INI-CET 2025 — Physiology
11 Previous Year Questions with Answers & Explanations
A single muscle twitch lasts 40 milliseconds. What is the minimum tetanization frequency required to produce a sustained (fused) contraction in this muscle?
Which type of pulse is based on the Frank-Starling law?
Which of the following tissues will not be able to take up glucose in insulin resistance/insulin absence/diabetes mellitus?
Which of the following is not a mechanism of action of ADH?
Patient presents to OPD with fever. Which area is most likely involved?
Which of the following is an example of feed forward mechanism?
In a normal awake person at rest with eyes closed, EEG waves that are reduced on opening the eyes:
Which of the following are features of Bezold Jarisch reflex? 1. Bradycardia 2. Hypertension 3. Coronary vasodilation 4. Tachycardia
Surface tension of the fluid lining the alveoli increases during:
Which of the following is seen in high altitude?
INI-CET 2025 - Physiology INI-CET Practice Questions and MCQs
Question 1: A single muscle twitch lasts 40 milliseconds. What is the minimum tetanization frequency required to produce a sustained (fused) contraction in this muscle?
- A. 10 Hz
- B. 20 Hz
- C. 25 Hz (Correct Answer)
- D. 40 Hz
Explanation: ***25 Hz*** - The **minimum tetanization frequency** (Critical Fusion Frequency) required to produce fused tetanus is calculated as the reciprocal of the total twitch duration: **f = 1/T** - With a complete muscle twitch duration of **40 milliseconds (0.04 seconds)**, the minimum frequency is: **1/0.04 s = 25 Hz** - At this frequency, each stimulus arrives **before the muscle can relax** from the previous contraction, causing **summation** and resulting in **smooth, sustained (fused) tetanus** - This represents the threshold where individual twitches fuse into continuous contraction *10 Hz* - This frequency provides one stimulus every **100 milliseconds (1/10 Hz)** - Since the twitch duration is only 40 ms, the muscle **completely relaxes between stimuli** - This results in **separate, discrete twitches** with no summation - Frequency is far below the critical fusion frequency of 25 Hz *20 Hz* - This frequency corresponds to a stimulus interval of **50 milliseconds (1/20 Hz)** - This interval is longer than the 40 ms twitch duration, allowing **partial relaxation** between stimuli - Results in **unfused (incomplete) tetanus** with visible oscillations in tension - Does not produce the smooth, sustained contraction characteristic of complete tetanus *40 Hz* - This frequency corresponds to an interval of **25 milliseconds (1/40 Hz)** between stimuli - While this frequency **does produce fused tetanus**, it exceeds the minimum requirement - At 40 Hz, stimuli arrive well before any relaxation occurs, but the question asks for the **minimum frequency required** - The minimum frequency for fused tetanus is 25 Hz, making this option incorrect as it is unnecessarily high
Question 2: Which type of pulse is based on the Frank-Starling law?
- A. Pulsus parvus
- B. Pulsus alternans (Correct Answer)
- C. Pulsus bisferiens
- D. Pulsus paradoxus
Explanation: ***Pulsus alternans*** - **Pulsus alternans** (alternating strong and weak pulse beats) is fundamentally explained by the **Frank-Starling law** because the weak beat is often followed by a cycle of slightly better ventricular filling, leading to a stronger subsequent contraction. - It results from severe left ventricular dysfunction (e.g., severe heart failure) where the ventricle cannot sustain uniform stroke volume, causing beat-to-beat variations in **stroke volume** and thus pulse amplitude. ***Pulsus bisferiens*** - This pulse is characterized by a pulse with **two palpable systolic peaks** and is typically associated with significant aortic regurgitation or combined aortic stenosis and regurgitation (AS/AR). - The mechanism is related to the specific timing and interaction of the rapid outflow and late recoil in the aorta, not primarily dictated by the Frank-Starling mechanism. ***Pulsus paradoxus*** - This refers to an exaggerated drop in the systolic blood pressure (more than 10 mmHg) during inspiration, commonly seen in conditions like **cardiac tamponade** or severe asthma. - The cause is increased right heart filling during inspiration, causing the interventricular septum to shift leftward, impeding left ventricular filling; this is a mechanical phenomenon, not a Frank-Starling abnormality. ***Pulsus parvus*** - **Pulsus parvus** means a pulse of small amplitude, often slow rising, classically associated with severe **aortic stenosis**. - The small pulse volume is due to fixed low stroke volume secondary to obstruction at the aortic valve, not a beat-to-beat fluctuation governed by the Frank-Starling relationship.
