hllj/quesmed huggingface dataset:
A 47 year old man with a BMI of 36 presents to the Emergency Department with severe right upper quadrant pain, yellowing of the skin, pale stools and dark urine.

An ultrasound scan reveals a gallstone in the common bile duct (CBD).

Which of the following biliary ducts join to form the CBD?

Options:
explanation: This is incorrect. The CBD forms after the cystic duct joins the common hepatic duct, not the right hepatic duct.
name: Cystic duct and right hepatic duct
label: e
answer: no
explanation: This is correct. The CBD is formed by the union of the cystic duct and common hepatic duct. It then joins with the pancreatic duct to form the hepatopancreatic ampulla of vater.
name: Cystic duct and common hepatic duct
label: a
answer: yes
explanation: This is incorrect. The common hepatic duct is formed by the union of the left and right hepatic ducts.
name: Left and right hepatic ducts
label: d
answer: no
explanation: This is incorrect. The CBD forms after the cystic duct joins the common hepatic duct, not the left hepatic duct.
name: Cystic duct and left hepatic duct
label: c
answer: no
explanation: This is incorrect. The common hepatic duct joins with the cystic duct, not the pancreatic duct.
name: Common hepatic duct and pancreatic duct
label: b
answer: no

Correct answer: a
A 78 year old woman is brought to the emergency department with bradycardia. She is given a dose of atropine.

Which of the following best describes the effect of atropine on salivary secretion and blood flow?

Options:
explanation: This is correct. Saliva is formed from parasympathetic stimulation from the chorda lingual nerve. Atropine blocks the muscarinic receptors in the salivary glands resulting in reduced saliva production. It does not affect blood flow.
name: Reduces secretions, no effect on blood flow
label: a
answer: yes
explanation: This is incorrect. Atropine blocks the muscarinic receptors in the salivary glands resulting in reduced saliva production. It does not affect blood flow.
name: No effect on secretions, reduces blood flow
label: e
answer: no
explanation: This is incorrect. Atropine blocks the muscarinic receptors in the salivary glands resulting in reduced saliva production. It does not affect blood flow.
name: Increases secretions and reduces blood flow
label: d
answer: no
explanation: This is incorrect. Atropine blocks the muscarinic receptors in the salivary glands resulting in reduced saliva production. It does not affect blood flow.
name: No effect on secretions or blood flow
label: b
answer: no
explanation: This is incorrect. Atropine blocks the muscarinic receptors in the salivary glands resulting in reduced saliva production. It does not affect blood flow.
name: Reduces secretions and reduces blood flow
label: c
answer: no

Correct answer: a
A 62 year old with a body weight of 82kg is given 400mg of a drug intravenously. After reaching equilibrium, the plasma concentration is 15mg/L.


What is the apparent volume of distribution (Vd), rounded to the nearest whole number?

Options:
explanation: This is incorrect. Vd can be calculated with the following formula:

Vd = Dose / Concentration

In this case, the dose is 400mg and the concentration is 15mg/L.

400/15 = 26.67L
name: 40L
label: d
answer: no
explanation: This is incorrect. Vd can be calculated with the following formula:

Vd = Dose / Concentration

In this case, the dose is 400mg and the concentration is 15mg/L.

400/15 = 26.67L
name: 35L
label: b
answer: no
explanation: This is correct. Vd can be calculated with the following formula:

Vd = Dose / Concentration

In this case, the dose is 400mg and the concentration is 15mg/L.

400/15 = 26.67L
name: 27L
label: a
answer: yes
explanation: This is incorrect. Vd can be calculated with the following formula:

Vd = Dose / Concentration

In this case, the dose is 400mg and the concentration is 15mg/L.

400/15 = 26.67L
name: 30L
label: c
answer: no
explanation: This is incorrect. Vd can be calculated with the following formula:

Vd = Dose / Concentration

In this case, the dose is 400mg and the concentration is 15mg/L.

400/15 = 26.67L
name: 20L
label: e
answer: no

Correct answer: a
A 45 year old male with a history of chronic kidney disease is admitted to the medical ward with deranged electrolyte levels. He is keen to learn more about the role of the kidney in regulating these electrolytes.

In the thick ascending limb of the loop of Henle, which of the following channels is responsible for the transport of sodium from the cell into the interstitium?

