Day 16 NEET PG

Chapter: Cardiovascular Physiology | Topic: Blood Pressure Regulation | Subtopic: Mean Arterial Pressure (MAP) and Determinants

Keywords

• Mean arterial pressure (MAP) — average arterial pressure during one cardiac cycle.

• Systolic blood pressure (SBP) — peak arterial pressure during ventricular systole.

• Diastolic blood pressure (DBP) — lowest arterial pressure during diastole.

• Pulse pressure — SBP minus DBP; reflects stroke volume and arterial compliance.

• Total peripheral resistance (TPR) — resistance to blood flow in systemic circulation.

• Cardiac output (CO) — stroke volume × heart rate; determines MAP with SVR.

• Autoregulation — intrinsic tissue control of blood flow within a pressure range.

• Arterial compliance — arterial elasticity influencing pressure changes.

• Hypertensive emergency — sudden BP rise with organ damage.

• Vasopressors/vasodilators — drugs altering vascular tone and MAP.

Lead Question - 2012

Mean arterial pressure is calculated as:

• a) (SBP + 2DBP) / 3

• b) (DBP + 2SBP) / 3

• c) (SBP + 3DBP) / 2

• d) (DBP + 3SBP) / 2

Explanation: The approximate formula is (SBP + 2×DBP)/3 because diastole occupies two-thirds of the cardiac cycle. This method is valid at normal heart rates and rhythms, making option a correct. MAP reflects tissue perfusion pressure, critical for organ blood supply and often targeted in critical care settings.

Q2. A 45-year-old hypertensive patient suddenly stands and feels dizzy. Which receptor mediates rapid correction?

• a) Chemoreceptors

• b) Baroreceptors

• c) Osmoreceptors

• d) Mechanoreceptors in joints

Explanation: Baroreceptors in carotid sinus and aortic arch sense stretch changes, activating reflexes to stabilize MAP. Upon standing, reduced venous return decreases stretch, leading to sympathetic activation and BP restoration. Correct answer is b. Dysfunction causes orthostatic hypotension, often seen in autonomic neuropathies or elderly patients.

Q3. During septic shock, which factor primarily lowers MAP?

• a) Increased TPR

• b) Decreased TPR

• c) Increased cardiac contractility

• d) Elevated SBP

Explanation: In septic shock, vasodilation due to inflammatory mediators decreases systemic vascular resistance (TPR), which in turn lowers MAP despite preserved or even elevated cardiac output. Thus, the correct answer is b. Management includes vasopressors to restore vascular tone and adequate tissue perfusion.

Q4. Which parameter has the greatest direct effect on mean arterial pressure?

• a) Stroke volume

• b) Cardiac output

• c) Venous return

• d) Systemic vascular resistance

Explanation: Mean arterial pressure is primarily determined by cardiac output × systemic vascular resistance. Both cardiac output and resistance contribute, but b (cardiac output) is the immediate determinant of blood flow and pressure, especially in clinical measurements. Drugs targeting either component affect MAP significantly in critical settings.

Q5. In a patient with chronic renal failure, MAP is often elevated due to:

• a) Reduced stroke volume

• b) Increased sympathetic tone

• c) Decreased vascular resistance

• d) Loss of baroreceptor reflex

Explanation: Chronic renal failure leads to sodium and water retention, activating renin-angiotensin and sympathetic pathways, elevating systemic vascular resistance. The result is higher MAP. Correct answer is b. This mechanism explains why antihypertensives targeting the RAAS system are especially effective in renal disease–related hypertension.

Q6. Which organ maintains constant blood flow across a wide MAP range due to autoregulation?

• a) Kidney

• b) Skin

• c) Spleen

• d) Muscle

Explanation: The kidney autoregulates blood flow across MAP of 80–180 mmHg, preserving GFR despite systemic fluctuations. This is critical for excretory function. Correct answer is a. Breakdown of autoregulation in shock or severe hypotension leads to acute kidney injury, making MAP support crucial in ICU settings.

Q7. In hypertensive emergencies, lowering MAP too rapidly may cause:

• a) Stroke

• b) Reflex tachycardia

• c) Organ hypoperfusion

• d) Increased cerebral perfusion

Explanation: In chronic hypertension, autoregulation shifts to higher MAP levels. Abrupt reduction can reduce perfusion below critical threshold, causing ischemia. The correct answer is c. Guidelines recommend gradual BP lowering by 20–25% within the first hour to prevent hypoperfusion of brain, heart, and kidneys.

Q8. A patient with tachycardia will have MAP estimation error because:

• a) Systolic occupies longer cycle time

• b) Diastolic shortens disproportionately

• c) Formula is independent of HR

• d) Stroke volume decreases

Explanation: MAP formula assumes diastole is two-thirds of cardiac cycle. In tachycardia, diastole shortens disproportionately, reducing accuracy of (SBP + 2×DBP)/3. The correct answer is b. In such cases, direct invasive arterial monitoring provides more accurate MAP estimation in intensive care.

Q9. Which drug increases MAP mainly by elevating systemic vascular resistance?

• a) Dobutamine

• b) Noradrenaline

• c) Nitroglycerin

• d) Milrinone

Explanation: Noradrenaline (norepinephrine) is a potent α-adrenergic agonist that increases vascular tone, raising systemic vascular resistance and MAP. Thus, the correct answer is b. It is first-line vasopressor in septic shock. Dobutamine and milrinone act more on cardiac contractility and vasodilation, while nitroglycerin reduces MAP.

Q10. MAP is best maintained in shock resuscitation above:

• a) 50 mmHg

• b) 60 mmHg

• c) 65 mmHg

• d) 75 mmHg

Explanation: Guidelines recommend maintaining MAP ≥65 mmHg to ensure vital organ perfusion during shock resuscitation. This target balances risks of underperfusion and excessive vasopressor use. Thus, the correct answer is c. Individualization may be required for patients with chronic hypertension or intracranial pathology.

Q11. A 60-year-old with head injury requires MAP support. Adequate MAP is essential primarily to maintain:

• a) Cerebral perfusion pressure

• b) Pulmonary artery pressure

• c) Right atrial pressure

• d) Venous return

Explanation: Cerebral perfusion pressure = MAP − intracranial pressure. Adequate MAP is critical to prevent secondary brain ischemia in head injury. Therefore, the correct answer is a. Critical care guidelines recommend maintaining CPP >60 mmHg, which depends on sustaining sufficient MAP alongside reducing raised intracranial pressure.

Chapter: Cardiovascular Physiology | Topic: Cardiac Function | Subtopic: Ejection Fraction

Keywords

• Ejection fraction (EF) — fraction of end-diastolic volume ejected during systole.

• Stroke volume (SV) — difference between end-diastolic and end-systolic volumes.

• Preload — ventricular end-diastolic volume or pressure.

• Afterload — resistance against which the ventricle ejects blood.

• Contractility — intrinsic myocardial ability to contract independently of preload and afterload.

• Frank-Starling mechanism — relationship between preload and stroke volume.

• Cardiac output (CO) — product of stroke volume and heart rate.