Question 3: Which of the following tissues will not be able to take up glucose in insulin resistance/insulin absence/diabetes mellitus?
- A. Kidney
- B. Skeletal muscle (Correct Answer)
- C. Brain
- D. Red blood cells
Explanation: ***Skeletal muscle*** - Skeletal muscle is an **insulin-dependent** tissue, meaning glucose uptake is facilitated by the insulin-driven translocation of the **GLUT4** transporter to the cell membrane. - In conditions of insulin resistance or insulin deficiency (diabetes mellitus), the translocation of **GLUT4** is impaired, severely reducing the muscle's ability to take up circulating glucose. *Red blood cells* - Glucose uptake by red blood cells (RBCs) is primarily mediated by the **GLUT1** transporter. - **GLUT1** is constitutively active and highly **insulin-independent**, ensuring that RBCs maintain their glucose supply regardless of the patient's insulin status. *Brain* - The brain relies on transporters like **GLUT1** and **GLUT3** (often considered the primary neuronal glucose transporter) for continuous glucose supply. - Glucose uptake in the brain is **insulin-independent** to guarantee stable energy provision to the central nervous system, even in high-demand states. *Kidney* - The kidney utilizes primarily **GLUT1** and **GLUT2** transporters for glucose uptake into its cells and for reabsorption of filtered glucose in the renal tubules. - These transporters operate independently of insulin levels, classifying the kidney as an **insulin-independent** tissue for glucose metabolism.
Question 4: Which of the following is not a mechanism of action of ADH?
- A. Increases absorption of NaCl in thin ascending limb
- B. Increases water permeability in collecting ducts
- C. Increases absorption of urea in medullary collecting duct
- D. Increases absorption of urea in descending limb of loop of Henle (Correct Answer)
Explanation: ***Increases absorption of urea in descending limb of loop of Henle*** - The mechanism of action of **Antidiuretic Hormone (ADH)** does not involve increasing urea absorption in the **descending limb** of the loop of Henle. - The descending limb is primarily permeable to **water only** and lacks ADH-responsive urea transporters. - This is **NOT** a mechanism of ADH action, making this the correct answer. *Increases water permeability in collecting ducts* - ADH binds to **V2 receptors** in the principal cells of the collecting ducts, triggering the insertion of **aquaporin-2 (AQP2)** channels into the luminal membrane. - This is the **primary mechanism** of ADH, allowing water reabsorption and urine concentration. *Increases absorption of urea in medullary collecting duct* - ADH stimulates the insertion of **urea transporters (UT-A1 and UT-A3)** in the inner medullary collecting duct (IMCD). - This passive diffusion of urea into the medullary interstitium helps maintain the high osmolarity required for maximal water reabsorption. - This is an established **direct mechanism** of ADH. *Increases absorption of NaCl in thin ascending limb* - While the thin ascending limb has passive NaCl permeability, ADH's effects on salt handling are primarily mediated through the **thick ascending limb (TAL)** where it enhances Na-K-2Cl cotransporter activity. - ADH contributes to medullary hypertonicity, which indirectly affects the concentration gradient for passive NaCl movement in the thin ascending limb. - This represents an **indirect effect** rather than a primary mechanism, but is still considered an ADH action in generating concentrated urine.
Question 5: Patient presents to OPD with fever. Which area is most likely involved?
- A. Periventricular hypothalamus
- B. Pre-optic nucleus (Correct Answer)
- C. Dorsomedial hypothalamus
- D. Insular cortex
Explanation: ***Pre-optic nucleus*** - The **pre-optic nucleus** in the anterior hypothalamus contains heat-sensitive and cold-sensitive neurons and functions as the body's primary **thermoregulatory center** or **thermostat**. - Fever results when **pyrogens** (like **IL-1, IL-6**, and **TNF-α**) raise the set-point of this nucleus, leading to heat production and conservation. *Insular cortex* - The insular cortex is involved in processing emotions, interoception (awareness of the body's internal state), and pain, not primarily in regulating core body temperature. - It has a role in complex functions like taste, visceral sensation, and autonomic control but is not the central area for initiating fever. *Periventricular hypothalamus* - The periventricular zone of the hypothalamus is involved in various neuroendocrine functions, including releasing hormones like **somatostatin** and **vasopressin**. - It is not the principal area responsible for setting the body's core temperature or initiating the febrile response. *Dorsomedial hypothalamus* - The **dorsomedial nucleus** of the hypothalamus mainly regulates gastrointestinal activity and some affective behaviors, like fear and aggression. - While the hypothalamus is a thermal regulation hub, this specific nucleus is not the primary target for pyrogens causing fever.
