Pathology
2 questionsWhat is the first cellular response observed after a sharp nerve cut?
Which of the following statements about peripheral nerve injury is false?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 541: What is the first cellular response observed after a sharp nerve cut?
- A. Chromatolysis (Correct Answer)
- B. Polymorphic arrangement
- C. Increased protein synthesis
- D. Macrophage activation
Explanation: ***Chromatolysis*** - **Chromatolysis** is the dissolution of the Nissl bodies (rough endoplasmic reticulum) in the neuron cell body following axonal injury, which is the **first observable cellular response** [1]. - This process is a preparatory step for neuronal regeneration, indicating the cell's attempt to repair the damaged axon [1]. *Polymorphic arrangement* - This term is not typically used to describe an immediate cellular response to a nerve cut; it might refer to diverse cell shapes or arrangements in different contexts but is not a recognized initial post-injury event. - The neuron's immediate response involves changes within the cell body, not a re-arrangement of its cellular structure with other cells. *Increased protein synthesis* - While increased protein synthesis does occur during neuronal repair and regeneration, it is a consequence of chromatolysis and part of a later, more sustained response, not the very first visible cellular change [1]. - **Chromatolysis precedes** and facilitates the subsequent increase in protein synthesis necessary for axonal regrowth [1]. *Macrophage activation* - **Macrophage activation** is a crucial part of the inflammatory response and debris clearance following nerve injury, but it is not the *first cellular response* of the neuron itself [2]. - Macrophages migrate to the site of injury hours to days after the initial insult, whereas chromatolysis begins within the neuron's cell body much earlier [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1254-1256. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 697-698.
Question 542: Which of the following statements about peripheral nerve injury is false?
- A. Wallerian degeneration starts in axonotmesis
- B. Neuropraxia is irreversible (Correct Answer)
- C. Neurotmesis is the most severe form of injury
- D. Epineurium is intact in axonotmesis
Explanation: This question asks which statement is **FALSE** about peripheral nerve injury. ***Neuropraxia is irreversible*** - This statement is **FALSE** (making it the correct answer to this question). - Neuropraxia represents the **mildest form** of peripheral nerve injury, characterized by local **demyelination** or temporary conduction block without axonal damage [2]. - Recovery from neuropraxia is typically **complete and rapid**, usually within **weeks to months**, as axonal continuity is preserved. - **No Wallerian degeneration** occurs because the axon remains intact. *Epineurium is intact in axonotmesis* - This statement is **TRUE**. In **axonotmesis**, there is disruption of the axon and myelin sheath, but the **connective tissue sheaths** (epineurium, perineurium, and endoneurium) remain intact. - The intact connective tissue provides a guide for **axonal regeneration**, which makes recovery possible, although often incomplete [1]. - Recovery occurs at approximately **1 mm/day** or **1 inch/month**. *Neurotmesis is the most severe form of injury* - This statement is **TRUE**. **Neurotmesis** involves complete severance of the nerve fiber, including the axon, myelin, and **all supporting connective tissue structures** (epineurium, perineurium, and endoneurium). - This type of injury has the **poorest prognosis** for recovery and usually requires **surgical intervention** to attempt repair [1]. *Wallerian degeneration starts in axonotmesis* - This statement is **TRUE**. **Wallerian degeneration** is a process that occurs when a nerve fiber is severed or severely injured, affecting the segment **distal to the injury** [1]. - In **axonotmesis**, the axon is disrupted, leading to degeneration of the distal axonal segment and its myelin sheath, which is characteristic of Wallerian degeneration. - Wallerian degeneration also occurs in **neurotmesis** but NOT in **neuropraxia**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 109-110. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, p. 1232.
Pharmacology
8 questionsThymidine is responsible for resistance to which antibiotic ?
Which antitubercular drug makes the patient non-infective the earliest?
Among the following statins, which has the longest half-life?
Which of the following is a characteristic of simvastatin?
What is the best method for treating methanol poisoning?
Ximelagatran is used as ?
Interstitial nephritis is associated with all of the following medications except:
What is the classification of Lorcaserin?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 541: Thymidine is responsible for resistance to which antibiotic ?
- A. Erythromycin
- B. Sulfonamide (Correct Answer)
- C. Tetracycline
- D. Nitrofurantoin
Explanation: ***Sulfonamide*** - **Thymidine** can contribute to **sulfonamide resistance** because sulfonamides interfere with **folate metabolism** and the subsequent synthesis of purines and pyrimidines, including thymidine. - An excess of thymidine can bypass the metabolic block caused by sulfonamides, allowing bacteria to continue DNA synthesis and grow. *Erythromycin* - **Erythromycin** resistance is primarily mediated by **methylation of ribosomal RNA**, which prevents the antibiotic from binding to the 50S ribosomal subunit. - It does not directly involve thymidine or the folate synthesis pathway. *Tetracycline* - Resistance to **tetracyclines** is commonly due to **efflux pumps** that actively pump the drug out of the bacterial cell or **ribosomal protection proteins** that prevent tetracycline binding. - Thymidine production or metabolism is not a mechanism of tetracycline resistance. *Nitrofurantoin* - **Nitrofurantoin** resistance typically involves **mutations** in bacterial enzymes (like **nitrofuran reductase**) that are responsible for activating the drug into its active form. - These mutations prevent the drug from becoming bactericidal, and thymidine does not play a role in this mechanism.
