose to
its effective dose (TD50/ED50). Explanation: A higher therapeutic index indicates a safer drug, as there
is a wider margin between effective and toxic doses.

, Pharmacology
pharmacodynamics
EXAM PREVIEW



7. What is receptor desensitization? Answer: It is the reduction in receptor responsiveness after
continuous or repeated exposure to an agonist. Explanation: Prolonged stimulation can lead to
decreased receptor numbers or signaling efficiency, reducing drug effectiveness over time.



8. What is the concept of a drug's ceiling effect? Answer: It is the maximum effect a drug can achieve,
beyond which no additional effect is observed, even with higher doses. Explanation: Some drugs have
a plateau in their dose-response curve, indicating their limited efficacy.



9. What role do ion channels play in pharmacodynamics? Answer: Ion channels regulate cellular ion
flow and are targets for drugs that modulate cell activity. Explanation: Drugs can open, block, or
modulate ion channels, influencing cellular responses like nerve conduction and muscle contraction.



10. How does receptor upregulation occur? Answer: Receptor upregulation happens when receptor
numbers increase in response to prolonged antagonist exposure. Explanation: Chronic antagonist use
blocks receptors, prompting cells to produce more receptors to maintain homeostasis.



11. What is receptor specificity in pharmacodynamics? Answer: Receptor specificity refers to the
ability of a drug to bind to a specific type of receptor. Explanation: Drugs that are highly specific
produce targeted effects with fewer side effects, while those with lower specificity may interact with
multiple receptor types.



12. What is the role of second messengers in drug action? Answer: Second messengers amplify the
signal from a drug-receptor interaction to produce cellular effects. Explanation: Examples include
cyclic AMP (cAMP), calcium ions, and inositol triphosphate (IP3). They propagate the signal within the
cell after receptor activation.
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