hllj/quesmed huggingface dataset:
What effect will repetitive skeletal muscle contraction have on the end diastolic volume and stroke volume of the heart?

Options:
explanation: This is incorrect as skeletal muscle contraction squeezes the blood through the veins back to the heart, increasing venous return, and hence increasing the end diastolic volume. Due to Starling's law, this will also increase the stroke volume.
name: Decreased end diastolic volume and decreased systolic volume
label: c
answer: no
explanation: Skeletal muscle contraction squeezes the blood through the veins back to the heart, increasing venous return, and hence increasing the end diastolic volume. Due to Starling's law, an increased end diastolic volume will stretch the myocardium, resulting in a greater force of contraction and hence larger stroke volume.
name: Increased end diastolic volume and increased systolic volume
label: a
answer: yes
explanation: Whilst this will indeed result in an increased end diastolic volume, this answer is incorrect as the systolic volume should also increase. Due to Starling's law, an increased end diastolic volume will stretch the myocardium, resulting in a greater force of contraction and hence larger stroke volume.
name: Increased end diastolic volume but no change in systolic volume
label: b
answer: no
explanation: This answer is wrong for two reasons. Firstly, skeletal muscle contraction squeezes the blood through the veins back to the heart, increasing venous return, and hence increasing the end diastolic volume. Secondly, Startling's law states that an increased end diastolic volume will increase the systolic volume, and vice versa. Therefore, if the end diastolic volume were to decrease, it would also result in a decreased systolic volume. In this question, however, the correct answer was an increased end diastolic and systolic volume.
name: Decreased end diastolic volume and increased systolic volume
label: e
answer: no
explanation: This answer is incorrect. Whilst there is a limit to Starling's law whereby such a large increase in end diastolic volume will start to decrease ventricular contraction, this will not be reached by skeletal muscle contraction alone. Therefore, both the end diastolic and systolic volumes will be increased.
name: Increased end diastolic volume and decreased systolic volume
label: d
answer: no

Correct answer: a
Annie, a 28-year-old female, is started on flecainide in the acute medical ward for the treatment of paroxysmal supraventricular tachycardia.

What is the mechanism of action of flecainide?

Options:
explanation: This is the mechanism of action of Class II antiarrhythmics, such as metoprolol. Flecainide targets sodium channels rather than beta-1-adrenergic receptors.
name: Inhibits beta-1-adrenergic receptors
label: d
answer: no
explanation: This is the mechanism of action of adenosine which opens potassium channels, resulting in hyperpolarisation and an increased refractory period. Flecainide targets sodium channels rather than potassium channels.
name: Opens potassium channels
label: e
answer: no
explanation: This is the mechanism of action of Class III antiarrhythmics, such as amiodarone. Flecainide targets sodium channels rather than potassium channels.
name: Inhibit potassium channels
label: c
answer: no
explanation: Flecainide is a Class I anti-arrhythmic. These drugs inhibit the voltage-gated sodium channels, slowing the steep depolarisation section of the ventricular myocyte action potentials. This increases the refractory period so increases the time between action potentials.
name: Inhibits voltage-gated sodium channels
label: a
answer: yes
explanation: This is the mechanism of action of Class IV antiarrhythmics, such as verapamil. Flecainide targets sodium channels rather than calcium channels.
name: Inhibit L-type calcium channels
label: b
answer: no

Correct answer: a
What effect does adenosine have on potassium channels in cells in the sinoatrial node?