Question 6: Which of the following is an example of feed forward mechanism?
- A. Temperature regulation (Correct Answer)
- B. Vasoconstriction in response to cooling
- C. Increase in cardiac output in response to anemia
- D. HR increases from supine to standing
Explanation: ***Temperature regulation*** - Temperature regulation is the correct answer because it demonstrates **feed-forward control** through **anticipatory mechanisms** that act *before* core body temperature changes. - Classic feed-forward example: When **skin thermoreceptors** detect intense sunlight or environmental heat, the body initiates protective responses (behavioral changes like seeking shade, peripheral vasodilation, sweating) *before* core temperature rises. - This anticipatory control contrasts with feedback mechanisms that respond *after* detecting changes in the regulated variable. - The feed-forward component uses **peripheral sensors** and central command signals to proactively maintain **homeostasis**, preventing disturbances rather than correcting them. *Incorrect: HR increases from supine to standing* - This is a classic **negative feedback loop** controlled by the **baroreflex**. - Sequence: Standing → blood pools → BP drops → baroreceptors detect change → HR increases to restore BP. - The response occurs *after* detecting the disturbance (reactive, not anticipatory). *Incorrect: Vasoconstriction in response to cooling* - This is **negative feedback** to maintain core body temperature. - **Peripheral thermoreceptors** detect temperature drop → hypothalamus responds → **vasoconstriction** via **sympathetic stimulation** minimizes heat loss. - The response follows detection of cooling (reactive mechanism). *Incorrect: Increase in cardiac output in response to anemia* - This is homeostatic **negative feedback** compensating for reduced **oxygen delivery**. - Tissue hypoxia from anemia → increased **sympathetic drive** → elevated **Cardiac Output (CO)** to maximize oxygen transport. - The compensation occurs *after* oxygen delivery becomes inadequate.
Question 7: In a normal awake person at rest with eyes closed, EEG waves that are reduced on opening the eyes:
- A. Theta waves
- B. Beta waves
- C. Alpha waves (Correct Answer)
- D. Delta waves
Explanation: ***Alpha waves*** - These waves (8-13 Hz) are characteristic of the **relaxed wakefulness** state, present chiefly over the occipital areas when the eyes are closed (the **Berger rhythm**). - When the eyes are opened or the person concentrates, the alpha waves are immediately abolished and replaced by fast, low-voltage **Beta waves**, a phenomenon known as **alpha block** or desynchronization. *Beta waves* - These waves (>13 Hz) are associated with **active concentration**, mental alertness, or the act of opening the eyes. - The opening of the eyes causes the brain activity to shift *towards* the Beta rhythm, thus they are increased, not reduced, in this scenario. *Theta waves* - Theta waves (4-7 Hz) are typically observed during **NREM sleep stages 1 and 2** (light sleep) and are usually infrequent in the normal awake, resting adult. - Their presence or absence is not primarily governed by the action of opening or closing the eyes in an awake individual; they reflect stages of sleep or deep emotional arousal. *Delta waves* - Delta waves (<4 Hz) are the slowest waves, typically dominating the EEG during **deep slow-wave sleep (N3)** or indicative of serious brain pathology when seen in an awake adult. - They are absent in the normal awake, resting state, so the act of opening the eyes does not lead to their reduction.
