Thermoregulation Practice Questions

Q: Fever is primarily due to which of the following cytokines?

Interleukin-1. **Explanation:** **Why Interleukin-1 (IL-1) is correct:** Fever (pyrexia) is a regulated rise in body temperature mediated by the hypothalamus. When the body encounters pathogens, phagocytic cells (monocytes and macrophages) release **endogenous pyrogens**. **Interleukin-1 (IL-1)** is the primary and most potent endogenous pyrogen. It travels via the bloodstream to the **OVLT (Organum Vasculosum of the Lamina Terminalis)** in the hypothalamus. Here, it triggers the release of **Prostaglandin E2 (PGE2)** through the induction of the enzyme Cyclooxygenase-2 (COX-2). PGE2 then acts on the preoptic area of the hypothalamus to "reset" the thermostatic set-point to a higher level, resulting in fever. **Why other options are incorrect:** * **Interleukin-2 (IL-2):** Primarily responsible for T-cell proliferation and activation (T-cell growth factor). It does not act as a primary pyrogen. * **Interleukin-3 (IL-3):** Acts as a colony-stimulating factor that supports the growth and differentiation of hematopoietic stem cells in the bone marrow. * **Interleukin-4 (IL-4):** Produced by Th2 cells; it promotes B-cell differentiation into IgE-producing plasma cells and is involved in allergic responses, not thermoregulation. **High-Yield Clinical Pearls for NEET-PG:** * **Major Endogenous Pyrogens:** IL-1 (most important), IL-6, TNF-α, and Interferon-gamma. * **Exogenous Pyrogen:** The most common is **Lipopolysaccharide (LPS)** or Endotoxin from Gram-negative bacteria, which stimulates the release of IL-1. * **Mechanism of Antipyretics:** Drugs like Paracetamol and NSAIDs reduce fever by inhibiting the COX enzyme, thereby blocking the synthesis of PGE2 in the hypothalamus. * **The "Master Switch":** PGE2 is the ultimate mediator of fever.

Q: Which of the following is NOT observed in newborns as a mechanism of thermogenesis?

Shivering. In newborns, thermogenesis is primarily achieved through **non-shivering thermogenesis**. The correct answer is **Shivering (A)** because neonates have an immature neuromuscular system and a high surface-area-to-volume ratio, making shivering an ineffective and physiologically impossible mechanism for them to generate heat. ### Why the other options are observed: * **Breakdown of brown fat (B):** This is the hallmark of neonatal thermogenesis. Brown adipose tissue (BAT), located in the interscapular and perirenal areas, is rich in mitochondria and the protein **UCP-1 (Thermogenin)**. When stimulated by norepinephrine, BAT uncouples oxidative phosphorylation to produce heat instead of ATP. * **Universal flexion (C):** Newborns adopt a "fetal position" or universal flexion to decrease the surface area exposed to the environment, thereby reducing heat loss via radiation and convection. * **Cutaneous vasoconstriction (D):** This is a sympathetic response to cold stress. By constricting peripheral blood vessels, the neonate shunts blood toward the core to conserve heat. ### NEET-PG High-Yield Pearls: * **Thermogenin (UCP-1):** The specific protein in brown fat mitochondria responsible for heat production. * **Neutral Thermal Environment (NTE):** The environmental temperature range where the baby maintains a normal body temperature with minimum metabolic rate and oxygen consumption. * **Cold Stress Danger:** In neonates, cold stress leads to increased oxygen consumption, which can result in **hypoxia, metabolic acidosis, and hypoglycemia**. * **Preterm Risk:** Preterm infants are at higher risk of hypothermia because they have minimal brown fat stores and lack the muscle tone for universal flexion.

Q: Which prostaglandin is responsible for causing fever?

