What is the nature of the relationship between insulin and glucose concentration in the human body?
What is Proaccelerin?
Inotropic effect of thyroid hormone is by ?
What is the average size of platelets in micrometers?
Which of the following is considered the most important intracellular buffer in human physiology?
Inhibition of heart by vagus is mediated by which receptors?
Penile erection is mediated by which system?
Somatomedin-C deficiency causes?
What is the respiratory quotient?
Cholecystokinin is produced from:
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 11: What is the nature of the relationship between insulin and glucose concentration in the human body?
- A. Linear
- B. Hyperbola
- C. Sigmoidal (Correct Answer)
- D. Bell Shaped
Explanation: ***Sigmoidal*** - The relationship between insulin and glucose concentration is best described as **sigmoidal**, characterized by a slow initial rise in insulin secretion at low glucose levels, followed by a steep increase at physiological glucose concentrations, and then a plateau at very high glucose levels. - This shape reflects the **beta cell's sensitivity to glucose**, where a minimal threshold of glucose is required to trigger insulin release, and then a maximal release capacity is reached. *Linear* - A **linear relationship** would imply that for every unit increase in glucose, there is a constant, proportional increase in insulin secretion, which is not physiologically accurate. - While insulin secretion does increase with glucose, the rate of increase varies significantly across different glucose concentrations. *Hyperbola* - A **hyperbolic relationship** typically suggests a rapid initial response that then gradually plateaus, often seen in enzyme kinetics. - While there is a plateau in insulin secretion at high glucose levels, the initial phase is not as rapid or proportionally inverse as a hyperbolic function would suggest. *Bell Shaped* - A **bell-shaped curve** describes a relationship where there is an optimal point, and deviations in either direction lead to a decrease in the response (e.g., enzyme activity vs. pH). - This is not characteristic of insulin secretion, as insulin levels generally continue to rise or plateau at higher glucose concentrations and do not decrease beyond an optimal point.
Question 12: What is Proaccelerin?
- A. Factor VII
- B. Factor II
- C. Factor V (Correct Answer)
- D. Factor X
Explanation: ***Factor V*** - **Factor V**, also known as **proaccelerin** or **labile factor**, is a **plasma protein** that plays a crucial role in the coagulation cascade. - It is activated by thrombin to **Factor Va**, which then combines with Factor Xa, calcium, and phospholipid to form the **prothrombinase complex**, significantly enhancing thrombin generation. *Factor II* - **Factor II** is **prothrombin**, a precursor to **thrombin**, which is central to coagulation. - It is not referred to as preaccelerin. *Factor VII* - **Factor VII** is primarily involved in the **extrinsic pathway** of coagulation, becoming activated to Factor VIIa upon contact with tissue factor. - It works to activate Factor IX and Factor X, but it is not preaccelerin. *Factor X* - **Factor X**, also known as **Stuart-Prower factor**, is a key enzyme in the **common pathway** of coagulation, converting prothrombin to thrombin. - It is distinct from Factor V, which acts as a cofactor.
Question 13: Inotropic effect of thyroid hormone is by ?
- A. Membrane receptors
- B. cAMP
- C. cGMP
- D. Enhancement of Catecholamines (Correct Answer)
Explanation: ***Enhancement of Catecholamines*** - Thyroid hormones **potentiate the effects of catecholamines** (like adrenaline and noradrenaline) on the heart, leading to increased heart rate and contractility, which is an **inotropic effect**. - This occurs by increasing the number and sensitivity of **beta-adrenergic receptors** on cardiac muscle cells. *Membrane receptors* - While thyroid hormones do have some rapid, non-genomic effects that may involve **membrane receptors**, their primary and well-established inotropic effect is mediated indirectly through catecholamine sensitivity. - The classic action of thyroid hormones is via intracellular receptors that modulate gene expression, not direct membrane receptor signaling for inotropic effects. *cAMP* - **cAMP** is a common second messenger for many hormones, particularly those acting via G protein-coupled receptors. - While catecholamines themselves act through cAMP to exert their cardiac effects, thyroid hormones *enhance the action* of catecholamines rather than directly using cAMP as their primary inotropic mechanism. *cGMP* - **cGMP** is a second messenger often associated with nitric oxide signaling and vasodilation, contributing to cGMP-dependent protein kinases. - It is not the primary mediator for the *positive inotropic effect* of thyroid hormones on the heart.
Question 14: What is the average size of platelets in micrometers?
