NEET-PG 2019 Practice Questions

Q: Joint involved in movement of head from left to right.

Atlanto axial. ***Atlanto axial*** - The **atlantoaxial joint** is responsible for the **rotation of the head**, allowing for movements such as shaking the head "no." - This joint is a **pivot joint** formed between the atlas (C1 vertebra) and the axis (C2 vertebra), specifically the **dens** of the axis articulating with the anterior arch of the atlas. *Atlanto occipital* - The **atlanto-occipital joint** primarily facilitates **flexion and extension of the head** (nodding "yes" movement). - This joint connects the **atlas (C1)** to the **occipital bone** of the skull. *C2- C3 Joint* - The **C2-C3 joint** is a typical **intervertebral joint** in the cervical spine. - While it contributes to overall cervical spine mobility, it does not primarily mediate the **rotational movement** of the head. *C3- C4 Joint* - The **C3-C4 joint** is another **intervertebral joint** in the cervical spine. - Its main roles include some degree of **flexion, extension, and lateral bending**, but it is not the primary joint for head rotation.

Q: Menkes disease is caused by a deficiency of which protein?

ATP7A (copper-transporting ATPase). ***ATP7A (copper-transporting ATPase)*** - **Menkes disease** is an X-linked recessive disorder caused by a mutation in the **ATP7A gene**, which encodes a copper-transporting ATPase. - This protein is essential for **copper absorption** from the intestines and its transport across cell membranes. *ATP7B (Wilson disease protein)* - Mutations in the **ATP7B gene** cause **Wilson disease**, characterized by **copper accumulation** in the liver, brain, and other organs due to impaired copper excretion. - Unlike Menkes disease, Wilson disease involves *too much* copper in tissues, not a deficiency due to poor absorption. *Ceruloplasmin* - **Ceruloplasmin** is a copper-carrying protein that transports copper in the blood and also acts as an oxidase. - While deficiencies in ceruloplasmin can lead to **aceruloplasminemia**, a disorder of iron metabolism, it is not the primary defect in Menkes disease. *Copper-zinc superoxide dismutase* - **Copper-zinc superoxide dismutase (SOD1)** is an enzyme that plays a crucial role in eliminating harmful **reactive oxygen species**. - Mutations in SOD1 are associated with some forms of **amyotrophic lateral sclerosis (ALS)**, not Menkes disease.

Q: In Krebs cycle and Urea cycle the linking amino acid is

Aspartate. ***Aspartate*** - **Aspartate** acts as the crucial amino acid link between the two cycles - In the urea cycle, aspartate condenses with citrulline to form **argininosuccinate** (via argininosuccinate synthetase) - When argininosuccinate is cleaved, it produces **fumarate**, which enters the Krebs cycle - In the Krebs cycle, fumarate is converted to malate, then to **oxaloacetate**, which can be transaminated back to aspartate - This creates the **aspartate-argininosuccinate shunt**, linking both cycles through nitrogen metabolism *Fumarate* - While **fumarate** is a key metabolic intermediate connecting both cycles, it is **not an amino acid** (it's a dicarboxylic acid) - It is produced in the urea cycle from argininosuccinate cleavage and feeds into the Krebs cycle - This is a common distractor since fumarate does link the cycles, but the question specifically asks for an amino acid *Alanine* - **Alanine** participates in the glucose-alanine cycle for nitrogen transport from muscle to liver - It does not directly link the Krebs cycle and urea cycle in the same manner as aspartate *Arginine* - **Arginine** is a urea cycle intermediate that is cleaved by arginase to produce urea and ornithine - While it's an amino acid in the urea cycle, it does not serve as the linking amino acid between the Krebs cycle and urea cycle

Q: Which measure indicates the diagnostic power of a test to correctly identify those with a disease?

Sensitivity. ***Positive predictive value*** - It refers to the probability that subjects with a positive test result truly have the disease, highlighting the test's **diagnostic accuracy** [1]. - A high positive predictive value indicates that the test is effective at diagnosing the disease in the population tested. *Sensitivity* - Sensitivity measures the ability of a test to correctly identify those with the disease (true positives), but does not account for the test result's predictive capability [1]. - It is important for screening, but **not directly the diagnostic power** for those already tested. *Negative predictive value* - This indicates the probability that subjects with a negative test result truly do not have the disease, focusing on true negatives rather than correct diagnosis of the condition [1]. - While informative, it does not assess the ability to correctly diagnose the disease when the result is positive. *Specificity* - Specificity is the measure of a test's ability to correctly identify those without the disease (true negatives), not diagnosing the disease accurately among those tested [1]. - It is essential for determining false positives but not for assessing the overall diagnostic power of a test. **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. 253-254.

Q: Which viral infection is known to cause a condition resembling erythroblastosis?

