Pediatrics
1 questionsA 6-year-old child presents to the emergency department with sudden onset of palpitations, shortness of breath, and dizziness. The child has no significant past medical history. On examination, the heart rate is 220 beats per minute, blood pressure is $90 / 60 \mathrm{mmHg}$, and the child appears anxious but is otherwise stable. An ECG confirms the diagnosis of paroxysmal supraventricular tachycardia (PSVT). What is the initial recommended dose of adenosine for this child?
NEET-PG 2024 - Pediatrics NEET-PG Practice Questions and MCQs
Question 201: A 6-year-old child presents to the emergency department with sudden onset of palpitations, shortness of breath, and dizziness. The child has no significant past medical history. On examination, the heart rate is 220 beats per minute, blood pressure is $90 / 60 \mathrm{mmHg}$, and the child appears anxious but is otherwise stable. An ECG confirms the diagnosis of paroxysmal supraventricular tachycardia (PSVT). What is the initial recommended dose of adenosine for this child?
- A. $0.1 \mathrm{mg} / \mathrm{kg}$ (Correct Answer)
- B. $0.2 \mathrm{mg} / \mathrm{kg}$
- C. $0.5 \mathrm{mg} / \mathrm{kg}$
- D. $1.0 \mathrm{mg} / \mathrm{kg}$
- E. $0.05 \mathrm{mg} / \mathrm{kg}$
Explanation: ***0.1 mg/kg*** - The initial recommended dose of **adenosine** for children with **PSVT** is **0.1 mg/kg** given as a rapid intravenous bolus. - This dose is typically followed by a saline flush to ensure rapid delivery to the heart and minimize peripheral metabolism. *0.05 mg/kg* - This dose is **too low** and is below the recommended initial dose for pediatric PSVT. - While it may be safer, it is unlikely to be effective in terminating the arrhythmia and would delay definitive treatment. - The standard starting dose of 0.1 mg/kg has been established to balance efficacy with safety. *0.2 mg/kg* - This dose is typically used as a **second dose** of adenosine if the initial 0.1 mg/kg dose is ineffective in converting PSVT. - The second dose can be **doubled** (e.g., from 0.1 mg/kg to 0.2 mg/kg), with a maximum single dose of 12 mg. *0.5 mg/kg* - This dose is **too high** for the initial administration of adenosine in a pediatric patient and could lead to significant side effects like profound bradycardia or asystole. - Gradual dose escalation is crucial to balance efficacy with safety in children. *1.0 mg/kg* - This dose is **excessively high** for pediatric adenosine administration and is not recommended as an initial or even subsequent dose. - Such a dose would greatly increase the risk of adverse cardiovascular effects.
Pharmacology
9 questionsIn which phase of clinical trials is drug dosing typically determined?
A patient with HIV who is currently on antiretroviral therapy consisting of zidovudine, lamivudine, and nevirapine is diagnosed with tuberculosis. Considering potential drug interactions, which of the following TB drugs should be changed in this patient?
Which of the following is commonly used for maintenance therapy in opioid abuse?
Caffeine is a widely used stimulant that promotes wakefulness. Which of the following mechanisms is responsible for this effect?
A 65-year-old patient presents with symptoms of bone pain, anemia, hypercalcemia, and renal impairment. A bone marrow biopsy confirms the diagnosis of multiple myeloma. The patient is started on a treatment regimen. Which of the following treatments is most likely associated with the reactivation of herpes zoster?
Which of the following is a selective norepinephrine reuptake inhibitor that can be used for the treatment of ADHD?
An 18-year-old boy from Rajasthan weighing 50 kg is diagnosed with mixed P . vivax and P . falciparum malaria. What is the appropriate treatment regimen on day 2?
Which of the following growth hormone analogues is not used for the treatment of GH deficiency but is used in the treatment of HIV associated lipodystrophy?
A 45-year-old patient with a history of depression was initially being treated with sertraline, but his symptoms were not adequately controlled. His medication regimen was changed to include an MAO inhibitor and amitriptyline. Shortly after the change in medication, the patient developed agitation, seizures, hyperreflexia, and tremor. Which of the following is the most appropriate treatment for this patient?
NEET-PG 2024 - Pharmacology NEET-PG Practice Questions and MCQs
Question 201: In which phase of clinical trials is drug dosing typically determined?
