NEET-PG 2012 Practice Questions

Q: Which enzyme is primarily associated with the reduction of NADP+ to NADPH in the pentose phosphate pathway?

G6PD. ***G6PD*** - **Glucose-6-phosphate dehydrogenase (G6PD)** catalyzes the first committed step in the pentose phosphate pathway, converting **glucose-6-phosphate** to **6-phosphogluconolactone**. - This reaction involves the reduction of **NADP+ to NADPH**, making G6PD the primary enzyme for NADPH production in this pathway. *APDH* - **APDH (adenosine phosphosulfate reductase)** is involved in sulfur metabolism and has no direct role in the pentose phosphate pathway or NADPH production. - This enzyme primarily functions in prokaryotes for the **reduction of APS (adenosine 5'-phosphosulfate)**. *α-keto glutarate dehydrogenases* - **Alpha-ketoglutarate dehydrogenase** is a mitochondrial enzyme part of the **Krebs cycle**, converting **alpha-ketoglutarate to succinyl-CoA**. - This enzyme is crucial for ATP production and generates **NADH**, not NADPH, in its reaction. *None of the options* - This option is incorrect because **G6PD** is indeed the primary enzyme responsible for NADPH generation in the pentose phosphate pathway.

Q: Which of the following pairs of compounds has the highest standard reduction potential?

Fe³⁺/Fe²⁺. ***Fe³⁺/Fe²⁺*** - The **Fe³⁺/Fe²⁺ couple** has a **standard reduction potential (E'0)** of **+0.77 V**, making it the highest among the given options. - A higher positive E'0 indicates a stronger tendency for the oxidized form to accept electrons and be reduced. *NADH/NAD+* - The **NADH/NAD+ couple** has a **standard reduction potential** of **-0.32 V**, indicating it is a strong reducing agent. - Its negative reduction potential means it readily donates electrons during metabolic processes. *Succinate/Fumarate* - The **succinate/fumarate couple** has a **standard reduction potential** of **+0.03 V**. - This pair is involved in the **TCA cycle**, where succinate is oxidized to fumarate, releasing electrons. *Ubiquinone/Ubiquinol* - The **ubiquinone/ubiquinol couple** has a **standard reduction potential** varying around **+0.05 to +0.10 V**, depending on the specific state. - It acts as a mobile electron carrier in the **electron transport chain**, accepting electrons from NADH and FADH2.

Q: Fluoroacetate inhibits?

Aconitase. ***Aconitase*** - **Fluoroacetate** is metabolically converted to **fluorocitrate**, which is a potent competitive inhibitor of **aconitase**. - **Aconitase** is the enzyme responsible for converting **citrate to isocitrate** in the **Krebs cycle**, and its inhibition blocks the cycle. *Citrate synthase* - This enzyme is responsible for the formation of **citrate** from **acetyl-CoA** and **oxaloacetate**. - While fluoroacetate indirectly affects the cycle, it does not directly inhibit **citrate synthase**. *Succinate dehydrogenase* - This enzyme is part of the **Krebs cycle** and the **electron transport chain**, converting **succinate to fumarate**. - **Malonate** is a competitive inhibitor of succinate dehydrogenase, not **fluoroacetate**. *Alpha-ketoglutarate dehydrogenase* - This enzyme catalyzes the conversion of **alpha-ketoglutarate to succinyl-CoA** in the **Krebs cycle**. - Specific inhibitors of this enzyme include **arsenite** and **mercury compounds**, but not fluoroacetate.

Q: Increased uric acid levels are seen in which glycogen storage disease ?

Type I (Von Gierke's disease). ***Type I (Von Gierke's disease)*** - In **Von Gierke's disease**, the deficiency of **glucose-6-phosphatase** leads to accumulation of glucose-6-phosphate in hepatocytes. - **Hyperuricemia** occurs due to: 1. **Increased purine degradation** - Metabolic stress leads to accelerated ATP breakdown and increased uric acid production 2. **Decreased renal excretion** - Lactic acidosis (from G6P → pyruvate → lactate) competitively inhibits uric acid secretion in renal tubules 3. **Enhanced purine synthesis** - Increased availability of ribose-5-phosphate from pentose phosphate pathway - Classic triad: **Hepatomegaly, hypoglycemia, and lactic acidosis with hyperuricemia** *Type II (Pompe disease)* - Caused by a deficiency of **acid alpha-glucosidase** (acid maltase), leading to glycogen accumulation in **lysosomes**. - Primarily affects the **heart**, **muscles**, and **liver**, but does not cause hyperuricemia. *Type IV (Andersen disease)* - Results from a deficiency of **glycogen branching enzyme**, leading to the formation of abnormal glycogen with long, unbranched chains. - Primarily affects the **liver** and **spleen**, causing cirrhosis and hepatic failure, but not hyperuricemia. *Type III (Cori disease)* - Caused by a deficiency of **glycogen debranching enzyme** (amylo-1,6-glucosidase), leading to abnormal accumulation of glycogen with short outer branches. - Presents with hepatomegaly, hypoglycemia, and muscle weakness, but **hyperuricemia is not a characteristic feature**.