Options:
explanation: This is correct. The Na+/K+ ATPase actively pumps 3 Na+ ions out of the cell and 2 K+ ions into the cell. The other channels listed are involved in other aspects of ion transport in the nephron but do not transport sodium into the interstitium from the thick ascending limb.
name: Na+/K+ ATPase
label: a
answer: yes
explanation: This is incorrect. These are ATP-dependent potassium channels that move potassium out of cells. They are involved in potassium recycling in the thick ascending limb and potassium secretion in the collecting duct. They do not transport sodium from the cell into the interstitium.
name: Renal outer medullary potassium (ROMK) channels
label: e
answer: no
explanation: This is incorrect. Chloride channels are important for stabilisation of cell membrane potential but do not transport sodium.
name: Chloride (Cl-) channels
label: d
answer: no
explanation: This is incorrect. These channels facilitate the movement of water across cell membranes. They do not transport sodium.
name: Aquaporin-1 (AQP-1) channels
label: b
answer: no
explanation: This is incorrect. These channels are located on the apical membrane of epithelial cells and facilitate the reabsorption of sodium ions across the apical membrane of epithelial cells in the distal nephron.
name: Epithelial Na+ (eNaC) channels
label: c
answer: no

Correct answer: a
A 60 year old patient with a history treatment-resistant of hypertension is reviewed in a cardiology clinic. The cardiologist explains the role of Nitric Oxide (NO) in regulating blood pressure and mentions that NO causes vasodilation by reducing intracellular calcium.

By which of the following mechanisms does NO reduce intracellular calcium?

Options:
explanation: This is incorrect. NO does not inhibit the action of calmodulin. Its primary mechanism of action is through the activation of guanylate cyclase and the subsequent increase in cGMP.
name: NO inhibits the action of the calcium-binding protein calmodulin, thereby reducing intracellular calcium levels
label: e
answer: no
explanation: This is incorrect. NO does not directly bind to calcium ions. Its primary mechanism of action is through the activation of guanylate cyclase and the subsequent increase in cGMP.
name: NO directly binds to calcium ions, neutralizing them and preventing them from contributing to cellular processes
label: b
answer: no
explanation: This is correct. Nitric oxide activates guanylate cyclase, which converts GTP to cGMP. Increased cGMP then activates protein kinase G (PKG), which acts to lower intracellular calcium through various mechanisms.
name: NO activates guanylate cyclase, which converts GTP to cGMP
label: a
answer: yes
explanation: This is incorrect. NO does not increase the activity of the Na+/K+ ATPase pump. Its primary mechanism of action is through the activation of guanylate cyclase and the subsequent increase in cGMP.
name: NO increases the activity of the Na+/K+ ATPase pump, indirectly leading to a decrease in intracellular calcium
label: d
answer: no
explanation: This is incorrect. NO does not block calcium release from the endoplasmic reticulum. NO does not directly bind to calcium ions. Its primary mechanism of action is through the activation of guanylate cyclase and the subsequent increase in cGMP.
name: NO blocks the release of calcium from the endoplasmic reticulum, thus reducing the amount of calcium available in the cell
label: c
answer: no

Correct answer: a
John, a 48-year-old gentleman, presents to the GP with a headache. As part of a routine check-up, a patient's blood pressure is recorded as 137/95 mmHg. Calculate the patient's mean arterial blood pressure.



Options:
explanation: This answer is closer to the systolic blood pressure than the diastolic blood pressure. Since we spend more time in diastole than systole, this must be reflected in the mean arterial blood pressure calculation by weighting the diastolic blood pressure more heavily. We must therefore add a third of the pulse pressure to the diastolic pressure (rather than taking a third away from the systolic pressure) in order to give an accurate average of the arterial blood pressure.
name: 123 mmHg
label: e
answer: no
explanation: The equation to calculate mean arterial blood pressure is (systolic blood pressure - diastolic blood pressure)/3 + diastolic blood pressure. In this case, we therefore do (137-95)/3 + 95 = 109.
name: 109 mmHg
label: a
answer: yes
explanation: This is just halfway between the systolic and diastolic blood pressure. Since we spend more time in diastole than systole, this must be reflected in the mean arterial blood pressure calculation by weighting the diastolic blood pressure more heavily. We must therefore add a third of the pulse pressure (not a half) to the diastolic pressure to give an accurate average of the arterial blood pressure.
name: 116 mmHg
label: b
answer: no
explanation: This is just the systolic blood pressure. In order to average the mean arterial blood pressure, we must also include the diastolic blood pressure. This is done by first, subtracting systolic - diastolic blood pressure, secondly, dividing by 3, and thirdly adding the diastolic blood pressure - (137-95)/3 + 95 = 109.
name: 137 mmHg
label: c
answer: no
explanation: This is just the diastolic blood pressure. In order to average the mean arterial blood pressure, we must also include the systolic blood pressure. This is done by first, subtracting systolic - diastolic blood pressure, secondly, dividing by 3, and thirdly adding the diastolic blood pressure - (137-95)/3 + 95 = 109.
name: 95 mmHg
label: d
answer: no

Correct answer: a
What is the mechanism through which vagus nerve activation decreases the heart rate?