- A. Phase 1 (Correct Answer)
- B. Phase 2
- C. Phase 3
- D. Phase 4
- E. Phase 0
Explanation: ***Phase 1*** - This phase involves a small group of **healthy volunteers** to assess the drug's safety, **pharmacokinetics (PK)**, and establish an initial dosing range. - The primary goal is to determine a **safe dosage level**, establish the **maximum tolerated dose (MTD)**, and identify potential side effects. - This is where drug dosing is **typically determined**. *Phase 0* - This is an exploratory phase involving **microdosing** studies with subtherapeutic doses. - The goal is to gather preliminary PK/PD data, but **not to determine therapeutic dosing**. *Phase 2* - This phase involves a larger group of **patients** with the condition to be treated. - The main goal is to evaluate the drug's **effectiveness** and further assess safety, but not primarily to determine initial dosing. *Phase 3* - This phase involves a large number of patients across multiple sites to confirm the drug's **efficacy** and monitor side effects in a broader population. - Dosing strategies have generally been established in earlier phases, and this phase primarily validates them. *Phase 4* - This phase occurs **after a drug has been approved** and marketed. - It involves ongoing surveillance to monitor long-term effects, collect additional information on safety, and identify new uses, but not initial dose determination.
Question 202: A patient with HIV who is currently on antiretroviral therapy consisting of zidovudine, lamivudine, and nevirapine is diagnosed with tuberculosis. Considering potential drug interactions, which of the following TB drugs should be changed in this patient?
- A. Isoniazid
- B. Rifampicin (Correct Answer)
- C. Ethambutol
- D. Streptomycin
- E. Pyrazinamide
Explanation: **Rifampicin** - **Rifampicin** is a potent **CYP450 enzyme inducer**, which significantly increases the metabolism of **nevirapine**, a non-nucleoside reverse transcriptase inhibitor (NNRTI), leading to subtherapeutic levels and potential treatment failure. - In patients on **nevirapine-based ART**, **rifampicin** is typically avoided or replaced with other rifamycins (like **rifabutin**), or the antiretroviral regimen is switched to one that is less affected by enzyme induction. *Isoniazid* - **Isoniazid** does not have significant, clinically problematic interactions with the antiretroviral regimen mentioned (zidovudine, lamivudine, nevirapine), and is generally well-tolerated. - It is a cornerstone of TB treatment and is usually continued without dose adjustment or substitution in this scenario. *Pyrazinamide* - **Pyrazinamide** is part of the standard first-line TB treatment regimen and does not have clinically significant drug interactions with zidovudine, lamivudine, or nevirapine. - It can be safely continued without dose adjustment in patients on this ART regimen. *Ethambutol* - **Ethambutol** primarily causes **optic neuritis** as a side effect and does not have significant pharmacokinetic interactions with the antiretroviral drugs listed. - Its use in TB treatment alongside this ART regimen is generally safe and does not require a change. *Streptomycin* - **Streptomycin** is an **aminoglycoside antibiotic** primarily used for multi-drug resistant TB or in specific situations, and its main toxicity is **ototoxicity** and **nephrotoxicity**. - It does not have known significant drug interactions with zidovudine, lamivudine, or nevirapine that would necessitate a change.
Question 203: Which of the following is commonly used for maintenance therapy in opioid abuse?
- A. Clonidine
- B. Buprenorphine (Correct Answer)
- C. Butorphanol
- D. Naloxone
- E. Methadone
Explanation: ***Buprenorphine*** - **Buprenorphine** is a **partial opioid agonist** commonly used for the maintenance treatment of **opioid use disorder** due to its ability to reduce cravings and prevent withdrawal symptoms. - It has a "ceiling effect," meaning that its opioid effects level off at higher doses, which contributes to its **safety profile** and lower risk of overdose compared to full agonists. - Preferred over methadone in many settings due to its **superior safety profile**, lower abuse potential, and ability to be prescribed in office-based settings. *Clonidine* - **Clonidine** is an **alpha-2 adrenergic agonist** primarily used to manage **autonomic symptoms** of opioid withdrawal (e.g., sweating, hypertension), but it does not address cravings or provide opioid effects. - It is not considered a primary maintenance therapy for opioid use disorder. *Butorphanol* - **Butorphanol** is a **mixed opioid agonist-antagonist** often used for pain relief, but its partial agonist activity and potential for withdrawal in opioid-dependent individuals make it unsuitable for maintenance therapy in opioid abuse. - It can precipitate **opioid withdrawal** in patients who are opioid-dependent. *Naloxone* - **Naloxone** is an **opioid antagonist** used to rapidly reverse the effects of opioid overdose by blocking opioid receptors. - While critical in overdose situations, it is not used for maintenance therapy as it would induce immediate and severe opioid withdrawal symptoms. *Methadone* - **Methadone** is a **full opioid agonist** that is also used for maintenance therapy in opioid use disorder, particularly in specialized opioid treatment programs. - However, it requires **daily supervised dosing** in most jurisdictions, has a higher risk of overdose, respiratory depression, and QT prolongation, making buprenorphine often the **preferred first-line agent** for maintenance therapy.
