Biochemistry
8 questionsWhich isoenzyme of lactate dehydrogenase (LDH) is predominantly elevated in liver injury?
Which of the following pairs of compounds has the highest standard reduction potential?
Increased uric acid levels are seen in which glycogen storage disease ?
Which hormone inhibits hormone-sensitive lipase?
What is the characteristic nitrogenous product of lecithin hydrolysis?
In ETC NADH generates -
Methionine can enter the TCA cycle at which level?
Which enzyme catalyzes the rate limiting step in the TCA cycle?
NEET-PG 2012 - Biochemistry NEET-PG Practice Questions and MCQs
Question 201: Which isoenzyme of lactate dehydrogenase (LDH) is predominantly elevated in liver injury?
- A. LDH-3
- B. LDH-5 (Correct Answer)
- C. LDH-1
- D. LDH-2
Explanation: ***LDH-5 isoenzyme most significant in hepatic conditions*** - **LDH-5** is the predominant isoenzyme found in the **liver** and skeletal muscle. - An elevation of **LDH-5** is highly indicative of **hepatocellular damage** or injury. *LDH-1 isoenzyme associated with cardiac tissue* - **LDH-1** is primarily present in the **heart** and red blood cells. - Its elevation suggests conditions like **myocardial infarction** or hemolytic anemia, not liver injury. *LDH-3 isoenzyme typical in respiratory system* - **LDH-3** is found in the **lungs**, kidneys, and other tissues. - While it can be elevated in **pulmonary embolism** or renal disease, it is not specific for liver injury. *LDH-2 isoenzyme linked to erythrocyte metabolism* - **LDH-2** is abundant in **red blood cells** and also found in the heart and kidneys. - Elevations are often seen in conditions involving **hemolysis** or myocardial damage, similar to LDH-1.
Question 202: Which of the following pairs of compounds has the highest standard reduction potential?
- A. NADH/NAD+
- B. Succinate/Fumarate
- C. Ubiquinone/Ubiquinol
- D. Fe³⁺/Fe²⁺ (Correct Answer)
Explanation: ***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.
Question 203: Increased uric acid levels are seen in which glycogen storage disease ?
- A. Type I (Von Gierke's disease) (Correct Answer)
- B. Type II (Pompe disease)
- C. Type IV (Andersen disease)
- D. Type III (Cori disease)
Explanation: ***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**.
Question 204: Which hormone inhibits hormone-sensitive lipase?
- A. Insulin (Correct Answer)
- B. GH
- C. ACTH
- D. Thyroid hormone
Explanation: ***Insulin*** - **Insulin** is a key anabolic hormone that promotes energy storage and inhibits catabolic processes, including the breakdown of triglycerides. - It directly inhibits **hormone-sensitive lipase (HSL)** activity, thus reducing the release of free fatty acids from adipose tissue. *Thyroid hormone* - **Thyroid hormones** (T3 and T4) generally promote catabolism and increase metabolic rate, including the mobilization of lipids. - They tend to **stimulate rather than inhibit** hormone-sensitive lipase expression and activity. *GH* - **Growth hormone (GH)** has lipolytic effects, meaning it promotes the breakdown of fats to provide energy. - GH typically **stimulates HSL activity** and increases the release of free fatty acids from adipocytes. *ACTH* - **Adrenocorticotropic hormone (ACTH)** primarily stimulates the adrenal cortex to produce cortisol. - **Cortisol** can have lipolytic effects in certain contexts and does not directly inhibit HSL; instead, catecholamines act as direct stimulators of HSL.
Question 205: What is the characteristic nitrogenous product of lecithin hydrolysis?
- A. Fatty acids
- B. Choline (Correct Answer)
- C. Glucose
- D. Phosphoric acid
Explanation: ***Choline*** - Lecithin is a type of **phospholipid** called **phosphatidylcholine**, meaning its head group contains choline. - Therefore, during hydrolysis, the **choline** component is released as the characteristic nitrogenous product. *Glucose* - **Glucose** is a simple sugar and a carbohydrate, not a component of lecithin. - It is a primary source of **energy** for cells but is not released during lipid hydrolysis. *Fatty acids* - While **fatty acids** are indeed components of lecithin (two fatty acid chains are attached to the glycerol backbone), they are not nitrogenous. - Fatty acids are **hydrophobic hydrocarbon chains** that make up a significant part of the lipid structure. *Phosphoric acid* - **Phosphoric acid** (or phosphate) is also a component of lecithin, connecting the glycerol backbone to the choline group. - However, it is an **inorganic acid** and does not contain nitrogen.
