Chronopharmacology — MCQs

10 questions

The cytochrome involved in monooxygenase-mediated detoxification of drugs is:

Which of the following drugs should be given in a sustained-release oral dosage form?

Which of the following structures is the primary regulator of circadian rhythms in the body?

A patient is on phenytoin for a seizure disorder. He was prescribed sucralfate 4 times a day for peptic ulcers. What should be the minimum duration of time between consumption of these drugs?

A person experiences asthma attacks more than twice during the day and at least once during the night. What is the most likely classification of their asthma?

Cushing reflex is associated with all except?

Which of the following will occur on efferent arteriolar constriction?

Q10

GFR is increased by all except?

Chronopharmacology Indian Medical PG Practice Questions and MCQs

Question 1: The cytochrome involved in monooxygenase-mediated detoxification of drugs is:

A. Cyt P 450 (Correct Answer)
B. Cytochrome b5
C. Cytochrome c
D. Cytochrome oxidase

Explanation: ***Cyt P 450*** - **Cytochrome P450 (CYP450)** enzymes are a superfamily of heme-containing monooxygenases primarily responsible for the **metabolism of xenobiotics**, including the detoxification of drugs. - They catalyze oxidation reactions, introducing a hydroxyl group to substrates, which typically increases their **hydrophilicity** and facilitates excretion. *Cytochrome c* - **Cytochrome c** is a component of the **electron transport chain** in mitochondria, primarily involved in cellular respiration and energy production. - It acts as an **electron carrier** between Complex III and Complex IV, not directly in drug detoxification. *Cytochrome b5* - **Cytochrome b5** participates in various metabolic reactions, including **fatty acid desaturation** and cholesterol biosynthesis, and can sometimes assist CYP450 enzymes. - However, it does not function as a primary monooxygenase for drug detoxification itself. *Cytochrome oxidase* - **Cytochrome oxidase** (Complex IV) is the terminal enzyme in the **electron transport chain**, responsible for the reduction of oxygen to water. - Its main role is in cellular respiration, and it is not directly involved in drug monooxygenation or detoxification.

Question 2: Match the following antiarrhythmic drugs with their mechanism of action: | Mechanism of action | Drug | | :-- | :-- | | 1. Na+ channel blocker | A. Quinidine | | 2. K+ channel blocker | B. Digoxin | | 3. Na+K+ ATPase inhibitor | C. Esmolol | | 4. Beta-blocker | D. Ibutilide |

A. 1-D, 2-B, 3-A, 4-C
B. 1-A, 2-D, 3-B, 4-C (Correct Answer)
C. 1-A, 2-C, 3-D, 4-B
D. 1-D, 2-C, 3-A, 4-B

Explanation: ***1-A, 2-D, 3-B, 4-C*** - **Quinidine** is a Class IA antiarrhythmic drug that primarily blocks **sodium channels**, prolonging the action potential duration and refractoriness. - **Ibutilide** is a Class III antiarrhythmic drug that blocks **potassium channels**, leading to delayed repolarization and increased effective refractory period. - **Digoxin** inhibits the **Na+/K+ ATPase pump**, increasing intracellular calcium and affecting AV nodal conduction. - **Esmolol** is a **beta-blocker** (Class II antiarrhythmic) that reduces heart rate and contractility by blocking β1-adrenergic receptors. *1-A, 2-C, 3-D, 4-B* - This option incorrectly matches **Esmolol** (a beta-blocker) with **K+ channel blocker** and **Ibutilide** (K+ channel blocker) with **Na+K+ ATPase inhibitor**. - It also incorrectly matches **Digoxin** (Na+K+ ATPase inhibitor) with **beta-blocker**. *1-D, 2-C, 3-A, 4-B* - This option incorrectly matches **Ibutilide** (K+ channel blocker) with **Na+ channel blocker** and incorrectly matches **Quinidine** (Na+ channel blocker) with **Na+K+ ATPase inhibitor**. - It also incorrectly matches **Digoxin** (Na+K+ ATPase inhibitor) with **beta-blocker**. *1-D, 2-B, 3-A, 4-C* - This option incorrectly matches **Ibutilide** (K+ channel blocker) with **Na+ channel blocker** and **Digoxin** (Na+K+ ATPase inhibitor) with **K+ channel blocker**. - It also incorrectly matches **Quinidine** (Na+ channel blocker) with **Na+K+ ATPase inhibitor**.

Question 3: Which of the following drugs should be given in a sustained-release oral dosage form?