Options:
explanation: This is correct. Adenosine is an anti-arrhythmic which works by opening potassium channels on cells in the sinoatrial node. This causes hyperpolarisation of the cell, meaning it is further from the threshold potential, therefore lengthening the refractory period and slowing conduction through the node.
name: It opens potassium channels causing hyperpolarisation
label: a
answer: yes
explanation: This is incorrect. Adenosine is an anti-arrhythmic which works by opening potassium channels on cells in the sinoatrial node. This causes hyperpolarisation of the cell, meaning it is further from the threshold potential, therefore lengthening the refractory period and slowing conduction through the node.
name: It does not affect potassium channels
label: e
answer: no
explanation: This is incorrect. Adenosine is an anti-arrhythmic which works by opening potassium channels on cells in the sinoatrial node. This causes hyperpolarisation of the cell, meaning it is further from the threshold potential, therefore lengthening the refractory period and slowing conduction through the node.
name: It closes potassium channels causing depolarisation
label: d
answer: no
explanation: Whilst adenosine does cause hyperpolarisation of the sinoatrial node cells, this is done via opening, not closing, potassium channels. Since potassium moves from inside the cell to outside, opening more potassium channels would result in more outward movement and hence further lower the membrane potential of the cell.
name: It closes potassium channels causing hyperpolarisation
label: c
answer: no
explanation: Whilst adenosine does open potassium channels, this would result in hyperpolarisation, not depolarisation. Since potassium moves from inside the cell to outside, opening more potassium channels would result in more outward movement and hence further lower the membrane potential of the cell.
name: It opens potassium channels causing depolarisation
label: b
answer: no

Correct answer: a
Which of the following describes the Windkessel effect?

Options:
explanation: This is not the right option. This describes Poiseuille's law.
name: The resistance in a blood vessel is directly proportional to both the viscosity of blood and the length of the vessel, but inversely proportional to the radius of the vessel
label: c
answer: no
explanation: This is not the right option. This describes the Frank-Starling law.
name: Increasing the left ventricular end-diastolic volume will stretch the myocytes, increasing their contractility, and hence giving a larger stroke volume
label: b
answer: no
explanation: This is not the right option. This describes Ohm's law.
name: The flow through a blood vessel can be calculated by the pressure gradient divided by the vascular resistance
label: e
answer: no
explanation: This is not the right option. This describes the law of Laplace.
name: The wall stress on a blood vessel is directly proportional to the blood pressure and vessel radius, but inversely proportional to the vessel wall thickness
label: d
answer: no
explanation: This is correct. This effect is an essential function of the aorta. By stretching during systole and recoiling during diastole, the aorta maintains the pressure giving continuous flow despite rhythmic contractions of the heart.
name: The elastic wall of the aorta stretches during systole, allowing it to recoil during diastole to propel the blood forward and maintain blood pressure
label: a
answer: yes

Correct answer: a
Which of the following correctly describes when Korotkoff sounds can be heard during a manual blood pressure reading?

Options:
explanation: This is incorrect. When you initially pump the cuff to a pressure above the systolic blood pressure, no sounds are heard as the artery is fully occluded. Korotkoff sounds are only heard when the cuff pressure is between the systolic and diastolic blood pressure as this is the period of turbulent flow.
name: Korotkoff sounds are only heard when the cuff pressure is above the systolic pressure
label: b
answer: no
explanation: This is incorrect as this is when no sounds are heard. When you initially pump the cuff to a pressure above the systolic blood pressure, no sounds are heard as the artery is fully occluded. Once the cuff pressure is below the systolic but above the diastolic pressure, there is turbulent flow through the artery, giving the characteristic Korotkoff sounds (due to the impact of the blood onto the vessel wall causing vibrations). Once the cuff pressure is below the diastolic pressure, the artery returns to laminar flow so no sounds are heard.
name: Korotkoff sounds are only heard when the cuff pressure is either above the systolic pressure or below the diastolic pressure
label: d
answer: no
explanation: This is correct. When you initially pump the cuff to a pressure above the systolic blood pressure, no sounds are heard as the artery is fully occluded. Once the cuff pressure is below the systolic but above the diastolic pressure, there is turbulent flow through the artery, giving the characteristic Korotkoff sounds (due to the impact of the blood onto the vessel wall causing vibrations). Once the cuff pressure is below the diastolic pressure, the artery returns to laminar flow and so no sounds are heard.
name: Korotkoff sounds are only heard when the cuff pressure is between the systolic and diastolic pressure
label: a
answer: yes
explanation: This is incorrect. Once the cuff pressure is below the diastolic pressure, there is normal laminar flow through the artery so no sounds are heard. Korotkoff sounds are only heard when the cuff pressure is between the systolic and diastolic blood pressure as this is the period of turbulent flow.
name: Korotkoff sounds are only heard when the cuff pressure is below the diastolic pressure
label: c
answer: no
explanation: This is incorrect. When you initially pump the cuff to a pressure above the systolic blood pressure, no sounds are heard as the artery is fully occluded. Once the cuff pressure is below the systolic but above the diastolic pressure, there is turbulent flow through the artery, giving the characteristic Korotkoff sounds (due to the impact of the blood onto the vessel wall causing vibrations). Once the cuff pressure is below the diastolic pressure, the artery returns to laminar flow so no sounds are heard.
name: Korotkoff sounds can be heard throughout the entire process
label: e
answer: no

Correct answer: a
Which of the following results in vasodilation of blood vessels?

