Internal Medicine
2 questionsWhich subtype of Acute Myeloid Leukemia (AML) is associated with the best prognosis?
Which of the following does not predispose to leukemia?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 471: Which subtype of Acute Myeloid Leukemia (AML) is associated with the best prognosis?
- A. Acute myelo monocytic leukemia.
- B. Acute monocytic leukemia.
- C. Erythro leukemia
- D. Acute promyeloblastic leukemia (M3) (Correct Answer)
Explanation: ***Acute promyeloblastic leukemia (M.3)*** [1] - **Best prognosis** in acute myeloid leukemia (AML) is associated with acute promyeloblastic leukemia due to its responsiveness to **all-trans retinoic acid (ATRA)** treatment. [1] - This type often presents with a **prominent coagulopathy**, but successful treatment can lead to **long-term remission**. *Acute monocytic leukemia* - Generally associated with **poor prognosis** and is characterized by a high white blood cell count and organ infiltration. - It lacks the favorable features seen in acute promyeloblastic leukemia, such as effective treatment outcomes. *Erythroleukemia* - Known for having a **poor prognosis** due to its aggressive nature and frequent association with complex chromosomal abnormalities. [1] - Treatment responses are often suboptimal compared to that of acute promyeloblastic leukemia. *Acute myelomonocytic leukemia* - Typically has an **intermediate prognosis** [1] and presents with a mixture of myeloid and monocytic features. - It does not have the same treatment responsiveness and favorable outcomes as seen in acute promyeloblastic leukemia.
Question 472: Which of the following does not predispose to leukemia?
- A. Smoking
- B. Chemical exposure
- C. Alcohol (Correct Answer)
- D. Genetic disorder
Explanation: ***Alcohol*** - Alcohol consumption does not have a well-established association with an increased risk of leukemia compared to other factors. - While excessive alcohol can impact overall health, it is not considered a primary risk factor for developing leukemia. *Chemical exposure* - Certain chemicals, such as **benzene** and **formaldehyde**, are known to be **leukemogenic** and can increase the risk of leukemia. [1] - Occupational exposure to these chemicals has been linked to **acute myeloid leukemia (AML)** and other types of leukemia. [1] *Smoking* - Smoking has been clearly associated with an increased risk of **acute myeloid leukemia (AML)** and other hematologic malignancies. [1] - The toxins in tobacco smoke can cause **DNA damage**, contributing to the development of leukemia. *Genetic disorder* - Certain genetic disorders, like **Down syndrome** and **Fanconi anemia**, are associated with an increased risk of leukemia. - Individuals with these genetic predispositions have a higher likelihood of developing various forms of leukemia.
Pathology
1 questionsWhich of the following is NOT seen in polycythemia vera?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 471: Which of the following is NOT seen in polycythemia vera?
- A. Increased erythropoietin (Correct Answer)
- B. Intrinsic abnormality of hematopoietic precursors
- C. Erythropoietin independent growth of red cell progenitors
- D. Most common cause of primary polycythemia
Explanation: ***Increased erythropoietin*** - In polycythemia vera, patients usually exhibit **low erythropoietin levels** due to feedback inhibition from increased red blood cell mass. - The condition is driven by a **myeloproliferative disorder** [2], not by increased erythropoietin stimulation. *Most common cause of polycythemia* - This option is incorrect because polycythemia vera is specifically a type of **primary polycythemia** [1], rather than the most common cause, which is often **secondary causes** such as hypoxia or abnormal erythropoietin production. - Other causes including chronic lung disease or renal tumors are more prevalent sources of increased red blood cell production. *Intrinsic abnormality of hematopoietic precursors* - While polycythemia vera indeed involves an **abnormality in hematopoietic stem cells** [1], it is not the only mechanism leading to polycythemia; many cases have secondary causes. - Hence, this option misrepresents the specific and more accurate characterization of polycythemia vera. *Erythropoietin independent growth of red cell progenitors* - Polycythemia vera is associated with **erythropoietin-independent** proliferation of hematopoietic cells [2], which is characteristic of the condition due to mutations in **JAK2** [2,3]. - This accurately reflects a significant feature of the disease, aligning closely with the pathophysiology. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 663-664. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 614-615. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 626-627.
Pharmacology
7 questionsBeta-blockers should be used with caution in patients with?
Which antimuscarinic drug is used in overactive bladder?
Maximum cycloplegic action of atropine is seen at ?
Which of the following is NOT a side effect of atropine?
Propranolol is most commonly prescribed as first-line therapy for which condition?
Which diuretic is known to cause the maximum potassium loss?
Hyoscine is an antagonist at which cholinergic receptor?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 471: Beta-blockers should be used with caution in patients with?