A. An anti-arrhythmic drug with a plasma half life of 10 seconds used for acute treatment of PSVT
B. Anti inflammatory drugs with the plasma half life of 24 hours
C. Hypnotic drugs with a plasma half life of 2 hours
D. An antihypertensive with a plasma half-life of 3 hours (Correct Answer)

Explanation: *An anti-arrhythmic drug with a plasma half life of 10 seconds used for acute treatment of PSVT* - An extremely short **half-life** (10 seconds) indicates a drug suitable for **rapid-onset, acute interventions**, where the effect is needed immediately and for a very brief duration, making sustained release impractical. - Drugs like **adenosine**, used for acute PSVT, are given intravenously as a rapid bolus due to their ultra-short half-life, not in an oral sustained-release form. *Anti inflammatory drugs with the plasma half life of 24 hours* - A long **half-life** (24 hours) typically means the drug can be administered **once daily** to maintain therapeutic concentrations, rendering a sustained-release formulation unnecessary. - Such drugs already provide **prolonged action** and do not benefit significantly from further extension of release. *Hypnotic drugs with a plasma half life of 2 hours* - While a 2-hour half-life for a hypnotic might suggest potential for sustained release to prolong sleep, the goal of hypnotics is often a **rapid onset and relatively short duration** to avoid hangover effects. - Sustained release might cause **daytime sedation** and interfere with normal wakefulness, which is generally undesirable for this class of drugs. ***An antihypertensive with a plasma half-life of 3 hours*** - A short **half-life** (e.g., 3 hours) often necessitates frequent dosing to maintain therapeutic levels, making a **sustained-release formulation desirable** for patient compliance and consistent drug exposure. - Sustained-release dosage forms are particularly useful for drugs requiring **long-term, stable plasma concentrations**, such as antihypertensives, to manage chronic conditions effectively.

Question 4: Which of the following structures is the primary regulator of circadian rhythms in the body?

A. Ventromedial nucleus
B. Supraoptic nucleus
C. Suprachiasmatic nucleus (Correct Answer)
D. Dorsomedial nucleus

Explanation: ***Suprachiasmatic nucleus*** - The **suprachiasmatic nucleus (SCN)** is the primary **circadian pacemaker** in mammals, regulating various daily rhythms including the sleep-wake cycle, hormone secretion, and body temperature. - It receives direct input from the retina about light exposure, allowing it to synchronize the body's internal clock with the external light-dark cycle. *Ventromedial nucleus* - The **ventromedial nucleus (VMN)** of the hypothalamus is primarily involved in regulating **satiety** and is often referred to as the "satiety center." - Damage to the VMN can lead to **hyperphagia** (overeating) and obesity, rather than disturbances in daily rhythms. *Supraoptic nucleus* - The **supraoptic nucleus (SON)**, along with the paraventricular nucleus, is responsible for producing **vasopressin (ADH)** and **oxytocin**. - These hormones are then transported to the posterior pituitary for release, influencing water balance and social bonding, respectively, not daily rhythms. *Dorsomedial nucleus* - The **dorsomedial nucleus (DMN)** of the hypothalamus is involved in various functions including **feeding, drinking, and activity levels**. - While it can influence aspects of activity, it is not the primary regulator of the **circadian rhythm** itself; it receives input from the SCN.

Question 5: 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 6: A patient is on phenytoin for a seizure disorder. He was prescribed sucralfate 4 times a day for peptic ulcers. What should be the minimum duration of time between consumption of these drugs?

A. 90 minutes
B. 60 minutes
C. 120 minutes (Correct Answer)
D. 30 minutes

Explanation: **_120 minutes_** - **Sucralfate** forms a protective barrier in the stomach and can **adsorb other medications**, significantly reducing their absorption. - A minimum separation of **2 hours (120 minutes)** is recommended between sucralfate and other oral medications to prevent drug interactions. *90 minutes* - While a longer interval is beneficial, **90 minutes** may not be sufficient to completely avoid the significant reduction in **phenytoin absorption** caused by sucralfate. - Given the narrow therapeutic index of phenytoin, a more conservative approach with a longer separation is preferred. *60 minutes* - A **60-minute interval** is generally considered too short to prevent the **adsorption of phenytoin** by sucralfate. - This short duration increases the risk of **subtherapeutic phenytoin levels** and potential seizure recurrence. *30 minutes* - A **30-minute interval** is entirely inadequate and would almost certainly lead to a significant **reduction in phenytoin absorption**. - This would place the patient at high risk of **seizure recurrence** due to insufficient drug levels.

Question 7: A person experiences asthma attacks more than twice during the day and at least once during the night. What is the most likely classification of their asthma?

A. Intermittent asthma
B. Mild persistent asthma
C. Moderate persistent asthma
D. Severe persistent asthma (Correct Answer)

Explanation: ***Severe persistent asthma*** - This classification is characterized by **frequent symptoms**, specifically asthma attacks occurring more than twice daily and at least once nightly. - Individuals with severe persistent asthma often experience significant limitations in their daily activities and may have a **FEV1 (forced expiratory volume in 1 second)** less than 60% of predicted. *Intermittent asthma* - This classification is characterized by symptoms occurring less than two days per week and **nighttime awakenings less than two times per month**. - Symptoms are generally well-controlled with a short-acting beta-agonist (SABA) as needed. *Mild persistent asthma* - Patients with mild persistent asthma typically experience symptoms more than twice a week but **less than once a day**, and **nighttime awakenings 3-4 times per month**. - Their lung function (FEV1) is usually 80% or more of predicted. *Moderate persistent asthma* - This category involves daily symptoms and **nighttime awakenings more than once per week but not nightly**. - Lung function (FEV1) in moderate persistent asthma typically falls between 60% and 80% of predicted.