• End-diastolic volume (EDV) — volume in ventricle before systole.

• End-systolic volume (ESV) — volume remaining after contraction.

• Heart failure — clinical syndrome with reduced EF in systolic type.

Lead Question - 2012

Calculate the ejection fraction from the given volume pressure curve:

• a) 40%

• b) 50%

• c) 55%

• d) 60%

Explanation: Ejection fraction = (EDV – ESV) / EDV × 100. A normal EF ranges from 55%–70%. On the curve, the calculated value is about 55%, making option c correct. EF is a key marker of left ventricular systolic function and important in diagnosing heart failure and cardiomyopathies.

Q1. A 60-year-old man with ischemic heart disease has EF of 35%. What type of heart failure is most likely?

• a) Heart failure with preserved EF

• b) Systolic heart failure

• c) Diastolic heart failure

• d) High-output failure

Explanation: An EF below 40% indicates systolic dysfunction where the ventricle fails to contract effectively. This is termed systolic heart failure. Diastolic failure occurs when EF is preserved but relaxation is impaired. Thus, option b is correct. Low EF is a major prognostic marker in ischemic cardiomyopathy.

Q2. Which factor directly increases stroke volume and ejection fraction?

• a) Increased afterload

• b) Increased preload

• c) Decreased contractility

• d) Increased heart rate

Explanation: Increasing preload within physiological limits enhances stroke volume by the Frank-Starling mechanism, thereby raising ejection fraction. Increased afterload reduces EF, while reduced contractility decreases EF. Tachycardia shortens filling time, lowering stroke volume. Correct answer is b. Preload optimization is key in volume-responsive patients.

Q3. In which condition is ejection fraction usually preserved?

• a) Dilated cardiomyopathy

• b) Hypertrophic cardiomyopathy

• c) Systolic heart failure

• d) Post-myocardial infarction scar

Explanation: Hypertrophic cardiomyopathy primarily causes impaired diastolic filling but systolic contraction is preserved or even hyperdynamic, so EF remains normal or high. Dilated cardiomyopathy and post-MI cause systolic dysfunction and reduced EF. Thus, correct answer is b. Clinical diagnosis relies on echocardiography.

Q4. A patient’s EDV is 120 mL and ESV is 60 mL. What is his EF?

• a) 40%

• b) 45%

• c) 50%

• d) 60%

Explanation: EF = (120 – 60) / 120 × 100 = 60 / 120 × 100 = 50%. This is at the lower end of normal. EF quantifies contractile function and is easily measured by echocardiography. Option c is correct. Values under 50% suggest borderline systolic impairment.

Q5. Which investigation most commonly measures ejection fraction in clinical practice?

• a) ECG

• b) Echocardiography

• c) Chest X-ray

• d) Coronary angiography

Explanation: Echocardiography is the most widely used, non-invasive, bedside method to estimate EF through Simpson’s biplane method or M-mode. ECG shows rhythm, chest X-ray shows size, and angiography evaluates coronaries but not EF directly. Correct answer is b. Cardiac MRI is gold standard but less available.

Q6. A patient on dobutamine infusion shows increased EF. The drug acts by:

• a) Decreasing preload

• b) Increasing contractility

• c) Reducing afterload

• d) Increasing heart rate only

Explanation: Dobutamine is a β1 agonist that increases myocardial contractility, thereby enhancing stroke volume and EF. It also slightly increases heart rate but the primary effect is inotropy. Correct answer is b. Used in acute decompensated heart failure and diagnostic stress echocardiography.

Q7. Which condition classically presents with reduced EF?

• a) Restrictive cardiomyopathy

• b) Aortic stenosis (chronic)

• c) Dilated cardiomyopathy

• d) Hypertrophic cardiomyopathy

Explanation: Dilated cardiomyopathy features stretched, weakened ventricles with impaired systolic contraction, leading to low EF. Restrictive and hypertrophic cardiomyopathy often show preserved EF but impaired filling. Aortic stenosis may reduce EF late but not initially. Correct answer is c. EF monitoring is key in prognosis and therapy.

Q8. Which of the following decreases ejection fraction?

• a) Increased sympathetic activity

• b) Positive inotropic drugs

• c) Acute myocardial infarction

• d) Exercise

Explanation: Acute myocardial infarction causes loss of functional myocardium, reducing contractility and EF. Sympathetic activation, inotropes, and exercise generally increase EF by enhancing contractility. Correct answer is c. Serial EF assessment post-MI helps guide therapy and detect ventricular remodeling.

Q9. A 70-year-old hypertensive diabetic patient has EF 60% but shows signs of heart failure. What is the likely diagnosis?

• a) Heart failure with reduced EF

• b) Right-sided failure

• c) Heart failure with preserved EF

• d) High-output failure

Explanation: HF with preserved EF (HFpEF) occurs when diastolic relaxation is impaired, as in elderly hypertensive diabetics with stiff ventricles. EF remains ≥50% but symptoms occur due to poor filling. Correct answer is c. Diagnosis requires echo showing preserved EF but diastolic dysfunction features.

Q10. Chemotherapy drug doxorubicin can cause cardiotoxicity. What EF change would you expect?

• a) Increased EF

• b) No effect on EF

• c) Reduced EF

• d) Transient rise in EF

Explanation: Doxorubicin-induced cardiomyopathy is a well-known cause of systolic dysfunction with reduced EF. Monitoring EF before and during therapy is standard. A significant fall necessitates discontinuation. Correct answer is c. EF decline reflects irreversible myocardial damage from oxidative stress caused by anthracycline therapy.

Chapter: Cardiovascular Physiology | Topic: Cardiac Preload & Hemodynamics | Subtopic: Preload Determinants

Keywords

• Preload — ventricular wall stress at end-diastole; approximated clinically by end-diastolic volume or pressure.

• End-diastolic volume (EDV) — volume in ventricle before systole; key preload measure.

• End-systolic volume (ESV) — volume remaining after systole; used to calculate stroke volume and EF.

• Stroke volume (SV) — EDV − ESV; influenced by preload, afterload, and contractility.

• Afterload — resistance against which the ventricle ejects; relates to arterial pressure and vascular tone.

• Venous return — primary determinant of preload; influenced by blood volume and venous tone.

• Frank-Starling law — increased preload increases stroke volume within physiological limits.

• Central venous pressure (CVP) — bedside surrogate for right-sided preload.

• Pulmonary capillary wedge pressure (PCWP) — surrogate for left-sided preload in invasive monitoring.

• Compliance — ventricular compliance affects pressure-volume relationship and preload interpretation.

Lead Question - 2012

Preload measures?

• a) End systolic volume

• b) End diastolic volume

• c) Peripheral resistance

• d) Stroke volume

Explanation: Preload reflects ventricular filling at end-diastole and is best approximated by end-diastolic volume (or pressure). End-systolic volume and peripheral resistance are not direct preload measures; stroke volume depends on preload but is not itself the preload. Hence the correct answer is b) End diastolic volume.

Q1. Which bedside measurement approximates left-sided preload in mechanically ventilated patients?

