NEET-PG 2019 Practice Questions

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: What does a decreased FEV1/FVC ratio typically indicate in pulmonary function tests?

Obstructive lung disease. ***Obstructive lung disease*** - A decreased **FEV1/FVC ratio** indicates that the amount of air forcefully exhaled in one second (FEV1) is disproportionately low compared to the total forced vital capacity (FVC) [1]. This is a hallmark of **airflow limitation**, distinguishing obstructive lung diseases. - This pattern suggests a problem with **airway narrowing** or obstruction, making it difficult to exhale air quickly, which is characteristic of conditions like **COPD** (emphysema, chronic bronchitis) or **asthma** [1]. *Normal pulmonary function* - In normal pulmonary function, the **FEV1/FVC ratio** would be within the expected reference range, typically **above 70%** (or 0.7) for adults [1]. - A low ratio explicitly indicates a deviation from normal airflow dynamics, not a state of healthy lung function. *Restrictive lung disease* - **Restrictive lung diseases** are characterized by a **reduced total lung volume** (decreased FVC), but the FEV1/FVC ratio is typically **normal or even increased**. - This is because the airways are generally not obstructed; instead, the problem lies with the lungs' inability to expand fully, leading to a proportional reduction in FEV1 and FVC. *Both obstructive and restrictive lung disease* - While it is possible to have both conditions, a **decreased FEV1/FVC ratio** primarily points to an **obstructive pattern**. - A definitive diagnosis of both would require further interpretation of other PFT parameters such as **total lung capacity (TLC)**, which would be normal or increased in obstruction and reduced in restriction.

Q: Which syndrome is associated with posterior inferior cerebellar artery thrombosis?

Wallenberg syndrome. No specific references from the provided list reached the relevance threshold (score >= 7) to be cited in the explanation. The original text remains unchanged. ***Wallenberg syndrome*** - Also known as **lateral medullary syndrome**, it is caused by **thrombosis of the posterior inferior cerebellar artery (PICA)** or its branches. - Symptoms include ipsilateral **ataxia**, **vertigo**, **nystagmus**, dysphagia, and contralateral loss of pain and temperature sensation. *Medial medullary syndrome* - This syndrome results from occlusion of the **anterior spinal artery** and paramedian branches of the **vertebral artery**. - Clinical features include contralateral **hemiparesis**, ipsilateral **tongue deviation**, and loss of position and vibration sensation. *Inferior alternating syndrome* - This is another name for **medial medullary syndrome**, caused by a lesion in the **medulla oblongata**. - It is characterized by ipsilateral cranial nerve signs and contralateral long tract signs, differentiating it from Wallenberg syndrome. *Dejerine syndrome* - Also known as **medial medullary syndrome**, it is linked to occlusion of the **anterior spinal artery**. - Symptoms primarily involve the **pyramidal tract**, **medial lemniscus**, and **hypoglossal nerve**.

Q: Calcitonin levels increased in

Medullary thyroid carcinoma. Medullary thyroid carcinoma - Calcitonin is a hormone produced by the parafollicular C cells of the thyroid gland. - Medullary thyroid carcinoma is a neuroendocrine tumor arising from these C cells, leading to excessive and unregulated calcitonin production. Hyperparathyroidism - This condition involves increased production of parathyroid hormone (PTH), which acts to increase serum calcium levels [2]. - Calcitonin secretion is typically decreased or normal in hyperparathyroidism, as calcitonin works to lower serum calcium. Hypoparathyroidism - This condition is characterized by insufficient production of parathyroid hormone (PTH), leading to low serum calcium levels [1]. - Calcitonin levels are generally unaffected or may even be slightly decreased in response to the low calcium, as its primary role is to lower calcium. Cushing Syndrome - Cushing Syndrome is caused by prolonged exposure to high levels of cortisol, a glucocorticoid. - While cortisol can affect bone metabolism, it does not directly impact calcitonin production or secretion, which is primarily regulated by serum calcium levels and C-cell activity.

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 are Gitter cells?

Modified macrophages in the CNS. ***Modified macrophages in CNS*** - Gitter cells are **modified macrophages** that have phagocytized lipid and other debris in the central nervous system (CNS), particularly in response to injury or disease [1][2]. - They play a crucial role in **cleaning up cellular debris** and are involved in the inflammatory response within the CNS [2]. *Macroglia* - Macroglia refers to **supportive cells** in the CNS, including astrocytes and oligodendrocytes, rather than being specifically modified macrophages. - It does not specifically describe the **phagocytic role** characteristic of Gitter cells. *Oligodendrocytes* - Oligodendrocytes primarily function to **myelinate axons** in the CNS and do not possess the same phagocytic capabilities as Gitter cells. - They are involved in **insulation** of neuronal axons rather than debris clearance. *Astrocytes* - Astrocytes are the principal **supportive glial cells** in the CNS and do not exhibit the characteristics of Gitter cells. - Their functions include **maintaining blood-brain barrier**, regulating blood flow, and supporting neuronal metabolism, not phagocytosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1255-1256. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 697-698.

Q: Which fluoroquinolone has the maximum bioavailability?