Question 542: Which antitubercular drug makes the patient non-infective the earliest?
- A. Ethambutol
- B. Pyrazinamide
- C. Isoniazid (INH) (Correct Answer)
- D. Rifampin
Explanation: ***Isoniazid (INH)*** - **Isoniazid** renders TB patients **non-infectious the fastest**, typically within **2-3 days** of starting treatment - It has the most **rapid bactericidal effect** against actively multiplying extracellular **Mycobacterium tuberculosis**, which are the primary organisms responsible for transmission - INH works by inhibiting **mycolic acid synthesis**, disrupting the bacterial cell wall of rapidly dividing bacilli - This makes it the most critical drug for **early infection control** and reducing community transmission *Rifampin* - While **rifampin** is highly bactericidal and has excellent sterilizing activity, it takes **slightly longer** than INH to render patients non-infectious - Rifampin is particularly effective against **semi-dormant organisms** and intracellular bacilli - It is the most important drug for **preventing relapse** and shortening treatment duration, but INH acts faster in reducing infectivity *Ethambutol* - **Ethambutol** is primarily **bacteriostatic**, inhibiting arabinosyl transferase and interfering with cell wall synthesis - Its main role is to **prevent emergence of drug resistance** rather than rapidly reducing bacterial load - Has minimal impact on early infectivity reduction *Pyrazinamide* - **Pyrazinamide** is most effective against **semi-dormant bacilli** within macrophages and in acidic environments - Its **sterilizing activity** helps shorten overall treatment duration but does not contribute significantly to rapid reduction in infectivity - Works slowly and is not bactericidal against actively multiplying extracellular organisms
Question 543: Among the following statins, which has the longest half-life?
- A. Pravastatin
- B. Simvastatin
- C. Lovastatin
- D. Rosuvastatin (Correct Answer)
Explanation: **Rosuvastatin** - **Rosuvastatin** has the longest half-life among the commonly used statins, approximately **19 hours**, allowing for consistent lipid-lowering effects. - Its prolonged presence in the body contributes to its effectiveness in reducing **LDL-C** at lower doses. *Pravastatin* - **Pravastatin** has a relatively short half-life of about **1.8 hours**, requiring daily dosing to maintain therapeutic concentrations. - Its hydrophilic nature means it is less likely to penetrate non-hepatic tissues, potentially reducing extrahepatic side effects. *Simvastatin* - **Simvastatin** has a short half-life of about **3 hours**, necessitating daily administration. - It is a **prodrug** that requires hepatic activation to its active beta-hydroxy acid form. *Lovastatin* - **Lovastatin** also has a short half-life, around **3 hours**, and is a **prodrug** like simvastatin. - It is often recommended to be taken in the evening due to the diurnal rhythm of cholesterol synthesis.
Question 544: Which of the following is a characteristic of simvastatin?
- A. Specific CYP3A4 substrate with high interaction potential
- B. Derived from fungal metabolite (Correct Answer)
- C. Prodrug requiring hepatic activation
- D. Short half-life requiring evening dosing
Explanation: ***Derived from fungal metabolite*** - **Simvastatin** and lovastatin are **naturally-derived statins** obtained from **fungal metabolites** (*Aspergillus terreus*), distinguishing them from synthetic statins like atorvastatin, rosuvastatin, and pravastatin [2]. - This is the **most distinguishing characteristic** for classification purposes, as it represents the drug's origin and places it in a specific subclass of HMG-CoA reductase inhibitors. - The discovery of fungal-derived statins led to the development of the entire statin drug class. *Prodrug requiring hepatic activation* - While **simvastatin** is a **lactone prodrug** requiring hepatic hydrolysis to its active beta-hydroxy acid form, this is a pharmacokinetic property shared with lovastatin [1]. - This is a characteristic but not the most distinguishing feature for classification. *Specific CYP3A4 substrate with high interaction potential* - **Simvastatin** is extensively metabolized by **CYP3A4**, leading to significant drug-drug interactions with CYP3A4 inhibitors (e.g., ketoconazole, erythromycin, grapefruit juice). - While clinically important, many drugs are CYP3A4 substrates, making this less distinctive as a defining characteristic. *Short half-life requiring evening dosing* - **Simvastatin** has a **short half-life** (2-3 hours) and is preferably administered in the evening because cholesterol synthesis is highest at night. - This is a dosing consideration based on pharmacokinetics rather than a fundamental distinguishing characteristic of the drug's identity.
Question 545: What is the best method for treating methanol poisoning?
