INI-CET 2021 — Pharmacology
15 Previous Year Questions with Answers & Explanations
Identify the correct 'organism-drug to which it is intrinsically resistant' pair.
What is the mechanism of action of local anesthetics?
Which of the following is not used to treat PCOD?
Which of the following is true regarding nicotine substitution therapy?
Hepatitis B subunit vaccine contains which of the following antigens?
Which of the following is false about the selection of essential drugs?
A patient who was diagnosed with epilepsy was put on retigabine TDS. Now phenytoin is being added. Which of the following changes should be made to retigabine?
A patient with history of ischemic stroke was started on clopidogrel. However, she had another attack of stroke after 6 months. Which of the following is likely to be responsible for the failure of clopidogrel in this patient?
Nivolumab is used as checkpoint inhibitor in
Antimicrobial combinations are used in all except
INI-CET 2021 - Pharmacology INI-CET Practice Questions and MCQs
Question 1: Identify the correct 'organism-drug to which it is intrinsically resistant' pair.
- A. Candida krusei - Fluconazole (Correct Answer)
- B. Candida albicans - Amphotericin B
- C. Aspergillus fumigatus - Micafungin
- D. Aspergillus niger - Voriconazole
Explanation: ***Candida krusei - Fluconazole*** - **Candida krusei** is intrinsically resistant to **fluconazole** due to reduced affinity of its target enzyme, **lanosterol 14-alpha demethylase**, for the drug. - This resistance is a natural characteristic of the species, meaning it is inherent and not acquired through exposure. *Aspergillus fumigatus - Micafungin* - **Aspergillus fumigatus** is generally susceptible to **micafungin**, an **echinocandin drug** that targets fungal cell wall synthesis. - While resistance can develop, it is not an intrinsic characteristic of *A. fumigatus* to micafungin. *Candida albicans - Amphotericin B* - **Candida albicans** is typically susceptible to **amphotericin B**, a polyene antifungal that binds to ergosterol in the fungal cell membrane. - Intrinsic resistance to amphotericin B in *C. albicans* is rare, though acquired resistance can occur. *Aspergillus niger - Voriconazole* - **Aspergillus niger** is usually susceptible to **voriconazole**, a broad-spectrum triazole antifungal. - There is no known intrinsic resistance of *A. niger* to voriconazole.
Question 2: What is the mechanism of action of local anesthetics?
- A. Block chloride channels
- B. Block calcium channels
- C. Block sodium channels (Correct Answer)
- D. Block potassium channels
Explanation: ***Block sodium channels*** - Local anesthetics work by **reversibly binding** to the alpha subunit of **voltage-gated sodium channels** on the neuronal membrane. - This binding prevents the influx of sodium ions, thereby inhibiting the **depolarization** of the neuron and **propagation of action potentials**. *Block chloride channels* - **Chloride channels** are primarily involved in **hyperpolarization** or stabilization of the resting membrane potential, and their blockade is not the primary mechanism of local anesthesia. - Drugs like **benzodiazepines** modulate GABA-gated chloride channels for their anxiolytic and sedative effects. *Block calcium channels* - **Calcium channels** are important for neurotransmitter release and muscle contraction, but their blockade is not the way local anesthetics exert their effects. - **Calcium channel blockers** are used in cardiovascular medicine (e.g., diltiazem, verapamil) to reduce heart rate and blood pressure. *Block potassium channels* - **Potassium channels** are crucial for repolarization of the neuronal membrane and maintaining the resting potential. - While some toxins block potassium channels, it is not the principal mechanism by which **local anesthetics** achieve their nerve blocking effect.
Question 3: Which of the following is not used to treat PCOD?