- A. Hypertension
- B. CHF
- C. Conduction defect (Correct Answer)
- D. Glaucoma
Explanation: ***Conduction defect*** - Beta-blockers **slow heart rate** and **decrease AV nodal conduction**, which can worsen pre-existing conduction defects like **AV block** or **sick sinus syndrome**. - Their use can lead to **symptomatic bradycardia** or complete heart block in susceptible individuals. - This represents a **strong relative contraindication** requiring significant caution. *Hypertension* - Beta-blockers are a **first-line treatment for hypertension**, effectively lowering blood pressure by reducing cardiac output and renin release. - They are generally **well-tolerated** and beneficial in most hypertensive patients. *Glaucoma* - Topical beta-blockers, such as **timolol**, are a common treatment for open-angle glaucoma as they **reduce aqueous humor production**, thereby lowering intraocular pressure. - Systemic use of beta-blockers does not typically worsen glaucoma and may even offer some benefit. *CHF* - While certain beta-blockers (**carvedilol, metoprolol succinate, bisoprolol**) are now proven beneficial in **chronic heart failure with reduced ejection fraction (HFrEF)**, they do require careful use. - They must be **initiated at low doses and carefully titrated** to avoid acute decompensation, and are **contraindicated in acute decompensated heart failure**. - However, **conduction defects** represent a **stronger contraindication** where beta-blockers can cause life-threatening bradycardia or complete heart block, making it the best answer for conditions requiring the most caution.
Question 472: Which antimuscarinic drug is used in overactive bladder?
- A. Trospium (Correct Answer)
- B. Atropine
- C. Tropicamide
- D. Pirenzepine
Explanation: ***Trospium*** - **Trospium** is a quaternary ammonium compound that acts as an **antimuscarinic agent** primarily used to treat **overactive bladder (OAB)**. - Its **polar nature** limits its ability to cross the blood-brain barrier, reducing central nervous system side effects common with other antimuscarinics. *Tropicamide* - **Tropicamide** is an **antimuscarinic** agent primarily used as a **mydriatic** (to dilate pupils) and **cycloplegic** (to paralyze the ciliary muscle) for ophthalmic examinations. - It has a short duration of action, making it unsuitable for chronic conditions like overactive bladder. *Atropine* - **Atropine** is a non-selective **muscarinic antagonist** with a wide range of uses, including bradycardia, organophosphate poisoning, and ophthalmic procedures. - While it has antimuscarinic effects on the bladder, its systemic side effects (e.g., dry mouth, blurred vision, tachycardia) limit its use for overactive bladder. *Pirenzepine* - **Pirenzepine** is a selective **M1 muscarinic antagonist** primarily used to treat **peptic ulcers** by reducing gastric acid secretion. - Its selectivity for M1 receptors means it has limited efficacy for relieving bladder symptoms, which are primarily mediated by M2 and M3 receptors.
Question 473: Maximum cycloplegic action of atropine is seen at ?
- A. 1-3 hours (Correct Answer)
- B. 1-2 weeks
- C. 4-6 hours
- D. 30-60 minutes
Explanation: ***1-3 hours*** - Atropine, a **non-selective muscarinic antagonist**, reaches its **peak cycloplegic effect** approximately 1 to 3 hours after topical administration. - This peak activity is crucial for accurate retinoscopy and **refractive error measurement** in children, as it effectively paralyzes the ciliary muscle. *4-6 hours* - While atropine's cycloplegic effect is still present at 4-6 hours, it is generally **past its peak action** by this time. - Slower-acting cycloplegics might have their peak around this window, but not atropine. *1-2 weeks* - The **duration of action** for atropine's cycloplegic and mydriatic effects can last for 1-2 weeks, but this is the total duration, not when the maximum action is observed. - Patients are often instructed about the **prolonged effects** and potential for blurred vision and photophobia over this period. *30-60 minutes* - While some mydriatic effects might start within 30-60 minutes, the **full cycloplegic effect** of atropine, which requires maximum paralysis of the ciliary muscle, is not achieved in this short timeframe. - Shorter-acting cycloplegics like **cyclopentolate** or **tropicamide** would show peak action within this earlier interval.
Question 474: Which of the following is NOT a side effect of atropine?
- A. Diarrhoea (Correct Answer)
- B. Urinary retention
- C. Confusion of elderly
- D. Blurring of vision
Explanation: ***Diarrhoea*** - Atropine is a **muscarinic antagonist** that blocks the action of **acetylcholine** on muscarinic receptors in the gastrointestinal tract. - This leads to **decreased GI motility** and **decreased secretions**, typically causing **constipation**, NOT diarrhoea. - Diarrhoea would be associated with **cholinergic agonists** or anticholinesterases, which increase GI motility. *Blurring of vision* - Atropine causes **mydriasis** (pupil dilation) and **cycloplegia** (paralysis of the ciliary muscle). - **Cycloplegia** impairs accommodation for near vision, leading to **blurring of vision**. - This is a common anticholinergic side effect. *Urinary retention* - Atropine blocks **M3 receptors** on the **detrusor muscle**, causing bladder relaxation and reduced contractility. - This leads to **urinary retention**, especially in patients with pre-existing conditions like **prostatic hypertrophy**. *Confusion in elderly* - Atropine can cross the **blood-brain barrier** and cause **CNS effects** including confusion, agitation, and delirium. - Elderly patients are particularly susceptible to these **central anticholinergic effects**.
