Community Medicine
1 questionsIndia started 2-dose vaccination strategy for measles, in -
NEET-PG 2013 - Community Medicine NEET-PG Practice Questions and MCQs
Question 691: India started 2-dose vaccination strategy for measles, in -
- A. 2008
- B. 2009
- C. 2010 (Correct Answer)
- D. 2011
Explanation: ***2010*** - India implemented the **two-dose measles vaccination strategy** as part of its Universal Immunization Program starting in **2010**. - This decision was based on recommendations to improve immunity and reduce measles incidence, moving from a single-dose to a more effective **two-dose schedule**. *2008* - While important immunization initiatives were ongoing, the specific policy of a **two-dose measles vaccination strategy** had not yet been introduced in India during 2008. - At this time, the focus was primarily on ensuring high coverage of the **first dose** of measles vaccine. *2009* - The year 2009 saw continued efforts to strengthen the Universal Immunization Program, but the official launch of the **two-dose measles vaccination strategy** in India occurred later. - Discussions and planning for the transition were likely underway, but implementation began in the subsequent year. *2011* - By 2011, the **two-dose measles vaccination strategy** was already being implemented across India, having been introduced in 2010. - This year marked a period of expanding coverage and consolidation of the new 2-dose schedule rather than its initial introduction.
Microbiology
2 questionsWhich of the following bacteria does not exhibit bipolar staining?
Which anticoagulant is used when blood is sent for blood culture?
NEET-PG 2013 - Microbiology NEET-PG Practice Questions and MCQs
Question 691: Which of the following bacteria does not exhibit bipolar staining?
- A. Haemophilus influenzae (Correct Answer)
- B. Yersinia pestis
- C. Calymmatobacterium granulomatis
- D. Francisella tularensis
Explanation: ***Haemophilus influenzae*** - *Haemophilus influenzae* is a **pleomorphic coccobacillus** that typically stains uniformly and does not exhibit characteristic **bipolar staining**. - Its presence is often identified by Gram stain showing small, Gram-negative rods, but without the distinctive safety pin appearance. *Calymmatobacterium granulomatis* - *Calymmatobacterium granulomatis* (now *Klebsiella granulomatis*) is known to exhibit **bipolar staining**, often described as a **"safety pin" appearance**, especially in tissue smears from granuloma inguinale lesions. - This characteristic staining is due to the concentration of stain at the ends of the rod-shaped bacteria. *Yersinia pestis* - *Yersinia pestis*, the causative agent of plague, is classically described as having **bipolar staining**, giving it a distinctive **"safety pin" appearance** under a microscope. - This finding is a key diagnostic feature, particularly when observed in Gram-stained smears of clinical samples. *Francisella tularensis* - *Francisella tularensis* is a small, Gram-negative coccobacillus that is known to exhibit **bipolar staining**, though it may be less prominent than in *Yersinia pestis*. - This characteristic can assist in the microscopic identification of the bacterium, which causes tularemia.
Question 692: Which anticoagulant is used when blood is sent for blood culture?
- A. Sodium citrate
- B. EDTA
- C. Oxalate
- D. SPS (Correct Answer)
Explanation: ***SPS*** - **SPS (Sodium Polyanethol Sulfonate)** is the preferred anticoagulant for blood cultures because it inhibits phagocytosis and complement activation, allowing microorganisms to survive and grow. - It also neutralizes the bactericidal effect of aminoglycoside antibiotics, which might be present in the patient's blood. *Sodium citrate* - **Sodium citrate** works by binding to calcium ions, preventing blood coagulation, and is typically used for coagulation studies. - It is not suitable for blood cultures as it does not have the anti-phagocytic or antibiotic-neutralizing properties of SPS. *EDTA* - **EDTA (Ethylenediaminetetraacetic acid)** is a strong chelator of calcium and is primarily used for hematology tests like complete blood counts (CBC) as it preserves cell morphology. - It can be toxic to some bacteria and would inhibit microbial growth, making it unsuitable for blood cultures. *Oxalate* - Various **oxalates** (e.g., potassium oxalate) also act as anticoagulants by precipitating calcium, and are commonly found in tubes for glucose testing when combined with a glycolytic inhibitor. - Oxalates are generally unsuitable for blood cultures because they can inhibit the growth of certain microorganisms.
Pharmacology
7 questionsWhich of the following medications is known to cause peripheral neuropathy?
Peripheral neuropathy as a side effect is caused by which of the following anticancer drugs?
Gynaecomastia is caused by which drug?
Which of the following medications is most likely to cause reflex tachycardia?
In which of the following conditions is Verapamil not typically used?
Botulinum toxin acts on
Which class of drugs does botulinum toxin mimic in its action?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 691: Which of the following medications is known to cause peripheral neuropathy?