Question 8: Which of the following are features of Bezold Jarisch reflex? 1. Bradycardia 2. Hypertension 3. Coronary vasodilation 4. Tachycardia
- A. 1,2,3
- B. 1,3,4
- C. All of the above
- D. 1,3 (Correct Answer)
Explanation: ***1, 3 (Correct Answer)*** - The **Bezold-Jarisch reflex (BJR)** is a cardio-inhibitory reflex initiated by stimulating cardiac sensory receptors (C-fibers, particularly in the inferoposterior wall of left ventricle). - The efferent limb is mediated by the **vagus nerve**, resulting in the classic triad: **bradycardia**, **hypotension**, and **coronary vasodilation**. - **Bradycardia (1)** occurs due to parasympathetic (vagal) stimulation of the SA node. - **Coronary vasodilation (3)** is a direct effect that helps reduce myocardial oxygen demand. - This reflex is protective, reducing cardiac workload during ischemic conditions. *1, 2, 3 (Incorrect)* - **Hypertension (2)** does not occur in BJR; instead, the reflex causes **hypotension** due to peripheral vasodilation and reduced cardiac output. - The BJR is fundamentally a depressor reflex, not a pressor reflex. *1, 3, 4 (Incorrect)* - **Tachycardia (4)** is the opposite of what occurs in BJR. - The reflex is mediated by parasympathetic activation, which decreases heart rate, not increases it. - Tachycardia would be a sympathetic response, contradicting the BJR mechanism. *All of the above (Incorrect)* - Since options 2 and 4 represent physiological responses opposite to BJR (hypertension and tachycardia), this cannot be correct. - The BJR produces bradycardia, hypotension, and coronary vasodilation only.
Question 9: Surface tension of the fluid lining the alveoli increases during:
- A. Inspiration
- B. Standing
- C. Expiration (Correct Answer)
- D. Supine
Explanation: ***Expiration*** - During expiration, the alveoli **decrease in size** and the alveolar radius becomes smaller. - As the surface area contracts, surfactant molecules become **compressed** and less effective at reducing surface tension. - According to the **Law of Laplace** (P = 2T/r), with a smaller radius and increased surface tension, alveoli would tend to collapse—surfactant normally prevents this, but surface tension is **highest at end-expiration**. - This physiological increase in surface tension during expiration is why **surfactant is critical** to prevent alveolar collapse, especially in premature infants with respiratory distress syndrome. *Incorrect: Inspiration* - During inspiration, alveoli **expand** and increase in radius. - Surfactant's unique property is that it **lowers surface tension more effectively** when spread over a larger surface area. - This dynamic behavior of surfactant ensures that surface tension actually **decreases during inspiration**, facilitating alveolar expansion and reducing the work of breathing. *Incorrect: Standing* - Standing affects the **distribution of ventilation and perfusion** (V/Q ratio) due to gravitational effects on blood flow and lung mechanics. - It does **not directly alter** the surface tension of the alveolar fluid lining on a molecular level. - Regional differences may occur, but there is no consistent, predictable increase in overall surface tension with standing. *Incorrect: Supine* - The supine position redistributes lung volumes and may cause some **airway closure** in dependent regions. - While functional residual capacity (FRC) may decrease slightly, this does **not cause a specific increase** in alveolar surface tension. - Effects on surface tension are indirect and not the primary physiological change with postural alterations.
Question 10: Which of the following is seen in high altitude?
- A. Respiratory alkalosis (Correct Answer)
- B. Respiratory acidosis
- C. Metabolic acidosis
- D. Metabolic alkalosis
Explanation: ***Respiratory alkalosis*** - High altitude exposure leads to **hypoxia** (low inspired oxygen), which stimulates peripheral chemoreceptors. - This stimulation increases the **respiratory rate and depth** (hyperventilation), resulting in excessive blowing off of **carbon dioxide (CO₂)**, which causes a decrease in arterial pCO₂ and elevates the blood pH (alkalosis). *Metabolic acidosis* - This is a condition where the blood pH is low due to a low bicarbonate (HCO₃⁻) concentration, which is not the primary immediate response to high altitude. - However, in a later stage, the kidneys attempt to compensate for respiratory alkalosis by **excreting bicarbonate**, leading to a compensatory metabolic acidosis. *Metabolic alkalosis* - This condition involves a high blood pH due to an excess of bicarbonate, which is typically seen in conditions like severe vomiting or use of diuretics, not acute high altitude exposure. - It is the opposite of the renal compensation mechanism seen in response to high altitude. *Respiratory acidosis* - Characterized by reduced ventilation (hypoventilation) leading to **retention of CO₂** (increased pCO₂), resulting in a lowered blood pH. - High altitude causes hyperventilation, not hypoventilation, and therefore results in respiratory *alkalosis*.