Question 475: Propranolol is most commonly prescribed as first-line therapy for which condition?
- A. Atrioventricular (AV) block
- B. Hypertension (high blood pressure)
- C. Cardiac arrest
- D. Thyrotoxicosis (excessive thyroid hormones) (Correct Answer)
Explanation: ***Thyrotoxicosis (excessive thyroid hormones)*** - **Propranolol** is commonly prescribed as **first-line symptomatic therapy** for **thyrotoxicosis** to manage symptoms such as **tachycardia, tremors, palpitations, and anxiety**. - It works by **blocking peripheral conversion of T4 to T3** and providing rapid **symptomatic relief** through beta-blockade. - While it does not treat the underlying thyroid disorder, it is the **immediate first-line agent** for symptom control while definitive treatment (antithyroid drugs, radioiodine, or surgery) is being arranged. - **Clinical pearl:** Propranolol is preferred over selective beta-blockers due to its additional effect on T4 to T3 conversion. *Hypertension (high blood pressure)* - **Propranolol** is **NOT a first-line agent** for hypertension in current guidelines (JNC 8, ESC/ESH). - First-line agents include **ACE inhibitors, ARBs, thiazide diuretics, and calcium channel blockers**. - Non-selective beta-blockers like propranolol are typically **third-line or later** due to unfavorable metabolic effects and side effect profile. - Selective beta-blockers (atenolol, metoprolol) may be used in specific hypertension scenarios, but propranolol is rarely first-line. *Atrioventricular (AV) block* - **Propranolol** is **absolutely contraindicated** in **AV block** as it further slows conduction through the AV node. - Beta-blockers can precipitate **complete heart block** in patients with pre-existing conduction abnormalities. *Cardiac arrest* - **Propranolol** is **contraindicated** in acute management of **cardiac arrest** as it reduces cardiac contractility and can worsen outcomes. - Cardiac arrest management involves **CPR, defibrillation, epinephrine, and amiodarone**.
Question 476: Which diuretic is known to cause the maximum potassium loss?
- A. Spironolactone
- B. Furosemide (Correct Answer)
- C. Thiazide diuretics
- D. Acetazolamide
Explanation: ***Furosemide*** - Furosemide is a **loop diuretic** that inhibits the Na-K-2Cl cotransporter in the **thick ascending limb of the loop of Henle**, leading to significant excretion of sodium, chloride, potassium, and water. - Its potent diuresis and impact on potassium reabsorption result in a **high risk of hypokalemia**. *Thiazide* - Thiazide diuretics inhibit the **Na-Cl cotransporter** in the **distal convoluted tubule**, causing moderate sodium and water excretion, and some potassium loss. - While they can cause hypokalemia, their effect on potassium excretion is generally **less pronounced than loop diuretics**. *Acetazolamide* - Acetazolamide is a **carbonic anhydrase inhibitor** that acts primarily in the **proximal tubule**, inhibiting bicarbonate reabsorption and leading to increased excretion of bicarbonate, sodium, potassium, and water. - The potassium loss is due to increased delivery of sodium to the collecting duct, leading to enhanced potassium secretion, but it is typically **less severe than with loop diuretics**. *Spironolactone* - Spironolactone is a **potassium-sparing diuretic** that acts as an **aldosterone antagonist** in the collecting duct, inhibiting sodium reabsorption and potassium secretion. - Instead of causing potassium loss, spironolactone actually **conserves potassium** and can lead to hyperkalemia.
Question 477: Hyoscine is an antagonist at which cholinergic receptor?
- A. Muscarinic (Correct Answer)
- B. Nicotinic
- C. Both
- D. None of the above
Explanation: ***Muscarinic*** - **Hyoscine** (scopolamine) is a well-known **antagonist** at **muscarinic cholinergic receptors**. - It blocks the action of **acetylcholine** at these receptors, leading to its anticholinergic effects like treating motion sickness and reducing secretions. *Nicotinic* - **Hyoscine** does not primarily act on **nicotinic cholinergic receptors**. - Drugs acting on nicotinic receptors include **neuromuscular blockers** (e.g., succinylcholine, rocuronium) and **ganglionic blockers**, which have different clinical applications. *Both* - While some drugs may have activity at both receptor types, **hyoscine's primary and clinically significant antagonism is at muscarinic receptors**. - Its therapeutic effects are attributed almost exclusively to its **muscarinic blockade**. *None of the above* - This option is incorrect because **hyoscine is a clear antagonist at muscarinic cholinergic receptors**. - Its widespread use in medicine is based on this specific pharmacological action.