• a) Central venous pressure (CVP)

• b) Pulmonary capillary wedge pressure (PCWP)

• c) Systolic blood pressure

• d) Heart rate

Explanation: Pulmonary capillary wedge pressure (PCWP) measured via a pulmonary artery catheter approximates left atrial pressure and left-sided preload. CVP estimates right-sided preload. Systolic BP and heart rate are not preload measures. Correct answer: b) PCWP. PCWP guides fluid vs. inotrope decisions in ICU care.

Q2. According to Frank-Starling mechanism, increasing preload within physiological limits causes:

• a) Decreased stroke volume

• b) Increased stroke volume

• c) No change in stroke volume

• d) Immediate decrease in contractility

Explanation: The Frank–Starling law states that increased preload stretches myocardial fibers, augmenting contractile force and stroke volume up to an optimal point. Thus increasing preload typically increases stroke volume. Correct answer: b) Increased stroke volume. Excessive preload, however, may cause congestion without further output gain.

Q3. Which clinical condition is characterized by low preload?

• a) Heart failure with volume overload

• b) Hypovolemic shock

• c) Constrictive pericarditis

• d) Cardiac tamponade

Explanation: Hypovolemic shock features reduced intravascular volume and thus low preload, lowering stroke volume and MAP. Constrictive pericarditis and tamponade impair filling but may show elevated venous pressures despite functional low filling. Volume overload increases preload. Correct answer: b) Hypovolemic shock.

Q4. Which intervention will most directly increase preload in a hypotensive patient?

• a) Intravenous fluid bolus

• b) Intravenous nitroprusside

• c) Intravenous furosemide

• d) Intravenous beta-blocker

Explanation: An IV fluid bolus increases intravascular volume and venous return, directly increasing preload and stroke volume in responsive patients. Vasodilators and diuretics reduce preload, and beta-blockers reduce heart rate/contractility. Correct answer: a) Intravenous fluid bolus. Fluid responsiveness should be assessed to avoid overload.

Q5. In cardiac tamponade preload is best described as:

• a) Increased EDV with normal pressures

• b) Reduced effective ventricular filling despite high venous pressures

• c) Increased stroke volume

• d) Elevated contractility

Explanation: Tamponade restricts diastolic filling producing high venous pressures but reduced effective ventricular volume and low stroke volume. Thus preload is functionally reduced despite raised filling pressures. Correct answer: b). Emergency pericardiocentesis restores filling and improves preload and cardiac output.

Q6. Which measurement is a right-sided preload surrogate often used at bedside?

• a) Pulmonary artery diastolic pressure

• b) Central venous pressure (CVP)

• c) Mean arterial pressure

• d) Left atrial pressure

Explanation: Central venous pressure (CVP) reflects right atrial pressure and serves as a bedside surrogate for right-sided preload, albeit with limitations. Pulmonary artery diastolic pressure and left atrial pressure better reflect left-sided filling. MAP is systemic pressure, not preload. Correct answer: b) CVP.

Q7. A patient with sepsis has vasodilation and relative hypovolemia; which change to preload is expected?

• a) Increased preload due to fluid shift into vessels

• b) Reduced preload due to venous pooling

• c) Unchanged preload

• d) Sudden increase in EDV

Explanation: Sepsis causes vasodilation and venous pooling, decreasing venous return and preload despite normal total blood volume. This lowers stroke volume and MAP unless corrected. Correct answer: b) Reduced preload due to venous pooling. Treatment includes fluids and vasopressors to restore preload and tone.

Q8. Which statement is true regarding afterload and preload?

• a) Preload is the same as afterload

• b) Increasing afterload increases stroke volume

• c) Preload depends on venous return; afterload depends on arterial resistance

• d) Neither affects cardiac output

Explanation: Preload is determined by venous return and filling volumes, while afterload is influenced by arterial resistance and arterial pressure. They are distinct and both modulate stroke volume and cardiac output. Correct answer: c). Therapeutic strategies vary: fluids for preload, vasopressors/vasodilators for afterload.

Q9. A patient with decreased ventricular compliance will have preload characterized by:

• a) Low filling pressures at large volumes

• b) High filling pressures at relatively small volumes

• c) No change in pressure-volume relation

• d) Reduced pulse pressure

Explanation: Reduced ventricular compliance means stiffer ventricle: small increases in volume cause large rises in diastolic pressure. Thus preload assessed by pressure may appear high despite modest volumes. Correct answer: b). This occurs in hypertrophy and restrictive cardiomyopathy and affects preload interpretation.

Q10. For fluid responsiveness assessment, which dynamic index best estimates preload responsiveness?

• a) Static CVP value

• b) Pulse pressure variation during mechanical ventilation

• c) Single MAP measurement

• d) Heart rate alone

Explanation: Pulse pressure variation (PPV) during controlled mechanical ventilation predicts fluid responsiveness by detecting preload-dependent stroke volume changes. Static CVP is a poor predictor. MAP and heart rate alone do not reliably indicate preload responsiveness. Correct answer: b) Pulse pressure variation.

Chapter: Cardiovascular Physiology | Topic: Cardiac Output and Stroke Volume | Subtopic: Determinants of Stroke Volume

Keywords

• Stroke volume — volume of blood ejected by left ventricle per beat.

• End-diastolic volume (EDV) — ventricular volume at end of filling.

• End-systolic volume (ESV) — ventricular volume at end of contraction.

• Ejection fraction (EF) — fraction of EDV ejected, SV/EDV × 100.

• Preload — ventricular stretch at end of diastole, approximated by EDV.

• Afterload — resistance the ventricle must overcome to eject blood.

• Contractility — intrinsic ability of myocardium to contract independent of preload/afterload.

• Frank-Starling law — stroke volume rises with increased venous return (EDV) up to a point.

• Cardiac output — stroke volume × heart rate.

• Clinical relevance — heart failure alters preload, afterload, and contractility, reducing stroke volume.

Lead Question - 2012

Stroke volume is increased by ?

• a) Increased end-diastolic and end-systolic volumes

• b) Decreased end-diastolic and end-systolic volumes

• c) Increased end-diastolic volume and decreased end-systolic volume

• d) Decreased end-diastolic volume and increased end-systolic volume

Explanation: Stroke volume depends on preload (EDV), afterload, and contractility. An increased EDV (greater filling) combined with a decreased ESV (stronger ejection) yields maximum stroke volume. Thus the correct answer is c. This mechanism reflects both the Frank-Starling effect and improved myocardial contractility.

Q2. A patient with severe mitral regurgitation typically has increased stroke volume because of:

• a) Increased preload

• b) Increased afterload

• c) Decreased contractility

• d) Reduced ejection fraction

Explanation: In mitral regurgitation, left ventricular volume overload increases EDV (preload). The Frank-Starling mechanism initially augments stroke volume despite regurgitation. Correct answer is a. Over time, chronic overload reduces contractility and ejection fraction.

Q3. Stroke volume decreases in which of the following clinical states?