- A. Sulfonamide
- B. Vincristine (Correct Answer)
- C. Amiodarone
- D. Paclitaxel
Explanation: ***Vincristine*** - **Vincristine** is a **vinca alkaloid chemotherapeutic agent** that is **notorious** for causing **peripheral neuropathy** as its **dose-limiting toxicity**. - It interferes with **microtubule function** during mitosis, leading to **axonal damage** and predominantly **sensorimotor neuropathy**. - Peripheral neuropathy occurs in **virtually all patients** receiving vincristine and typically manifests as **distal paresthesias**, **loss of deep tendon reflexes**, and **motor weakness**. - This is the **most characteristic adverse effect** of vincristine. *Paclitaxel* - **Paclitaxel** is a **taxane chemotherapeutic agent** that also causes **peripheral neuropathy** as a significant adverse effect. - It stabilizes **microtubules**, preventing their depolymerization, leading to neurotoxicity. - While peripheral neuropathy is common with paclitaxel, it shares prominence with other major toxicities like **myelosuppression** and **hypersensitivity reactions**. *Sulfonamide* - **Sulfonamide antibiotics** are primarily associated with **hypersensitivity reactions**, **crystalluria**, **skin rashes**, and **hematologic abnormalities**. - Peripheral neuropathy is not a recognized or common adverse effect of sulfonamides. *Amiodarone* - **Amiodarone** is an **antiarrhythmic drug** with multiple adverse effects including **pulmonary fibrosis**, **thyroid dysfunction**, **corneal deposits**, and **hepatotoxicity**. - While rare cases of **peripheral neuropathy** have been reported, it is **not a characteristic or common adverse effect** of amiodarone.
Question 692: Peripheral neuropathy as a side effect is caused by which of the following anticancer drugs?
- A. Cyclophosphamide
- B. Etoposide
- C. Irinotecan
- D. Vincristine (Correct Answer)
Explanation: ***Vincristine*** - **Vincristine** is a **vinca alkaloid** that works by inhibiting **microtubule formation**, which is essential for cell division [1], [3]. - Its major dose-limiting toxicity is **peripheral neuropathy**, manifesting as paresthesias, weakness, and loss of reflexes due to damage to neuronal microtubules [1], [2]. *Cyclophosphamide* - **Cyclophosphamide** is an **alkylating agent** that forms cross-links in DNA, leading to cell death. - Its most common side effects include **myelosuppression**, hemorrhagic cystitis, and alopecia; **peripheral neuropathy** is generally not a prominent adverse effect. *Etoposide* - **Etoposide** is a **topoisomerase II inhibitor** that causes DNA strand breaks. - Key toxicities include **myelosuppression** and **gastrointestinal disturbances**, but it is not typically associated with significant peripheral neuropathy. *Irinotecan* - **Irinotecan** is a **topoisomerase I inhibitor** that causes DNA damage during replication. - Its primary dose-limiting toxicities are **diarrhea** and **myelosuppression**, not peripheral neuropathy.
Question 693: Gynaecomastia is caused by which drug?
- A. Spironolactone (Correct Answer)
- B. Rifampicin
- C. Thiazide
- D. Propranolol
Explanation: ***Spironolactone*** - Spironolactone is a **well-established cause of gynaecomastia**, occurring in 5-10% of patients in a dose-dependent manner. - It acts as an **anti-androgen** by blocking androgen receptors and inhibiting testosterone synthesis, thereby increasing the estrogen to androgen ratio. - It is a **potassium-sparing diuretic** and aldosterone antagonist, commonly used in heart failure, hypertension, and conditions requiring androgen blockade. *Rifampicin* - Rifampicin is an **antibiotic** primarily used to treat tuberculosis and acts as a **strong inducer of cytochrome P450 enzymes**. - While rare hormonal effects have been reported, it is **not a recognized common cause** of gynaecomastia. - Main side effects include hepatotoxicity, orange discoloration of bodily fluids, and drug interactions. *Thiazide* - Thiazide diuretics work by inhibiting the **sodium-chloride cotransporter** in the distal convoluted tubule. - They are **not commonly associated** with gynaecomastia; typical side effects include hypokalemia, hyponatremia, and hyperglycemia. *Propranolol* - Propranolol is a **non-selective beta-blocker** used for hypertension, angina, arrhythmias, and anxiety. - While beta-blockers have rarely been implicated, propranolol is **not a well-established cause** of gynaecomastia compared to spironolactone. - Common side effects include bradycardia, fatigue, and bronchospasm.
Question 694: Which of the following medications is most likely to cause reflex tachycardia?