PGE2. ### Explanation **Correct Option: B (PGE2)** The hypothalamus acts as the body’s thermostat. During an infection or inflammation, exogenous pyrogens (like bacterial endotoxins) stimulate immune cells to release endogenous pyrogens, primarily **Interleukin-1 (IL-1)**, **IL-6**, and **TNF-α**. These cytokines travel to the **OVLT (Organum Vasculosum of the Lamina Terminalis)** in the brain, where they induce the enzyme **Cyclooxygenase-2 (COX-2)**. COX-2 facilitates the synthesis of **Prostaglandin E2 (PGE2)**. PGE2 then acts on **EP3 receptors** in the preoptic area of the hypothalamus, triggering a reset of the thermal set-point to a higher level, resulting in fever. This is why NSAIDs (like Aspirin or Paracetamol) are effective antipyretics; they inhibit COX enzymes, thereby reducing PGE2 levels. **Analysis of Incorrect Options:** * **PGF2α:** Primarily involved in uterine contractions (induction of labor) and bronchoconstriction. It does not play a significant role in central thermoregulation. * **PGE1:** While it has vasodilatory and cytoprotective properties (used clinically to keep the ductus arteriosus open), it is not the primary mediator of the febrile response. * **PGT2:** This is not a standard physiological prostaglandin involved in the inflammatory or thermoregulatory pathways. **High-Yield Clinical Pearls for NEET-PG:** * **Site of Action:** The **OVLT** is a circumventricular organ lacking a blood-brain barrier, allowing cytokines to trigger the hypothalamus. * **Key Enzyme:** COX-2 is the inducible isoform responsible for PGE2 production during fever. * **Antipyretic Mechanism:** Steroids inhibit Phospholipase A2, while NSAIDs inhibit COX, both ultimately preventing PGE2 synthesis. * **Hyperthermia vs. Fever:** Fever involves a change in the hypothalamic set-point (mediated by PGE2); hyperthermia (e.g., heat stroke) does not.

Q: Which of the following substances is primarily responsible for producing fever?

Prostaglandin E2 (PGE2). **Explanation:** The regulation of body temperature is controlled by the **hypothalamus**, specifically the preoptic area. Fever (pyrexia) occurs when the hypothalamic "set-point" is elevated. This process is initiated by exogenous pyrogens (like bacterial toxins) which trigger the release of endogenous pyrogens (IL-1, IL-6, TNF-α). These cytokines act on the *organum vasculosum of the lamina terminalis* (OVLT) to induce the synthesis of **Prostaglandin E2 (PGE2)** via the cyclooxygenase (COX-2) pathway. PGE2 then binds to EP3 receptors on hypothalamic neurons, leading to increased heat production and conservation. **Analysis of Options:** * **Prostaglandin E2 (PGE2):** This is the principal mediator of fever. It is the only prostaglandin that significantly crosses the blood-brain barrier or is produced locally in the hypothalamus to reset the thermostat. * **Prostaglandin F2 alpha (PGF2a):** Primarily involved in uterine contractions (oxytocic action) and luteolysis; it does not play a role in central thermoregulation. * **Prostacyclin (PGI2):** Produced by vascular endothelium, its main functions are vasodilation and inhibition of platelet aggregation. * **Prostaglandin D2 (PGD2):** Primarily involved in smooth muscle contraction, allergic responses (mast cells), and sleep induction, but not the febrile response. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Antipyretics:** Drugs like Paracetamol and NSAIDs reduce fever by inhibiting the **COX enzyme**, thereby blocking the synthesis of PGE2. * **The "Thermostat":** The **Preoptic area of the Anterior Hypothalamus** is the primary site for temperature integration. * **Cytokine Trigger:** **IL-1** is often cited as the most potent endogenous pyrogen that stimulates PGE2 production.

Q: All of the following can occur in a neonate for heat production, except?