Levofloxacin. ***Levofloxacin*** - **Levofloxacin** exhibits high oral bioavailability, approximately 99%, meaning nearly all of the administered dose reaches systemic circulation [1]. - This high bioavailability allows for seamless transition from intravenous to oral administration without significant changes in drug exposure [1]. *Moxifloxacin* - **Moxifloxacin** has a high bioavailability of approximately 90%, which is slightly lower than levofloxacin's almost complete absorption [1]. - While excellent, it is not the absolute highest among fluoroquinolones. *Gatifloxacin* - **Gatifloxacin** has good oral bioavailability, around 96%, but it is still generally considered slightly less than that of levofloxacin [1]. - This difference, though small, makes levofloxacin the one with the highest overall bioavailability. *Ciprofloxacin* - **Ciprofloxacin** has the lowest oral bioavailability among the listed fluoroquinolones, ranging from 70% to 80% [1]. - Its absorption can be significantly impaired by co-administration with multivalent cations, leading to reduced systemic concentrations.

Q: Tubuloglomerular feedback control is useful for which one of the following?

GFR. ***GFR*** - **Tubuloglomerular feedback (TGF)** is a critical autoregulatory mechanism that maintains a relatively constant **glomerular filtration rate (GFR)** despite fluctuations in arterial blood pressure. - The **macula densa** cells at the end of the thick ascending limb of the loop of Henle sense the **volume** and **sodium chloride concentration** of the tubular fluid and release paracrine factors to adjust afferent arteriolar resistance. *Plasma sodium* - While TGF senses the **sodium chloride concentration** in the filtrate, its primary role is to regulate GFR, not directly control systemic plasma sodium levels. - Plasma sodium is primarily regulated by hormones like **ADH** and **aldosterone**, which influence water reabsorption and sodium excretion. *Plasma volume* - **Plasma volume** is regulated predominantly by hormonal mechanisms (e.g., **renin-angiotensin-aldosterone system**, **ADH**, **ANP**) and control over overall sodium and water balance, rather than by the acute, intrinsic GFR regulation of TGF. - Changes in plasma volume can indirectly affect GFR, but TGF is not the direct control mechanism for plasma volume itself. *Determining tubular secretion* - **Tubular secretion** is the process by which solutes are actively transported from the peritubular capillaries into the tubular lumen. - TGF influences **glomerular filtration**, not directly the rates of tubular secretion, which are regulated by specific transport proteins and physiological needs.

Q: Boot shape of heart in TOF is due to:

Right ventricular hypertrophy. ***Right ventricular hypertrophy*** - The characteristic **boot-shaped heart (coeur en sabot)** seen in Tetralogy of Fallot (TOF) on a chest X-ray is primarily due to **right ventricular hypertrophy** and the small pulmonary artery. - The hypertrophied right ventricle lifts the cardiac apex, while the concavity in the area of the pulmonary artery (due to **pulmonary stenosis**) gives the heart its distinctive shape. *Enlargement of the left atrium* - Left atrial enlargement is not a feature of **Tetralogy of Fallot**; in fact, chronic pulmonary outflow obstruction often leads to a relatively normal or small left atrium. - This condition involves right-sided heart abnormalities, and left atrial enlargement would suggest increased left-sided pressures, which are not typical for TOF. *Enlargement of the right atrium* - While right atrial enlargement can occur in severe cases of TOF due to increased resistance to blood flow, it is **right ventricular hypertrophy** that is the primary determinant of the classic boot-shaped cardiac silhouette. - Right atrial enlargement alone does not create the specific "boot" appearance which is largely due to the ventricular contour. *Hypertrophy of both ventricles* - In Tetralogy of Fallot, the primary ventricular abnormality is **right ventricular hypertrophy**, driven by the need to pump blood through a stenosed pulmonary artery. - The left ventricle typically maintains a normal size and function, as it primarily pumps into the systemic circulation and is not directly affected by the primary defects in the same way as the right ventricle.

Question 1

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 2

In Krebs cycle and Urea cycle the linking amino acid is

Accepted Answer

Aspartate

Answer

Fumarate

Answer

Alanine

Answer

Arginine

Question 3

What does a decreased FEV1/FVC ratio typically indicate in pulmonary function tests?

Accepted Answer

Obstructive lung disease

Answer

Normal pulmonary function

Answer

Restrictive lung disease

Answer

Both obstructive and restrictive lung disease

Question 4

Which syndrome is associated with posterior inferior cerebellar artery thrombosis?

Accepted Answer

Wallenberg syndrome

Answer

Medial medullary syndrome

Answer

Inferior alternating syndrome

Answer

Dejerine syndrome

Question 5

Calcitonin levels increased in

Accepted Answer

Medullary thyroid carcinoma

Answer

Hypoparathyroidism

Answer

Cushing Syndrome

Answer

Hyperparathyroidism

Question 6

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

Accepted Answer

Parvovirus B19

Answer

EBV

Answer

CMV

Answer

HSV

Question 7

What are Gitter cells?

Accepted Answer

Modified macrophages in the CNS

Answer

Microglia

Answer

Astrocytic cells

Answer

Oligodendrocytic cells

Question 8

Which fluoroquinolone has the maximum bioavailability?

Accepted Answer

Levofloxacin

Answer

Gatifloxacin

Answer

Ciprofloxacin

Answer

Moxifloxacin

Question 9

Tubuloglomerular feedback control is useful for which one of the following?

Accepted Answer

GFR

Answer

Plasma sodium

Answer

Plasma volume

Answer

Determining tubular secretion

Question 10

Boot shape of heart in TOF is due to:

Accepted Answer

Right ventricular hypertrophy

Answer

Enlargement of the left atrium

Answer

Enlargement of the right atrium

Answer

Hypertrophy of both ventricles

NEET-PG 2019

Biochemistry

Internal Medicine

Microbiology

Pathology

Pharmacology

Physiology

Radiology