- A. Calcium gluconate
- B. BAL
- C. Fomepizole (Correct Answer)
- D. Deferoxamine
Explanation: ***Fomepizole*** - **Fomepizole** (Antizol) is a potent inhibitor of **alcohol dehydrogenase**, the enzyme responsible for metabolizing methanol into toxic metabolites like formic acid [1]. - By inhibiting this enzyme, fomepizole prevents the formation of these harmful metabolites, thus halting the progression of methanol toxicity and reducing mortality [1]. - It is the **gold standard** antidote for methanol poisoning. *Calcium gluconate* - **Calcium gluconate** is primarily used to treat **hypocalcemia** and magnesium toxicity. - It has no role in the direct treatment or detoxification of methanol poisoning. *Deferoxamine* - **Deferoxamine** is a **chelating agent** used to treat **iron toxicity** by binding to iron and facilitating its excretion [3]. - It is not effective for methanol poisoning as it does not interact with methanol or its toxic metabolites. *BAL* - **BAL** (British Anti-Lewisite, dimercaprol) is a chelating agent primarily used for poisoning by **heavy metals** such as arsenic, mercury, and gold [2]. - It has no therapeutic role in methanol poisoning, which involves a different toxicological mechanism.
Question 546: Ximelagatran is used as ?
- A. Anticoagulant (Correct Answer)
- B. Fibrinolytic
- C. Platelet inhibitor
- D. Clot buster
Explanation: ***Anticoagulant*** - Ximelagatran is a **direct thrombin inhibitor**, meaning it directly blocks the action of thrombin, a key enzyme in the coagulation cascade. - By inhibiting thrombin, it prevents the formation of **fibrin clots**, thus acting as an anticoagulant. *Platelet inhibitor* - **Platelet inhibitors** prevent platelets from clumping together to form a clot, often by targeting pathways like ADP receptors or COX-1 enzyme. - Examples include **aspirin** and **clopidogrel**, which have different mechanisms of action than Ximelagatran. *Clot buster* - **Clot busters** are also known as thrombolytic agents, which actively dissolve existing blood clots. - They work by activating **plasminogen** to produce plasmin, an enzyme that breaks down fibrin. *Fibrinolytic* - **Fibrinolytics** are a class of drugs that enhance **fibrinolysis**, the natural process of breaking down blood clots. - **Thrombolytics** are a subset of fibrinolytic drugs used therapeutically to dissolve clots.
Question 547: Interstitial nephritis is associated with all of the following medications except:
- A. INH (Correct Answer)
- B. Diuretics
- C. Allopurinol
- D. Beta-lactam antibiotics
Explanation: ***INH*** - **Isoniazid (INH)** is primarily associated with **hepatotoxicity** (liver damage) and **peripheral neuropathy**, not typically interstitial nephritis. - While many drugs can rarely cause various adverse effects, INH is not a recognized common cause of **drug-induced interstitial nephritis**. *Beta-lactam antibiotics* - **Beta-lactam antibiotics**, including penicillins and cephalosporins, are among the most common causes of **drug-induced acute interstitial nephritis (AIN)**. - AIN is an **allergic hypersensitivity reaction** characterized by inflammation of the kidney's tubules and interstitium. *Diuretics* - Certain **diuretics**, particularly **thiazide diuretics** and **loop diuretics**, have been implicated in causing **acute interstitial nephritis**. - The mechanism is thought to be an **allergic or hypersensitivity reaction** within the renal tubules and interstitium. *Allopurinol* - **Allopurinol**, used to treat gout and hyperuricemia, is a known cause of **drug-induced acute interstitial nephritis**. - Renal involvement with allopurinol can range from mild tubular dysfunction to severe **acute kidney injury** due to AIN.
Question 548: What is the classification of Lorcaserin?
- A. Anti-anxiety
- B. Anti-smoking
- C. Anti-helminthic
- D. Anti-obesity (Correct Answer)
Explanation: ***Anti-obesity*** - Lorcaserin is a selective **serotonin 5-HT₂C receptor agonist** that works by promoting satiety and reducing food intake. - It is prescribed as a long-term treatment for **weight management** in adults who are obese or overweight with at least one weight-related comorbidity. *Anti-anxiety* - Anti-anxiety medications, such as **benzodiazepines** or **SSRIs**, primarily target neurotransmitters like GABA or serotonin 5-HT₁A receptors to reduce anxiety symptoms. - Lorcaserin's primary mechanism of action is distinct, focusing on the 5-HT₂C receptor for appetite regulation, not anxiety. *Anti-smoking* - Anti-smoking medications, like **varenicline** or **bupropion**, are designed to reduce nicotine cravings and withdrawal symptoms. - Their mechanisms often involve nicotinic acetylcholine receptors or dopamine and norepinephrine reuptake inhibition, which differs from lorcaserin's action. *Anti-helminthic* - Anti-helminthic drugs are used to treat **parasitic worm infections** by paralyzing or killing the worms. - Common examples include **albendazole** or **mebendazole**, which have no relation to appetite control or obesity treatment.