- A. Tamoxifen (Correct Answer)
- B. OCP
- C. Metformin
- D. Clomiphene citrate
Explanation: ***Tamoxifen*** - **Tamoxifen** is a selective estrogen receptor modulator (SERM) primarily used in the treatment of **estrogen receptor-positive breast cancer**. - While other SERMs like clomiphene citrate are used in PCOD for ovulation induction, tamoxifen is not a standard treatment for **PCOD** itself. *OCP* - **Oral contraceptive pills (OCPs)** are a common first-line treatment for managing various symptoms of PCOD, such as **menstrual irregularities** and **hirsutism**. - They work by suppressing ovarian androgen production and providing regular withdrawal bleeds. *Metformin* - **Metformin** is an insulin-sensitizing agent often used in PCOD, especially in women with **insulin resistance** or impaired glucose tolerance. - It helps improve **menstrual regularity** and can facilitate ovulation in some patients by reducing insulin levels. *Clomiphene citrate* - **Clomiphene citrate** is a selective estrogen receptor modulator (SERM) commonly used as an **ovulation induction agent** in women with PCOD who are trying to conceive. - It works by blocking estrogen receptors in the hypothalamus, leading to increased release of **gonadotropins** (FSH and LH).
Question 4: Which of the following is true regarding nicotine substitution therapy?
- A. Preferably given by gastrointestinal route.
- B. Varenicline comes with a black box warning of cardiovascular death
- C. There should be a 15-minute gap between nicotine gum and coffee/soda/acidic food as they decrease its absorption (Correct Answer)
- D. Nicotine chewing gum is better for constant use as it gives 25% higher blood level than lozenges
Explanation: ***There should be a 15-minute gap between nicotine gum and coffee/soda/acidic food as they decrease its absorption*** - **Acidic beverages** like coffee, soda, and fruit juices can alter the pH of the mouth and stomach, which significantly **reduces the absorption of nicotine** from gum. - This recommendation ensures optimal **nicotine delivery** and effectiveness of the therapy in reducing withdrawal symptoms. *Preferably given by gastrointestinal route* - Nicotine has poor bioavailability when taken orally due to **extensive first-pass metabolism** in the liver. - Nicotine substitution therapies are therefore preferentially administered via **transdermal**, **buccal** (gum, lozenges), or **nasal routes** to bypass first-pass metabolism and achieve therapeutic blood levels more effectively. *Varenicline comes with a black box warning of cardiovascular death* - Varenicline (Chantix) previously had a black box warning for **neuropsychiatric side effects**, including suicidal ideation and depression, which has since been removed due to further studies. - It does not carry a black box warning specifically for **cardiovascular death**, though cardiovascular events have been a subject of study, particularly in patients with pre-existing cardiovascular conditions. *Nicotine chewing gum is better for constant use as it gives 25% higher blood level than lozenges* - While both nicotine gum and lozenges are effective, the **blood levels achieved are comparable**, and the choice often depends on patient preference and proper technique. - Nicotine gum is best used with a **"chew and park" technique** to allow buccal absorption, and constant chewing can lead to excessive swallowing of nicotine, causing gastrointestinal upset.
Question 5: Hepatitis B subunit vaccine contains which of the following antigens?
- A. HbeAg
- B. HbsAg (Correct Answer)
- C. HbcAg
- D. HBV DNA
Explanation: ***HbsAg*** - The Hepatitis B vaccine is a **subunit vaccine** that contains recombinant **hepatitis B surface antigen (HBsAg)**. - This antigen is highly immunogenic and elicits a protective antibody response (anti-HBs) that neutralizes the virus. *HbeAg* - **HBeAg** indicates active viral replication and high infectivity, but it is not the antigen used in the vaccine. - While important for diagnostic purposes, antibodies to HBeAg (anti-HBe) indicate reduced viral replication. *HbcAg* - **HBcAg (hepatitis B core antigen)** is an internal component of the virion and is not found in the subunit vaccine. - Antibodies to HBcAg (anti-HBc) indicate past or current infection but do not confer protective immunity. *HBV DNA* - **HBV DNA** represents the viral genetic material and is a marker of active viral replication and infectivity. - It is not an antigen and therefore not included in a subunit vaccine designed to induce an immune response to viral proteins.
Question 6: Which of the following is false about the selection of essential drugs?