• a) Hemorrhagic shock

• b) Athlete’s heart

• c) Sympathetic stimulation

• d) Increased venous return

Explanation: Hemorrhage reduces preload (EDV) due to hypovolemia, leading to reduced stroke volume despite compensatory tachycardia. Correct answer is a. In contrast, exercise, sympathetic drive, and increased venous return augment stroke volume.

Q4. A hypertensive patient with high afterload will most likely have:

• a) Increased stroke volume

• b) Decreased stroke volume

• c) No effect on stroke volume

• d) Increased preload

Explanation: Increased afterload (arterial resistance) makes ejection more difficult, raising ESV and lowering stroke volume. Correct answer is b. Chronic high afterload may also lead to concentric LV hypertrophy.

Q5. In septic shock, stroke volume is often:

• a) Increased due to reduced afterload

• b) Decreased due to low preload

• c) Unchanged

• d) Increased due to sympathetic stimulation

Explanation: Septic shock features vasodilation and capillary leak. Although afterload decreases, low preload and impaired myocardial contractility often lower stroke volume. Correct answer is b. Fluids and vasopressors are used to restore volume and perfusion.

Q6. Which of the following increases stroke volume physiologically?

• a) Beta-adrenergic stimulation

• b) Beta-blocker therapy

• c) Acidosis

• d) Myocardial ischemia

Explanation: Beta-adrenergic stimulation enhances myocardial contractility, reducing ESV and increasing stroke volume. Correct answer is a. Beta-blockers, ischemia, and acidosis depress contractility, reducing stroke volume.

Q7. Stroke volume is most reduced in which of the following?

• a) Acute myocardial infarction

• b) Athlete’s bradycardia

• c) Moderate exercise

• d) Positive inotrope infusion

Explanation: In acute myocardial infarction, contractility falls acutely, causing a rise in ESV and a fall in stroke volume. Correct answer is a. In athletes, stroke volume is preserved or enhanced despite slower heart rates.

Q8. Stroke volume increases during exercise due to:

• a) Increased EDV and sympathetic stimulation

• b) Decreased EDV and afterload

• c) Decreased contractility

• d) Increased ESV

Explanation: Exercise boosts venous return (increasing preload) and sympathetic activity (enhancing contractility), lowering ESV and raising stroke volume. Correct answer is a. This adaptation supports higher cardiac output during physical activity.

Q9. Which condition decreases stroke volume most significantly?

• a) Cardiac tamponade

• b) Exercise

• c) Sympathetic stimulation

• d) Early pregnancy

Explanation: Cardiac tamponade impairs diastolic filling by external compression of the heart, reducing preload and stroke volume. Correct answer is a. Exercise, sympathetic drive, and pregnancy normally increase stroke volume.

Q10. Stroke volume is increased by which pharmacological agent?

• a) Dobutamine

• b) Beta-blockers

• c) Calcium channel blockers (verapamil)

• d) Digoxin toxicity

Explanation: Dobutamine, a beta-1 agonist, enhances myocardial contractility and reduces ESV, increasing stroke volume. Correct answer is a. Other listed agents impair contractility or conduction and reduce stroke volume.

Q11. Which of the following is used clinically as a surrogate measure of stroke volume?

• a) Pulse pressure

• b) Diastolic pressure

• c) Heart rate

• d) Central venous pressure

Explanation: Pulse pressure (SBP–DBP) is proportional to stroke volume when arterial compliance is constant. Thus it serves as a surrogate measure. Correct answer is a. Diastolic pressure, HR, or CVP do not directly reflect stroke volume.

Chapter: Cardiovascular Physiology

Topic: Cardiac Action Potential

Subtopic: Plateau Phase Mechanism

Keywords

- Plateau phase: Sustained depolarization of cardiac action potential.

- Calcium channels: L-type Ca2+ channels allowing inward current.

- Potassium permeability: Decreased during plateau maintaining depolarization.

- Sodium influx: Occurs early, not during plateau.

- Excitation-contraction coupling: Calcium influx triggers muscle contraction.

Lead Question – 2012

The plateau phase of this graph is due to:

a) The movement of fewer sodium ions across the cell membrane

b) The calcium channels remaining open longer than the sodium channels

c) The increased membrane permeability to potassium ion

d) A decrease in the amount of calcium diffusing across the membrane

Explanation: The plateau phase of the cardiac action potential is primarily maintained by the prolonged opening of L-type calcium channels, while potassium efflux is reduced. This sustained calcium influx prolongs depolarization, essential for contraction. Hence, the correct answer is (b) The calcium channels remaining open longer than the sodium channels.

Guessed Questions

1) Which ion influx is most critical for triggering myocardial contraction?

a) Sodium

b) Calcium

c) Potassium

d) Chloride

Explanation: Myocardial contraction is dependent on calcium influx during the plateau phase, which binds to troponin to initiate contraction. Thus, calcium is the essential ion. Answer: (b) Calcium.

2) A patient receiving verapamil therapy would show reduced:

a) Sodium influx

b) Calcium influx

c) Potassium efflux

d) Chloride influx

Explanation: Verapamil blocks L-type calcium channels, reducing calcium influx, shortening plateau, and decreasing contractility. The answer is (b) Calcium influx.

3) Which phase of the cardiac action potential is most affected by calcium channel blockers?

a) Phase 0

b) Phase 1

c) Phase 2

d) Phase 3

Explanation: Calcium channel blockers reduce calcium entry during phase 2 (plateau phase), altering contraction strength. The correct answer is (c) Phase 2.

4) The refractory period of cardiac muscle is prolonged due to:

a) Rapid sodium influx

b) Calcium influx during plateau

c) Potassium efflux

d) Chloride movement

Explanation: The plateau phase extends depolarization and refractory period, preventing tetany. This is mediated by calcium influx. Answer: (b) Calcium influx during plateau.

5) A drug that increases potassium efflux during phase 2 will:

a) Prolong plateau phase

b) Shorten plateau phase

c) Increase calcium entry

d) Increase refractory period

Explanation: Increased potassium efflux would counter depolarization, leading to early repolarization and shortening of the plateau. The answer is (b) Shorten plateau phase.

6) In pacemaker cells, the plateau phase is:

a) Prominent

b) Absent

c) Longer than in ventricular cells

d) Stronger than atrial cells

Explanation: Pacemaker cells (SA node) do not have a distinct plateau phase; instead, they exhibit gradual depolarization. Thus, the answer is (b) Absent.

7) The plateau phase in ventricular myocytes ensures:

a) Summation of contractions

b) Sustained contraction for effective ejection

c) Prevention of depolarization

d) Immediate relaxation

Explanation: Plateau phase sustains depolarization, allowing sufficient contraction for ejection of blood and preventing rapid re-excitation. The answer is (b) Sustained contraction for effective ejection.

8) Which ion is mainly responsible for repolarization following the plateau?

a) Sodium influx

b) Calcium influx

c) Potassium efflux

d) Chloride efflux

Explanation: Repolarization after the plateau is mediated by increased potassium efflux, which restores resting membrane potential. The answer is (c) Potassium efflux.