Question 204: Caffeine is a widely used stimulant that promotes wakefulness. Which of the following mechanisms is responsible for this effect?
- A. Adenosine antagonism (Correct Answer)
- B. Increased discharge of norepinephrine from the locus ceruleus
- C. Release of histamine
- D. Inhibition of phosphodiesterase
- E. Dopamine reuptake inhibition
Explanation: ***Adenosine antagonism*** - Caffeine acts as a **competitive antagonist** at **adenosine receptors** (primarily A1 and A2A) in the brain. - **Adenosine** is an inhibitory neurotransmitter that promotes drowsiness and reduces neuronal activity; by blocking its receptors, caffeine prevents this sedation and promotes wakefulness. - This is the **primary mechanism** responsible for caffeine's stimulant effects at typical dietary doses. *Increased discharge of norepinephrine from the locus ceruleus* - While increased **norepinephrine** can promote wakefulness, it is not the primary direct mechanism by which caffeine exerts its stimulant effects. - Caffeine may indirectly affect norepinephrine release as a downstream consequence of adenosine receptor blockade, but this is a secondary effect. *Release of histamine* - **Histamine** is indeed a neurotransmitter involved in wakefulness and arousal, but caffeine does not primarily promote wakefulness by directly causing histamine release. - Some antihistamines cause drowsiness by blocking central histamine receptors, but caffeine's mechanism is distinct from the histaminergic system. *Inhibition of phosphodiesterase* - Caffeine does inhibit **phosphodiesterase (PDE)** enzymes, leading to increased intracellular **cAMP** levels. - However, PDE inhibition occurs at significantly **higher concentrations** than those required for adenosine receptor antagonism, making it a less important mechanism for caffeine's typical stimulant effects at common dietary doses (1-3 cups of coffee). *Dopamine reuptake inhibition* - While some CNS stimulants (e.g., **methylphenidate**, **cocaine**) work primarily through dopamine reuptake inhibition, this is **not** caffeine's primary mechanism. - Caffeine may have minor indirect effects on dopamine neurotransmission through its adenosine receptor antagonism, but direct dopamine reuptake inhibition is not a significant mechanism of action.
Question 205: A 65-year-old patient presents with symptoms of bone pain, anemia, hypercalcemia, and renal impairment. A bone marrow biopsy confirms the diagnosis of multiple myeloma. The patient is started on a treatment regimen. Which of the following treatments is most likely associated with the reactivation of herpes zoster?
- A. Bortezomib (Correct Answer)
- B. Lenalidomide
- C. Daratumumab
- D. Melphalan
- E. Dexamethasone
Explanation: ***Bortezomib*** - **Bortezomib**, a **proteasome inhibitor**, is known to increase the risk of herpes zoster reactivation in patients with multiple myeloma due to its immunosuppressive effects. - Prophylaxis with antiviral agents (e.g., acyclovir) is often recommended during bortezomib treatment to prevent this complication. - Studies show herpes zoster incidence of 10-15% in bortezomib-treated patients without prophylaxis. *Lenalidomide* - While lenalidomide is an **immunomodulatory drug** used in multiple myeloma, it is generally associated with a lower risk of herpes zoster reactivation compared to proteasome inhibitors. - It primarily acts by inhibiting angiogenesis and stimulating T-cell and natural killer cell activity. *Daratumumab* - **Daratumumab** is a **monoclonal antibody** targeting CD38 on myeloma cells, leading to their destruction. - Although it has immunosuppressive effects, it is less commonly associated with herpes zoster reactivation than bortezomib. *Melphalan* - **Melphalan** is an **alkylating agent** used in chemotherapy for multiple myeloma, particularly in conditioning regimens for stem cell transplantation. - While it causes myelosuppression and general immunosuppression, the direct association with herpes zoster reactivation is not as prominent or specific as with bortezomib. *Dexamethasone* - **Dexamethasone** is a **corticosteroid** commonly used in combination regimens for multiple myeloma (e.g., RVD, VCD). - While corticosteroids cause immunosuppression and can increase infection risk, the specific association with herpes zoster reactivation is less pronounced than with bortezomib.
Question 206: Which of the following is a selective norepinephrine reuptake inhibitor that can be used for the treatment of ADHD?
