Biochemistry
6 questionsWhich of the following statements about LDL is false?
Which of the following lipoproteins is most strongly associated with an increased risk of cardiovascular diseases and is commonly referred to as "bad cholesterol"?
Krabbe's disease is due to deficiency of ?
What is essential for the transfer of fatty acid across the mitochondrial membrane?
Ketone body formation without glycosuria is seen in ?
Ketone bodies are not used by?
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 131: Which of the following statements about LDL is false?
- A. More dense than chylomicron
- B. Transports maximum amount of lipid (Correct Answer)
- C. Contains maximum cholesterol
- D. Smaller than VLDL
Explanation: ***Transports maximum amount of lipid*** - This statement is false because **chylomicrons**, not LDL, are primarily responsible for transporting the **maximum amount of dietary lipids** (triglycerides) from the intestines to various tissues. - While LDL does transport lipids, its primary role is to deliver **cholesterol** to cells, and it contains a lower proportion of triglyceride compared to chylomicrons and VLDL. *More dense than chylomicron* - This statement is true; **LDL is denser than chylomicrons** because it has a higher protein-to-lipid ratio. - **Chylomicrons** are the least dense lipoproteins due to their very high triglyceride content. *Smaller than VLDL* - This statement is true; **LDL is smaller than VLDL** (Very Low-Density Lipoprotein). - VLDL particles are larger and contain more triglycerides, which are gradually removed, leading to the formation of smaller LDL particles. *Contains maximum cholesterol* - This statement is true; **LDL contains the highest proportion of cholesterol** (specifically, **cholesterol esters**) among the lipoproteins. - This characteristic makes LDL the primary carrier for delivering cholesterol to peripheral tissues.
Question 132: Which of the following lipoproteins is most strongly associated with an increased risk of cardiovascular diseases and is commonly referred to as "bad cholesterol"?
- A. VLDL
- B. Chylomicron
- C. Lp (a)
- D. LDL (Correct Answer)
Explanation: ***LDL*** - **Low-density lipoprotein (LDL)** is commonly referred to as "bad" cholesterol because elevated levels are the **primary driver** of atherosclerotic plaque buildup in arterial walls. - LDL particles transport cholesterol from the liver to peripheral tissues; when present in excess, they infiltrate the arterial intima and undergo oxidative modification, triggering inflammatory responses that lead to atherosclerosis. - **Clinical significance:** LDL cholesterol is the primary target of lipid-lowering therapy in cardiovascular disease prevention. *VLDL* - **Very low-density lipoprotein (VLDL)** primarily transports endogenously synthesized **triglycerides** from the liver to peripheral tissues. - While elevated VLDL levels do contribute to cardiovascular risk (particularly through conversion to small, dense LDL particles), it is not the primary lipoprotein targeted in cardiovascular risk assessment. *Chylomicron* - **Chylomicrons** transport **dietary lipids** (triglycerides and cholesterol) from the intestines to tissues after meals. - They are rapidly cleared from circulation (half-life of 5-10 minutes) and are typically not present during fasting, making their contribution to chronic atherosclerotic plaque formation minimal. *Lp(a)* - **Lipoprotein(a) [Lp(a)]** is structurally similar to LDL but contains an additional apolipoprotein(a) molecule, which has homology to plasminogen and may interfere with fibrinolysis. - While Lp(a) is an independent cardiovascular risk factor, it is less commonly measured in routine clinical practice, and **LDL remains the cornerstone lipoprotein** for cardiovascular risk stratification and management.
Question 133: Krabbe's disease is due to deficiency of ?