9) Digitalis toxicity prolongs plateau by increasing:

a) Calcium influx

b) Sodium influx

c) Potassium efflux

d) Chloride entry

Explanation: Digitalis increases intracellular calcium by inhibiting Na+/K+ ATPase, prolonging the plateau and contraction. The answer is (a) Calcium influx.

10) A mutation causing prolonged opening of calcium channels may lead to:

a) Tachyarrhythmia

b) Short QT syndrome

c) Long QT syndrome

d) Increased potassium clearance

Explanation: Prolonged calcium entry prolongs action potential duration, predisposing to long QT syndrome. Answer: (c) Long QT syndrome.

11) During exercise, sympathetic stimulation increases calcium influx, which results in:

a) Decreased stroke volume

b) Increased contractility

c) Shortened plateau phase

d) Reduced cardiac output

Explanation: Sympathetic activity increases calcium influx, strengthening contraction and raising stroke volume. Answer: (b) Increased contractility.

Chapter: Cardiovascular Physiology

Topic: Autonomic Regulation of Blood Vessels

Subtopic: Cutaneous Circulation

Keywords

- Vasoconstriction: Narrowing of blood vessels reducing blood flow.

- Sympathetic system: Autonomic nervous system division controlling vasoconstriction.

- Parasympathetic system: Autonomic division with minimal role in skin vessels.

- Wheal and flare: Triple response due to histamine release.

- Thermoregulation: Adjustments in blood flow to skin for heat balance.

Lead Question – 2012

Vasoconstriction in skin?

a) Sympathetic

b) Parasympathetic

c) Wheal and flare

d) Warm climate

Explanation: Skin vasoconstriction is mediated by sympathetic adrenergic activity via norepinephrine acting on α1-receptors. Parasympathetic innervation is negligible in skin. Vasoconstriction conserves heat in cold climates. Thus, the correct answer is (a) Sympathetic.

Guessed Questions

1) A patient with spinal cord injury at T1 loses vasoconstrictor tone in skin below the lesion. This occurs because:

a) Parasympathetic denervation

b) Sympathetic denervation

c) Histamine release

d) Loss of local autoregulation

Explanation: Sympathetic fibers originate from thoracolumbar segments; interruption leads to loss of vasoconstriction below the lesion. The answer is (b) Sympathetic denervation.

2) During hemorrhage, cutaneous vasoconstriction helps by:

a) Increasing blood flow to skin

b) Redirecting blood to vital organs

c) Activating parasympathetic tone

d) Preventing sweating

Explanation: In shock, sympathetic vasoconstriction reduces skin perfusion, shunting blood to heart and brain. This is a protective response. The answer is (b) Redirecting blood to vital organs.

3) Administration of α-blocker (e.g., phentolamine) would cause skin vessels to:

a) Constrict

b) Dilate

c) Show no change

d) Collapse

Explanation: Blocking α1-receptors prevents sympathetic vasoconstriction, leading to vasodilation and flushing of skin. The correct answer is (b) Dilate.

4) In cold exposure, skin appears pale due to:

a) Parasympathetic constriction

b) Sympathetic vasoconstriction

c) Histamine effect

d) Increased nitric oxide

Explanation: Cold triggers sympathetic adrenergic vasoconstriction, decreasing skin blood flow and causing pallor. This conserves heat. Answer: (b) Sympathetic vasoconstriction.

5) A burn patient develops erythema around the wound due to:

a) Sympathetic tone

b) Histamine-mediated vasodilation

c) Parasympathetic reflex

d) Loss of autoregulation

Explanation: Burn injury releases histamine and other mediators causing local vasodilation and erythema (flare response). Correct answer is (b) Histamine-mediated vasodilation.

6) Vasoconstrictor fibers to the skin mainly release:

a) Acetylcholine

b) Norepinephrine

c) Dopamine

d) Serotonin

Explanation: Sympathetic adrenergic fibers release norepinephrine, activating α1-receptors to constrict vessels. The correct answer is (b) Norepinephrine.

7) Emotional stress causing pallor in face is due to:

a) Parasympathetic cholinergic activity

b) Sympathetic adrenergic vasoconstriction

c) Histamine release

d) Serotonin effect

Explanation: Stress triggers sympathetic activation, leading to facial skin vasoconstriction and pallor. The answer is (b) Sympathetic adrenergic vasoconstriction.

8) In Raynaud’s phenomenon, exaggerated vasoconstriction of fingers is triggered by:

a) Heat

b) Cold or stress

c) Infection

d) Exercise

Explanation: Raynaud’s is a disorder with excessive sympathetic-mediated vasoconstriction in response to cold or stress, causing pallor, cyanosis, and pain. Answer is (b) Cold or stress.

9) Which of the following drugs causes cutaneous vasodilation?

a) Phenylephrine

b) Atropine

c) Nitroprusside

d) Norepinephrine

Explanation: Sodium nitroprusside releases nitric oxide, causing potent vasodilation including cutaneous vessels. The answer is (c) Nitroprusside.

10) A soldier in desert heat collapses with flushed, dilated skin vessels. The mechanism is:

a) Sympathetic cholinergic vasodilation

b) Parasympathetic activation

c) Histamine response

d) α-receptor stimulation

Explanation: Heat stress activates sympathetic cholinergic fibers in skin, causing vasodilation and sweating for thermoregulation. Correct answer: (a) Sympathetic cholinergic vasodilation.

11) A patient with pheochromocytoma often has cold extremities due to:

a) Increased sympathetic vasoconstriction

b) Increased parasympathetic tone

c) Reduced adrenergic activity

d) Loss of histamine response

Explanation: Excess catecholamines in pheochromocytoma overstimulate α1-receptors, causing persistent vasoconstriction and cold extremities. Answer: (a) Increased sympathetic vasoconstriction.

Chapter: General Physiology

Topic: Body Fluid Compartments

Subtopic: Interstitial Fluid Dynamics

Keywords

- Interstitial pressure: Pressure exerted by interstitial fluid outside the capillaries.

- Capillary hydrostatic pressure: Force pushing fluid out of capillaries.

- Plasma oncotic pressure: Osmotic force pulling fluid into capillaries due to plasma proteins.

- Lymphatic drainage: Mechanism that prevents fluid accumulation in tissues.

- Edema: Swelling caused by excessive fluid in interstitial spaces.

Lead Question – 2012

Normal interstitial pressure is?

a) 10 to 15 mmHg

b) -5 to 0 mmHg

c) 20 to 30 mmHg

d) -10 to -20 mmHg

Explanation: Interstitial pressure is normally slightly negative, about -5 to 0 mmHg. This negative value maintains continuous absorption of excess fluid by lymphatics. Positive interstitial pressure may cause edema. Thus, the correct answer is (b) -5 to 0 mmHg.

Guessed Questions

1) A patient develops generalized edema in nephrotic syndrome due to:

a) Increased interstitial pressure

b) Reduced plasma oncotic pressure

c) Increased lymphatic drainage

d) Decreased capillary hydrostatic pressure

Explanation: Nephrotic syndrome causes protein loss, lowering plasma oncotic pressure, reducing fluid reabsorption into capillaries, and leading to edema. Correct answer: (b) Reduced plasma oncotic pressure.

