Week 13 / Pharmacology 4 Flashcards
Q1: What are the two main types of variation in drug responsiveness under its scope?
Q2: What are the possible consequences of variation in drug responsiveness?
Q3: What are the possible mechanisms of variation in drug responsiveness?
Q4: How does inter-patient variation occur in drug responsiveness?
Q5: How does intra-patient variation occur in drug responsiveness?
A1:
1. Inter-patient variation: Differences in drug responsiveness between individuals.
2. Intra-patient variation: Differences in drug responsiveness within the same individual over time.
A2:
1. Lack of efficacy: The drug does not produce the intended therapeutic effect.
2. Unexpected side effects: The drug causes adverse or unintended reactions.
A3:
1. Pharmacokinetic mechanisms: Variations in drug absorption, distribution, metabolism, or excretion affecting drug concentration at the target site.
2. Pharmacodynamic mechanisms: Variations in the interaction between the drug and its target, including receptor sensitivity and signal transduction pathways.
A4: It occurs due to differences in genetics, age, gender, diet, or health conditions between individuals.
A5: It occurs due to changes in the individual’s health, concurrent medications, or environmental factors over time.
Flashcards: Types of Variation in Drug Responsiveness
Q1: What are the two main types of variation in drug responsiveness?
Q2: What is hyper-responsiveness in quantitative variation?
Q3: What is hypo-responsiveness in quantitative variation?
Tolerance in Drug Responsiveness
Q4: What are the two types of tolerance?
Q5: What is the difference between tolerance and tachyphylaxis?
A1:
1. Qualitative variations: Differences in the type of response, such as a completely unexpected or opposite effect (e.g., allergic reactions).
2. Quantitative variations: Differences in the magnitude of response, including hyper-responsiveness or hypo-responsiveness.
A2: Hyper-responsiveness is an exaggerated response to a standard dose of a drug.
A3: Hypo-responsiveness (or tolerance) is a reduced response to a standard dose of a drug over time or initially.
A4:
1. Innate tolerance: A pre-existing, genetically determined low response to a drug.
2. Acquired tolerance: A decreased response to a drug that develops with repeated exposure over time.
A5:
- Tolerance: Gradual reduction in drug responsiveness over days to weeks due to repeated use.
- Tachyphylaxis: A rapid reduction in drug responsiveness occurring after a few doses or within a short period.
What is acquired tolerance?
What are the mechanisms of acquired tolerance?
A1: An acquired state of progressively decreasing responsiveness to a drug due to prior or repeated exposure to the drug or a similar one.
Pharmacodynamic: Changes at the drug’s target, such as receptor desensitization.
Metabolic: Increased drug metabolism reduces its concentration at the target site.
Exhaustion/Depletion of mediators: Depletion of substances necessary for the drug’s effect.
Physiological adaptation: The body compensates to counteract the drug’s effects.
Flashcards: Mechanisms of Acquired Tolerance
Q1: What is pharmacodynamic tolerance?
Q2: What is receptor down-regulation?
Q3: What is receptor uncoupling?
Q4: What is metabolic tolerance?
Let me know if you’d like adjustments! 😊
A1: A mechanism of acquired tolerance where changes occur at the drug’s target site, such as receptor down-regulation or uncoupling.
A2: A reduction in receptor density on the cell surface, decreasing the drug’s effect (e.g., β1-adrenergic receptor).
A3: The uncoupling of receptors from their effector systems, making them less responsive to the drug (e.g., β2-adrenergic receptor).
A4: Enhanced metabolism of the drug due to the induction of metabolizing enzymes, leading to reduced drug concentration at the target site (e.g., alcohol, barbiturates).
Flashcards: Mechanisms of Acquired Tolerance
Q1: What is the exhaustion or depletion of mediators mechanism in acquired tolerance?
Q2: What type of drugs commonly cause depletion of mediators?
Q3: What is physiological adaptation in acquired tolerance?
