Biochemistry
1 questionsWhat is the mechanism by which mercury causes damage?
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 291: What is the mechanism by which mercury causes damage?
- A. Causes toxicity through various mechanisms
- B. Binds to -SH groups of enzymes (Correct Answer)
- C. Inhibits electron transport chain
- D. Inhibits protein synthesis
Explanation: ***Binds to -SH groups of enzymes*** - Mercury, particularly its inorganic and organic forms, has a high affinity for **sulfhydryl (-SH) groups** found in **cysteine residues** of proteins and enzymes. - This binding disrupts the **tertiary structure** and **catalytic activity** of vital enzymes, leading to widespread cellular dysfunction and toxicity. *Causes toxicity through various mechanisms (not specific to -SH binding)* - While mercury can indeed cause toxicity through various mechanisms, the **most prominent and fundamental mechanism** underpins many of these downstream effects. - This option is too general and does not pinpoint the primary molecular interaction responsible for mercury's widespread cellular damage. *Indirectly inhibits the electron transport chain (ETC) by enzyme disruption* - This statement is partially true in that mercury's enzyme disruption can affect the ETC, but it's an **indirect consequence** rather than the primary mechanism itself. - The direct mechanism involves the initial binding to -SH groups, which then leads to the dysfunction of enzymes, including those involved in the ETC. *Indirectly inhibits protein synthesis by disrupting enzyme function* - Similar to ETC inhibition, mercury's disruption of enzyme function can ultimately impair protein synthesis, but this is an **effect down the causal chain**. - The initial and direct molecular interaction is the binding to sulfhydryl groups of key enzymes involved in various cellular processes, including protein synthesis.
Pathology
5 questionsLocalized Langerhans cell histiocytosis affecting head and neck is?
MALT lymphoma is positive for which of the following markers?
Centrilobular necrosis of the liver may be seen with?
Which of the following statements is false regarding hereditary spherocytosis?
Which of the following is not a germ cell tumor?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 291: Localized Langerhans cell histiocytosis affecting head and neck is?
- A. Eosinophilic granuloma (Correct Answer)
- B. Letterer-siwe disease
- C. Pulmonary Langerhans cell histiocytosis
- D. Hand-Schuller-Christian disease
Explanation: ***Eosinophilic granuloma*** - This is a localized form of **Langerhans cell histiocytosis** that typically presents in the head and neck region, often affecting areas like the skull and mandible [1]. - Characterized by **bone lesions** and may present with **pain or swelling** in the affected area, making it a prominent form in children and young adults. *Pulmonary langerhans cell histiocytosis* - Primarily affects the **lungs** and is associated with **cough, dyspnea**, and pulmonary nodules, not the head and neck region. - Occurs predominantly in **smokers** and involves interstitial lung disease patterns on imaging studies. *Hand-schuller-christian disease* - This condition is a systemic form of Langerhans cell histiocytosis that affects multiple systems rather than being localized, commonly presenting with **diabetes insipidus** and bone lesions. - It is often associated with **exophthalmos** and may involve lymphadenopathy, affecting older children and adults, not localized head and neck involvement. *Letterer-siwe disease* - This represents the acute, disseminated form of Langerhans cell histiocytosis, affecting infants, and is marked by systemic symptoms like **fever**, **rash**, and **hepatosplenomegaly** [1]. - Typically presents with serious manifestations and not specifically localized in the **head and neck area** as seen in eosinophilic granuloma. **References:** [1] 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, p. 630.
Question 292: MALT lymphoma is positive for which of the following markers?