Options:
explanation: This is correct. Nitric oxide reduces the levels of Ca2+ in smooth muscle cells, causing relaxation and hence vasodilation.
name: Nitric oxide
label: a
answer: yes
explanation: This is incorrect. Cold temperature results in vasoconstriction to conserve body heat by reducing the volume of blood reaching the skin.
name: Cold temperature
label: e
answer: no
explanation: This is incorrect. Endothelins do the reverse of nitric oxide. They increase the level of Ca2+ in smooth muscle cells, causing them to contract, resulting in vasoconstriction
name: Endothelin
label: b
answer: no
explanation: This is incorrect. Sympathetic nervous system activation is part of the 'fight or flight' response and causes vasoconstriction via the action of the noradrenaline neurotransmitter.
name: Sympathetic nervous system activation
label: d
answer: no
explanation: This is incorrect. Angiotensin II is a vasoconstriction released as part of the renin-angiotensin-aldosterone system to increase blood pressure.
name: Angiotensin II
label: c
answer: no

Correct answer: a
Which of the following is the correct explanation for how sympathetic activation affects blood vessel tone?

Options:
explanation: This is incorrect. Sympathetic activation results in the release of noradrenaline. This binds to alpha-1 receptors on endothelial cells to cause vasoconstriction. Noradrenaline also binds to beta-2 receptors which results in vasodilation, however, the binding to beta-2 receptors is weaker than to alpha-1 receptors. The overall effect is therefore vasoconstriction in response to sympathetic activation.
name: Binding of noradrenaline from sympathetic fibres to alpha-1 receptors outweighs the binding to beta-2 receptors, resulting in vasodilation
label: b
answer: no
explanation: This is correct. Sympathetic activation results in the release of noradrenaline. This binds to alpha-1 receptors on endothelial cells to cause vasoconstriction. Noradrenaline also binds to beta-2 receptors which results in vasodilation, however, the binding to beta-2 receptors is weaker than to alpha-1 receptors. The overall effect is therefore vasoconstriction in response to sympathetic activation.
name: Binding of noradrenaline from sympathetic fibres to alpha-1 receptors outweighs the binding to beta-2 receptors, resulting in vasoconstriction
label: a
answer: yes
explanation: This is incorrect as it is the binding to alpha-1 receptors which causes vasoconstriction whereas binding to beta-2 receptors causes vasodilation. Hence, binding to alpha-1 must outweigh binding to beta-2 to give vasoconstriction overall.
name: Binding of noradrenaline from sympathetic fibres to beta-2 receptors outweighs the binding to alpha-1 receptors, resulting in vasoconstriction
label: c
answer: no
explanation: This is incorrect. Sympathetic activation results in the release of noradrenaline. This binds to alpha-1 receptors on endothelial cells to cause vasoconstriction. Noradrenaline also binds to beta-2 receptors which results in vasodilation, however, the binding to beta-2 receptors is weaker than to alpha-1 receptors. The overall effect is therefore vasoconstriction in response to sympathetic activation.
name: Binding of noradrenaline from sympathetic fibres to beta-2 receptors outweighs the binding to alpha-1 receptors, resulting in vasodilation
label: d
answer: no
explanation: This is incorrect as noradrenaline is the neurotransmitter released from sympathetic fibres, not acetylcholine.
name: Binding of acetylcholine from sympathetic fibres to alpha-1 receptors outweighs the binding to beta-2 receptors, resulting in vasoconstriction
label: e
answer: no

Correct answer: a
What is the mechanism of action of digoxin?