Q: Which of the following is required for fatty acid synthesis ?

NADPH. ***NADPH*** - **NADPH** is crucial for fatty acid synthesis, providing the **reducing power** needed for the successive reduction steps. - The enzymes involved, such as **fatty acid synthase**, utilize **NADPH** for the conversion of keto groups to hydroxyl groups and then to saturated methylene groups. *NADH* - **NADH** plays a primary role in **oxidative phosphorylation** and the electron transport chain to generate ATP. - It is generally produced during **catabolic reactions** and is not primarily used as a reducing agent in anabolic processes like fatty acid synthesis. *FADH* - **FADH2** (reduced form of FAD, not FADH) is a coenzyme involved in redox reactions, particularly in the **Krebs cycle** and beta-oxidation of fatty acids. - Like NADH, it is mostly involved in **catabolic processes** that generate energy, rather than anabolic processes requiring reducing equivalents for synthesis. *None of the options* - This option is incorrect because **NADPH** is indeed required for fatty acid synthesis, serving as the essential reducing agent. - The other coenzymes mentioned (NADH, FADH) have different metabolic roles, primarily in energy production rather than biosynthesis.

Q: All of the following statements about the third heart sound (S3) are true, except:

Seen in Constrictive Pericarditis. ***Seen in Constrictive Pericarditis*** - While constrictive pericarditis can lead to a diastolic sound, it's typically a **pericardial knock**, which is sharper and occurs earlier than an S3, due to abrupt halting of ventricular filling. - A true S3 is a low-pitched sound caused by turbulent blood flow into an overly compliant or volume-overloaded ventricle, which is not the primary mechanism in constrictive pericarditis. *Occurs due to rapid filling of the ventricles during early diastole.* - The S3 heart sound is precisely caused by the **rapid inflow of blood** into a dilated or poorly compliant ventricle during the early, rapid filling phase of diastole [1]. - This rapid distension causes vibrations in the ventricular wall, audible as S3, and is often associated with conditions causing **volume overload** or **ventricular dysfunction**. *Seen in Atrial Septal Defect (ASD)* - Patients with a large ASD have increased blood flow through the tricuspid valve, leading to **right ventricular volume overload** [2]. - This increased volume can cause an **S3** sound, particularly a **right ventricular S3**, due to rapid filling of the overloaded right ventricle [2]. *Seen in Ventricular Septal Defect (VSD)* - A significant VSD leads to a **left-to-right shunt**, increasing blood flow to the pulmonary circulation and subsequently returning to the left atrium and left ventricle. - This **left ventricular volume overload** can result in an audible **left ventricular S3**, reflecting rapid filling of the dilated left ventricle.

Q: The primary site of vasopressin synthesis is

Supraoptic nucleus. ***Supraoptic nucleus*** - The **supraoptic nucleus** of the hypothalamus is the **primary site** for the synthesis of **vasopressin** (also known as antidiuretic hormone or ADH). - Approximately **80% of vasopressin** is produced by the neurosecretory cells in this nucleus. - The synthesized vasopressin is transported down axons to the posterior pituitary for storage and release. *Preoptic nucleus* - The **preoptic nucleus** is involved in various homeostatic functions, including **thermoregulation** and **sleep regulation**, but not the synthesis of vasopressin. - While it has neuronal connections to the hypothalamus, it does not produce ADH. *Paraventricular nucleus* - The **paraventricular nucleus** also synthesizes **both vasopressin and oxytocin**, accounting for approximately **20% of vasopressin production**. - While it does produce vasopressin, the **supraoptic nucleus remains the primary site**, making it the correct answer to this question. - The PVN also plays important roles in stress response and various autonomic functions. *Posterior pituitary* - The **posterior pituitary** (neurohypophysis) is responsible for the **storage and release** of vasopressin and oxytocin, not their synthesis. - These hormones are produced in the hypothalamic nuclei (supraoptic and paraventricular) and then transported down axonal tracts to the posterior pituitary.

Q: Which mechanism is primarily responsible for the transport of glucose in renal tubular cells?

Sodium-glucose cotransport. ***Sodium-glucose cotransport*** - Glucose reabsorption in the renal tubules, particularly in the **proximal tubule**, occurs primarily via **secondary active transport** involving **sodium-glucose cotransporters (SGLTs)**. - SGLT proteins use the **sodium concentration gradient** (maintained by the Na+/K+-ATPase on the basolateral membrane) to move glucose against its concentration gradient from the tubular lumen into the cell. *Glucose diffusion* - While passive diffusion may play a minor role, it is insufficient to reabsorb the large amounts of **filtered glucose** - Diffusion would lead to significant **glucose loss in urine**, even at normal blood glucose levels. *Sodium antiport* - Antiport systems move two different ions or molecules in **opposite directions** across a membrane. - While present in renal cells, sodium antiport mechanisms are not the primary means of **glucose reabsorption**; rather, glucose transport is mostly symport. *Facilitated diffusion* - Facilitated diffusion involves carrier proteins (like **GLUT transporters**) that move molecules down their **concentration gradient**. - While GLUT transporters are present on the **basolateral membrane** of tubular cells to move glucose into the interstitium, they are not the primary mechanism for glucose uptake from the tubular lumen, which occurs against a concentration gradient.

