Biochemistry
5 questionsWhich protein does the domain of plasminogen resemble?
How many molecules of Acetyl CoA are produced from β-oxidation of palmitic acid?
What primarily forms the core of chylomicrons?
Transport of lipids from the intestine to other tissues is by -
Most important carbohydrate store for maintaining blood glucose homeostasis -
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 231: Which protein does the domain of plasminogen resemble?
- A. Fibrinogen (a clotting protein)
- B. LDL receptor (a lipid metabolism protein)
- C. Apolipoprotein (a) (a lipoprotein) (Correct Answer)
- D. Prothrombin (a coagulation protein)
Explanation: ***Apolipoprotein (a) (a lipoprotein)*** - **Plasminogen** and **apolipoprotein (a)** share structural homology, specifically due to the presence of **kringle domains**. - This structural similarity suggests a potential for apolipoprotein (a) to **interfere with plasminogen’s fibrinolytic activity**, contributing to **atherosclerosis**. *Fibrinogen (a clotting protein)* - While plasmin acts on fibrinogen (and its derivative fibrin), its domain structure does not **resemble fibrinogen**. - **Fibrinogen** is a large, multi-domain glycoprotein crucial for **clot formation**, distinct from plasminogen's primarily **kringle-rich structure**. *LDL receptor (a lipid metabolism protein)* - The **LDL receptor** is involved in **cholesterol uptake** by cells and has structural features like ligand-binding repeats and epidermal growth factor (EGF) repeats. - Its domain structure is **not similar to plasminogen**, which is characterized by **kringle domains** and a protease domain. *Prothrombin (a coagulation protein)* - **Prothrombin** is a precursor to thrombin, featuring **gla domains**, kringle-like domains (though structurally distinct from plasminogen's), and a serine protease domain. - While both are involved in coagulation/fibrinolysis, their **overall domain arrangements and specific kringle structures differ** significantly.
Question 232: How many molecules of Acetyl CoA are produced from β-oxidation of palmitic acid?
- A. 3 acetyl CoA
- B. 16 Acetyl CoA
- C. 6 acetyl CoA
- D. 8 acetyl CoA (Correct Answer)
Explanation: ***8 acetyl CoA*** - Palmitic acid is a **16-carbon saturated fatty acid (C16:0)**. During β-oxidation, each cycle cleaves two carbons as **acetyl CoA**. - The formula for acetyl CoA produced is **n/2**, where n = number of carbons. For palmitic acid: 16/2 = **8 acetyl CoA molecules**. - Alternatively: Palmitic acid undergoes **7 cycles of β-oxidation** [(n/2) - 1 = 7], each producing 1 acetyl CoA (7 total), plus the final 2-carbon fragment forming the 8th acetyl CoA. *3 acetyl CoA* - This number is too low for a 16-carbon fatty acid. **Short-chain fatty acids** would produce fewer acetyl CoA molecules. - This value corresponds to β-oxidation of a **6-carbon fatty acid** (hexanoic acid), not palmitic acid. *6 acetyl CoA* - This number is also too low for a 16-carbon fatty acid. - This quantity would be produced from a **12-carbon fatty acid** (lauric acid), not palmitic acid. *16 Acetyl CoA* - This number is too high and would incorrectly imply that each carbon forms an acetyl CoA independently. - Sixteen acetyl CoA molecules would be produced from a **32-carbon fatty acid**, which is extremely rare in biological systems.
Question 233: What primarily forms the core of chylomicrons?
- A. Triglycerides and Cholesterol together
- B. Triglycerides (Correct Answer)
- C. Free fatty acids
- D. Triglyceride, Cholesterol and Phospholipids
Explanation: ***Triglycerides*** - Chylomicrons are primarily responsible for transporting **dietary triglycerides** from the intestines to other tissues. - Their large core, composed mainly of **triglycerides**, allows efficient transport of these hydrophobic molecules. *Triglycerides and Cholesterol together* - While **cholesterol** is present in chylomicrons, it is less abundant than **triglycerides** and primarily exists as **cholesterol esters** in the core. - The core is not an equal mixture; **triglycerides** overwhelmingly dominate the volume. *Free fatty acids* - **Free fatty acids** are transported in the blood primarily bound to **albumin**, not within the core of chylomicrons. - Chylomicrons typically carry **esterified fatty acids** as part of triglycerides. *Triglyceride, Cholesterol and Phospholipids* - **Phospholipids** form the outer monolayer of the chylomicron, along with apoproteins, making them **amphipathic**. - They do not constitute a core component but rather the **surface interface** with the aqueous environment.