Options:
explanation: This is incorrect. This is the mechanism of action of phosphodiesterase inhibitors such as milrinone.
name: Inhibition of phosphodiesterase
label: b
answer: no
explanation: This is correct. Digoxin inhibits the Na+/K+ ATPase which prevents Na+ efflux from the cell, causing a rise in intracellular Na+. This lowers the Na+ gradient across the cell which makes the Na+/Ca2+ exchanger less effective, preventing Ca2+ efflux. This, therefore increases the Ca2+ levels in the cell, increasing contractility.
name: Inhibition of the Na+/K+ ATPase
label: a
answer: yes
explanation: This is incorrect. This is the mechanism of action of beta-blockers such as bisoprolol.
name: Inhibition of beta-adrenergic receptors
label: d
answer: no
explanation: This is incorrect. This is the mechanism of action of ivabradine.
name: Inhibition of the funny currents
label: c
answer: no
explanation: This is incorrect. This is the mechanism of action of angiotensin II receptor blockers (ARBs) such as losartan.
name: Inhibition of angiotensin II receptor
label: e
answer: no

Correct answer: a
Which of the following correctly describes the mechanism through which phosphodiesterase inhibitors act as inotropic drugs?

Options:
explanation: This is incorrect. Phosphodiesterase inhibitors work by preventing cAMP and cGMP degradation, increasing their intracellular levels. This in turn increases the release of Ca2+ from the sarcoplasmic reticulum, increasing the contractility of the muscle cell.
name: Through inhibiting phosphodiesterases, they increase Ca2+ clearance from the cell
label: e
answer: no
explanation: This is incorrect. Since phosphodiesterases degrade cAMP and cGMP, by inhibiting them, these drugs increase cAMP and cGMP levels. This then increases Ca2+ release from the sarcoplasmic reticulum.
name: Through inhibiting phosphodiesterases, they decrease the levels of cAMP and cGMP which increases Ca2+ release from the sarcoplasmic reticulum
label: b
answer: no
explanation: This is correct. Phosphodiesterases (PDEs) breakdown the secondary messengers cAMP and cGMP. Phosphodiesterase inhibitors therefore work by preventing cAMP and cGMP degredation, increasing their intracellular levels. This in turn increases the release of Ca2+ from the sarcoplasmic reticulum, increasing the contractility of the muscle cell.
name: Through inhibiting phosphodiesterases, they increase the levels of cAMP and cGMP which increases Ca2+ release from the sarcoplasmic reticulum
label: a
answer: yes
explanation: This is incorrect. Phosphodiesterase inhibitors work by preventing cAMP and cGMP degradation, increasing their intracellular levels. This in turn increases the release of Ca2+ from the sarcoplasmic reticulum, increasing the contractility of the muscle cell.
name: Through inhibiting phosphodiesterases, they decrease intracellular Na+ which reduces the Na+/Ca2+ exchanger activity, increasing intracellular Ca2+
label: d
answer: no
explanation: This is incorrect. This description is more similar to the mechanism of action of digoxin which blocks the Na+/K+ ATPase to increase intracellular Na+. Phosphodiesterase inhibitors work by preventing cAMP and cGMP degradation, increasing their intracellular levels. This in turn increases the release of Ca2+ from the sarcoplasmic reticulum, increasing the contractility of the muscle cell.
name: Through inhibiting phosphodiesterases, they increase intracellular Na+ which reduces the Na+/Ca2+ exchanger activity, increasing intracellular Ca2+
label: c
answer: no

Correct answer: a
Which of the following conditions would result in an increased level of adenosine in myocardial tissue?

Options:
explanation: This is correct. Adenosine in a vasodilator which increases blood flow to the heart. During times of increased metabolic activity, decreased blood flow, or decreased myocardial pO2, the heart requires a greater flow of blood and hence adenosine is released.
name: Increased myocyte metabolic activity
label: a
answer: yes
explanation: This is incorrect. Adenosine is a vasodilator and hence will be released when there is a drop in blood flow to the heart, not an increase.
name: Increased blood flow to the heart
label: b
answer: no
explanation: This is incorrect. Since adenosine causes vasodilation, it is produced when a greater flow of blood is needed to the heart. A drop in oxygenation of the myocardial tissue would be an example of this, as opposed to an increased oxygen partial pressure as suggested in the question.
name: Increased oxygen partial pressure in myocardial tissue
label: c
answer: no
explanation: This is incorrect. Since adenosine causes vasodilation, it is produced when a greater flow of blood is needed to the heart. An increase in myocardial oxygen demand would therefore be an example of this, not a decrease.
name: Decreased myocardial oxygen demand
label: d
answer: no
explanation: This is incorrect. Adenosine is a vasodilator and so will not be produced if the coronary arteries have already dilated.
name: Coronary artery dilation
label: e
answer: no