- A. Sphingomyelinase
- B. Beta galactocerebrosidase (Correct Answer)
- C. Hexosaminidase
- D. Arylsulfatase
Explanation: ***Beta galactocerebrosidase*** - Krabbe's disease is specifically caused by a deficiency of **beta-galactocerebrosidase**, leading to the accumulation of toxic substances in the brain [1]. - This disease predominantly affects the **myelin sheath**, resulting in severe neurological deterioration [1]. *Arylsulfatase* - Deficiency of **arylsulfatase** is associated with **metachromatic leukodystrophy**, not Krabbe's disease. - Symptoms and pathology differ significantly, primarily affecting **sulfatides** rather than galactocerebrosides. *Sphingomyelinase* - A deficiency of **sphingomyelinase** is linked to **Niemann-Pick disease**, characterized by splenomegaly and liver involvement. - This condition does not involve the same neurological deterioration seen in Krabbe's disease. *Hexosaminidase* - Hexosaminidase deficiency is associated with **Tay-Sachs disease**, primarily affecting the **GM2 gangliosides** [2]. - This results in different clinical manifestations, such as **cherry-red spots** and progressive neurodegeneration, rather than the symptoms of Krabbe's disease [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1304-1305. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 161.
Question 134: What is essential for the transfer of fatty acid across the mitochondrial membrane?
- A. Creatinine
- B. Carnitine (Correct Answer)
- C. Biotin
- D. Creatine
Explanation: ***Carnitine*** - **Carnitine** is crucial for transporting **long-chain fatty acids** into the mitochondrial matrix for **beta-oxidation**. - It forms **acylcarnitine** by esterifying with fatty acids, allowing passage through the inner mitochondrial membrane via the **carnitine-acylcarnitine translocase**. *Creatinine* - **Creatinine** is a waste product formed from the breakdown of **creatine phosphate** in muscles and is excreted by the kidneys. - It serves as a marker for **kidney function** and has no role in fatty acid transport. *Biotin* - **Biotin** is a vitamin cofactor essential for **carboxylase enzymes**, including acetyl-CoA carboxylase in **fatty acid synthesis**. - While involved in lipid metabolism, it plays no role in the transport of fatty acids across mitochondrial membranes. *Creatine* - **Creatine** is a nitrogenous organic acid that helps supply energy to cells, primarily muscle, by facilitating the regeneration of **ATP**. - It plays no direct role in the facilitated transport of fatty acids across the mitochondrial membrane.
Question 135: Ketone body formation without glycosuria is seen in ?
- A. Diabetes mellitus
- B. Diabetes insipidus
- C. Starvation (Correct Answer)
- D. Obesity
Explanation: ***Starvation*** - During **starvation**, the body depletes its **glycogen stores** and begins to break down **fat for energy**. This process leads to the production of **ketone bodies** (acetoacetate, beta-hydroxybutyrate, and acetone) as an alternative fuel source for the brain and other tissues. - Since there is no underlying problem with **insulin production** or action, blood glucose levels are typically low or normal, and therefore, **glycosuria** (glucose in the urine) is absent. *Diabetes mellitus* - In **uncontrolled diabetes mellitus**, especially Type 1, the body cannot effectively use **glucose** due to lack of insulin, leading to high blood glucose levels (**hyperglycemia**) and subsequently **glycosuria**. - The body then compensates by breaking down **fats**, leading to the formation of **ketone bodies** (**diabetic ketoacidosis**), which results in both **ketonuria** and **glycosuria**. *Diabetes insipidus* - **Diabetes insipidus** is a condition characterized by the inability to conserve water due to insufficient **antidiuretic hormone (ADH)** production or action, leading to excessive urination and thirst. - It does not involve abnormalities in **glucose metabolism** or **ketone body production** and therefore does not typically present with ketonuria or glycosuria. *Obesity* - While **obesity** can lead to **insulin resistance** and is a risk factor for Type 2 Diabetes, it does not directly cause **ketone body formation** in the absence of metabolic derangements such as those seen in uncontrolled diabetes or prolonged starvation. - In most cases of obesity without diabetes, **glucose metabolism** is still adequate enough to prevent significant reliance on **fat breakdown** for energy, meaning there is usually no ketonuria or glycosuria.
Question 136: Ketone bodies are not used by?