- A. Cost to benefit has to be considered
- B. Fixed drug combination is preferred over single drugs (Correct Answer)
- C. An adequate safety profile needs to be established
- D. Disease prevalence is considered
Explanation: ***Fixed drug combination is preferred over single drugs*** - The statement that **fixed-drug combinations (FDCs)** are preferred over single drugs for essential drug selection is false. Generally, **single drugs are preferred** to allow for individual dose adjustments and minimize potential adverse effects from unnecessary components. - FDCs are only considered essential when they offer specific advantages, such as **improved adherence** (e.g., in tuberculosis treatment) or a **synergistic effect** not achievable with individual drugs. *Cost to benefit has to be considered* - This statement is true; the **cost-effectiveness** and **cost-benefit ratio** are crucial factors in selecting essential drugs. - Essential drugs aim to provide the most public health benefit at an **affordable cost**, ensuring access for a broad population. *An adequate safety profile needs to be established* - This statement is true; essential drugs must have a **well-established safety profile** with acceptable risks. - The benefits of the drug must significantly outweigh its potential harms, with minimal serious **adverse reactions**. *Disease prevalence is considered* - This statement is true; essential drugs are selected based on their ability to address the **most prevalent diseases** and health needs of a population. - Prioritizing drugs for common conditions ensures that public health resources are effectively allocated to where they are most needed.
Question 7: A patient who was diagnosed with epilepsy was put on retigabine TDS. Now phenytoin is being added. Which of the following changes should be made to retigabine?
- A. Stop the drug
- B. Stop retigabine and start on carbamazepine
- C. Increase the dose (Correct Answer)
- D. Decrease the dose
Explanation: ***Increase the dose*** - **Phenytoin** is a potent **enzyme inducer** that induces hepatic enzymes including **UGT (glucuronidation) enzymes**. - **Retigabine** is primarily metabolized by **N-acetylation and glucuronidation** (not significantly by CYP450 enzymes). - Phenytoin induces UGT enzymes, which **increases retigabine metabolism and clearance**, leading to **decreased plasma concentrations**. - To maintain therapeutic levels and seizure control, the **dose of retigabine needs to be increased** when co-administered with phenytoin. *Stop the drug* - There is no clinical indication to completely **stop retigabine** simply because phenytoin is being added, as both can be used concurrently with dose adjustment. - Doing so might lead to a **loss of seizure control** if retigabine was providing effective seizure management. *Stop retigabine and start on carbamazepine* - This is an unnecessary and unindicated change; there is no medical reason to **switch from retigabine to carbamazepine** due to phenytoin addition. - Like phenytoin, **carbamazepine is also a strong enzyme inducer**, so similar drug interactions would occur. *Decrease the dose* - **Decreasing the dose** would be appropriate if phenytoin were an enzyme inhibitor, leading to higher retigabine levels. - Since phenytoin is an **enzyme inducer**, decreasing the dose would further reduce retigabine's therapeutic concentration, potentially leading to **breakthrough seizures**.
Question 8: A patient with history of ischemic stroke was started on clopidogrel. However, she had another attack of stroke after 6 months. Which of the following is likely to be responsible for the failure of clopidogrel in this patient?
- A. Upregulation of CYP1A1
- B. Downregulation of CYP2E1
- C. Downregulation of CYP2C19 (Correct Answer)
- D. Downregulation of CYP2D6
Explanation: ***Reduced function/Loss of function of CYP2C19*** - **Clopidogrel** is a **prodrug** that requires activation by **hepatic cytochrome P450 (CYP) enzymes**, primarily **CYP2C19**, to its active metabolite. - **Genetic polymorphisms** causing **reduced function or loss of function of CYP2C19** (e.g., CYP2C19*2, *3 alleles) result in insufficient conversion of clopidogrel to its active form, leading to **clopidogrel resistance** and increased risk of thrombotic events like recurrent stroke. - These **poor metabolizers** have significantly reduced antiplatelet response to standard clopidogrel doses. *Upregulation of CYP1A1* - **CYP1A1** is involved in the metabolism of various xenobiotics but plays a **minimal role** in clopidogrel activation. - Upregulation of CYP1A1 would not be a primary factor in clopidogrel failure as it is not the main enzyme responsible for its bioactivation. *Downregulation of CYP2E1* - **CYP2E1** is primarily involved in the metabolism of small organic molecules, some drugs, and toxins, and has **no significant role** in the bioactivation of clopidogrel. - Therefore, changes in its expression would not impact clopidogrel's efficacy. *Downregulation of CYP2D6* - **CYP2D6** is a major enzyme involved in the metabolism of many psychoactive drugs, beta-blockers, and opioids, but plays only a **minor role** in clopidogrel activation compared to CYP2C19. - Downregulation of CYP2D6 would not be the primary cause of clopidogrel failure.