Q: Substance that is completely reabsorbed from the kidney?

Glucose. ***Glucose*** - In a healthy individual, **virtually all filtered glucose** is reabsorbed in the proximal convoluted tubule via **sodium-glucose cotransporters (SGLTs)**. - This complete reabsorption ensures that this vital energy source is conserved and not excreted in the urine. *Na+* - While a large proportion of filtered **Na+** is reabsorbed to maintain fluid and electrolyte balance, not all of it is reabsorbed; some is excreted in urine. - The reabsorption of Na+ is **regulated** by hormones like **aldosterone** to fine-tune its excretion based on the body's needs. *K+* - **K+** undergoes both reabsorption and secretion in different parts of the nephron, and its excretion is tightly regulated. - Net reabsorption of K+ is not complete; its handling ensures appropriate plasma levels are maintained for muscle and nerve function. *Urea* - Approximately **50% of filtered urea undergoes reabsorption** in the renal tubules, while the other half is excreted. - Urea reabsorption is important for generating the **medullary osmotic gradient**, which is essential for concentrating urine, but it is never completely reabsorbed.

Q: What is the primary mechanism of heat loss in a modern X-ray tube?

Radiation. ***Radiation*** - The **primary mechanism** of heat loss in a modern X-ray tube is **radiation** (infrared emission). - The anode surface reaches extremely high temperatures (>1000°C) during X-ray production, causing it to emit significant **infrared radiation**. - Modern X-ray tubes use **high-emissivity materials** (tungsten-rhenium alloys) on the anode to maximize radiative heat transfer. - Since the tube operates in a **vacuum**, radiation is the only effective mechanism for heat dissipation from the anode itself. *Evaporation* - **Evaporation** requires a liquid-to-gas phase change, which is not applicable in the solid-state environment of an X-ray tube anode. - The **vacuum environment** inside the tube prevents any evaporative cooling. - This mechanism is irrelevant for heat loss from the anode. *Conduction* - **Conduction** does transfer heat from the focal spot through the anode body to the rotor bearings. - However, this is heat transfer *within* the tube components, not the primary mechanism for heat loss *from the tube*. - Heat conducted through components must ultimately be dissipated by **radiation** (from anode) or **convection** (from housing via cooling oil). *Convection* - **Convection** requires fluid movement (liquid or gas), which cannot occur in the **vacuum** inside the X-ray tube envelope. - While cooling oil outside the tube uses convection to remove heat from the housing, this is secondary heat removal, not the primary mechanism of heat loss from the anode. - The anode loses heat primarily via **radiation** first, then that heat may be further managed by convection in the cooling system.

Question 1

Which enzyme is primarily associated with the reduction of NADP+ to NADPH in the pentose phosphate pathway?

Accepted Answer

G6PD

Answer

APDH

Answer

α-keto glutarate dehydrogenases

Answer

None of the options

Question 2

Which of the following pairs of compounds has the highest standard reduction potential?

Accepted Answer

Fe³⁺/Fe²⁺

Answer

NADH/NAD+

Answer

Succinate/Fumarate

Answer

Ubiquinone/Ubiquinol

Question 3

Fluoroacetate inhibits?

Accepted Answer

Aconitase

Answer

Citrate synthase

Answer

Succinate dehydrogenase

Answer

Alpha-ketoglutarate dehydrogenase

Question 4

Increased uric acid levels are seen in which glycogen storage disease ?

Accepted Answer

Type I (Von Gierke's disease)

Answer

Type II (Pompe disease)

Answer

Type IV (Andersen disease)

Answer

Type III (Cori disease)

Question 5

Which of the following is required for fatty acid synthesis ?

Accepted Answer

NADPH

Answer

NADH

Answer

FADH₂

Answer

None of the options

Question 6

All of the following statements about the third heart sound (S3) are true, except:

Accepted Answer

Seen in Constrictive Pericarditis

Answer

Seen in Atrial Septal Defect (ASD)

Answer

Seen in Ventricular Septal Defect (VSD)

Answer

Occurs due to rapid filling of the ventricles during early diastole.

Question 7

The primary site of vasopressin synthesis is

Accepted Answer

Supraoptic nucleus

Answer

Preoptic nucleus

Answer

Paraventricular nucleus

Answer

Posterior pituitary

Question 8

Which mechanism is primarily responsible for the transport of glucose in renal tubular cells?

Accepted Answer

Sodium-glucose cotransport

Answer

Facilitated diffusion

Answer

Glucose diffusion

Answer

Sodium antiport

Question 9

Substance that is completely reabsorbed from the kidney?

Accepted Answer

Glucose

Answer

Na+

Answer

K+

Answer

Urea

Question 10

What is the primary mechanism of heat loss in a modern X-ray tube?

Accepted Answer

Radiation

Answer

Evaporation

Answer

Conduction

Answer

Convection

NEET-PG 2012

Biochemistry

Internal Medicine

Physiology

Radiology