- A. Reboxetine
- B. Methylphenidate
- C. Guanfacine
- D. Modafinil
- E. Atomoxetine (Correct Answer)
Explanation: ***Atomoxetine*** - **Atomoxetine** is a **selective norepinephrine reuptake inhibitor (SNRI)** that is **FDA-approved specifically for the treatment of ADHD** in children, adolescents, and adults. - It works by **selectively blocking the presynaptic norepinephrine transporter**, increasing norepinephrine availability in the prefrontal cortex and other brain regions involved in attention and impulse control. - Unlike stimulant medications, atomoxetine is **not a controlled substance** and is considered a first-line **non-stimulant option** for ADHD treatment. - It is particularly useful in patients with comorbid anxiety, tic disorders, or substance abuse concerns. *Reboxetine* - While **reboxetine** is technically a **selective norepinephrine reuptake inhibitor**, it is primarily used as an **antidepressant** and is **not approved for ADHD treatment**. - It has been investigated off-label for ADHD, but it is not a standard or recommended treatment option. - Reboxetine has **limited global availability** and has been withdrawn from many markets due to efficacy concerns. *Methylphenidate* - **Methylphenidate** is a **stimulant** medication that inhibits the reuptake of both **dopamine and norepinephrine**, making it **non-selective**. - It is a first-line treatment for ADHD, but its mechanism of action involves dual monoamine reuptake inhibition, not selective norepinephrine reuptake. *Guanfacine* - **Guanfacine** is an **alpha-2 adrenergic agonist**, not a norepinephrine reuptake inhibitor. - It works by stimulating postsynaptic alpha-2A receptors in the prefrontal cortex, which enhances prefrontal cortex function and improves attention and impulse control. *Modafinil* - **Modafinil** is a wakefulness-promoting agent with a **complex, non-selective mechanism** involving dopamine, norepinephrine, histamine, and orexin systems. - It is primarily used for **narcolepsy** and excessive daytime sleepiness, not as a primary ADHD treatment. - It is **not classified as a selective norepinephrine reuptake inhibitor**.
Question 207: An 18-year-old boy from Rajasthan weighing 50 kg is diagnosed with mixed P . vivax and P . falciparum malaria. What is the appropriate treatment regimen on day 2?
- A. Artesunate 50 mg (4 tablets) + Primaquine 2.5 mg ( 6 tablets)
- B. Artesunate 50 mg (4 tablets) + Primaquine 7.5 mg (6 tablets)
- C. Artesunate 50 mg (4 tablets) + Sulfadoxine/ pyrimethamine ( 750/37.5 mg ) (2 tablets) + Primaquine 2.5 mg ( 6 tablets) (Correct Answer)
- D. Artesunate 50 mg (4 tablets) + Sulfadoxine/ pyrimethamine ( 750/37.5 mg ) (2 tablets) + Primaquine 7.5 mg ( 6 tablets)
- E. Artesunate 50 mg (4 tablets) only
Explanation: ***Artesunate 50 mg (4 tablets) + Sulfadoxine/pyrimethamine (750/37.5 mg) (2 tablets) + Primaquine 2.5 mg (6 tablets)*** - For **mixed P. vivax and P. falciparum malaria**, the standard treatment regimen in India includes **Artesunate, Sulfadoxine/Pyrimethamine (SP)**, and **Primaquine**. - **Artesunate** and **SP** target the erythrocytic stages of P. falciparum, while **Primaquine** is essential for killing P. vivax hypnozoites (to prevent relapse) and P. falciparum gametocytes (to reduce transmission). - On **Day 2**, the patient continues with Artesunate along with SP (if given as single dose on Day 0, this would not be repeated; if following a specific protocol where Day 2 includes all three drugs, this represents the complete regimen). - The dosage of Primaquine of **2.5 mg** (0.25 mg/kg for 50 kg individual) daily for 14 days is appropriate for P. vivax radical cure. *Artesunate 50 mg (4 tablets) + Primaquine 2.5 mg (6 tablets)* - This regimen is incomplete for **mixed infections** as it lacks **Sulfadoxine/Pyrimethamine (SP)**, which is crucial for effective treatment of P. falciparum infections. - While Primaquine is included, the absence of SP would likely lead to treatment failure or recrudescence of **P. falciparum**. *Artesunate 50 mg (4 tablets) + Primaquine 7.5 mg (6 tablets)* - This regimen also omits **Sulfadoxine/Pyrimethamine (SP)**, which is necessary for the treatment of P. falciparum in mixed infections. - The **Primaquine dosage of 7.5 mg** is higher than typically used for P. vivax radical cure in this context (usually 0.25 mg/kg), and the absence of SP makes this regimen inadequate for mixed malaria. *Artesunate 50 mg (4 tablets) + Sulfadoxine/pyrimethamine (750/37.5 mg) (2 tablets) + Primaquine 7.5 mg (6 tablets)* - While this option includes **Artesunate** and **SP** for P. falciparum, the **Primaquine dose of 7.5 mg** is too high for the standard daily dose required for P. vivax radical cure in a 50 kg individual (which is 2.5 mg/day). - An inappropriately high dose of Primaquine for daily use for 14 days increases the risk of side effects, especially in individuals with **G6PD deficiency**, and is not the recommended regimen for mixed malaria in India. *Artesunate 50 mg (4 tablets) only* - While Artesunate is a key component of treatment, using it **alone on Day 2** without SP is inadequate for **P. falciparum** and does not address **P. vivax hypnozoites**. - This incomplete regimen would not provide radical cure for P. vivax and lacks the partner drug (SP) necessary for effective clearance of P. falciparum parasites.