- A. 4-5 µm
- B. 3-4 µm
- C. 2-3 µm (Correct Answer)
- D. 1-2 µm
Explanation: ***2-3 µm*** - Platelets, also known as **thrombocytes**, are small, anucleated cell fragments crucial for **hemostasis**, and their average diameter generally falls within the range of 2-3 micrometers. - This **small size** allows them to easily navigate through capillaries and aggregate rapidly at sites of vascular injury. *3-4 µm* - While platelets can vary slightly in size, an average of 3-4 µm is generally considered a bit on the larger side and not the typical average diameter. - Larger platelets might be seen in certain conditions like **idiopathic thrombocytopenic purpura (ITP)**, but this is not the average normal size. *4-5 µm* - This range is significantly larger than the typical size of normal circulating platelets. - Platelets this large would be considered **macroplatelets** and could indicate specific pathological conditions or inherited platelet disorders. *1-2 µm* - This size range is generally considered smaller than the average normal platelet size. - Very small platelets might be seen in some specific conditions, but it's not the usual average for healthy individuals.
Question 15: Which of the following is considered the most important intracellular buffer in human physiology?
- A. Albumin protein
- B. Ammonia buffer
- C. Bicarbonate buffer
- D. Phosphate buffer (Correct Answer)
Explanation: ***Phosphate buffer*** - The **phosphate buffer system (H₂PO₄⁻/HPO₄²⁻)** is the most important intracellular buffer due to relatively high concentrations of inorganic phosphates within cells - The pKa₂ of approximately **6.8 is close to intracellular pH** (~7.0-7.2), providing optimal buffering capacity - Plays a crucial role in buffering acids and bases generated by metabolic processes within cells and is also important in renal tubular buffering *Albumin protein* - **Proteins**, including albumin, are important **extracellular buffers** in plasma due to their abundant ionizable amino acid residues - While proteins do contribute to intracellular buffering (especially hemoglobin in RBCs), the **phosphate system is more significant** for general intracellular pH regulation *Ammonia buffer* - The **ammonia buffer system (NH₃/NH₄⁺)** is primarily a **renal buffer system** that plays a crucial role in acid excretion via urine - It is not considered the primary intracellular buffer for metabolic acid-base balance within cells *Bicarbonate buffer* - The **bicarbonate buffer system (HCO₃⁻/H₂CO₃)** is the **most important extracellular buffer system**, critical for maintaining blood pH - Although present intracellularly, its buffering capacity is less prominent than phosphate within cells due to lower intracellular bicarbonate concentration and its pKa of 6.1 being further from intracellular pH
Question 16: Inhibition of heart by vagus is mediated by which receptors?
- A. M1
- B. M2 (Correct Answer)
- C. NN
- D. NM
Explanation: ***M2*** - The **vagus nerve** primarily mediates its inhibitory effects on the heart through **muscarinic M2 receptors**. - Activation of M2 receptors by **acetylcholine** (released from the vagus nerve) decreases heart rate and contractility. *M1* - **M1 receptors** are primarily found in neuronal tissue and glands, playing a role in **gastric acid secretion** and cognitive functions. - They are not the primary muscarinic subclass responsible for vagal inhibition of the heart. *NN* - **NN receptors** are **nicotinic receptors** found on postganglionic neurons in autonomic ganglia. - They are involved in **ganglionic transmission** and are not directly responsible for efferent vagal effects on the heart. *NM* - **NM receptors** are **nicotinic receptors** found at the **neuromuscular junction** of skeletal muscles. - Their activation leads to **skeletal muscle contraction**, and they have no role in regulating heart function.
Question 17: Penile erection is mediated by which system?
- A. Parasympathetic system via muscarinic receptors (Correct Answer)
- B. Parasympathetic system via nicotinic receptors
- C. Sympathetic system via α-receptors
- D. Sympathetic system via β-receptors
Explanation: ***Parasympathetic system via muscarinic receptors*** - Penile erection is primarily a **parasympathetic response** mediated by the **pelvic splanchnic nerves (S2-S4)**. - The key mechanism involves **nitric oxide (NO)** release from non-adrenergic, non-cholinergic (NANC) neurons, which activates guanylate cyclase → increases cGMP → smooth muscle relaxation in the **corpora cavernosa**. - **Acetylcholine acting on muscarinic receptors** plays a **supportive role** by enhancing NO release and contributing to vasodilation. - For exam purposes, the parasympathetic system (with its cholinergic muscarinic component) is the recognized answer. *Parasympathetic system via nicotinic receptors* - **Nicotinic receptors** are located at **autonomic ganglia** and **neuromuscular junctions**, not at the effector sites in penile vasculature. - While nicotinic transmission occurs at the parasympathetic ganglia, the post-ganglionic fibers act on **muscarinic receptors** and release **NO** at the target tissue. - This option confuses the ganglionic transmission with the effector mechanism. *Sympathetic system via α-receptors* - The **sympathetic nervous system** via **α1-adrenergic receptors** causes **vasoconstriction** and maintains penile **flaccidity** (detumescence). - Sympathetic activation is responsible for **ejaculation** and the resolution phase after orgasm. - Activation of α-receptors opposes erection by causing smooth muscle contraction. *Sympathetic system via β-receptors* - **β-adrenergic receptors** are involved in functions like **cardiac stimulation** and **bronchodilation**, but play no significant role in penile erection. - The sympathetic system's role in sexual function is primarily through **α-receptors** (detumescence and ejaculation), not β-receptors.
