Anatomy
2 questionsWhich carpal bone does not articulate with the radius?
Posterior cardinal veins develop into:
NEET-PG 2015 - Anatomy NEET-PG Practice Questions and MCQs
Question 11: Which carpal bone does not articulate with the radius?
- A. Pisiform (Correct Answer)
- B. Scaphoid
- C. Lunate
- D. Triquetrum
Explanation: ***Pisiform*** - The **pisiform** is a sesamoid bone located within the tendon of the **flexor carpi ulnaris** muscle. - It articulates only with the **triquetrum**, not directly with the radius. *Scaphoid* - The **scaphoid** is one of the carpal bones that directly articulates with the radius, forming part of the **radiocarpal joint**. - It is located in the **proximal row** of carpal bones on the lateral side. *Lunate* - The **lunate** is another bone in the proximal carpal row that articulates directly with the **radius**, alongside the scaphoid. - It plays a crucial role in wrist movement and stability. *Triquetrum* - The **triquetrum** is a carpal bone in the proximal row, located medially. - Although it is in the proximal row, it primarily articulates with the **ulnar articular disc** (triangular fibrocartilage complex), which separates it from the distal ulna, and does not directly articulate with the radius.
Question 12: Posterior cardinal veins develop into:
- A. Parts of inferior vena cava
- B. Common iliac vein (Correct Answer)
- C. Hemiazygos vein
- D. Azygos vein
Explanation: ***Common iliac vein*** - The **posterior cardinal veins** are paired primitive veins in the embryo that drain the caudal body. - The **caudal portions** of the posterior cardinal veins persist and directly form the **common iliac veins** and contribute to the internal iliac veins [1]. - This is the **primary and most direct derivative** of the posterior cardinal veins, making it the best answer. *Azygos vein* - The **azygos vein** develops from the **right supracardinal vein** + **cranial portion of the right posterior cardinal vein**. - While posterior cardinal veins do contribute to its formation, this is not the primary derivative. - The middle portions of posterior cardinal veins regress, and the supracardinal contribution is more significant. *Hemiazygos vein* - The **hemiazygos vein** is derived from the **left supracardinal vein** + **cranial portion of the left posterior cardinal vein**. - Similar to the azygos, posterior cardinal veins contribute but are not the primary source. - The supracardinal vein provides the major contribution. *Parts of inferior vena cava* - The **IVC** forms from multiple embryonic veins: right vitelline vein (hepatic segment), right subcardinal vein (renal segment), right supracardinal vein (infrarenal segment), and hepatic veins. - While the common iliac veins (derived from posterior cardinal veins) drain into the IVC, the posterior cardinal veins themselves do **not directly form the IVC proper**. - The posterior cardinal veins largely regress in their middle portions.
Community Medicine
1 questionsWhich blinding technique is considered the most effective in clinical trials?
NEET-PG 2015 - Community Medicine NEET-PG Practice Questions and MCQs
Question 11: Which blinding technique is considered the most effective in clinical trials?
- A. Double blinding (Correct Answer)
- B. Triple blinding
- C. No blinding
- D. Single blinding
Explanation: **Double blinding** - Involves both the **participants** and the **researchers/investigators** being unaware of the treatment assignment. - This method effectively minimizes bias from both **subject expectation** (placebo effect) and **observer expectation** (detection bias). *Single blinding* - Only the **participant** is unaware of the treatment they are receiving, while the investigator knows. - While it reduces participant bias, it can still introduce bias from the investigator regarding **outcome assessment** or **patient interaction**. *Triple blinding* - Extends blinding to include the **data analyst** who is also unaware of the treatment assignments during analysis. - While theoretically offering an additional layer of protection against bias, its practical benefits over double blinding are often marginal and it's less commonly implemented due to **complexity**. *No blinding* - Both the **participants** and the **researchers** are aware of the treatment assignments (open-label study). - This approach is highly susceptible to **bias** from both participant and researcher expectations, significantly compromising the study's validity and reliability.
Internal Medicine
2 questionsAbsence of the intrahepatic bile ducts leads to which syndrome?
Which of the following statements about Wilson's disease is true?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 11: Absence of the intrahepatic bile ducts leads to which syndrome?
- A. Polycystic Liver Disease
- B. Caroli Disease
- C. Von Meyenburg Complexes
- D. Alagille Syndrome (Correct Answer)
Explanation: ***Alagille Syndrome*** - Characterized by the **absence of intrahepatic bile ducts**, leading to cholestasis and liver dysfunction. - Often associated with **cardiac defects** and **skeletal abnormalities**, as well as distinct **facial features**. *Von Meyenburg Complexes* - Refers to **bile duct hamartomas**, which are developmental abnormalities but do not lead to complete absence of ducts. - Typically discovered incidentally and are not associated with syndromic presentations like Alagille syndrome. *Caroli Disease* - Involves **dilated intrahepatic bile ducts** [1] and does not result in their absence; thus, it leads to **recurrent cholangitis**. - More associated with **cysts** and can lead to biliary complications rather than complete duct loss. *Polycystic Liver Disease* - Characterized by the presence of multiple **cysts** in the liver, but the intrahepatic bile ducts are typically present. - It is often associated with **kidney cysts** and systemic manifestations, not the absence of bile ducts.