Question 206: In ETC NADH generates -
- A. 1 ATPs
- B. 4 ATPs
- C. 3 ATPs (Correct Answer)
- D. 2 ATPs
Explanation: ***3 ATPs*** - Each molecule of **NADH** donates electrons to **Complex I** of the electron transport chain (ETC), resulting in the pumping of enough protons to generate approximately **3 ATP molecules** via **oxidative phosphorylation**. - This high yield is due to NADH's ability to activate multiple proton pumps along the ETC, maximizing the **proton gradient** for ATP synthesis. *1 ATPs* - This is an incorrect yield for NADH; **FADH2** typically generates fewer ATPs (around 2) because it enters the ETC at a later stage, bypassing the initial proton pump. - Generating only 1 ATP from NADH would be very inefficient and is not physiologically accurate for oxidative phosphorylation. *2 ATPs* - While closer, 2 ATPs is the approximate yield for **FADH2**, which enters the ETC at **Complex II**, bypassing Complex I and thus pumping fewer protons. - NADH enters at Complex I, which provides enough energy for a higher ATP yield. *4 ATPs* - 4 ATPs is an overestimation of the ATP yield from NADH in the electron transport chain. - The maximum theoretical yield from NADH via oxidative phosphorylation is typically considered to be 3 ATPs.
Question 207: Methionine can enter the TCA cycle at which level?
- A. Fumarate
- B. Oxaloacetate
- C. Succinyl-CoA (Correct Answer)
- D. Citrate
Explanation: ***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.
Question 208: Which enzyme catalyzes the rate limiting step in the TCA cycle?
- A. Fumarase
- B. Aconitase
- C. Thiokinase
- D. α-ketoglutarate dehydrogenase (Correct Answer)
Explanation: **α-ketoglutarate dehydrogenase** - The **α-ketoglutarate dehydrogenase complex** catalyzes the oxidative decarboxylation of α-ketoglutarate to succinyl-CoA, producing NADH and CO2. - This step is a **major control point** in the TCA cycle and is highly regulated by: - **Product inhibition**: Succinyl-CoA and NADH - **Calcium ions**: Activate the enzyme - Along with isocitrate dehydrogenase and citrate synthase, it represents one of the three key regulatory enzymes of the TCA cycle. *Fumarase* - **Fumarase** catalyzes the reversible hydration of fumarate to L-malate. - This enzyme is **not a regulatory step** in the TCA cycle; its activity is typically high and not a control point for the overall flux of the cycle. *Aconitase* - **Aconitase** catalyzes the reversible isomerization of citrate to isocitrate, via the intermediate cis-aconitate. - While important for the cycle's progression, aconitase activity is **not considered a rate-limiting step** for the overall regulation of the TCA cycle. *Thiokinase* - The term **thiokinase** (or succinyl-CoA synthetase) catalyzes the reversible conversion of succinyl-CoA to succinate, coupled with GTP/ATP production. - This enzyme is responsible for **substrate-level phosphorylation** in the TCA cycle but does not represent a primary regulatory or rate-limiting step.
Physiology
2 questionsWhich tract is responsible for the loss of proprioception and fine touch?
In bladder injury, pain is referred to which of the following areas?
NEET-PG 2012 - Physiology NEET-PG Practice Questions and MCQs
Question 201: Which tract is responsible for the loss of proprioception and fine touch?
- A. Anterior spinothalamic tract
- B. Lateral spinothalamic tract
- C. Dorsal column (Correct Answer)
- D. Corticospinal tract
Explanation: ***Dorsal column*** - The **dorsal column-medial lemniscus pathway** is responsible for transmitting **fine touch**, **vibration**, and **proprioception** from the body to the cerebral cortex. - Damage to this tract (e.g., in **tabes dorsalis** or **vitamin B12 deficiency**) leads to a loss of these sensations. *Anterior spinothalamic tract* - This tract primarily conveys crude touch and pressure sensations. - While it carries tactile information, it does not transmit the fine discriminative touch or proprioception associated with the dorsal columns. *Lateral spinothalamic tract* - This pathway is responsible for transmitting **pain** and **temperature** sensations. - It does not play a role in proprioception or fine touch. *Corticospinal tract* - The **corticospinal tract** is a **motor pathway** responsible for voluntary movement. - It has no role in transmitting sensory information such as proprioception or fine touch.
Question 202: In bladder injury, pain is referred to which of the following areas?
- A. Flank
- B. Upper part of thigh
- C. Lower abdominal wall (Correct Answer)
- D. Penis
Explanation: ***Correct Option: Lower abdominal wall*** - **Referred pain** from the bladder is typically felt in the **suprapubic region** of the lower abdominal wall due to shared visceral and somatic afferent innervation. - The **parietal peritoneum** overlying the bladder is innervated by somatic nerves that also supply the abdominal wall. - This convergence of visceral afferents from the bladder and somatic afferents from the abdominal wall at the spinal cord level (particularly S2-S4) results in referred pain to the suprapubic area. *Incorrect Option: Upper part of thigh* - Pain in the upper thigh is more commonly associated with conditions affecting the **hip joint**, **femoral nerve**, or **inguinal region**. - Bladder innervation does not primarily refer pain to the upper thigh. *Incorrect Option: Flank* - Flank pain is typically associated with conditions of the **kidneys** or **ureters**, such as **nephrolithiasis** or **pyelonephritis**. - The bladder's referred pain pattern does not usually extend to the flank. *Incorrect Option: Penis* - While bladder irritation can sometimes cause sensations in the penis, it is more often associated with conditions like **urethritis**, **cystitis**, or **prostatitis**. - Direct referred pain from bladder injury to the penis is less common than to the lower abdominal wall.