Parvovirus B19. ***Parvovirus B19*** - **Parvovirus B19** has a specific tropism for **erythroid progenitor cells** in the bone marrow. - In the fetus, congenital infection causes **severe anemia** due to destruction of red blood cell precursors, leading to **hydrops fetalis** with massive compensatory erythropoiesis. - This results in circulating **nucleated red blood cells (erythroblasts)**, hepatosplenomegaly from extramedullary hematopoiesis, and severe anemia - a picture closely **resembling erythroblastosis fetalis**. - Unlike the immune-mediated hemolysis in Rh isoimmunization, parvovirus causes direct viral destruction of erythroid precursors with similar clinical manifestations. *CMV* - **Cytomegalovirus (CMV)** is the most common congenital infection and can cause hepatosplenomegaly, jaundice, and thrombocytopenia. - However, CMV typically causes **direct hyperbilirubinemia** from hepatocellular damage rather than the hemolytic anemia pattern seen in erythroblastosis. - While CMV can affect hematopoiesis, it does not characteristically produce the massive erythroblast response and hydrops pattern typical of erythroblastosis fetalis. *EBV* - **Epstein-Barr virus (EBV)** primarily causes **infectious mononucleosis** in older children and adults, with atypical lymphocytosis. - EBV is rare in neonates and does not cause fetal hydrops or an erythroblastosis-like syndrome. - Associated with lymphoproliferative disorders and post-transplant complications rather than fetal anemia. *HSV* - **Herpes simplex virus (HSV)** causes disseminated neonatal infection with encephalitis, hepatitis, and mucocutaneous lesions. - HSV does not have tropism for erythroid precursors and does not cause the anemia, hydrops, or erythroblastosis-like picture. - Typically acquired perinatally rather than causing congenital infection with hematologic manifestations.

Q: What is the drug of choice (DOC) for a scorpion sting bite?

Prazosin. ***Prazosin*** - **Prazosin** is an **alpha-1 adrenergic antagonist** that effectively counteracts the symptoms of scorpion envenomation, particularly **autonomic hyperactivity** like hypertension and tachycardia. - It works by blocking the effects of norepinephrine released by the scorpion venom, helping to stabilize vital signs and reduce cardiovascular complications. *EDTA* - **EDTA (ethylenediaminetetraacetic acid)** is a **chelating agent** primarily used to treat **heavy metal poisoning**, such as lead or mercury. - It binds to metal ions, forming a stable complex that can then be excreted from the body; it has no role in scorpion envenomation. *Neostigmine* - **Neostigmine** is an **acetylcholinesterase inhibitor** used to treat conditions like myasthenia gravis or to reverse the effects of neuromuscular blocking agents. - It increases acetylcholine levels at the neuromuscular junction; it is not indicated for the management of scorpion stings. *N-acetylcysteine* - **N-acetylcysteine (NAC)** is primarily used as an **antidote for acetaminophen overdose** and as a mucolytic agent in respiratory conditions. - It replenishes glutathione stores, helping to detoxify harmful metabolites; it has no direct role in treating scorpion venom effects.

Q: Which of the following drugs is used in SIADH?

Tolvaptan. ***Tolvaptan*** - **Tolvaptan** is a **vasopressin receptor antagonist** that blocks the action of **antidiuretic hormone (ADH)** at the **V2 receptors** in the kidneys [1]. - This action promotes **water excretion (aquaresis)** without significantly affecting electrolyte balance, thereby increasing serum sodium levels in patients with **SIADH** [1]. *Desmopressin* - **Desmopressin** is a synthetic analog of **ADH** that primarily acts on **V2 receptors**, promoting water reabsorption [3], [4]. - It is used in conditions like **diabetes insipidus** [3], [4] or **hemophilia** [2] to increase ADH activity or clotting factors, which is contrary to the goal in SIADH. *Von Willebrand factor* - **Von Willebrand factor** is a **glycoprotein** involved in **hemostasis**, promoting platelet adhesion and carrying **factor VIII**. - It plays no role in the direct management of **SIADH** or fluid balance disorders. *Terlipressin* - **Terlipressin** is an analog of **vasopressin** that primarily acts on **V1 receptors**, causing vasoconstriction [5]. - It is used in conditions like **hepatorenal syndrome** or **esophageal variceal bleeding**, not for treating **SIADH**.

Q: A drug with high plasma protein binding property has which of the following properties?

Lower volume of distribution. ***Lower volume of distribution*** - Drugs with high plasma protein binding are largely confined to the **vascular compartment** as they bind to proteins (e.g., albumin, alpha-1-acid glycoprotein), making them less available to distribute into tissues. - This confinement within the plasma compartment results in a **smaller apparent volume of distribution**. *Less drug interaction* - High plasma protein binding actually increases the potential for **drug-drug interactions** through displacement. - If a second drug displaces the first from its binding sites, it can increase the **free fraction** and potentially lead to toxicity. *Reduced renal clearance* - While highly protein-bound drugs are generally not easily filtered by the glomeruli, their primary route of elimination is often through **hepatic metabolism** or **active tubular secretion**, rather than reduced renal elimination. - Many highly protein-bound drugs still undergo significant renal excretion via **active secretion**, if they are substrates for active transporters. *Less tubular secretion* - Plasma protein binding does not inherently reduce tubular secretion; in some cases, the drug-protein complex can dissociate rapidly at the secretory sites, allowing for efficient secretion of the **free drug**. - In fact, many drugs that undergo significant tubular secretion are also highly protein-bound, as protein binding helps **maintain a concentration gradient** for and delivery of the drug to the secretion transporters.