- A. Nifedipine (Correct Answer)
- B. Verapamil
- C. Propranolol
- D. Amlodipine
Explanation: ***Nifedipine*** - Nifedipine is a **dihydropyridine calcium channel blocker** that causes significant peripheral vasodilation, leading to a rapid drop in blood pressure. - This sudden drop in blood pressure triggers a **baroreflex response**, compensatory increase in heart rate. *Verapamil* - Verapamil is a **non-dihydropyridine calcium channel blocker** that primarily acts on the cardiac pacemaker cells and slows AV nodal conduction. - While it can cause vasodilation, its direct negative chronotropic effect on the heart often **blunts or prevents reflex tachycardia**. *Propranolol* - Propranolol is a **non-selective beta-blocker** that blocks beta-1 and beta-2 adrenergic receptors. - It directly **decreases heart rate and myocardial contractility**, thereby preventing reflex tachycardia. *Amlodipine* - Amlodipine is a **dihydropyridine calcium channel blocker**, similar to nifedipine, but it has a **slower onset of action and a longer half-life**. - Its more gradual onset of vasodilation often results in a significantly **less pronounced or absent reflex tachycardia** compared to nifedipine.
Question 695: In which of the following conditions is Verapamil not typically used?
- A. Angina pectoris
- B. Atrial fibrillation
- C. Ventricular tachycardia (Correct Answer)
- D. Hypertension
Explanation: ***Ventricular tachycardia*** - Verapamil, a **non-dihydropyridine calcium channel blocker**, can worsen hemodynamics in patients with **ventricular tachycardia (VT)** by causing profound hypotension or precipitating cardiac arrest. - VT often requires prompt treatment with **antiarrhythmics like amiodarone** or **electrical cardioversion**, as it can be life-threatening. - Verapamil is **contraindicated in VT** due to its negative inotropic effects and risk of hemodynamic collapse. *Angina pectoris* - Verapamil is effectively used to treat angina pectoris by **decreasing myocardial oxygen demand** through negative chronotropic and inotropic effects, and by causing **coronary vasodilation**, improving blood flow. - Its effects help to reduce the frequency and severity of anginal episodes, particularly in **stable angina**. *Atrial fibrillation* - Verapamil is commonly used for **rate control in atrial fibrillation** by **slowing conduction through the AV node**, which decreases the ventricular response rate. - It helps to manage symptoms and prevent complications related to rapid heart rates in this arrhythmia. *Hypertension* - Verapamil is used in the treatment of **hypertension** through its vasodilatory effects and reduction in peripheral vascular resistance. - It is particularly useful in patients who cannot tolerate other antihypertensive agents or as part of combination therapy.
Question 696: Botulinum toxin acts on
- A. Synapse (Correct Answer)
- B. Smooth muscle of intestine
- C. Central nervous system
- D. Sensory nerves
Explanation: ***Synapse*** - **Botulinum toxin** acts by inhibiting the release of **acetylcholine** at the **neuromuscular junction**, which is a type of synapse. - This blockade of neurotransmitter release at the **presynaptic terminal** prevents muscle contraction, leading to paralysis. *Smooth muscle of intestine* - While botulinum toxin can affect smooth muscle indirectly by paralyzing the motor nerves innervating them, its primary site of action is the **synapse** itself, not directly on the muscle fibers. - The toxin primarily targets the nerve endings, rather than the mechanical contractility of the muscle cell. *Central nervous system* - **Botulinum toxin** does not readily cross the **blood-brain barrier**, meaning its primary effects are peripheral. - Its therapeutic and toxic effects are localized to the **peripheral nervous system** and neuromuscular junctions. *Sensory nerves* - **Botulinum toxin** specifically targets **motor nerve endings** to inhibit acetylcholine release, leading to muscle paralysis. - It does not directly affect the function of **sensory nerve transmission** or pain perception in the same way.
Question 697: Which class of drugs does botulinum toxin mimic in its action?
- A. Adrenergics
- B. Antiadrenergic
- C. Cholinergics
- D. Anticholinergics (Correct Answer)
Explanation: ***Anticholinergics*** - **Botulinum toxin** inhibits the release of **acetylcholine** from **presynaptic nerve terminals** [2] by preventing vesicle fusion, leading to muscle paralysis [1]. - While the **mechanism differs** (botulinum acts presynaptically, anticholinergics act postsynaptically at receptors), the **functional outcome** is similar: reduced cholinergic neurotransmission. - In terms of **clinical effect** at the neuromuscular junction, both reduce acetylcholine's action, making anticholinergics the closest functional parallel among the given options. *Cholinergics* - **Cholinergics** enhance acetylcholine activity, either by increasing its release, mimicking its effects at receptors, or inhibiting its breakdown. - This is the **opposite** of botulinum toxin's action, which reduces acetylcholine's impact. *Adrenergics* - **Adrenergics** stimulate the **sympathetic nervous system** via **adrenergic receptors** (α and β receptors). - They act on **norepinephrine/epinephrine pathways**, not the cholinergic system where botulinum toxin acts. *Antiadrenergic* - **Antiadrenergic drugs** block **adrenergic receptors** or inhibit sympathetic activity. - These are unrelated to botulinum toxin's effect on **cholinergic neuromuscular transmission**.