Metabolic Rate and Basal Metabolism — MCQs
Energy expenditure in the resting state mainly depends on which of the following parameters?
Post-mortem caloricity is not seen in which of the following conditions?
A cold exposure which is expected to bring the body temperature from 37°C to 20°C, actually brings it down to only 36.5°C. Calculate the 'Gain' of the thermoregulatory system.
All the following are causes of hyperthermia except
Which of the following is false about starvation ketoacidosis?
Metabolic changes seen in starvation include all of the following except?
The maximum allowable sweat rate during intense physical exercise for a healthy adult is approximately:
BMR is increased in all except:
Final common pathway of metabolism of carbohydrate, lipids, and protein metabolism is?
The hormone associated with cold adaptation is:
Metabolic Rate and Basal Metabolism Indian Medical PG Practice Questions and MCQs
Question 1: Energy expenditure in the resting state mainly depends on which of the following parameters?
- A. Exercise
- B. Lean body mass (Correct Answer)
- C. Resting heart rate
- D. Adipose tissue
Explanation: ***Lean body mass*** - **Lean body mass** (muscle, organs, bone) is metabolically active and requires significant energy, making it a primary determinant of Basal Metabolic Rate (BMR) or **resting energy expenditure**. - Tissues like **muscle** have a higher metabolic rate even at rest compared to adipose tissue. *Exercise* - **Exercise** accounts for the most variable component of daily energy expenditure, but it does not determine the energy expenditure in the **resting state**. - While physical activity consumes significant energy, that is separate from the baseline energy required to sustain life at rest. *Resting heart rate* - **Resting heart rate** is an indicator of cardiovascular fitness and sympathetic nervous system activity, but it is not a direct measure or primary determinant of total resting energy expenditure. - While a higher heart rate often correlates with a slightly elevated metabolic rate, the **amount of metabolically active tissue** is a more fundamental driver. *Adipose tissue* - **Adipose tissue** (fat) is metabolically less active than lean body mass, contributing minimally to resting energy expenditure compared to muscle or organ mass. - Although it does have some metabolic activity, its contribution is minor relative to the **energy demands of essential organs and muscle tissue**.
Question 2: Post-mortem caloricity is not seen in which of the following conditions?
- A. Pontine haemorrhage
- B. Bacteremia
- C. Status epilepticus
- D. Post-mortem glycogenolysis (Correct Answer)
Explanation: ***Post-mortem glycogenolysis*** - **Post-mortem glycogenolysis** is a **normal biochemical process** that occurs after death, involving the breakdown of glycogen in tissues. - It is **NOT a pre-death pathological condition** and does not cause the body temperature to rise after death. - **Post-mortem caloricity** occurs due to ante-mortem conditions with intense metabolic activity or thermoregulatory dysfunction, not from normal post-mortem biochemical changes. - This is the **correct answer** as it does NOT cause post-mortem caloricity. *Pontine haemorrhage* - **Pontine haemorrhage** causes damage to the **thermoregulatory centers** in the brainstem. - This leads to dysregulation and **uncontrolled heat generation**, resulting in hyperthermia. - The elevated metabolic state can persist briefly after death, causing **post-mortem caloricity**. *Bacteremia* - **Bacteremia** and **sepsis** trigger a massive **inflammatory response** with increased metabolic activity. - The heightened metabolic state generates significant heat before and immediately after death. - This contributes to elevated body temperature observed as **post-mortem caloricity**. *Status epilepticus* - **Status epilepticus** involves **prolonged, intense muscle contractions** and widespread neuronal activity. - This extreme metabolic demand generates substantial heat through continuous muscle activity. - The heat generation can persist briefly post-mortem, leading to **post-mortem caloricity**.
Question 3: A cold exposure which is expected to bring the body temperature from 37°C to 20°C, actually brings it down to only 36.5°C. Calculate the 'Gain' of the thermoregulatory system.
- A. 33 (Correct Answer)
- B. 34
- C. 16.5
- D. 66
Explanation: ***33*** - The **error signal** (or uncorrected temperature drop) is the difference between the actual drop and the expected drop without regulation. Here, the expected drop is 37°C - 20°C = 17°C. The actual drop is 37°C - 36.5°C = 0.5°C. So, the error signal caused by the regulatory system's action is 36.5°C - 20°C = 16.5°C. Alternatively calculated as 17°C (expected) - 0.5°C (actual) = 16.5°C. - The **gain** of a thermoregulatory system is calculated as the expected change in temperature (without regulation) divided by the actual observed change in temperature after regulation when the body resists the change. Here, the body would have cooled by 17°C (37°C - 20°C) without compensation, but it only cooled by 0.5°C (37°C - 36.5°C). The gain is therefore 16.5 / 0.5 = 33. *34* - This answer likely arises from a miscalculation of the error signal or the expected temperature drop. - The key is to correctly identify the **change that would have occurred without regulation** and the **change that actually occurred.** *16.5* - This value represents the **change in temperature that was prevented by the thermoregulatory system** (17°C expected drop minus 0.5°C actual drop), but it is not the gain. - The gain is a ratio, not an absolute temperature difference. *66* - This value would result from an incorrect calculation, possibly by inverting the gain formula or multiplying by an incorrect factor. - The gain is specifically the ratio of the "corrected" change to the "uncorrected" error.