Question 12: Which of the following statements about Wilson's disease is true?
- A. Low serum ceruloplasmin and low urinary copper
- B. Low serum ceruloplasmin and high urinary copper (Correct Answer)
- C. High serum ceruloplasmin and low urinary copper
- D. High serum ceruloplasmin and high urinary copper
Explanation: ***Low serum ceruloplasmin and high urinary copper*** - In **Wilson's disease**, there is a defect in **copper transport**, leading to impaired incorporation of copper into ceruloplasmin and reduced biliary excretion. - This results in **low serum ceruloplasmin** levels (since ceruloplasmin is the main copper-carrying protein in the blood) and **increased urinary copper excretion** as the body attempts to eliminate excess free copper. *Low serum ceruloplasmin and low urinary copper* - While **low serum ceruloplasmin** is characteristic, **low urinary copper** would indicate adequate copper elimination or a different condition, which is not the case for Wilson's disease. - Patients with Wilson's disease have **excess copper accumulation**, and increased urinary excretion is a compensatory mechanism [1]. *High serum ceruloplasmin and low urinary copper* - **High serum ceruloplasmin** is inconsistent with Wilson's disease, as ceruloplasmin levels are typically low due to the impaired copper binding. - **Low urinary copper** excretion would indicate normal or low total body copper, which contradicts the copper overload seen in Wilson's disease. *High serum ceruloplasmin and high urinary copper* - **High serum ceruloplasmin** would suggest normal or increased ceruloplasmin synthesis or release, which is contrary to the pathophysiology of Wilson's disease. - Although **high urinary copper** is a feature, it isn't accompanied by high ceruloplasmin in this condition, as ceruloplasmin is primarily involved in carrying copper in the blood rather than excreting excess copper [1].
Ophthalmology
1 questionsCataract is caused by all except:
NEET-PG 2015 - Ophthalmology NEET-PG Practice Questions and MCQs
Question 11: Cataract is caused by all except:
- A. Ultraviolet radiation
- B. Infrared radiation
- C. Microwave radiation
- D. MRI (Correct Answer)
Explanation: ***MRI*** - Magnetic Resonance Imaging (MRI) uses powerful **magnetic fields** and radio waves to generate images, which are not known to cause cataracts. - The energy used in MRI is **non-ionizing** and does not directly damage lens proteins. *Ultraviolet radiation* - Prolonged exposure to **UV-B radiation** is a significant risk factor for the development of various types of cataracts, especially cortical and posterior subcapsular cataracts. - UV radiation can cause oxidative damage to lens proteins and lipids, leading to their aggregation and opacification. *Infrared radiation* - Chronic exposure to high levels of **infrared (IR) radiation**, such as that experienced by glassblowers or steelworkers, can lead to "glassblower's cataract" or "heat cataract." - IR radiation causes thermal damage to the lens, particularly the anterior capsule and subcapsular region. *Microwave radiation* - High-intensity **microwave radiation** has been implicated in the formation of cataracts, particularly in occupational exposure scenarios. - It causes thermal effects within the lens due to absorption of energy, leading to protein denaturation and opacification.
Pediatrics
1 questionsNewborns typically lose how much weight in the first week?
NEET-PG 2015 - Pediatrics NEET-PG Practice Questions and MCQs
Question 11: Newborns typically lose how much weight in the first week?
- A. 5-10% (Correct Answer)
- B. 1-2%
- C. 11-15%
- D. 15-20%
Explanation: ***5-10%*** - **Physiologic weight loss** of 5-10% of birth weight is normal in newborns during the first week of life. - This loss is primarily due to the **mobilization of extracellular fluid** and delayed onset of full milk production (lactogenesis). - Most infants regain their birth weight by **10-14 days** of age. *1-2%* - A weight loss of only 1-2% in the first week would be **less than expected** and might suggest the infant is retaining excess fluid. - While not necessarily pathological, it's at the **lower end of the normal range** and less typical than the 5-10% range. *11-15%* - A weight loss greater than **10%** is generally considered **excessive** and indicates inadequate feeding or possible dehydration. - Weight loss of 11-15% typically requires **closer monitoring**, feeding assessment, and possible lactation support or supplementation. *15-20%* - A weight loss of 15-20% is significantly **above the normal physiological range** and represents a serious concern for **severe dehydration** or inadequate nutritional intake. - This degree of weight loss would warrant **immediate medical evaluation** and intervention, including possible hospitalization.