- A. CD20 (Correct Answer)
- B. CD19
- C. CD43
- D. CD5
Explanation: ***CD20*** - MALT lymphoma is a type of **B-cell non-Hodgkin lymphoma**, and CD20 is a **pan B-cell marker consistently expressed** in MALT lymphomas. - CD20 positivity is **crucial for diagnosis** and is the **primary therapeutic target** for anti-CD20 monoclonal antibody therapy (Rituximab). - In diagnostic practice, **CD20 is the most important B-cell marker** for identifying MALT lymphoma and guiding treatment decisions. *CD19* - CD19 is also a **pan B-cell marker** and is **typically positive in MALT lymphoma** along with CD20. - However, in the context of this question, **CD20 is the preferred answer** because it is the **standard diagnostic marker emphasized in clinical practice** and the **primary therapeutic target**. - Both markers are positive, but CD20 has greater **clinical and therapeutic significance** in MALT lymphoma management. *CD43* - CD43 is primarily a **T-cell and myeloid marker**, but can show **aberrant expression in 40-50% of MALT lymphomas**. - While it may be positive in some cases, it is **not a defining B-cell lineage marker** and is not used as a primary diagnostic criterion for MALT lymphoma. - Its variable expression makes it **less reliable** than consistent B-cell markers like CD20. *CD5* - CD5 is typically associated with **T-cells** and certain B-cell lymphomas, particularly **chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL)** and **mantle cell lymphoma**. - **MALT lymphoma is characteristically CD5-negative**, which is an important feature for **differentiating it from CD5+ B-cell lymphomas**.
Question 293: Centrilobular necrosis of the liver may be seen with?
- A. Arsenic
- B. Ethanol
- C. CCl4 (Correct Answer)
- D. Phosphorus
Explanation: ***CCl4*** - **Carbon tetrachloride (CCl4)** is the **classic and prototypical** hepatotoxin that causes **centrilobular (zone 3) necrosis**. - The **centrilobular zone (zone 3)** is particularly vulnerable due to its high concentration of **cytochrome P450 enzymes**, which metabolize CCl4 into **toxic free radicals (trichloromethyl radicals)**. - This is the **most characteristic** cause of centrilobular necrosis in toxicology and is the preferred answer for exam purposes. *Ethanol* - **Ethanol** can also cause **centrilobular necrosis** in **alcoholic hepatitis**, as zone 3 is most susceptible to hypoxic injury and oxidative stress. - However, alcoholic liver disease presents with a **spectrum of changes** including steatosis (earliest), hepatitis with ballooning degeneration and Mallory-Denk bodies, and eventual cirrhosis. - While centrilobular necrosis occurs in alcoholic hepatitis, **CCl4 remains the prototype** for pure centrilobular necrosis in exam contexts. *Phosphorus* - **Elemental phosphorus** toxicity causes **periportal (zone 1) necrosis**, which is the opposite pattern from centrilobular necrosis. - It also causes widespread fatty change and hemorrhagic necrosis within the liver. *Arsenic* - **Arsenic poisoning** causes **diffuse/generalized hepatocellular necrosis** and cholestasis, rather than the specific centrilobular pattern. - Chronic exposure is associated with non-cirrhotic portal fibrosis and portal hypertension.
Question 294: Which of the following statements is false regarding hereditary spherocytosis?
- A. Defect in ankyrin
- B. Reticulocytosis
- C. Decreased MCHC (Correct Answer)
- D. Normal to increased MCV
Explanation: ***Decreased MCHC*** - Hereditary spherocytosis typically presents with an **increased MCHC** due to the spherocytes being more concentrated. - MCHC is a measure of the hemoglobin concentration in red blood cells, and in spherocytosis, this value is often elevated rather than decreased. *Defect in ankyrin* - This is a true statement; hereditary spherocytosis is associated with a defect in **ankyrin**, a protein that helps maintain the cell's membrane structure [2]. - Mutations in ankyrin lead to instability of the red blood cell membrane, resulting in spherocyte formation [2]. *Decreased MCV* - In hereditary spherocytosis, MCV is often **normal or slightly increased**, as it reflects the volume of red blood cells, which can be misinterpreted due to the presence of spherocytes. - Spherocytes are smaller cells, which can mistakenly suggest a falsely decreased MCV if not properly interpreted [1]. *Reticulocytosis* - This condition typically presents with **reticulocytosis** as a response to hemolysis, indicating the bone marrow is producing more red blood cells to compensate [1]. - The presence of reticulocytosis is a common finding in hereditary spherocytosis due to increased destruction of spherocytes. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 640-641.