Question 4: All the following are causes of hyperthermia except
- A. Hypothyroidism (Correct Answer)
- B. Cerebral hemorrhage
- C. Succinyl Choline
- D. Pheochromocytoma
Explanation: ***Hypothyroidism*** - Hypothyroidism is characterized by a **reduced metabolic rate** and **decreased heat production**, leading to **cold intolerance** and sometimes **hypothermia**, not hyperthermia [1]. - The body's inability to generate sufficient heat due to low thyroid hormone levels makes hyperthermia an unlikely presentation. *Cerebral hemorrhage* - **Cerebral hemorrhage**, especially in the **hypothalamus** or brainstem, can disrupt the body's **thermoregulation center**, leading to **uncontrolled hyperthermia** [1]. - This is a neurogenic cause of hyperthermia, often refractory to antipyretics. *Succinyl Choline* - **Succinylcholine** can trigger **malignant hyperthermia** in susceptible individuals, particularly when combined with volatile anesthetics [2]. - Malignant hyperthermia is a severe, rapid increase in body temperature due to uncontrolled muscle contractions. *Pheochromocytoma* - **Pheochromocytoma** causes the excessive release of **catecholamines** (epinephrine and norepinephrine), which increase the **metabolic rate** and lead to peripheral vasoconstriction. - This heightened metabolic activity and reduced heat dissipation can result in **hyperthermia** [2].
Question 5: Which of the following is false about starvation ketoacidosis?
- A. Smell of acetone in breath
- B. Metabolic acidosis
- C. Benedict's test +ve (Correct Answer)
- D. Rothera's test +ve
Explanation: ***Benedict's test +ve (FALSE)*** - **Benedict's test** detects the presence of **reducing sugars** (glucose) in the urine. - In starvation ketoacidosis, there is **no significant glucose in the urine** because blood glucose levels are low to normal. - The body is in a state of **prolonged fasting** with depleted glycogen stores, utilizing **fats for energy** instead of carbohydrates. - Unlike diabetic ketoacidosis where glucosuria occurs due to hyperglycemia, starvation ketoacidosis typically presents with **hypoglycemia or normoglycemia**. - Therefore, Benedict's test would be **negative**, making this statement FALSE. *Smell of acetone in breath (TRUE)* - During starvation, the body breaks down fats into **ketone bodies** (beta-hydroxybutyrate, acetoacetate, and acetone). - **Acetone** is volatile and exhaled through the lungs, producing a characteristic **fruity or sweet smell** on the breath. - This is a classic clinical feature of ketoacidosis. *Metabolic acidosis (TRUE)* - The accumulation of **beta-hydroxybutyrate** and **acetoacetate** (both acidic ketone bodies) in the blood leads to decreased pH. - This results in **high anion gap metabolic acidosis** as the excess acids consume the body's **bicarbonate buffer system**. - The anion gap increases due to unmeasured anions (ketone bodies). *Rothera's test +ve (TRUE)* - **Rothera's test** specifically detects **ketone bodies**, particularly **acetoacetate**, in urine. - In starvation ketoacidosis, there is significant production and excretion of ketone bodies. - This causes a **positive Rothera's test**, confirming ketonuria.
Question 6: Metabolic changes seen in starvation include all of the following except?
- A. Ketogenesis
- B. Protein degradation
- C. Increased gluconeogenesis
- D. Increased glycolysis (Correct Answer)
Explanation: ***Increased glycolysis*** - In starvation, the body's primary goal is to conserve **glucose** for essential organs like the brain, as glucose supply is limited. Therefore, glycolysis, the breakdown of glucose, is *decreased*, not increased. - The body shifts to using alternative fuels such as **fatty acids** and **ketone bodies** to spare glucose. *Increased gluconeogenesis* - **Gluconeogenesis**, the synthesis of glucose from non-carbohydrate precursors like amino acids and glycerol, is *increased* during starvation to maintain blood glucose levels. - This process is crucial for providing glucose to tissues that primarily rely on it, such as the brain and red blood cells. *Ketogenesis* - **Ketogenesis**, the production of ketone bodies from fatty acids, is significantly *increased* during prolonged starvation. - **Ketone bodies** become a major energy source for the brain and other tissues when glucose is scarce, helping to spare muscle protein. *Protein degradation* - **Protein degradation** (proteolysis) is *increased* during starvation, especially in the initial phases, to provide amino acids for gluconeogenesis. - Muscle protein is a primary source of these amino acids, contributing to muscle wasting observed in prolonged starvation.
