Drug Tolerance and Tachyphylaxis — MCQs
Pharmacodynamics deals with:-
Which sympathomimetic drug is primarily known to increase heart rate?
A female was given morphine sulphate during labour for pain but she developed respiratory distress. Which of the following will be the correct antidote?
Which of the following best demonstrates the variability in drug responsiveness among individuals?
Which of the following actions is NOT associated with tricyclic antidepressants?
Which of the following pairs are considered physiological antagonists in pharmacology?
What does the term 'tolerance' refer to in pharmacology?
Match the following drugs in Column A with their contraindications in Column B. | Column A | Column B | | :-- | :-- | | 1. Morphine | 1. QT prolongation | | 2. Amiodarone | 2. Thromboembolism | | 3. Vigabatrin | 3. Pregnancy | | 4. Estrogen preparations | 4. Head injury |
Which of the following is NOT a primary function of histamine antagonists as a drug class?
What do A and B represent in the curve shown below?
Drug Tolerance and Tachyphylaxis Indian Medical PG Practice Questions and MCQs
Question 1: Pharmacodynamics deals with:-
- A. Latency of onset
- B. Mechanism of action of a drug (Correct Answer)
- C. Transport of drug across the biological membranes
- D. Mode of excretion of a drug
Explanation: Detailed study of the **Mechanism of action of a drug** [1][2] - **Pharmacodynamics** describes what the **drug does to the body**, including its **molecular targets** and biochemical effects [3]. - This involves the study of the drug's mechanisms to produce its therapeutic or toxic effects [2]. *Latency of onset* - **Latency of onset** refers to the time it takes for a drug to start producing its effects, which is a pharmacokinetic rather than a pharmacodynamic parameter. - It deals with the drug's absorption and distribution rather than its interaction with the body once it reaches its site of action. *Transport of drug across the biological membranes* - The **transport of drugs across biological membranes** is a key aspect of **pharmacokinetics**, specifically absorption and distribution [1]. - This process determines how much drug reaches its target site, not how it interacts with the target. *Mode of excretion of a drug* - The **mode of excretion** of a drug (e.g., renal, hepatic) falls under **pharmacokinetics**, addressing how the body gets rid of the drug. - This process influences the drug's duration of action and elimination half-life, not its mechanism of action.
Question 2: Which sympathomimetic drug is primarily known to increase heart rate?
- A. Isoprenaline (Correct Answer)
- B. Phenylephrine
- C. Noradrenaline
- D. Adrenaline
Explanation: ***Isoprenaline*** - **Isoprenaline** (isoproterenol) is a non-selective beta-adrenergic agonist, with a strong affinity for **β1 and β2 receptors** [1]. - Its activation of **β1 receptors** in the heart leads to a significant increase in **heart rate (positive chronotropy)** and contractility (positive inotropy) [1]. - It is the **most potent chronotropic agent** among sympathomimetics and is primarily known for increasing heart rate [2]. *Phenylephrine* - **Phenylephrine** is a selective **α1 adrenergic agonist** that causes vasoconstriction [4]. - It increases blood pressure but typically causes **reflex bradycardia** (decreased heart rate) due to baroreceptor activation. - Does NOT directly increase heart rate. *Noradrenaline* - **Noradrenaline** (norepinephrine) primarily acts on **α1 receptors** causing vasoconstriction, and to a lesser extent on **β1 receptors** [3]. - While it can stimulate β1 receptors, its predominant effect is to increase **mean arterial pressure** through vasoconstriction, often causing **reflex bradycardia** [3]. *Adrenaline* - **Adrenaline** (epinephrine) acts on **α1, β1, and β2 receptors** [4]. While it does increase heart rate via **β1 receptor** stimulation, it also causes significant **vasoconstriction** (via α1) and **vasodilation** (via β2). - Its cardiovascular effects are more complex and dose-dependent compared to isoprenaline's specific chronotropic action.
Question 3: A female was given morphine sulphate during labour for pain but she developed respiratory distress. Which of the following will be the correct antidote?
- A. Naloxone (Correct Answer)
- B. Epinephrine
- C. Pralidoxime
- D. Atropine
Explanation: ***Naloxone*** - **Naloxone** is a pure opioid antagonist that rapidly reverses the effects of **opioid overdose** [1, 3], including **respiratory depression** [2], by competitively binding to opioid receptors [1]. - Its short half-life may necessitate repeated doses, especially with longer-acting opioids like morphine, to prevent recurrence of respiratory depression [1]. *Epinephrine* - **Epinephrine** is an adrenergic agonist used to treat **anaphylaxis** and severe allergic reactions, as it causes **vasoconstriction** and **bronchodilation**. - It is not an antidote for opioid-induced respiratory depression, which primarily results from central nervous system effects rather than allergic reactions. *Pralidoxime* - **Pralidoxime** is a **cholinesterase reactivator** used to treat poisoning by **organophosphates**, which inhibit acetylcholinesterase, leading to cholinergic crisis. - It works by restoring the function of the enzyme, thereby breaking down excess acetylcholine, and is not indicated for opioid overdose. *Atropine* - **Atropine** is an **anticholinergic agent** that blocks muscarinic acetylcholine receptors, used to treat **bradycardia** and **organophosphate poisoning**. - It would not reverse opioid-induced respiratory depression, as it primarily affects the parasympathetic nervous system and does not antagonize opioid receptor effects.
