NEET-PG 2012 Practice Questions

Q: The primary defect which leads to sickle cell anemia is:

Replacement of glutamate by valine in β-chain of HbA. ***Replacement of glutamate by valine in β-chain of HbA*** - The primary defect in sickle cell anemia is a **point mutation** that leads to the replacement of **glutamic acid** with **valine** in the **sixth position** of the β-globin chain [1]. - This mutation causes the hemoglobin (HbS) to polymerize under low oxygen conditions, resulting in the characteristic **sickle-shaped red blood cells** [1]. *A nonsence mutation in the I3-chain of HbA* - A nonsense mutation leads to a **premature stop codon**, which is not the mechanism behind sickle cell anemia. - This mutation does not involve the β-globin chain, which is critical in this specific disorder. *Substitution of valine by glutamate in the a-chain of HbA* - This statement is incorrect as sickle cell anemia specifically involves the **β-chain**, not the **α-chain**. - Substituting valine with glutamate does not cause sickling but rather the opposite of the actual defect observed in this condition. *An abnormality in porphyrin part of hemoglobin* - Sickle cell anemia does not arise from **porphyrin metabolism issues**, which are related to conditions like **porphyrias**. - The primary defect is a change in the amino acid sequence, not in the porphyrin structure of hemoglobin. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599.

Q: Which of the following is not a precursor in the synthesis of pyrimidines?

Thymidine. ***Thymidine*** - **Thymidine** is a *nucleoside* consisting of deoxyribose and thymine. It is a *product* and a component of DNA, not a precursor in the *de novo synthesis* of pyrimidine bases. - While it can be incorporated into DNA via the *salvage pathway*, it does not serve as an initial building block for the pyrimidine ring itself. *Glutamine* - **Glutamine** provides the **nitrogen atoms** crucial for the formation of the pyrimidine ring, specifically N3 in the pyrimidine base. - It is a key donor of *amino groups* in various anabolic pathways, including nucleotide synthesis. *Carbon dioxide (CO2)* - **Carbon dioxide (CO2)** contributes one of the carbon atoms (C2) to the pyrimidine ring. - It combines with **ammonia** (derived from glutamine) to form **carbamoyl phosphate**, an essential intermediate. *Aspartic acid* - **Aspartic acid** provides four atoms (N1, C4, C5, C6) of the pyrimidine ring. - Its carbon skeleton and amino group are directly incorporated into the pyrimidine structure during the *de novo synthesis* pathway.

Q: In the electron transport chain (ETC), which enzyme does cyanide inhibit?

Cytochrome c oxidase (Complex IV). ***Cytochrome c oxidase (Complex IV)*** - Cyanide binds to the **ferric iron (Fe3+)** in the heme a3 component of cytochrome c oxidase, blocking the final transfer of electrons to oxygen. - This inhibition effectively halts the entire **electron transport chain** and **oxidative phosphorylation**, leading to rapid cellular energy depletion. *Complex I (NADH dehydrogenase)* - While other toxins can inhibit Complex I (e.g., rotenone, amytal), **cyanide specifically targets Complex IV**. - Inhibition here prevents the entry of electrons from **NADH** into the ETC, but it's not cyanide's primary site of action. *Complex III (Cytochrome bc1 complex)* - Complex III is involved in transferring electrons from **ubiquinol** to cytochrome c, but it is not directly inhibited by cyanide. - Antimycin A is a well-known inhibitor of Complex III. *Complex II (Succinate dehydrogenase)* - Complex II directly receives electrons from **succinate** in the citric acid cycle and passes them to ubiquinone, bypassing Complex I. - Cyanide does not inhibit Complex II; inhibitors of this complex include malonate.

Q: What is the rate-controlling enzyme of fatty acid synthesis?

Acetyl-CoA carboxylase. ***Acetyl-CoA carboxylase*** - **Acetyl-CoA carboxylase (ACC)** catalyzes the committed step in fatty acid synthesis, converting **acetyl-CoA** to **malonyl-CoA**. - This enzyme is subject to both allosteric regulation (e.g., activation by **citrate** and inhibition by **long-chain fatty acyl-CoA**) and hormonal regulation (e.g., phosphorylation by glucagon and dephosphorylation by insulin). *Thioesterase* - **Thioesterase** is the enzyme responsible for releasing the completed fatty acid chain from the **fatty acid synthase complex**. - While essential for the termination of synthesis, it does not regulate the initiation or overall rate of the pathway. *Transacetylase* - **Transacetylase** (specifically, acetyl-CoA-ACP transacetylase and malonyl-CoA-ACP transacetylase) is involved in transferring acetyl and malonyl groups to the **acyl carrier protein (ACP)** within the fatty acid synthesis complex. - This is an intermediary step, but not the primary **rate-controlling** or committed step. *Ketoacyl synthase* - **Ketoacyl synthase (or β-ketoacyl-ACP synthase)** is responsible for condensing the growing acyl chain with malonyl-ACP, leading to the formation of a **β-ketoacyl-ACP**. - This is a crucial chain elongation step within the fatty acid synthase complex, but not the enzyme that controls the overall commitment to fatty acid synthesis.