Question 9: Nivolumab is used as checkpoint inhibitor in
- A. Hodgkin's lymphoma (Correct Answer)
- B. Medulloblastoma
- C. Retinoblastoma
- D. Pleuropulmonary blastoma
Explanation: ***Hodgkin's lymphoma*** - **Nivolumab** is an **immune checkpoint inhibitor** targeting **PD-1**. It has shown significant efficacy in treating relapsed or refractory Hodgkin's lymphoma, particularly in patients who have failed prior therapies. - Hodgkin's lymphoma cells, specifically **Reed-Sternberg cells**, often overexpress PD-L1, which allows them to evade the immune system, making PD-1 blockade a rational therapeutic strategy. *Medulloblastoma* - **Medulloblastoma** is a common malignant brain tumor in children, and while immunotherapy research is ongoing, Nivolumab is **not a standard treatment** for this condition. - Treatment typically involves **surgery, radiation, and chemotherapy**, with targeted therapies under investigation. *Retinoblastoma* - **Retinoblastoma** is a malignant tumor of the retina, most commonly affecting young children. Treatment usually involves **chemotherapy, laser therapy, cryotherapy, or enucleation**. - There is **no established role for Nivolumab** or PD-1 inhibitors in the routine management of retinoblastoma. *Pleuropulmonary blastoma* - **Pleuropulmonary blastoma** is a rare, malignant lung tumor of childhood. Treatment primarily consists of **surgery and chemotherapy**. - While experimental, there is **no current evidence** supporting the use of Nivolumab as a standard treatment for pleuropulmonary blastoma.
Question 10: Antimicrobial combinations are used in all except
- A. Intra abdominal infections
- B. Malaria
- C. Tuberculosis
- D. Gonorrhea (Correct Answer)
Explanation: ***Gonorrhea*** - While **gonorrhea** treatment has evolved to include **dual therapy** (e.g., ceftriaxone + azithromycin), this is primarily for co-treatment of potential Chlamydia co-infection and to combat emerging resistance, given as a **single-session treatment**. - Unlike the other conditions, gonorrhea does not require a **prolonged multi-drug regimen** with true synergy or prevention of resistance development during treatment. - The combination is more about empiric co-coverage and resistance concerns rather than the classic indications for antimicrobial combinations (synergy, preventing resistance emergence during therapy, polymicrobial coverage). - This distinguishes it from conditions requiring extended combination therapy. *Intra-abdominal infections* - Involve **polymicrobial etiology** requiring combination therapy to cover both aerobic (e.g., Enterobacteriaceae) and anaerobic bacteria (e.g., Bacteroides fragilis). - Combination therapy ensures broad-spectrum coverage for mixed infections and prevents treatment failures in complex intra-abdominal sepsis. *Malaria* - **Artemisinin-based combination therapies (ACTs)** are the standard first-line treatment for uncomplicated *Plasmodium falciparum* malaria. - Combination therapy reduces drug resistance risk and improves cure rates by targeting different mechanisms of action against the parasite. *Tuberculosis* - Treatment always involves **multi-drug regimen** (isoniazid, rifampicin, pyrazinamide, ethambutol) to prevent emergence of drug-resistant strains. - Multi-drug therapy is essential because *Mycobacterium tuberculosis* rapidly develops resistance if exposed to single agents during the prolonged treatment course.