Q: Vasopressin acts through which aquaporin channels in the collecting duct?

Aquaporin 2. ***Aquaporin 2*** - Vasopressin (ADH) stimulates the insertion of **Aquaporin 2 (AQP2)** channels into the apical membrane of collecting duct cells, increasing water reabsorption. - This process is crucial for the kidney's ability to concentrate urine and maintain **water balance**. *Aquaporin 1* - **Aquaporin 1 (AQP1)** is predominantly found in the proximal tubules and descending limb of the loop of Henle, where **constitutive water reabsorption** occurs, independent of vasopressin. - It plays a role in bulk water reabsorption rather than regulated fine-tuning. *Aquaporin 3* - **Aquaporin 3 (AQP3)** is located on the **basolateral membrane** of collecting duct cells, facilitating the exit of water from the cell into the interstitial fluid. - While essential for water movement, its insertion into the membrane is **not directly regulated by vasopressin** in the same way as AQP2. *Aquaporin 4* - **Aquaporin 4 (AQP4)** is also found on the **basolateral membrane** of collecting duct cells and in other tissues like the brain. - Similar to AQP3, it allows water to leave the cell but is not the primary target for vasopressin-mediated regulation of water permeability.

Q: Functional residual capacity (FRC) is defined as the volume of air remaining in the lungs at which specific moment in the respiratory cycle?

After normal expiration. ***After normal expiration*** - **Functional residual capacity (FRC)** is the volume of air remaining in the lungs at the end of a **normal, passive expiration**. - It represents the sum of the **expiratory reserve volume (ERV)** and the **residual volume (RV)**. *During active expiration* - **Active expiration** involves the use of accessory muscles to force more air out of the lungs than during normal expiration. - This process would result in a lung volume less than FRC, closer to the **residual volume**. *At peak inspiration* - **Peak inspiration** represents the total lung capacity (TLC), which is the maximum volume of air the lungs can hold after a maximal inspiratory effort. - This is the largest lung volume, significantly greater than FRC. *During active inspiration* - **Active inspiration** is the process of inhaling air, which increases lung volume. - FRC is a static volume measured at the end of expiration, not during the dynamic process of inhaling.

Question 1

Joint involved in movement of head from left to right.

Accepted Answer

Atlanto axial

Answer

Atlanto occipital

Answer

C2- C3 Joint

Answer

C3- C4 Joint

Question 2

Menkes disease is caused by a deficiency of which protein?

Accepted Answer

ATP7A (copper-transporting ATPase)

Answer

ATP7B (Wilson disease protein)

Answer

Ceruloplasmin

Answer

Copper-zinc superoxide dismutase

Question 3

In Krebs cycle and Urea cycle the linking amino acid is

Accepted Answer

Aspartate

Answer

Fumarate

Answer

Alanine

Answer

Arginine

Question 4

Which measure indicates the diagnostic power of a test to correctly identify those with a disease?

Accepted Answer

Sensitivity

Answer

Negative predictive value

Answer

Specificity

Answer

Positive predictive value

Question 5

Which viral infection is known to cause a condition resembling erythroblastosis?

Accepted Answer

Parvovirus B19

Answer

EBV

Answer

CMV

Answer

HSV

Question 6

What is the drug of choice (DOC) for a scorpion sting bite?

Accepted Answer

Prazosin

Answer

EDTA

Answer

Neostigmine

Answer

N-acetylcysteine

Question 7

Which of the following drugs is used in SIADH?

Accepted Answer

Tolvaptan

Answer

Desmopressin

Answer

Terlipressin

Answer

Von Willebrand factor

Question 8

A drug with high plasma protein binding property has which of the following properties?

Accepted Answer

Lower volume of distribution

Answer

Reduced renal clearance

Answer

Less drug interaction

Answer

Less tubular secretion

Question 9

Vasopressin acts through which aquaporin channels in the collecting duct?

Accepted Answer

Aquaporin 2

Answer

Aquaporin 1

Answer

Aquaporin 4

Answer

Aquaporin 3

Question 10

Functional residual capacity (FRC) is defined as the volume of air remaining in the lungs at which specific moment in the respiratory cycle?

Accepted Answer

After normal expiration

Answer

During active expiration

Answer

At peak inspiration

Answer

During active inspiration

NEET-PG 2019

Anatomy

Biochemistry

Community Medicine

Pediatrics

Pharmacology

Physiology