2) In right heart failure, interstitial fluid accumulates primarily due to:

a) Increased plasma oncotic pressure

b) Decreased capillary hydrostatic pressure

c) Increased capillary hydrostatic pressure

d) Reduced lymphatic return

Explanation: Right heart failure elevates venous pressure, raising capillary hydrostatic pressure, pushing fluid into the interstitial space, and causing peripheral edema. Correct answer: (c) Increased capillary hydrostatic pressure.

3) In lymphatic obstruction (e.g., filariasis), edema occurs because:

a) Interstitial pressure becomes negative

b) Capillary hydrostatic pressure falls

c) Interstitial fluid cannot be drained

d) Plasma oncotic pressure rises

Explanation: Blockage of lymphatic drainage prevents removal of interstitial fluid, leading to lymphedema even when hydrostatic and oncotic pressures are normal. Correct answer: (c) Interstitial fluid cannot be drained.

4) Pulmonary edema in acute left heart failure is due to:

a) Reduced plasma oncotic pressure

b) Increased pulmonary capillary hydrostatic pressure

c) Increased lymphatic flow

d) Negative interstitial pressure

Explanation: Left heart failure raises pulmonary venous pressure, increasing capillary hydrostatic pressure, forcing fluid into alveolar interstitium, causing pulmonary edema. Correct answer: (b) Increased pulmonary capillary hydrostatic pressure.

5) A burn patient develops massive edema because of:

a) Loss of plasma proteins

b) Reduced interstitial volume

c) Increased lymphatic return

d) Positive interstitial pressure

Explanation: Burns increase capillary permeability, causing plasma protein leakage into interstitial fluid, reducing plasma oncotic pressure and favoring edema formation. Correct answer: (a) Loss of plasma proteins.

6) Interstitial pressure becomes positive when:

a) Tissue edema develops

b) Plasma oncotic pressure increases

c) Lymphatic drainage accelerates

d) Capillary hydrostatic pressure decreases

Explanation: In early edema, interstitial pressure rises from its normal negative value to positive, which further promotes fluid leakage into tissue. Correct answer: (a) Tissue edema develops.

7) The main safety factor against edema under normal physiology is:

a) Positive interstitial pressure

b) Negative interstitial pressure

c) High hydrostatic pressure

d) Low lymph flow

Explanation: Negative interstitial pressure maintains fluid absorption into lymphatics, preventing excessive accumulation. This acts as a protective mechanism. Correct answer: (b) Negative interstitial pressure.

8) In severe liver cirrhosis, ascites develops due to:

a) Increased plasma protein synthesis

b) Reduced plasma oncotic pressure

c) Negative interstitial pressure

d) Reduced capillary hydrostatic pressure

Explanation: Cirrhosis reduces albumin production, lowering plasma oncotic pressure, favoring movement of fluid into peritoneal cavity, causing ascites. Correct answer: (b) Reduced plasma oncotic pressure.

9) During prolonged standing, dependent edema occurs due to:

a) Reduced capillary hydrostatic pressure

b) Increased capillary hydrostatic pressure in legs

c) Increased plasma oncotic pressure

d) Negative interstitial pressure

Explanation: Standing increases venous pressure in lower limbs, raising capillary hydrostatic pressure, leading to filtration of fluid into interstitial space and edema. Correct answer: (b) Increased capillary hydrostatic pressure in legs.

10) The Starling equilibrium is maintained by balance between:

a) Hydrostatic and oncotic pressures

b) Interstitial and lymphatic pressures

c) Capillary and interstitial pressures only

d) Oncotic and osmotic pressures only

Explanation: Starling forces describe fluid exchange across capillaries based on balance between hydrostatic and oncotic pressures on both plasma and interstitial sides. Correct answer: (a) Hydrostatic and oncotic pressures.

11) An anaphylactic reaction causes edema mainly by:

a) Increased capillary permeability

b) Reduced plasma oncotic pressure

c) Negative interstitial pressure

d) Increased lymphatic drainage

Explanation: Histamine release in anaphylaxis increases capillary permeability, allowing plasma proteins and fluid to leak into interstitial space, causing angioedema. Correct answer: (a) Increased capillary permeability.

Chapter: Central Nervous System

Topic: Basal Ganglia

Subtopic: Striatum and Memory Functions

Keywords

- Striatum: Part of basal ganglia involved in motor control and habit learning.

- Procedural memory: Memory for skills and habits, dependent on basal ganglia.

- Explicit memory: Conscious recall of facts and events, mediated by hippocampus.

- Short-term memory: Temporary information storage lasting seconds to minutes.

- Long-term memory: Stable memory stored for days to years.

- Parkinsonism: Clinical syndrome due to basal ganglia dysfunction.

Lead Question – 2012

Striatum damage affects primarily?

a) Procedural memory

b) Short term memory

c) Long term memory

d) Explicit memory

Explanation: The striatum, part of the basal ganglia, regulates procedural memory linked to skills and habits. Unlike hippocampus-driven explicit memory, striatal injury impairs motor learning such as riding a bicycle or typing, while short- and long-term declarative memories remain intact. Correct answer: (a) Procedural memory.

Guessed Questions

1) A Parkinson’s patient struggles with buttoning his shirt. Which memory type is impaired?

a) Procedural memory

b) Explicit memory

c) Short term memory

d) Episodic memory

Explanation: Parkinson’s disease impairs basal ganglia circuits, particularly the striatum, which controls learned motor skills. Patients lose smooth execution of habitual actions. Declarative and episodic recall remain intact. Correct answer: (a) Procedural memory.

2) A stroke involving the hippocampus mainly affects:

a) Habit learning

b) Procedural skills

c) Explicit memory

d) Reflex conditioning

Explanation: The hippocampus is essential for consolidation of declarative memories, including facts and events. Stroke injury here produces severe anterograde amnesia for explicit memory, but motor habits and reflex learning remain intact. Correct answer: (c) Explicit memory.

3) Which memory remains unaffected in striatal lesions?

a) Motor habits

b) Procedural skills

c) Explicit memory

d) Skill learning

Explanation: Striatal lesions disrupt motor habits and procedural learning. Explicit memory, mediated by hippocampus and temporal cortex, stays preserved in such patients. They can recall events but struggle with habit execution. Correct answer: (c) Explicit memory.

4) A patient can recall his wedding day but cannot play the piano anymore after basal ganglia injury. This reflects loss of:

a) Explicit memory

b) Procedural memory

c) Short term memory

d) Semantic memory

Explanation: Piano playing is a learned skill relying on procedural memory, dependent on striatal circuits. Episodic recall, like remembering wedding details, involves hippocampus and remains unaffected. Correct answer: (b) Procedural memory.

5) In Huntington’s disease, degeneration of the striatum causes early:

a) Loss of semantic memory

b) Loss of episodic recall

c) Impaired procedural memory

d) Impaired short-term storage

Explanation: Huntington’s disease selectively damages the caudate and putamen (striatum). Patients show impaired motor learning and skill execution due to loss of procedural memory, while semantic and episodic memory are relatively intact early. Correct answer: (c) Impaired procedural memory.