Question 4: Which of the following best demonstrates the variability in drug responsiveness among individuals?
- A. Potency
- B. Quantal Dose Response Curve (Correct Answer)
- C. Efficacy
- D. Graded Dose Response Curve
Explanation: ***Quantal Dose Response Curve*** - A **quantal dose-response curve** plots the percentage of individuals exhibiting a discrete, all-or-none effect against the log dose of a drug. - This curve directly illustrates the **variability in drug responsiveness** within a population by showing the range of doses required to produce a specific effect in different individuals. *Efficacy* - **Efficacy** refers to the maximum effect a drug can produce, regardless of the dose. - While efficacy is an important pharmacological parameter, it describes the drug's overall therapeutic potential, not the **individual variability** in response. *Potency* - **Potency** is a measure of the amount of drug needed to produce an effect of given intensity. - It relates to the absolute dose required for a particular effect but does not directly demonstrate the **inter-individual differences** in biological response. *Graded Dose Response Curve* - A **graded dose-response curve** depicts the relationship between the dose of a drug and the **magnitude of the effect** in a **single biological unit** (e.g., an individual, a tissue, or a cell). - This curve reflects the relationship between drug concentration and effect intensity, but not the **variability in response among different individuals** in a population.
Question 5: Which of the following actions is NOT associated with tricyclic antidepressants?
- A. Block 5-HT or NE reuptake
- B. Anticholinergic action
- C. MAO inhibition (Correct Answer)
- D. Causes sedation
Explanation: ***MAO inhibition*** - Tricyclic antidepressants (TCAs) primarily exert their effects by inhibiting the reuptake of **norepinephrine** and **serotonin**, not by inhibiting monoamine oxidase (MAO). - **MAO inhibitors** are a distinct class of antidepressants with a different mechanism of action and side effect profile. *Anticholinergic action* - Many TCAs have significant **anticholinergic effects**, blocking muscarinic receptors and leading to side effects like dry mouth, constipation, and blurred vision. - These effects contribute to the **adverse event profile** of TCAs, especially in elderly patients. *Block 5-HT or NE reuptake* - The primary mechanism of action of TCAs involves the **inhibition of serotonin (5-HT)** and **norepinephrine (NE) reuptake** into presynaptic neurons. - This action increases the concentration of these neurotransmitters in the **synaptic cleft**, thereby potentiating their effects. *Causes sedation* - TCAs frequently cause **sedation**, particularly the more histaminergic ones (e.g., amitriptyline, doxepin), due to their **histamine H1 receptor antagonism**. - This side effect can be beneficial for patients with insomnia but can be problematic for daytime functioning.
Question 6: Which of the following pairs are considered physiological antagonists in pharmacology?
- A. Adrenaline and Isoprenaline
- B. Isoprenaline and Propranolol
- C. Histamine and Adrenaline (Correct Answer)
- D. All of the options
Explanation: ***Histamine and Adrenaline*** - **Physiological antagonism** occurs when two drugs produce opposite effects by acting on different receptors or pathways. - **Histamine** causes bronchoconstriction and vasodilation, while **adrenaline** causes bronchodilation and vasoconstriction, counteracting each other's effects through different mechanisms. *Adrenaline and Isoprenaline* - Both **adrenaline** and **isoprenaline** are **adrenergic agonists** that produce similar physiological effects, primarily through beta-adrenergic receptor activation. - They are not physiological antagonists but rather have **synergistic** or similar pharmacological actions. *Isoprenaline and Propranolol* - **Isoprenaline** is a **beta-adrenergic agonist**, while **propranolol** is a **beta-adrenergic antagonist**. - This is an example of **pharmacological antagonism (receptor antagonism)**, where one drug blocks the effect of another at the same receptor site, rather than physiological antagonism.
Question 7: What does the term 'tolerance' refer to in pharmacology?
- A. Increased effect of drug on the same dose
- B. Decreased effect of drug on the same dose (Correct Answer)
- C. Same effect at lower doses
- D. No effect
Explanation: ***Decreased effect of drug on the same dose*** - **Tolerance** is a state in which the body's response to a drug is **reduced** over time, requiring higher doses to achieve the same effect. - This phenomenon often develops with **repeated exposure** to a drug, leading to a need for dose escalation. *Increased effect of drug on the same dose* - This describes **sensitization** or **reverse tolerance**, where the body becomes more responsive to the drug over time, which is the opposite of tolerance. - It is not a characteristic feature of pharmacological tolerance. *Same effect at lower doses* - This would imply an **increased sensitivity** to the drug, meaning that less drug is needed to achieve the desired effect. - This is contrary to the definition of tolerance, which requires higher doses for the same effect. *No effect* - While extreme tolerance can lead to a point where a drug has minimal or no clinical effect at standard doses, "no effect" itself is not the primary definition of tolerance. - Tolerance refers to the gradual **reduction in effect**, rather than an immediate absence of effect.