- A. Brain
- B. Muscle
- C. RBC (Correct Answer)
- D. Renal cortex
Explanation: ***RBC*** - Red blood cells **lack mitochondria**, which are essential organelles for the **oxidation of ketone bodies** (acetoacetate and β-hydroxybutyrate) for energy production. - Their primary energy source is **anaerobic glycolysis** of glucose. *Muscle* - **Skeletal and cardiac muscles** readily utilize **ketone bodies** as an alternative fuel source, especially during prolonged fasting or starvation. - This helps to conserve glucose for other tissues, particularly the brain. *Brain* - The brain can adapt to use **ketone bodies** for energy when glucose supply is limited, such as during prolonged fasting or in cases of uncontrolled diabetes. - This process is crucial for brain function when glucose levels are low. *Renal cortex* - The **renal cortex** is capable of utilizing **ketone bodies** for energy, particularly during starvation. - The kidney is also involved in the **synthesis of glucose** (gluconeogenesis) and the excretion of ketone bodies.
Physiology
4 questionsDeoxygenated blood is not seen in which of the following?
When blood pressure falls below 40 mm Hg, which mechanism of regulation is working?
Which of the following stimuli is primarily responsible for triggering the Bezold-Jarisch reflex?
Which of the following best describes hypoxic pulmonary vasoconstriction?
NEET-PG 2013 - Physiology NEET-PG Practice Questions and MCQs
Question 131: Deoxygenated blood is not seen in which of the following?
- A. Pulmonary artery
- B. Umbilical artery
- C. Pulmonary vein (Correct Answer)
- D. Right atrium
Explanation: ***Pulmonary vein*** - The pulmonary veins carry **oxygenated blood** from the lungs back to the left atrium of the heart. - Their primary function is to transport blood that has undergone **gas exchange** in the lungs, making it rich in oxygen. *Pulmonary artery* - The pulmonary artery carries **deoxygenated blood** from the right ventricle of the heart to the lungs. - This is an exception to the general rule that arteries carry oxygenated blood, as its purpose is to deliver blood for **oxygenation**. *Right atrium* - The right atrium receives **deoxygenated blood** from the systemic circulation via the superior and inferior vena cava. - It acts as a collecting chamber for blood that has supplied oxygen to the body's tissues before it is pumped to the lungs. *Umbilical artery* - The umbilical arteries carry **deoxygenated blood** and waste products from the fetus to the placenta. - In fetal circulation, these arteries are responsible for removing metabolic wastes and carbon dioxide from the fetal circulation.
Question 132: When blood pressure falls below 40 mm Hg, which mechanism of regulation is working?
- A. CNS ischemic reflex (Correct Answer)
- B. Chemoreceptor response
- C. Baroreceptor response
- D. None of the options
Explanation: ***CNS ischemic reflex*** - The **CNS ischemic reflex** is activated when blood pressure falls below 60 mmHg, with maximal activation below 40 mmHg, indicating severe ischemia in the brain's vasomotor center. - This reflex elicits an intense **sympathetic vasoconstriction** and cardiac stimulation to prioritize blood flow to the brain even at the expense of other organs. *Chemoreceptor response* - The chemoreceptor reflex is primarily activated by a decrease in **arterial pO2**, an increase in **pCO2**, or a decrease in **pH**. - While it can increase blood pressure, it is not the primary or most profound regulatory mechanism specifically triggered by extremely low blood pressure (below 40 mmHg) to prevent brain ischemia. *Baroreceptor response* - **Baroreceptors** are most sensitive to changes in blood pressure within the normal to moderately hypotensive range (e.g., 60-180 mmHg). - At very low pressures (below 40-50 mmHg), baroreceptors become **less sensitive** or "saturated," and their effectiveness in raising blood pressure significantly diminishes. *None of the options* - This option is incorrect because the **CNS ischemic reflex** specifically functions as a powerful, last-ditch mechanism to maintain cerebral blood flow during severe hypotension which is a life saving reflex during conditions like hemorrhage.