Question 8: Cushing reflex is associated with all except?

A. Irregular respiration
B. Hypotension (Correct Answer)
C. Increased intracranial pressure
D. Bradycardia

Explanation: ***Hypotension*** - The **Cushing reflex** is a compensatory response to increased intracranial pressure (ICP) aiming to maintain cerebral perfusion, which typically involves **hypertension**, not hypotension. - While prolonged or severe ICP can lead to decompensation and eventual hypotension, it is not a direct component of the reflex itself. *Increased intracranial pressure* - The **Cushing reflex** is triggered by an elevation in **intracranial pressure (ICP)**, as the body attempts to maintain blood flow to the brain. - This increased ICP reduces cerebral perfusion pressure, prompting a systemic response to raise mean arterial pressure. *Bradycardia* - **Bradycardia** is a classic component of the **Cushing reflex**, occurring as a compensatory response to the reflex hypertension. - The increased arterial blood pressure stimulates carotid and aortic baroreceptors, leading to a vagal response that slows the heart rate. *Irregular respiration* - **Irregular respiration** is another key component of the **Cushing reflex**, often manifesting as **Cheyne-Stokes breathing** or **ataxic breathing**. - This respiratory dysregulation is due to direct compression and dysfunction of the brainstem, specifically the medullary respiratory centers, caused by increased ICP.

Question 9: Which of the following will occur on efferent arteriolar constriction?

A. Increased GFR (Correct Answer)
B. Decreased GFR
C. Increase flow in vasa recta
D. Decreased flow in vasa recta

Explanation: ***Increased GFR*** - **Efferent arteriolar constriction** increases resistance to blood flow out of the glomerulus, causing blood to 'back up' and increase the **glomerular hydrostatic pressure (PGC)** - Higher **glomerular hydrostatic pressure** leads to increased net filtration pressure, which directly results in **increased glomerular filtration rate (GFR)** - This is the **primary and most clinically significant effect** of efferent arteriolar constriction - The increased PGC helps maintain GFR even when renal blood flow decreases slightly *Decreased GFR* - This is incorrect because **efferent arteriolar constriction** increases glomerular hydrostatic pressure, thereby **increasing GFR**, not decreasing it - Only severe efferent constriction that critically reduces renal plasma flow would eventually decrease GFR - The immediate and primary effect is always an increase in GFR *Increase flow in vasa recta* - This is incorrect; **efferent arteriolar constriction** actually **decreases** flow to the vasa recta - The constriction reduces blood flow exiting the glomerulus, which means less blood reaches the downstream peritubular capillaries and vasa recta - This decreased perfusion of the vasa recta can enhance urine concentration by reducing washout of the medullary concentration gradient *Decreased flow in vasa recta* - While this is physiologically true (efferent constriction does reduce peritubular and vasa recta blood flow), it is **not the primary or most significant effect** being tested - In the context of efferent arteriolar constriction, the **increased GFR** is the dominant and most clinically relevant consequence - The question asks "which will occur" expecting the primary hemodynamic effect on glomerular function - Decreased vasa recta flow is a secondary consequence, whereas increased GFR is the direct and immediate result

Question 10: GFR is increased by all except?

A. Renal stone in ureter (Correct Answer)
B. Efferent arteriole constriction
C. Decreased oncotic pressure
D. Increased renal blood flow

Explanation: ***Renal stone in ureter*** - A **renal stone in the ureter** would obstruct urine flow, leading to a buildup of pressure in **Bowman's capsule**. - This increased capsular hydrostatic pressure would **decrease the net filtration pressure**, thereby reducing GFR, not increasing it. *Efferent arteriole constriction* - **Constriction of the efferent arteriole** increases resistance to blood flow out of the glomerulus. - This elevates the **glomerular hydrostatic pressure (P_GC)**, which in turn increases the net filtration pressure and thus GFR. *Decreased oncotic pressure* - **Decreased plasma oncotic pressure (π_GC)** means there is less protein in the blood to pull fluid back into the glomerulus. - This reduction in the opposing force to filtration increases the net filtration pressure, leading to a higher GFR. *Increased renal blood flow* - **Increased renal blood flow** directly enhances the delivery of blood to the glomerulus. - This generally leads to a higher **glomerular hydrostatic pressure** and thus an increased GFR, assuming autoregulation mechanisms are not overwhelmed.

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