Pharmacology
3 questionsDrug not used in pulmonary hypertension is:
What is the cause of cough and angioedema in a patient receiving ACE inhibitors?
What is the mechanism of action of ticagrelor?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 11: Drug not used in pulmonary hypertension is:
- A. Endothelin receptor antagonist
- B. Prostacyclin
- C. Alpha blocker (Correct Answer)
- D. Calcium channel blocker
Explanation: ***Alpha blocker*** - Alpha-blockers primarily cause **systemic vasodilation** [1] and are not indicated for the specific pulmonary vascular remodeling and vasoconstriction seen in pulmonary hypertension. [2] - Their use could lead to an undesirable drop in **systemic blood pressure** [3] without adequately addressing the pulmonary arterial pressure. *Calcium channel blocker* - **Calcium channel blockers** (namely **dihydropyridines** like nifedipine and amlodipine) are used in a small subset of pulmonary hypertension patients who are **vasoreactive** on acute testing. - They work by relaxing pulmonary arterial smooth muscle, reducing **pulmonary vascular resistance**. *Endothelin receptor antagonist* - **Endothelin receptor antagonists** (e.g., bosentan, ambrisentan) block the effects of **endothelin-1**, a potent vasoconstrictor and smooth muscle proliferator involved in pulmonary hypertension. - They improve hemodynamics, exercise capacity, and clinical outcomes by preventing **vasoconstriction** and **vascular remodeling**. *Prostacyclin* - **Prostacyclin analogs** (e.g., epoprostenol, treprostinil) are potent **vasodilators** and inhibitors of platelet aggregation. - They are highly effective in treating severe pulmonary hypertension by relaxing pulmonary arteries and preventing **thrombosis**.
Question 12: What is the cause of cough and angioedema in a patient receiving ACE inhibitors?
- A. Bradykinin
- B. Increased renin levels
- C. Increased angiotensin-II levels
- D. Bradykinin accumulation (Correct Answer)
Explanation: ***Bradykinin accumulation*** - **ACE inhibitors** block the enzyme **angiotensin-converting enzyme (ACE)**, which is responsible for degrading **bradykinin**. - The resulting **accumulation of bradykinin** is a potent vasodilator and increases capillary permeability, leading to **cough** (5-20% of patients) and **angioedema** (0.1-0.7%). - This is the most **precise answer** as it specifies the mechanism: impaired degradation leading to accumulation. *Bradykinin (alone)* - While **bradykinin** is the mediator involved, this option is **less precise** than "bradykinin accumulation." - **Bradykinin** is naturally present in the body; the problem with ACE inhibitors is specifically the **accumulation** due to impaired degradation. - The correct answer requires understanding that it's the **excess levels**, not just the presence, that causes symptoms. *Increased renin levels* - **ACE inhibitors** block the conversion of **angiotensin I to angiotensin II**, leading to reduced negative feedback. - This causes **compensatory increase in renin secretion** from the juxtaglomerular apparatus. - However, increased renin is **not responsible** for cough or angioedema—these are bradykinin-mediated effects. *Increased angiotensin-II levels* - **ACE inhibitors** actually **decrease angiotensin-II levels**, which is their primary **antihypertensive mechanism**. - This option is **incorrect** as ACE inhibitors reduce (not increase) angiotensin-II. - The reduction in angiotensin-II does not cause cough or angioedema.
Question 13: What is the mechanism of action of ticagrelor?
- A. P2Y12 receptor antagonist (Correct Answer)
- B. Cox inhibition
- C. Inhibition of thromboxane synthase
- D. GPIIb/IIIa inhibition
Explanation: ***P2Y12 receptor antagonist*** - **Ticagrelor** is an **oral antiplatelet drug** that reversibly binds to the **P2Y12 ADP receptor** on platelet surfaces. - By blocking this receptor, it prevents **ADP-mediated platelet activation** and subsequent aggregation, reducing the risk of thrombotic events. *Cox inhibition* - **COX inhibitors** like **aspirin** prevent the synthesis of **thromboxane A2**, a powerful platelet aggregator. - This mechanism is characteristic of **NSAIDs** and **aspirin**, not ticagrelor. *GPIIB/IIIA inhibition* - **GPIIb/IIIa inhibitors** (e.g., abciximab, eptifibatide, tirofiban) directly block the final common pathway for platelet aggregation by preventing **fibrinogen binding** to the GPIIb/IIIa receptor. - While also an antiplatelet mechanism, this is distinct from ticagrelor's action on the P2Y12 receptor. *Inhibition of thromboxane synthase* - Inhibition of **thromboxane synthase** would reduce the production of **thromboxane A2**, similar to the effect of COX inhibition. - This is not the primary mechanism of action for ticagrelor; drugs like **dazoxiben** or **picotamide** act through this pathway.