Q: Methionine can enter the TCA cycle at which level?

Succinyl-CoA. ***Succinyl - CoA*** - Methionine is a **glucogenic amino acid** that is catabolized to propionyl-CoA, which is then converted to **methylmalonyl-CoA** and finally to **succinyl-CoA**. - **Succinyl-CoA** is an intermediate of the **TCA cycle**, allowing methionine-derived carbons to enter the cycle. *Fumarate* - Fumarate is an intermediate of the TCA cycle, but methionine catabolism does not directly produce **fumarate**. - Amino acids like **phenylalanine** and **tyrosine** can be catabolized to fumarate. *Oxaloacetate* - **Oxaloacetate** is a TCA cycle intermediate and can be formed from **pyruvate** (via pyruvate carboxylase) or from certain amino acids like **aspartate** and **asparagine**. - Methionine does not directly convert to oxaloacetate. *Citrate* - **Citrate** is the first intermediate formed in the TCA cycle when **acetyl-CoA** combines with **oxaloacetate**. - Methionine catabolism does not lead to the direct formation of citrate.

Q: Nutmeg liver is associated with which condition?

Right sided heart failure. ***Right sided heart failure*** - **Nutmeg liver** is a classic finding associated with **congestion** in the liver due to **right-sided heart failure**, leading to the characteristic mottled appearance [1][2]. - **Impaired venous return** from the systemic circulation causes hepatic congestion, resulting in **enlargement and fibrosis** of the liver over time [2]. *Left sided heart failure* - Left-sided heart failure primarily affects the **lungs**, leading to pulmonary congestion rather than hepatic changes. - While it can cause secondary effects on the liver over time, it does not directly cause **nutmeg liver**. *Increased pulmonary pressure* - Increased pulmonary pressure is generally associated with conditions like **pulmonary hypertension**, affecting primarily the **lungs** rather than the liver directly. - It does not lead to the **congestive changes** observed in nutmeg liver [1], which is related to right heart function. *Decreased pulmonary pressure* - Decreased pulmonary pressure would typically improve pulmonary blood flow, therefore having no association with liver congestion. - It does not contribute to the **venous stasis** seen in right heart failure, which is pivotal for nutmeg liver. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 126. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 870-872.

Q: What is the normal range for the CSF/plasma glucose ratio?

0.6 - 0.8. ***Correct: 0.6 - 0.8*** - This ratio indicates that cerebrospinal fluid (CSF) glucose concentration is typically 60-80% of plasma glucose concentration - This range is crucial for identifying metabolic or infectious pathologies affecting the central nervous system - Normal CSF glucose is approximately 50-80 mg/dL when plasma glucose is 70-120 mg/dL *Incorrect: 0.2 - 0.4* - A ratio in this range indicates significantly low CSF glucose, suggesting conditions like bacterial meningitis or hypoglycorrhachia - This is well below the normal physiological proportion of glucose in the CSF relative to plasma - Seen in bacterial/tuberculous meningitis, fungal infections, or malignancy *Incorrect: 1.0 - 1.2* - A CSF/plasma glucose ratio close to or above 1.0 would imply that CSF glucose levels are equal to or higher than plasma levels, which is physiologically impossible under normal conditions - Glucose transport into the CSF is regulated by GLUT-1 transporters and typically results in lower concentrations than in plasma - The blood-brain barrier maintains this gradient *Incorrect: 1.2 - 1.6* - This range is even more exaggerated and physiologically impossible, as CSF glucose cannot exceed plasma glucose in a healthy individual - Such a high ratio would contradict the mechanisms of glucose transport across the blood-brain barrier - Would suggest laboratory error if observed

Q: Which of the following is the MOST accurate statement about CSF?

Formed by the choroid plexus in the ventricles.. ***Formed by the choroid plexus in the ventricles.*** * The **choroid plexus**, located in the ventricles of the brain, is primarily responsible for the production of **cerebrospinal fluid (CSF)**. * Specialized epithelial cells of the choroid plexus filter blood plasma to produce CSF, which then circulates through the central nervous system. *Normally contains no neutrophils* * Normal CSF should contain **virtually no neutrophils**; their presence typically indicates an inflammatory or infectious process, such as **bacterial meningitis**. * While normal CSF doesn't have neutrophils, this option isn't as broadly accurate as the choroid plexus statement because the presence of other cell types like lymphocytes in small numbers is normal. *pH is less than that of plasma* * The pH of CSF is typically **slightly lower than that of plasma** (around 7.31 compared to 7.40), but the statement "less than" is broad and the degree of difference can be variable and is a less defining characteristic than its formation site. * This slight difference in pH is important for regulating **respiration** through chemoreceptors, but it's not the most accurate or fundamental statement about CSF properties. *Removal of CSF during dural tap can cause a headache due to the change in pressure.* * A **post-dural puncture headache** (PDPH) is a well-known complication of a dural tap (lumbar puncture), caused by the leakage of CSF from the puncture site, leading to **intracranial hypotension**, not simply a change in pressure. * This decrease in CSF volume and pressure causes a traction on pain-sensitive structures within the cranium, resulting in a headache that is typically **worse when upright** and relieved by lying down.