Question 295: Which of the following is not a germ cell tumor?
- A. Embryonal carcinoma
- B. Endodermal sinus
- C. Seminoma
- D. Leydig cell tumor (Correct Answer)
Explanation: ***Leydig cell tumor*** - Leydig cell tumors are classified as **sex-cord stromal tumors**, not germ cell tumors [1]. - These tumors are derived from **Leydig cells** which produce androgens, affecting the endocrine function rather than germ cell lineage [1]. *Endodermal sinus* - Endodermal sinus tumors, or **yolk sac tumors**, are indeed germ cell tumors characterized by **alpha-fetoprotein (AFP)** production [2]. - They typically arise in the testis or ovaries and are known for rapid growth and aggressiveness. *Embryonal carcinoma* - Embryonal carcinoma is a type of **germ cell tumor** commonly associated with elevated levels of **beta-hCG** [2]. - It primarily affects the testes in males and can occur in the ovaries, and it is known for its aggressive behavior. *Seminoma* - Seminomas are classic examples of **germ cell tumors**, noted for their sensitivity to radiation and chemotherapy [3]. - They usually present with **increased beta-hCG** levels and can coexist with non-seminomatous germ cell tumors [3]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 510-514. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 979-980. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 980-982.
Pharmacology
3 questionsWhich beta-1 antagonist is used in congestive cardiac failure?
Which antiglaucomatous drug is known to cause spasm of accommodation?
Which of the following is classified as a Type E adverse reaction?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 291: Which beta-1 antagonist is used in congestive cardiac failure?
- A. Atenolol
- B. Metoprolol (Correct Answer)
- C. Esmolol
- D. Bisoprolol
Explanation: ***Metoprolol*** - **Metoprolol succinate** (extended-release formulation) is a selective **beta-1 antagonist** proven to reduce mortality and hospitalizations in **chronic heart failure with reduced ejection fraction (HFrEF)**. - It works by **reducing heart rate, myocardial oxygen demand**, and preventing adverse cardiac remodeling through inhibition of chronic sympathetic activation. - Along with **bisoprolol and carvedilol**, it is one of the **three beta-blockers with proven mortality benefit** in heart failure trials. *Atenolol* - While atenolol is a selective beta-1 antagonist, it **lacks evidence for mortality benefit** in heart failure. - It has **high hydrophilicity** and renal elimination, leading to less favorable pharmacokinetics compared to metoprolol. - More commonly used for **hypertension and angina** rather than heart failure management. *Esmolol* - **Esmolol** is an ultra-short-acting selective beta-1 antagonist used for **acute control of heart rate** in perioperative and critical care settings. - Its **very short half-life (9 minutes)** makes it unsuitable for chronic management of heart failure. - Administered only **intravenously** and requires continuous infusion. *Bisoprolol* - While **bisoprolol is also approved** for heart failure and has proven mortality benefit (CIBIS-II trial), this question likely expects **metoprolol** as the answer given the historical context. - Both bisoprolol and metoprolol are acceptable answers, but **metoprolol** has been more widely studied and is more commonly cited in Indian medical exams. - Bisoprolol has **greater beta-1 selectivity** than metoprolol but similar clinical outcomes in heart failure.
Question 292: Which antiglaucomatous drug is known to cause spasm of accommodation?