Question 18: Somatomedin-C deficiency causes?
- A. Growth retardation (Correct Answer)
- B. Genetic dwarfism
- C. Congenital hypothyroidism
- D. Type 1 diabetes mellitus
Explanation: ***Growth retardation*** - **Somatomedin-C** (also known as **Insulin-like Growth Factor 1 or IGF-1**) is a crucial mediator of **growth hormone's** effects on growth. - A deficiency in Somatomedin-C, therefore, directly leads to **impaired growth** and **stature**, manifesting as **growth retardation**. *Genetic dwarfism* - This term generally refers to dwarfism caused by various **genetic conditions** (e.g., achondroplasia), which may or may not involve the **growth hormone/IGF-1 axis**. - While Somatomedin-C deficiency can be genetic, "genetic dwarfism" is a broader term and not the most precise answer for the direct consequence. *Congenital hypothyroidism* - This condition results from **deficient thyroid hormone production** from birth. - It leads to neurological impairment and **growth failure**, but it is due to **thyroid hormone deficiency**, not Somatomedin-C deficiency. *Type 1 diabetes mellitus* - This is an **autoimmune disease** characterized by the **destruction of pancreatic beta cells**, leading to **insulin deficiency**. - It is entirely unrelated to **Somatomedin-C** or the growth hormone axis.
Question 19: What is the respiratory quotient?
- A. CO2 released to O2 consumed (Correct Answer)
- B. CO2 consumed to O2 released
- C. O2 released to CO2 consumed
- D. O2 consumed to CO2 released
Explanation: **CO2 released to O2 consumed** - The **respiratory quotient (RQ)** is a ratio used in metabolism to describe the proportion of **carbon dioxide (CO2) produced** by the body relative to the **oxygen (O2) consumed**. - It is calculated as the **volume of CO2 released** divided by the **volume of O2 consumed** over a specific period. - RQ = VCO2/VO2, where VCO2 is CO2 production and VO2 is O2 consumption. *CO2 consumed to O2 released* - This option is incorrect as it reverses the correct order and refers to **CO2 consumption and O2 release**, which are not the standard components of the RQ calculation. - The body primarily **releases CO2** and **consumes O2** during cellular respiration. *O2 released to CO2 consumed* - This option is also incorrect because it inverts both the gases and the direction of their metabolic flow (release vs. consumption). - Metabolic processes involve **O2 consumption** and **CO2 release**, not the other way around. *O2 consumed to CO2 released* - This option incorrectly reverses the numerator and denominator in the RQ formula. - The standard definition places **CO2 production** in the numerator and **O2 consumption** in the denominator.
Question 20: Cholecystokinin is produced from:
- A. Hepatocyte
- B. Gastric mucosa
- C. Duodenal mucosa (Correct Answer)
- D. Epithelial cells of distal common bile duct
Explanation: ***Duodenal mucosa*** - **Cholecystokinin (CCK)** is primarily secreted by **I cells**, which are specialized enteroendocrine cells located in the **mucosa of the duodenum** and jejunum. - The release of CCK is stimulated by the presence of **fatty acids** and **amino acids** in the small intestine. *Hepatocyte* - **Hepatocytes** are the main functional cells of the liver, responsible for bile production, metabolism, and detoxification. - They **do not produce regulatory hormones** like cholecystokinin. *Gastric mucosa* - The **gastric mucosa** primarily produces **gastrin**, hydrochloric acid, and pepsinogen, which are involved in gastric digestion. - It does **not secrete cholecystokinin**, which is involved in stimulating gallbladder contraction and pancreatic enzyme release. *Epithelial cells of distal common bile duct* - The **epithelial cells of the common bile duct** are involved in bile transport and modification, but **not in hormone production**. - Their primary role is to line the duct and contribute to the composition of bile.