Correct answer: a
Which of the following is the primary function of countercurrent exchange in the cutaneous circulation?

Options:
explanation: This is correct. Countercurrent exchange is a mechanism to conserve heat. Heat from warm blood in arteries travelling towards to skin is transferred to veins travelling back towards the trunk. This maintains the trunk temperature while preventing heat loss from the skin.
name: Transfer heat from arteries to adjacent veins
label: a
answer: yes
explanation: This is incorrect. Countercurrent exchange helps with heat conservation, not oxygen transfer. Heat from warm blood in arteries travelling towards to skin is transferred to veins travelling back towards the trunk. This maintains the trunk temperature while preventing heat loss from the skin.
name: Transfer oxygen from arteries to adjacent veins
label: c
answer: no
explanation: This is incorrect. Countercurrent exchange helps with heat conservation, not blood pressure regulation. Heat from warm blood in arteries travelling towards to skin is transferred to veins travelling back towards the trunk. This maintains the trunk temperature while preventing heat loss from the skin.
name: Regulate blood pressure
label: e
answer: no
explanation: This is incorrect. Countercurrent exchange helps with heat conservation, not oxygen transfer. Heat from warm blood in arteries travelling towards to skin is transferred to veins travelling back towards the trunk. This maintains the trunk temperature while preventing heat loss from the skin.
name: Transfer oxygen from veins to adjacent arteries
label: d
answer: no
explanation: This is incorrect. In countercurrent exchange, heat from warm blood in arteries travelling towards to skin is transferred to veins travelling back towards the trunk. This maintains the trunk temperature while preventing heat loss from the skin.
name: Transfer heat from veins to adjacent arteries
label: b
answer: no

Correct answer: a
At the venous end of a capillary, the net movement of fluid is from the interstitium back into the capillary.

Which of the following is the predominant force driving this reabsorption?

Options:
explanation: This is incorrect. The capillary hydrostatic pressure is the force coming from the heart contraction which drives fluid out of the capillary. Along the course of the capillary, this force drops significantly due to resistance in the vessel, meaning it is very small by the venous end of the capillary. Furthermore, if this force was significant, it would push fluid out of the capillary, whereas the question asked for the force driving the reabsorption of fluid back into the capillary.
name: Capillary hydrostatic pressure
label: c
answer: no
explanation: Oncotic pressure is the osmotic force of large molecules, such as proteins, in a solution. The capillary oncotic pressure is therefore the force of large proteins within the capillary pulling fluid from the interstitium back into the capillary. At the arterial end of the capillary, the capillary hydrostatic force outweighs the capillary oncotic pressure, and hence fluid moves out into the interstitium. At the venous end of the capillary, however, the capillary hydrostatic force is much lower and hence the capillary oncotic pressure predominates, pulling fluid back from the interstitium into the capillary.
name: Capillary oncotic pressure
label: a
answer: yes
explanation: This is incorrect. Whilst this force does indeed aid in pushing fluid back into the capillary, it is insignificant in comparison to the size of the capillary oncotic pressure.
name: Tissue hydrostatic pressure
label: d
answer: no
explanation: This is incorrect. It is the capillary oncotic pressure which primarily drives fluid reabsorption back into the capillary at the venous end.
name: None of the above
label: e
answer: no
explanation: This is incorrect. The tissue oncotic pressure is essentially 0 in a healthy state as there shouldn't be any protein in the interstium. Furthermore, if this force was significant, it would pull fluid out of the capillary, whereas the question asked for the force driving the reabsorption of fluid back into the capillary.
name: Tissue oncotic pressure
label: b
answer: no

Correct answer: a