- A. Timolol
- B. Pilocarpine (Correct Answer)
- C. Dorzolamide
- D. Latanoprost
Explanation: ***Pilocarpine*** - **Pilocarpine** is a **direct-acting muscarinic agonist** that contracts the **ciliary muscle**. - Contraction of the ciliary muscle leads to **accommodation spasm** and a forward movement of the **iris-lens diaphragm**, which also helps to open the **trabecular meshwork**, facilitating aqueous outflow. *Timolol* - **Timolol** is a **beta-blocker** that reduces aqueous humor production by blocking beta-adrenergic receptors on the ciliary epithelium. - It does not directly affect the **ciliary muscle** or cause accommodation spasm. *Dorazolamide* - **Dorzolamide** is a **carbonic anhydrase inhibitor** that reduces aqueous humor production. - Its mechanism of action does not involve the ciliary body's mechanical action and therefore does not cause **accommodation spasm**. *Latanoprost* - **Latanoprost** is a **prostaglandin analog** that increases uveoscleral outflow of aqueous humor. - It does not directly affect the ciliary muscle's contraction or cause **accommodation spasm**.
Question 293: Which of the following is classified as a Type E adverse reaction?
- A. Toxicity
- B. Augmented effect
- C. Teratogenesis
- D. Rebound effect due to drug withdrawal (Correct Answer)
Explanation: ***Rebound effect due to drug withdrawal*** - Type E adverse reactions are related to **end-of-treatment effects**, specifically withdrawal phenomena. - The **rebound effect** after drug cessation, such as worsened angina after stopping beta-blockers, is a classic example of a Type E reaction. *Toxicity* - This is a general term for adverse effects from excessive drug doses and is **not a specific type** in the ABCDEF classification. - Dose-dependent toxic effects typically align with **Type A** (augmented) reactions, which are predictable and related to the drug's pharmacology. *Augmented effect* - An **augmented effect** is classified as a Type A adverse drug reaction, meaning it is **dose-dependent**, predictable from the drug's known pharmacology, and common. - Examples include bleeding with anticoagulants or hypotension with antihypertensives. *Teratogenesis* - **Teratogenesis** refers to drug-induced fetal malformations and is categorized as a **Type D** (delayed) adverse drug reaction. - These effects are often severe, occur after prolonged exposure, and are rare.
Physiology
1 questionsWhich of the following statements about thyroid hormone receptors is correct?
NEET-PG 2013 - Physiology NEET-PG Practice Questions and MCQs
Question 291: Which of the following statements about thyroid hormone receptors is correct?
- A. They directly bind to thyrotropin-releasing hormone (TRH)
- B. They directly bind to thyroid-stimulating hormone (TSH)
- C. They cause nuclear transcription after binding with T4
- D. They are intracellular receptors that mediate gene transcription after binding with T3 or T4, but their primary action is through T3. (Correct Answer)
Explanation: ***They are intracellular receptors that mediate gene transcription after binding with T3 or T4, but their primary action is through T3.*** - **Thyroid hormone receptors** are indeed **intracellular** and act as **ligand-activated transcription factors**, regulating gene expression. - While both **T3** and **T4** can bind, **T3 (triiodothyronine)** is the more potent and active form, binding with much higher affinity to the receptors to exert its primary metabolic effects. *They directly bind to thyrotropin-releasing hormone (TRH)* - **TRH (thyrotropin-releasing hormone)** is produced by the hypothalamus and acts on the **pituitary gland** to stimulate TSH release, not directly on thyroid hormone receptors. - Thyroid hormone receptors bind to thyroid hormones (**T3 and T4**), not to the hypothalamic releasing hormones like TRH. *They directly bind to thyroid-stimulating hormone (TSH)* - **TSH (thyroid-stimulating hormone)** is produced by the pituitary gland and primarily acts on receptors located on the **thyroid gland cells** to stimulate thyroid hormone synthesis and release. - Thyroid hormone receptors are distinct from TSH receptors and bind to the hormones themselves (**T3/T4**), not the stimulating hormone TSH. *Causes nuclear transcription after binding with T4* - While **T4 (thyroxine)** can bind to thyroid hormone receptors, it is primarily a **prohormone**. - T4 is largely converted to the more active **T3** within target cells, and **T3** is the main mediator of nuclear transcription through these receptors.