Question 234: Transport of lipids from the intestine to other tissues is by -
- A. Chylomicrons (Correct Answer)
- B. LDL
- C. HDL
- D. VLDL
Explanation: ***Chylomicrons*** - **Chylomicrons** are the **largest lipoprotein particles** that transport **dietary (exogenous) lipids** from the **intestine** to peripheral tissues - They are synthesized in **intestinal enterocytes** after fat absorption and enter the bloodstream via the **lymphatic system (thoracic duct)** - They carry **triglycerides (85-95%), cholesterol, phospholipids, and fat-soluble vitamins** (A, D, E, K) - **Apolipoprotein B-48** is the characteristic structural protein of chylomicrons - After delivering triglycerides to tissues (via lipoprotein lipase), chylomicron remnants are taken up by the **liver** *LDL (Low-Density Lipoprotein)* - LDL transports **cholesterol from the liver to peripheral tissues** (not from intestine) - It carries **endogenous cholesterol**, not dietary lipids from the intestine - Often called "**bad cholesterol**" due to its role in atherosclerosis - Contains **Apolipoprotein B-100** *HDL (High-Density Lipoprotein)* - HDL performs **reverse cholesterol transport** - moving excess cholesterol from peripheral tissues **back to the liver** - It does **not transport lipids from the intestine** to tissues - Called "**good cholesterol**" for its protective cardiovascular role - Contains **Apolipoprotein A-I and A-II** *VLDL (Very-Low-Density Lipoprotein)* - VLDL is synthesized in the **liver** (not intestine) and transports **endogenous triglycerides** to peripheral tissues - It carries lipids **from the liver**, not from the intestine - VLDL is converted to IDL and then LDL after losing triglycerides - Contains **Apolipoprotein B-100**
Question 235: Most important carbohydrate store for maintaining blood glucose homeostasis -
- A. Blood glucose
- B. Glycogen in adipose tissue
- C. Hepatic glycogen (Correct Answer)
- D. None of the options
Explanation: ***Hepatic glycogen*** - The liver contains **100-120g of glycogen**, which is the most crucial carbohydrate store for **maintaining blood glucose homeostasis**. - **Hepatic glycogen** can be mobilized and released as glucose into the bloodstream to supply all body tissues, especially during fasting. - Although muscle glycogen is quantitatively larger (~400-500g), it cannot contribute to blood glucose as muscle lacks glucose-6-phosphatase. - The liver's unique ability to release free glucose makes hepatic glycogen the **most metabolically important** carbohydrate store. *Blood glucose* - **Blood glucose** (~5g total in circulation) represents carbohydrates available for immediate energy, not a storage form. - This is far too small to be considered a major carbohydrate reserve. *Glycogen in adipose tissue* - **Adipose tissue** primarily stores **fat (triglycerides)**, with negligible glycogen content. - Adipose tissue plays virtually no role in carbohydrate storage. *None of the options* - This is incorrect because **hepatic glycogen** is indeed the most important carbohydrate store for glucose homeostasis.
Forensic Medicine
1 questionsWhat is defined as a negative autopsy?
NEET-PG 2015 - Forensic Medicine NEET-PG Practice Questions and MCQs
Question 231: What is defined as a negative autopsy?
- A. Cause is apparent on gross examination but not on histopathological examination.
- B. Gross findings are minimal.
- C. Cause is apparent on gross examination but not found due to constraints on the part of the doctor.
- D. No cause of death is found after both gross and histopathological examination. (Correct Answer)
Explanation: ***No cause of death is found after both gross and histopathological examination.*** - A **negative autopsy** is declared when comprehensive examination, including both macroscopic (gross) and microscopic (histopathological) assessment, fails to identify a definitive **cause of death**. - This outcome can be due to various reasons, such as death from **functional disturbances** (e.g., arrhythmias, metabolic imbalances) or processes not evident morphologically. *Cause is apparent on gross examination but not on histopathological examination.* - This scenario describes situations where a cause might be evident visually (e.g., a large hemorrhage) but further microscopic investigation is still needed for confirmation or detailed understanding. - It does not align with a "negative" autopsy, as a cause has already been *grossly identified*. *Gross findings are minimal.* - While minimal gross findings might precede a negative autopsy, this statement alone is insufficient to define it. - A negative autopsy specifically requires the absence of a cause of death even after subsequent **histopathological examination**. *Cause is apparent on gross examination but not found due to constraints on the part of the doctor.* - This option refers to a failure in diagnostic process due to external factors or limitations by the examiner, not an inherent lack of discernible cause. - It suggests a missed diagnosis, not that a cause could not be found through comprehensive investigation.
Pathology
1 questionsWhat is the primary process involved in Wallerian degeneration?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 231: What is the primary process involved in Wallerian degeneration?