Q4: How does physiological adaptation affect drug effectiveness?
Does this format work for you? 😊
A1: It occurs when indirectly-acting drugs deplete endogenous stores of mediators required for their action (e.g., amphetamine, nitrates).
A2: Indirectly-acting drugs, which rely on endogenous stores to exert their effects.
A3: The evocation of compensatory or homeostatic mechanisms by the body that blunt or cancel the drug’s effects (e.g., diuretics, nitrates).
A4: It reduces the drug’s effects by triggering the body’s mechanisms to maintain balance or homeostasis.
Flashcards: Drug Receptor Concepts
Q1: What is the difference between absolute and relative selectivity in drug receptors?
Q2: What is the difference between therapeutic effects and adverse effects?
Q3: What is the concept of the therapeutic index?
Q4: What does clinical selectivity refer to?
Let me know if you need further details! 😊
A1:
- Absolute selectivity: The drug exclusively binds to one receptor type, with no binding to others.
- Relative selectivity: The drug binds preferentially to one receptor type, but also has some affinity for other receptors.
A2:
- Therapeutic effects: The desired, beneficial outcomes of drug treatment.
- Adverse effects: Undesirable, harmful reactions to the drug, also known as side effects.
A3: The therapeutic index is the ratio between the dose of a drug that causes toxicity and the dose that produces the desired therapeutic effect. A higher therapeutic index indicates a safer drug.
A4: Clinical selectivity refers to a drug’s ability to produce therapeutic effects while minimizing adverse effects by selectively targeting specific receptors or pathways.
Flashcards: Absolute vs Relative Selectivity
Q1: Why is relative selectivity used instead of absolute selectivity in drug action?
Q2: What is the definition of relative selectivity?
Q3: What is the concept of clinical selectivity?
Would you like more details on clinical selectivity? 😊
A1: No drug has only one single, specific effect. Drugs produce a spectrum of effects, so selectivity is considered relative—the degree to which a drug acts upon a given site relative to all possible sites of interaction.
A2: Relative selectivity is the degree to which a drug acts upon a given site relative to all possible sites of interaction.
A3: Clinical selectivity refers to a drug’s ability to achieve its therapeutic effects while minimizing side effects by targeting specific sites or receptors more effectively than others.
Flashcards: Therapeutic vs Undesirable (Side) Effects
Q1: How are drug effects split?
Q2: How do undesirable effects arise?
Q3: What is clinical selectivity in relation to therapeutic vs. undesirable effects?
Would you like to expand on any of these examples? 😊
A1: Drug effects are split into therapeutic effects (desired) and undesirable effects (side effects).
A2: Undesirable effects can occur in various ways:
1. Same receptor-effector mechanism: Both therapeutic and undesirable effects may be mediated by the same receptor-effector mechanism (e.g., nitrates, insulin, warfarin).
2. Same receptors in different tissues: Both effects may be mediated by identical receptors located in different tissues (e.g., haloperidol, verapamil).
3. Different types of receptors: Both effects may be mediated by different types of receptors (e.g., salbutamol, propranolol).
A3: Clinical selectivity refers to the ability of a drug to produce its therapeutic effects while minimizing undesirable or side effects, typically by targeting specific receptors or tissues more effectively.
Flashcards: Concept of Therapeutic Index
Q1: How is the therapeutic index determined?
Q2: What does the therapeutic index measure?
Q3: What is an example of drugs with different therapeutic indices?
A1: The therapeutic index is determined by the ratio of the median toxic dose (TD50) to the median effective dose (ED50).
Therapeutic Index = TD50 / ED50
A2: The therapeutic index provides a measure of:
1. The margin of safety of a drug.
2. The benefit to risk ratio of a drug.
A3:
- Penicillin: Has a high therapeutic index, meaning it is safer with a large difference between effective and toxic doses.
- Warfarin: Has a low therapeutic index, meaning the difference between the effective and toxic doses is small, increasing the risk of adverse effects.