Q: IVC filter is used in the following situations except -

As primary treatment for acute DVT. ***As primary treatment for acute DVT*** - The **primary treatment** for **acute deep vein thrombosis (DVT)** is **anticoagulation therapy** (heparin, warfarin, or DOACs) to prevent clot propagation and embolization. - An **IVC filter** is **NOT primary therapy**—it is reserved for specific situations and does not treat the underlying thrombosis. - **Indications for IVC filter include:** - Absolute **contraindication to anticoagulation** (active bleeding, recent hemorrhagic stroke) - **Recurrent PE despite adequate anticoagulation** - Complications from anticoagulation therapy - Therefore, using IVC filter as primary treatment for acute DVT is **incorrect and not indicated**. *Negligible size of emboli* - While IVC filters trap **large emboli**, the concept of "negligible size emboli" is not a standard clinical consideration for filter placement. - IVC filters are indicated based on **risk of PE** and **contraindications to anticoagulation**, not based on emboli size assessment. *To reduce symptoms* - **IVC filters** do not reduce symptoms of DVT such as pain, swelling, or discomfort. - They function as a **mechanical barrier** to prevent emboli from reaching pulmonary circulation. - Symptom management requires anticoagulation, compression therapy, and leg elevation. *To prevent progress of native blood vessel disease* - IVC filters do not influence progression of underlying **vascular disease** such as atherosclerosis or chronic venous insufficiency. - Their sole function is **mechanical prevention of PE**, not disease modification.

Question 1

The primary defect which leads to sickle cell anemia is:

Accepted Answer

Replacement of glutamate by valine in β-chain of HbA

Answer

An abnormality in porphyrin part of hemoglobin

Answer

A nonsense mutation in the β-chain of HbA

Answer

Substitution of valine by glutamate in the α-chain of HbA

Question 2

Which of the following is not a precursor in the synthesis of pyrimidines?

Accepted Answer

Thymidine

Answer

Glutamine

Answer

Carbon dioxide (CO2)

Answer

Aspartic acid

Question 3

In the electron transport chain (ETC), which enzyme does cyanide inhibit?

Accepted Answer

Cytochrome c oxidase (Complex IV)

Answer

Complex II (Succinate dehydrogenase)

Answer

Complex I (NADH dehydrogenase)

Answer

Complex III (Cytochrome bc1 complex)

Question 4

What is the rate-controlling enzyme of fatty acid synthesis?

Accepted Answer

Acetyl-CoA carboxylase

Answer

Thioesterase

Answer

Transacetylase

Answer

Ketoacyl synthase

Question 5

Methionine can enter the TCA cycle at which level?

Accepted Answer

Succinyl-CoA

Answer

Fumarate

Answer

Oxaloacetate

Answer

Citrate

Question 6

Nutmeg liver is associated with which condition?

Accepted Answer

Right sided heart failure

Answer

Increased pulmonary pressure

Answer

Decreased pulmonary pressure

Answer

Left sided heart failure

Question 7

What is the normal range for the CSF/plasma glucose ratio?

Accepted Answer

0.6 - 0.8

Answer

1.2 - 1.6

Answer

0.2 - 0.4

Answer

1.0 - 1.2

Question 8

Which of the following is the MOST accurate statement about CSF?

Accepted Answer

Formed by the choroid plexus in the ventricles.

Answer

Normally contains no neutrophils

Answer

pH is less than that of plasma

Answer

Removal of CSF during dural tap can cause a headache due to the change in pressure.

Question 9

The plateau phase of this graph is due to:

Accepted Answer

The calcium channels remaining open longer than the sodium channels

Answer

Increased membrane permeability to potassium ions

Answer

A decrease in calcium diffusion across the membrane

Answer

The movement of fewer sodium ions across the cell membrane

Question 10

IVC filter is used in the following situations except -

Accepted Answer

As primary treatment for acute DVT

Answer

To reduce symptoms

Answer

Negligible size of emboli

Answer

To prevent progress of native blood vessel disease

NEET-PG 2012

Biochemistry

Pathology

Physiology

Surgery