Question 208: Which of the following growth hormone analogues is not used for the treatment of GH deficiency but is used in the treatment of HIV associated lipodystrophy?
- A. Tesamorelin (Correct Answer)
- B. Sermorelin
- C. Somatropin
- D. Pegvisomant
- E. Mecasermin
Explanation: ***Tesamorelin*** - **Tesamorelin** is a **growth hormone-releasing hormone (GHRH) analogue** approved specifically for the treatment of **HIV-associated lipodystrophy**. - It works by stimulating the natural production and release of endogenous growth hormone, which helps reduce **visceral adipose tissue** observed in this condition. - **Key distinction:** NOT used for GH deficiency, but specifically for lipodystrophy. *Sermorelin* - **Sermorelin** is also a **GHRH analogue**, but it is primarily used to diagnose and treat **growth hormone deficiency** in children. - It is not approved for lipodystrophy and works by stimulating the pituitary to secrete growth hormone. *Somatropin* - **Somatropin** is the recombinant form of **human growth hormone (GH)** itself, used to treat **growth hormone deficiency** in both children and adults. - While it can affect body composition, its primary indication is not HIV-associated lipodystrophy. *Mecasermin* - **Mecasermin** is recombinant **insulin-like growth factor-1 (IGF-1)** used to treat severe primary IGF-1 deficiency. - It is used for growth failure in children with GH gene deletion or GH receptor defects, not for HIV-associated lipodystrophy. *Pegvisomant* - **Pegvisomant** is a **growth hormone receptor antagonist** used to treat **acromegaly**, a condition caused by excessive growth hormone. - It works by blocking the action of growth hormone at its receptor, directly opposing the therapeutic goal for lipodystrophy.
Question 209: A 45-year-old patient with a history of depression was initially being treated with sertraline, but his symptoms were not adequately controlled. His medication regimen was changed to include an MAO inhibitor and amitriptyline. Shortly after the change in medication, the patient developed agitation, seizures, hyperreflexia, and tremor. Which of the following is the most appropriate treatment for this patient?
- A. Cyproheptadine (Correct Answer)
- B. Lorazepam
- C. L-carnitine
- D. Leucovorin
- E. Dantrolene
Explanation: ***Cyproheptadine*** - This patient exhibits symptoms of **serotonin syndrome** (agitation, seizures, hyperreflexia, tremor) due to the combination of an **MAO inhibitor** and **amitriptyline**. - **Cyproheptadine** is a **serotonin antagonist** and is the most appropriate treatment for reversing the effects of serotonin syndrome. - Treatment also includes discontinuing offending agents and supportive care. *Lorazepam* - **Lorazepam** is a **benzodiazepine** that can help manage agitation and seizures, but it does not address the underlying serotonin overstimulation. - It would be used as an adjunct for symptom control, not as the primary treatment for serotonin syndrome. *Dantrolene* - **Dantrolene** is a **muscle relaxant** used for **neuroleptic malignant syndrome (NMS)** and **malignant hyperthermia**. - While NMS and serotonin syndrome can have overlapping features (hyperthermia, rigidity), dantrolene is not indicated for serotonin syndrome. - Cyproheptadine is the specific serotonin antagonist needed for this condition. *L-carnitine* - **L-carnitine** is a supplement often used for conditions like **carnitine deficiency** or certain **metabolic disorders**. - It has no role in the treatment of serotonin syndrome. *Leucovorin* - **Leucovorin** (folinic acid) is used to **rescue bone marrow** from the toxic effects of **methotrexate** or to enhance the effects of **fluorouracil**. - It is not indicated for the treatment of serotonin syndrome.