Shivering. **Explanation:** In neonates, the primary mechanism for heat production is **Non-Shivering Thermogenesis (NST)**. Unlike adults, neonates **cannot shiver** effectively because their skeletal muscles are immature and they lack the neurological coordination required to produce heat through involuntary muscle contractions. Therefore, **Option A** is the correct "except" choice. **Analysis of Options:** * **Option B (Brown Fat & Adrenaline):** This is the hallmark of neonatal thermogenesis. Neonates possess **Brown Adipose Tissue (BAT)**, located between the scapulae and around the kidneys. Cold stress triggers the sympathetic nervous system to release **Norepinephrine/Adrenaline**, which activates the protein **Thermogenin (UCP-1)** in brown fat, uncoupling oxidative phosphorylation to produce heat instead of ATP. * **Option C (Universal Flexion):** Neonates instinctively adopt a "fetal position" (flexion of limbs) to reduce the surface area exposed to the environment, thereby minimizing heat loss via radiation and convection. * **Option D (Cutaneous Vasoconstriction):** This is a reflex sympathetic response to cold. By constricting peripheral blood vessels, the neonate shunts blood toward the core, reducing heat loss through the skin. **High-Yield Clinical Pearls for NEET-PG:** * **Brown Fat:** Highly vascularized and contains a high density of mitochondria (giving it the brown color). * **Thermogenin (UCP-1):** The specific protein responsible for heat production in BAT. * **Surface Area to Volume Ratio:** Neonates are at high risk for hypothermia because they have a large surface area relative to their body mass and thin subcutaneous fat. * **Neutral Thermal Environment (NTE):** The environmental temperature range where a neonate maintains a normal body temperature with minimum metabolic expenditure.

Question 1

Hyperthermia is defined as:

Accepted Answer

Uncontrolled increase in body temperature despite a normal hypothalamic temperature setting

Answer

Core temperature > 40.0°C

Answer

Core temperature > 41.5°C

Answer

Elevated temperature that normalizes with antipyretic drugs

Question 2

Fever is primarily due to which of the following cytokines?

Accepted Answer

Interleukin-1

Answer

Interleukin-2

Answer

Interleukin-3

Answer

Interleukin-4

Question 3

Which of the following is NOT observed in newborns as a mechanism of thermogenesis?

Accepted Answer

Shivering

Answer

Breakdown of brown fat

Answer

Universal flexion

Answer

Cutaneous vasoconstriction

Question 4

Which prostaglandin is responsible for causing fever?

Accepted Answer

PGE2

Answer

PGF2

Answer

PGE1

Answer

PGT2

Question 5

During high temperatures, how is the body prevented from overheating?

Accepted Answer

Increased cutaneous vasodilation and cooling effect of sweat

Answer

Cutaneous vasodilation

Answer

Cooling effect of sweat

Answer

Shivering

Question 6

Which of the following substances is primarily responsible for producing fever?

Accepted Answer

Prostaglandin E2 (PGE2)

Answer

Prostaglandin F2 alpha (PGF2a)

Answer

Prostacyclin (PGI2)

Answer

Prostaglandin D2 (PGD2)

Question 7

All of the following can occur in a neonate for heat production, except?

Accepted Answer

Shivering

Answer

Breakdown of brown fat with adrenaline secretion

Answer

Universal flexion like a fetus

Answer

Cutaneous vasoconstriction

Question 8

On exposure to cold, all are seen EXCEPT:

Accepted Answer

Cutaneous vasodilation

Answer

Increased adrenaline

Answer

Shivering

Answer

Increased thyroxine

Question 9

Compared to an unacclimatized person, what physiological changes occur in a person acclimatized to cold?

Accepted Answer

Various combinations of the above, depending on the environment that produced acclimatization.

Answer

Higher metabolic rate in the cold to produce more heat.

Answer

Lower metabolic rate in the cold to conserve metabolic energy.

Answer

Lower peripheral blood flow in the cold to retain heat.

Question 10

The range of environmental temperature at which the basal metabolic rate (BMR) of a baby is at a minimum, oxygen consumption is at least, and the baby maintains its normal body temperature is called?

Accepted Answer

Thermoneutral environment

Answer

Normothermic environment

Answer

Basal environment

Answer

Anabolic environment

Thermoregulation — MCQs

Thermoregulation — MCQs

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