Question 7: The maximum allowable sweat rate during intense physical exercise for a healthy adult is approximately:
- A. 21 ltrs
- B. 2.5 ltrs (Correct Answer)
- C. 3.5 ltrs
- D. 4.5 ltrs
Explanation: ***2.5 ltrs*** - A healthy adult's body can typically **cool itself effectively** through sweating up to an average rate of **2.5 liters per hour** during intense physical exercise. - This rate balances **effective thermoregulation** with the body's capacity to replenish fluids and electrolytes to maintain **homeostasis**. *3.5 ltrs* - While individuals can sweat at rates exceeding 2.5 L/hr, consistently higher rates like **3.5 L/hr** over prolonged periods of intense exercise would put a significant strain on the body's **fluid balance** and electrolyte regulation, increasing the risk of **dehydration** and heat-related illness. - Such rates are often seen in **elite athletes** under extreme conditions and are not a sustainable maximum for general healthy adults. *21 ltrs* - A sweat rate of **21 liters per hour** is physiologically impossible and would lead to immediate, severe, and life-threatening **dehydration**. - The human body simply cannot produce sweat at this volume nor could it sustain such a rapid fluid loss. *4.5 ltrs* - Sweating at **4.5 liters per hour** is an extremely high rate that would be difficult to sustain and would rapidly lead to **severe dehydration** and **electrolyte imbalances** in virtually any individual. - This rate is far beyond what the body can safely manage during prolonged intense exercise without rapid and aggressive fluid replenishment.
Question 8: BMR is increased in all except:
- A. Fever
- B. Exercise
- C. Hypothyroidism (Correct Answer)
- D. Hyperthyroidism
Explanation: ***Hypothyroidism*** - **Hypothyroidism** leads to a **decreased metabolic rate** due to insufficient thyroid hormone production, thus **reducing BMR**. - Symptoms like **weight gain**, **fatigue**, and **cold intolerance** are consistent with a lower metabolic rate. *Fever* - **Fever** causes an **increase in body temperature**, which directly elevates the **metabolic rate** as the body expends more energy to combat infection. - Each degree Celsius rise in body temperature increases BMR by approximately **13%**. *Exercise* - **Chronic exercise training** leads to an **increase in muscle mass**, which is metabolically more active than fat tissue. - This increased muscle mass contributes to a **higher resting metabolic rate (BMR)** over time, even when at rest. - The adaptive response to regular physical activity permanently elevates baseline energy expenditure. *Hyperthyroidism* - **Hyperthyroidism** results in an **overproduction of thyroid hormones**, significantly **increasing the metabolic rate**. - This leads to symptoms such as **weight loss**, **heat intolerance**, and **tachycardia**, all indicative of an elevated BMR.
Question 9: Final common pathway of metabolism of carbohydrate, lipids, and protein metabolism is?
- A. Gluconeogenesis
- B. TCA (Correct Answer)
- C. HMP pathway
- D. Glycolysis
Explanation: ***TCA (Tricarboxylic Acid Cycle)*** - The **TCA cycle** (also called Krebs cycle or citric acid cycle) is the **final common oxidative pathway** where all three macronutrients converge - **Carbohydrates** → Pyruvate → **Acetyl-CoA** (via pyruvate dehydrogenase) - **Lipids** → Fatty acids → **Acetyl-CoA** (via beta-oxidation) - **Proteins** → Amino acids → **Acetyl-CoA or TCA intermediates** (via deamination/transamination) - Complete oxidation of acetyl-CoA occurs in the TCA cycle, producing **NADH, FADH2, and GTP** for energy production *Gluconeogenesis* - This is a **biosynthetic pathway** that synthesizes glucose from non-carbohydrate precursors (lactate, glycerol, amino acids) - It is an **anabolic process**, not the catabolic final common pathway for energy production from all macronutrients *Glycolysis* - **Carbohydrate-specific pathway** that converts glucose to pyruvate - It is only the initial breakdown pathway for carbohydrates, not the common pathway where lipids and proteins also converge - Pyruvate from glycolysis must enter TCA cycle for complete oxidation *HMP pathway (Pentose Phosphate Pathway)* - Parallel pathway to glycolysis that generates **NADPH** (for biosynthesis and antioxidant defense) and **ribose-5-phosphate** (for nucleotide synthesis) - Processes only **glucose-6-phosphate** from carbohydrate metabolism - Not involved in lipid or protein metabolism integration
Question 10: The hormone associated with cold adaptation is:
- A. Melanocyte Stimulating Hormone
- B. Insulin
- C. Growth hormone
- D. Thyroxine (Correct Answer)
Explanation: ***Thyroxine*** - **Thyroxine (T4)** and **triiodothyronine (T3)**, produced by the thyroid gland, play a crucial role in regulating basal metabolic rate and heat production. - In cold environments, the release of these **thyroid hormones** increases, stimulating metabolism and generating more body heat to maintain core temperature. *Melanocyte Stimulating Hormone* - **Melanocyte-stimulating hormone (MSH)** primarily regulates **melanin production** in the skin, which determines skin pigmentation. - It has no direct significant role in **cold adaptation** or thermoregulation. *Insulin* - **Insulin** is essential for **glucose metabolism** by facilitating glucose uptake into cells from the bloodstream. - While energy metabolism is relevant to heat production, insulin's primary role is not direct **cold adaptation**. *Growth hormone* - **Growth hormone (GH)** is critical for **growth**, development, and metabolism of proteins, carbohydrates, and fats. - While it has some metabolic effects that contribute to overall energy balance, it is not a primary hormone specifically associated with **cold adaptation**.
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