Question 8: Match the following drugs in Column A with their contraindications in Column B. | Column A | Column B | | :-- | :-- | | 1. Morphine | 1. QT prolongation | | 2. Amiodarone | 2. Thromboembolism | | 3. Vigabatrin | 3. Pregnancy | | 4. Estrogen preparations | 4. Head injury |
- A. A-1, B-3, C-2, D-4
- B. A-4, B-1, C-3, D-2 (Correct Answer)
- C. A-3, B-2, C-4, D-1
- D. A-2, B-4, C-1, D-3
Explanation: ***A-4, B-1, C-3, D-2*** - **Morphine** is contraindicated in **head injury** as it can increase intracranial pressure and mask neurological symptoms. - **Amiodarone** is contraindicated in patients with **QT prolongation** due to its risk of inducing more severe arrhythmias like Torsades de Pointes. - **Vigabatrin** is contraindicated during **pregnancy** due to its potential for teratogenicity and adverse effects on fetal development. - **Estrogen preparations** are contraindicated in patients with a history of **thromboembolism** due to their increased risk of blood clot formation. *A-1, B-3, C-2, D-4* - This option incorrectly matches **Morphine** with QT prolongation and **Estrogen preparations** with head injury, which are not their primary contraindications. - It also incorrectly links **Vigabatrin** with thromboembolism and **Amiodarone** with pregnancy. *A-3, B-2, C-4, D-1* - This choice incorrectly associates **Morphine** with pregnancy and **Vigabatrin** with head injury, which are not the most critical or direct contraindications. - It also misaligns **Amiodarone** with thromboembolism and **Estrogen preparations** with QT prolongation. *A-2, B-4, C-1, D-3* - This option incorrectly matches **Morphine** with thromboembolism and **Amiodarone** with head injury, which are not their most significant contraindications. - It also incorrectly links **Vigabatrin** with QT prolongation and **Estrogen preparations** with pregnancy.
Question 9: Which of the following is NOT a primary function of histamine antagonists as a drug class?
- A. Antipruritic
- B. Sedation
- C. Inhibition of gastric acid secretion
- D. Antivertigo (Correct Answer)
Explanation: ***Antivertigo*** - While some first-generation **H1-antihistamines** like dimenhydrinate and meclizine have **antivertigo** properties due to their anticholinergic and sedative effects, this is a specific *effect* of certain histamine antagonists, not a general *function* that all antagonists exhibit. - The question asks for an exception to the *general functions* of histamine antagonists. **Antivertigo** is not a primary, universal effect of histamine antagonism in the way the other options describe. *Antipruritic* - **H1-antihistamines** block the action of **histamine** on **H1 receptors**, which are involved in mediating itching (**pruritus**). - This is a common and primary function of **H1-antagonists** in treating allergic reactions and skin conditions. *Sedation* - First-generation **H1-antihistamines** readily cross the **blood-brain barrier** and block **H1 receptors** in the brain, leading to drowsiness and **sedation**. - This is a well-known side effect and, in some cases, a therapeutic use of these drugs. *Inhibition of gastric acid secretion* - **H2-antihistamines** (e.g., ranitidine, cimetidine) specifically block **histamine H2 receptors** on **parietal cells** in the stomach, thereby reducing **gastric acid secretion**. - This is a primary function of a distinct class of histamine antagonists used to treat acid-related disorders.
Question 10: What do A and B represent in the curve shown below?
- A. A= Median effective dose, B= Median lethal dose (Correct Answer)
- B. A= Therapeutic index, B= Median efficacy
- C. A= Median lethal dose, B= Median effective dose
- D. A= Median efficacy, B= Therapeutic index
Explanation: ***A= Median effective dose, B= Median lethal dose*** - **A** corresponds to the **median effective dose (ED50)**, which is the dose that produces a therapeutic effect in 50% of the population - The purple curve represents the dose-response for efficacy; at A, 50% of individuals are responding effectively - **B** corresponds to the **median lethal dose (LD50)**, which is the dose that is lethal to 50% of the population - The red curve represents the dose-response for toxicity/lethality; at B, 50% of individuals are experiencing a lethal outcome *A= Therapeutic index, B= Median efficacy* - The **therapeutic index** is a ratio (LD50/ED50), not a specific dose represented on the x-axis - **Median efficacy** is not a standard pharmacological term to represent a point on a dose-response curve; rather, efficacy refers to the maximal effect a drug can produce *A= Median lethal dose, B= Median effective dose* - This option reverses the correct identification of A and B - **Median effective dose (ED50)** is typically expected at lower doses, while **median lethal dose (LD50)** is at higher doses, indicating toxicity - In the provided graph, the curve for A occurs at a much lower dose range than the curve for B, making it the effective dose, not the lethal dose *A= Median efficacy, B= Therapeutic index* - **Median efficacy** is not a specific dose value represented this way on a dose-response curve - The **therapeutic index** is a ratio, not a dose point on the graph
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