Question 133: Which of the following stimuli is primarily responsible for triggering the Bezold-Jarisch reflex?
- A. Parasympathetic withdrawal
- B. Decreased venous return
- C. Increased sympathetic stimulation
- D. Activation of cardiac C-fiber afferents (Correct Answer)
Explanation: ***Activation of cardiac C-fiber afferents*** - The **Bezold-Jarisch reflex** is primarily triggered by stimulation of **cardiac mechanoreceptors and chemoreceptors** located in the ventricles, particularly the inferoposterior wall of the left ventricle. - These receptors have **unmyelinated vagal C-fiber afferents** that transmit signals to the medullary cardiovascular centers. - Activation of these afferents leads to the characteristic triad: **bradycardia, hypotension, and vasodilation** via increased parasympathetic activity and withdrawal of sympathetic tone. - Common triggers include vigorous ventricular contraction with decreased filling, certain drugs (veratridine), myocardial ischemia (especially inferior wall MI), and reperfusion. *Decreased venous return* - While **decreased venous return** creates the hemodynamic context (ventricular underfilling) that can lead to vigorous contraction of a relatively empty ventricle, it is not itself the *trigger* of the reflex. - The actual trigger is the activation of the ventricular receptors sensing this abnormal contraction pattern, which then signal via C-fiber afferents. - Decreased venous return alone, without receptor activation, would not produce the reflex. *Parasympathetic withdrawal* - **Parasympathetic withdrawal** would cause tachycardia and is opposite to the Bezold-Jarisch reflex, which involves **increased parasympathetic activity**. - This is a compensatory response seen in other reflexes like the baroreceptor reflex during hypotension. *Increased sympathetic stimulation* - **Increased sympathetic stimulation** produces tachycardia, increased contractility, and vasoconstriction—effects opposite to the Bezold-Jarisch reflex. - The reflex actually causes **sympathetic withdrawal** along with parasympathetic activation.
Question 134: Which of the following best describes hypoxic pulmonary vasoconstriction?
- A. Reversible pulmonary vasoconstriction due to hypoxia (Correct Answer)
- B. Irreversible pulmonary vasoconstriction due to hypoxia
- C. Redirects blood to well-ventilated areas
- D. Occurs immediately in response to hypoxia
Explanation: ***Reversible pulmonary vasoconstriction due to hypoxia*** - Hypoxic pulmonary vasoconstriction (HPV) is a physiological response in which **pulmonary arterioles constrict** in areas of the lung with low oxygen levels. - This mechanism is **reversible**, meaning that when oxygen levels improve, the constricted vessels will dilate again. - The underlying mechanism involves hypoxia-induced inhibition of voltage-gated K⁺ channels in pulmonary arterial smooth muscle, leading to membrane depolarization, Ca²⁺ influx, and smooth muscle contraction. *Irreversible pulmonary vasoconstriction due to hypoxia* - This statement is incorrect because HPV is fundamentally a **reversible process**, designed to adapt to transient changes in alveolar oxygen. - Irreversible vasoconstriction typically occurs in chronic hypoxia, leading to **pulmonary hypertension** and structural remodeling (vascular remodeling with medial hypertrophy), which is a pathological state rather than the acute physiological response of HPV. *Redirects blood to well-ventilated areas* - While this is the **physiological purpose** and overall effect of hypoxic pulmonary vasoconstriction, it describes the functional outcome rather than what HPV fundamentally is. - The redirection of blood flow is the **consequence** of vasoconstriction in hypoxic areas, which optimizes ventilation-perfusion matching. *Occurs immediately in response to hypoxia* - While HPV does begin rapidly in response to hypoxia (within seconds to minutes), this describes the **timing characteristic** rather than what HPV is. - This statement is also somewhat imprecise, as the response involves intracellular signaling pathways that take time to manifest fully, though the onset is relatively quick compared to other vascular responses.