6) Procedural memory is best tested by:

a) Word recall

b) Mirror tracing task

c) Object naming

d) Sentence repetition

Explanation: Procedural memory is assessed through tasks requiring skill learning, such as mirror tracing or rotary pursuit. Word recall and object naming depend on explicit memory and language centers. Correct answer: (b) Mirror tracing task.

7) A patient retains ability to solve arithmetic problems but forgets new motor skills after basal ganglia injury. Which is intact?

a) Procedural memory

b) Habit learning

c) Explicit memory

d) Reflex motor learning

Explanation: Arithmetic skills and fact-based knowledge depend on explicit memory stored in the cortex and hippocampus. These remain intact despite striatal injury. Procedural learning is impaired. Correct answer: (c) Explicit memory.

8) Which brain structure primarily encodes explicit long-term memory?

a) Striatum

b) Hippocampus

c) Amygdala

d) Cerebellum

Explanation: The hippocampus consolidates explicit long-term memory such as facts and events. The striatum mediates procedural memory, the amygdala processes emotional memory, and the cerebellum handles motor coordination. Correct answer: (b) Hippocampus.

9) Striatal injury spares which of the following?

a) Habit learning

b) Skill acquisition

c) Declarative recall

d) Motor sequence learning

Explanation: Declarative recall (explicit memory) is dependent on hippocampal circuits and not the striatum. Therefore, patients with striatal lesions can still recall facts but fail to perform acquired habits. Correct answer: (c) Declarative recall.

10) A medical student learns to perform venipuncture. Which memory system is reinforced?

a) Procedural memory

b) Short term memory

c) Semantic memory

d) Episodic memory

Explanation: Skill-based learning such as venipuncture is stored in procedural memory, relying on striatal and cerebellar circuits. Over time, repetition strengthens habit execution independent of conscious recall. Correct answer: (a) Procedural memory.

11) A patient with amnesia can still play the guitar skillfully. Which memory is preserved?

a) Explicit memory

b) Procedural memory

c) Episodic memory

d) Semantic memory

Explanation: Amnesia typically impairs explicit (declarative) memory while sparing procedural memory. Thus, the patient cannot recall past events but continues to perform learned motor skills such as guitar playing. Correct answer: (b) Procedural memory. 

Chapter: Central Nervous System | Topic: Somatosensory System | Subtopic: Cortical Sensory Functions

Keywords

• Primary somatosensory cortex — postcentral gyrus; processes discriminative touch and proprioception.

• Stereognosis — recognition of objects by touch; cortical function.

• Two-point discrimination — spatial acuity mediated by S1.

• Graphesthesia — recognizing writing on skin; cortical sensory test.

• Astereognosis — inability to identify objects by touch; indicates cortical lesion.

• Thalamus — relay station for somatic sensory pathways to cortex.

• Spinothalamic tract — transmits pain and temperature to thalamus/cortex.

• Proprioception — limb position sense; dorsal columns and cortex.

• Neglect — parietal lobe dysfunction causing inattention to one side.

• Localization — identifying site of tactile stimulus; a cortical discriminative ability.

Lead Question - 2012

Somatosensory cortex lesion will cause ?

• a) Pain

• b) Temperature

• c) Localization

• d) Vibration

Explanation: The primary somatosensory cortex is essential for discriminative touch tasks such as localization, two-point discrimination, stereognosis and graphesthesia. A cortical lesion impairs the ability to localize stimuli despite preserved basic pain and temperature sensation. Correct answer is c) Localization.

Q2. A patient cannot identify an object by touch but can feel it; this sign is called:

• a) Anosmia

• b) Astereognosis

• c) Hemianopia

• d) Agraphia

Explanation: Astereognosis is the inability to recognize objects by touch despite intact primary sensation, indicating contralateral parietal or postcentral gyrus dysfunction. It reflects impaired cortical processing of tactile information. Correct answer: b) Astereognosis. This helps localize lesions to somatosensory cortex.

Q3. Loss of two-point discrimination on the right hand suggests lesion in:

• a) Left primary somatosensory cortex

• b) Right dorsal column

• c) Left cerebellum

• d) Peripheral nerve only

Explanation: Two-point discrimination is a cortical function processed in the contralateral primary somatosensory cortex. Loss on the right hand indicates a lesion in the left postcentral gyrus. Peripheral lesions can reduce sensation but cortical loss specifically impairs spatial discrimination. Correct answer: a).

Q4. In a pure postcentral gyrus infarct, which sensation is most likely preserved?

• a) Stereognosis

• b) Pain perception

• c) Two-point discrimination

• d) Graphesthesia

Explanation: Basic pain perception often remains because spinothalamic pathways reach thalamus and brainstem centers; however discriminative tasks (stereognosis, two-point discrimination, graphesthesia) require cortical processing and are impaired. Thus pain perception may be relatively preserved; correct answer: b).

Q5. A lesion of the secondary somatosensory cortex most affects:

• a) Conscious pain detection

• b) Integration and recognition of complex tactile patterns

• c) Spinal reflexes

• d) Muscle tone

Explanation: Secondary somatosensory cortex integrates tactile information for higher functions like texture discrimination and object recognition. Lesions impair complex tactile perception but not basic detection. Correct answer: b). Clinical tests include stereognosis and graphesthesia to detect such deficits.

Q6. Hemineglect (inattention to one side) most commonly results from lesion in:

• a) Dominant parietal lobe

• b) Nondominant parietal lobe

• c) Occipital lobe

• d) Brainstem

Explanation: Hemineglect is typically due to damage of the nondominant (usually right) parietal cortex, causing inattention to the contralateral side. It affects awareness more than primary sensation. Correct answer: b). This is tested by cancellation tasks and sensory stimulation.

Q7. Graphesthesia testing assesses which function?

• a) Pain localization

• b) Ability to recognize writing on skin

• c) Vibration sense

• d) Proprioception

Explanation: Graphesthesia is recognizing letters or numbers traced on the skin and depends on intact cortical sensory areas. Loss suggests parietal lobe dysfunction. Correct answer: b). It complements stereognosis and two-point discrimination in cortical assessment.

Q8. A thalamic stroke most commonly causes which sensory deficit?

• a) Pure motor weakness only

• b) Contralateral hemisensory loss including pain and temperature

• c) Ipsilateral loss of vibration only

• d) Loss of smell

Explanation: The thalamus relays most somatic sensory modalities to cortex; a thalamic stroke causes contralateral hemisensory loss affecting pain, temperature, touch and proprioception. Correct answer: b). Thalamic pain syndrome can follow with chronic dysesthesia.

Q9. Dissociation of pain and touch (lost pain but preserved touch) indicates lesion in:

• a) Dorsal columns

• b) Spinothalamic tract

• c) Peripheral nerves only

• d) Primary motor cortex

Explanation: Loss of pain and temperature with preserved dorsal column modalities suggests spinal cord lesion affecting the spinothalamic tract (e.g., syringomyelia). Correct answer: b). Cortical lesions typically affect discriminative touch rather than abolish pain selectively.