- A. Nerve degeneration (Correct Answer)
- B. Muscle degeneration
- C. Nerve regeneration
- D. Muscle regeneration
Explanation: ***Nerve degeneration*** - **Wallerian degeneration** specifically refers to the process of **axon degeneration** that occurs distal to the site of injury when a nerve fiber is severed [2]. - This process involves the breakdown of the **axon** and its myelin sheath, leading to loss of function [1]. *Muscle degeneration* - While prolonged nerve degeneration can lead to muscle **atrophy** due to denervation, **muscle degeneration itself** is not the primary process of Wallerian degeneration. - Wallerian degeneration focuses on the **nerve itself**, not the target tissue. *Nerve regeneration* - **Nerve regeneration** is the process where damaged nerves attempt to regrow and re-establish connections [2]. - This is a subsequent, and not always successful, event that can occur *after* Wallerian degeneration has cleared the debris [1]. *Muscle regeneration* - **Muscle regeneration** refers to the repair and regrowth of damaged muscle tissue, typically involving satellite cells. - It is unrelated to Wallerian degeneration, which is a process affecting the **nerve**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 697-698. [2] 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. 109-110.
Physiology
3 questionsWhat physiological mechanism is responsible for the increase in the duration of expiration?
Which of the following statements is true regarding smooth muscle contraction?
What does the transient response observed during the insertion of an electrode in electromyography (EMG) indicate?
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 231: What physiological mechanism is responsible for the increase in the duration of expiration?
- A. J-reflex
- B. Head's paradoxical reflex
- C. Proprioceptors
- D. Hering-Breuer reflex (Correct Answer)
Explanation: ***Hering-Breuer reflex*** - The **Hering-Breuer reflex** is initiated by **stretch receptors in the bronchi and bronchioles** which are activated during lung inflation. - This reflex **inhibits inspiration** and **prolongs expiration**, preventing overinflation of the lungs. *J-reflex* - The **J-reflex** is stimulated by **juxtacapillary (J) receptors** in the alveolar walls, usually in response to pulmonary edema or congestion. - It typically causes **rapid, shallow breathing** and **bronchoconstriction**, not prolonged expiration. *Head's paradoxical reflex* - **Head's paradoxical reflex** (also known as the **inflation reflex** in newborns) involves an inspiratory effort triggered by lung inflation, often overcoming the Hering-Breuer reflex in specific conditions. - It tends to **increase respiratory rate** and depth, not prolong expiration. *Proprioceptors* - **Proprioceptors** are sensory receptors in muscles, tendons, and joints that provide information about body position and movement. - While they can influence respiration during exercise, they are not primarily responsible for directly **increasing the duration of expiration** as a reflex mechanism against overinflation.
Question 232: Which of the following statements is true regarding smooth muscle contraction?
- A. None of the options.
- B. Calmodulin plays no role in smooth muscle contraction.
- C. Phosphorylation of myosin is essential for contraction. (Correct Answer)
- D. Troponin plays a significant role in smooth muscle contraction.
Explanation: **Phosphorylation of myosin is essential for contraction.** - In **smooth muscle**, the **myosin light chain (MLC)** must be phosphorylated by **myosin light chain kinase (MLCK)** to enable interaction with actin and initiate contraction. - This phosphorylation causes a conformational change in the **myosin head**, increasing its ATPase activity and allowing cross-bridge cycling. *Calmodulin plays no role in smooth muscle contraction.* - **Calmodulin (CaM)** is crucial for smooth muscle contraction, as it binds **calcium ions (Ca²⁺)** forming a Ca²⁺-CaM complex. - This complex then activates **myosin light chain kinase (MLCK)**, which phosphorylates myosin, triggering contraction. *None of the options.* - This statement is incorrect because one of the provided options, "Phosphorylation of myosin is essential for contraction," is indeed true. *Troponin plays a significant role in smooth muscle contraction.* - Unlike **striated muscle (skeletal and cardiac)**, **smooth muscle** does not contain **troponin**. - Regulation of smooth muscle contraction is primarily **calcium-calmodulin-dependent**, with roles for **MLCK** and **MLCP**, rather than troponin.
Question 233: What does the transient response observed during the insertion of an electrode in electromyography (EMG) indicate?
- A. Spontaneous muscle activity
- B. Voluntary muscle contraction
- C. Cell membrane disruption (Correct Answer)
- D. Induced muscle contraction
Explanation: **Cell membrane disruption** - The **transient response** observed during electrode insertion in **EMG** is caused by the mechanical trauma of the needle disrupting the **muscle fiber cell membranes**. - This disruption leads to a brief depolarization and subsequent repolarization of the affected fibers, generating characteristic electrical activity. *Spontaneous muscle activity* - **Spontaneous muscle activity**, such as **fibrillation potentials** or **positive sharp waves**, occurs independently of electrode insertion. - While observed during EMG, these are indicative of **denervation** or **myopathy** and are not directly caused by the act of insertion itself. *Voluntary muscle contraction* - **Voluntary muscle contraction** is recorded when the patient actively contracts the muscle and results in **motor unit action potentials (MUAPs)**. - This is a distinct process from the transient activity produced by electrode insertion. *Induced muscle contraction* - **Induced muscle contraction** typically refers to activity caused by **nerve stimulation** (e.g., in nerve conduction studies) or direct electrical stimulation of the muscle. - This is not the mechanism for the transient response during simple electrode insertion.