Q10. A patient with cortical sensory loss will most likely fail which bedside test?

• a) Reflex hammer tendon reflex

• b) Two-point discrimination

• c) Muscle strength testing

• d) Pupillary light reflex

Explanation: Two-point discrimination depends on cortical sensory processing; cortical lesions impair this test. Tendon reflexes and muscle strength reflect spinal and motor pathways. Pupillary reflex is brainstem mediated. Correct answer: b). This helps distinguish cortical from peripheral sensory loss.

Q11. Which sign suggests parietal lobe (cortical) sensory dysfunction rather than peripheral neuropathy?

• a) Stocking-glove numbness

• b) Astereognosis

• c) Diminished ankle reflex

• d) Burning pain in feet

Explanation: Astereognosis (inability to recognize objects by touch) indicates cortical parietal dysfunction. Peripheral neuropathies produce distal symmetric sensory loss and reflex changes. Correct answer: b). Identifying astereognosis localizes lesion to somatosensory cortex.

Chapter: Central Nervous System | Topic: Motor System | Subtopic: Motor Planning & Postural Set

Keywords

• Supplementary motor area (SMA) — medial frontal region involved in planning, initiating complex and bimanual movements and setting postural tone.

• Premotor cortex — lateral frontal area organizing movements in response to external cues and sensory guidance.

• Primary motor cortex (M1) — executes voluntary movements; somatotopically organized.

• Postural set — anticipatory adjustment of posture before voluntary movement to maintain balance.

• Motor planning — preparation and sequencing of movement components prior to execution.

• Apraxia — impairment of learned purposeful movements despite intact strength and comprehension.

• Basal ganglia — selection/gating of motor programs and modulation of movement initiation.

• Cerebellum — timing, coordination, and adaptive control of movements and posture.

• Feedforward control — anticipatory motor adjustments based on predicted outcomes.

• Pharmacologic/lesion effects — focal lesions produce specific deficits in planning or execution.

Lead Question - 2012

Setting posture before planned movement ?

• a) Premotor cortex

• b) Motor cortex

• c) Frontal

• d) Supplementary motor cortex

Explanation: The supplementary motor area (SMA) is primarily responsible for internally generated movement planning and anticipatory postural adjustments (postural set) before voluntary actions, especially for bimanual and sequential tasks. Lesions cause impaired initiation and postural preparation. Correct answer: d) Supplementary motor cortex.

Q2. A patient cannot initiate a self-paced sequence of movements but moves normally to external cues. Which area is likely affected?

• a) Primary motor cortex

• b) Premotor cortex

• c) Supplementary motor area

• d) Somatosensory cortex

Explanation: SMA lesions impair internally generated, self-initiated sequences while externally cued movements remain relatively preserved due to premotor circuits. Patients show akinesia or difficulty initiating learned sequences. Correct answer: c) Supplementary motor area. Rehabilitation uses external cues to bypass SMA deficits.

Q3. Which structure provides timing and coordination for anticipatory postural adjustments?

• a) Cerebellum

• b) Broca’s area

• c) Hippocampus

• d) Occipital lobe

Explanation: The cerebellum refines timing and coordination of both movement execution and anticipatory postural adjustments by integrating sensory inputs and motor plans. Cerebellar lesions produce dysmetria and impaired postural control. Correct answer: a) Cerebellum. It works with SMA for smooth movement onset.

Q4. A lesion in the lateral premotor cortex most likely impairs:

• a) Internally-generated bimanual sequencing

• b) Response to external sensory cues

• c) Primary muscle strength

• d) Long-term memory

Explanation: The lateral premotor area is important for selecting and preparing movements guided by external sensory cues. Lesions reduce cue-driven responses and impair reaching based on visual instructions. Correct answer: b) Response to external sensory cues; strength (M1) and memory are not primarily affected.

Q5. Which clinical sign suggests SMA dysfunction?

• a) Contralateral spastic weakness only

• b) Difficulty performing learned sequences without cues

• c) Pure sensory loss

• d) Visual field defect

Explanation: SMA damage causes difficulty initiating learned motor sequences and impaired bimanual coordination; actions may be performed with external prompting. While M1 lesions cause weakness, SMA lesions mainly affect initiation and sequencing. Correct answer: b). Assess by asking patient to perform self-initiated tasks.

Q6. Deep brain structures that gate motor programs and influence postural set include:

• a) Basal ganglia

• b) Optic chiasm

• c) Medulla oblongata only

• d) Corpus callosum

Explanation: Basal ganglia circuits select and facilitate appropriate motor programs and modulate posture and initiation. Dysfunction causes bradykinesia, rigidity, and impaired preparatory postural adjustments. Correct answer: a) Basal ganglia. They interact with SMA and premotor areas for smooth motor control.

Q7. Which test assesses anticipatory postural adjustments related to SMA function?

• a) Ask patient to raise one arm quickly while observing weight shift

• b) Visual acuity chart

• c) Pure tone audiometry

• d) Deep tendon reflex testing

Explanation: Observing compensatory weight shift when a patient rapidly raises an arm evaluates anticipatory postural adjustments. SMA dysfunction yields inadequate preparatory shifts and imbalance. Correct answer: a). This bedside test reveals impaired feedforward control of posture.

Q8. A patient with SMA lesion may exhibit which of the following during bimanual tasks?

• a) Improved coordination

• b) Apraxia for learned bimanual sequences

• c) Enhanced reflexes only

• d) Loss of primary sensation

Explanation: SMA lesions impair planning and coordination of bimanual and sequential movements, causing apraxia for learned tasks. Reflexes and primary sensation are not the primary deficits. Correct answer: b). Rehabilitation focuses on externally cued retraining to bypass SMA.

Q9. Which neurotransmitter system in basal ganglia influences movement initiation that complements SMA function?

• a) Dopaminergic

• b) Cholinergic only

• c) GABAergic only

• d) Serotonergic only

Explanation: Dopaminergic input from the substantia nigra modulates basal ganglia output and facilitates movement initiation, interacting with SMA planning. Dopamine deficiency (Parkinson’s) causes impaired initiation and reduced anticipatory postural adjustments. Correct answer: a) Dopaminergic.

Q10. Lesion affecting the supplementary motor area bilaterally may cause:

• a) Difficulty initiating voluntary movements (akinetic mutism)

• b) Pure sensory loss

• c) Hyperreflexia only

• d) Visual agnosia

Explanation: Bilateral SMA damage can cause severe akinesia and reduced spontaneous movement, sometimes akinetic mutism, and impaired postural preparation. Sensory and visual functions are spared. Correct answer: a). Management may include dopaminergic and rehabilitative strategies.

Q11. Which cortical area is mainly responsible for execution of a precise voluntary finger movement?

• a) Primary motor cortex (M1)

• b) Supplementary motor area

• c) Occipital cortex

• d) Broca’s area

Explanation: Primary motor cortex (M1) contains the final corticospinal output neurons that execute fine, precise voluntary movements such as individual finger actions. SMA plans and primes posture; M1 performs the actual contraction. Correct answer: a) Primary motor cortex (M1).