Options:
explanation: This answer was incorrect as increasing sodium influx would speed up depolarisation and so increase the heart rate.
name: Vagal activation increases sodium influx into the sinoatrial node cells
label: c
answer: no
explanation: The pacemaker potential is the section of slow depolarisation between two action potentials. It occurs when the movement of sodium and calcium ions into the nerve cells exceeds the outward movement of potassium ions, causing an overall increase in voltage inside the cells. When the vagus nerve is activated, it increases potassium efflux from the sinoatrial node cells, slowing the pacemaker potential incline. This means it takes longer for the voltage to reach the threshold potential, increasing the length of time between action potentials and so, decreasing the heart rate.
name: Vagal activation increases potassium efflux from the sinoatrial node cells
label: a
answer: yes
explanation: This answer was incorrect as even though decreasing sodium influx would slow down depolarisation of the pacemaker potential, the vagus nerve does not affect sodium channels.
name: Vagal activation decreases sodium influx into the sinoatrial node cells
label: d
answer: no
explanation: This answer was incorrect as increasing calcium influx would speed up depolarisation of the sinoatrial node cells and so increase heart rate.
name: Vagal activation increases calcium influx into the sinoatrial node cells
label: e
answer: no
explanation: This answer was incorrect as decreasing potassium efflux would speed up depolarisation of the pacemaker potential and so increase the heart rate.
name: Vagal activation decreases potassium efflux from the sinoatrial node cells
label: b
answer: no

Correct answer: a
What is the mechanism through which raised levels of circulating adrenaline increase the heart rate?

Options:
explanation: The pacemaker potential is the section of slow depolarisation between two action potentials. It occurs when the movement of sodium and calcium ions into the nerve cells exceeds the outward movement of potassium ions, causing an overall increase in voltage inside the cells. Adrenaline binds to beta-1 receptors causing increased calcium influx, hence speeding up the depolarisation of the pacemaker potential. This reduces the time taken for the cell to reach threshold potential. It occurs through L-type calcium channels.
name: Adrenaline binds to beta-1 receptors causing increased calcium influx through L-type calcium channels into the sinoatrial node cells
label: a
answer: yes
explanation: The binding of adrenaline to Beta-1 receptors increases calcium influx, not efflux. Increasing the calcium efflux would slow down the depolarisation of the pacemaker potential, reducing the heart rate. Furthermore, the movement of calcium during the pacemaker potential is through L-type calcium channels, not T-type.
name: Adrenaline binds to beta-1 receptors causing increased calcium efflux through T-type calcium channels into the sinoatrial node cells
label: c
answer: no
explanation: Whilst adrenaline does indeed increase calcium influx, this is not done primarily via binding to beta-2 receptors. Beta-2 receptors are found mainly in vascular and bronchial smooth muscle. Whilst they are present in cardiac muscle, they are considerably less numerous and functionally important at that site than beta-1 receptors. Furthermore, the movement of calcium during the pacemaker potential is through L-type calcium channels, not T-type,
name: Adrenaline binds to beta-2 receptors causing increased calcium influx through T-type calcium channels into the sinoatrial node cells
label: d
answer: no
explanation: Whilst adrenaline does indeed increase calcium influx through L-type calcium channels, this is not done primarily via binding to beta-2 receptors. Beta-2 receptors are found mainly in vascular and bronchial smooth muscle. Whilst they are present in cardiac muscle, they are considerably less numerous and functionally important at that site than beta-1 receptors.
name: Adrenaline binds to beta-2 receptors causing increased calcium influx through L-type calcium channels into the sinoatrial node cells
label: b
answer: no
explanation: Whilst adrenaline does bind to beta-1 receptors, this does not affect potassium movement. Instead, adrenaline binding results in increased calcium influx into sinoatrial node cells, hence speeding up the depolarisation of the pacemaker potential, reducing the time taken for the cell to reach threshold potential. Furthermore, increasing potassium efflux would slow down the depolarisation of the pacemaker potential, reducing the heart rate.
name: Adrenaline binds to beta-1 receptors causing increased potassium efflux out of the sinoatrial node cells
label: e
answer: no

Correct answer: a
Which of the following is the correct explanation for the plateau phase of the ventricular myocyte action potential?

Options:
explanation: This is incorrect as once the cell has depolarised, potassium moves outward (not inward) to begin repolarisation. At that point, L-type calcium channels open causing calcium influx, which balances the potassium efflux to bring about the plateau phase.
name: Balanced calcium efflux and potassium influx
label: c
answer: no
explanation: This is incorrect as this unopposed potassium efflux describes the ion movement during repolarisation. This occurs briefly after depolarisation (during the partial rapid repolarisation phase) and after the plateau phase during terminal repolarisation. The plateau phase is caused by the balanced outward movement of potassium ions with the inward movement of calcium ions through L-type calcium channels.
name: Potassium efflux
label: e
answer: no
explanation: This is incorrect as once the cell has depolarised, sodium channels are deactivated so sodium influx stops. The plateau phase is caused by the balanced outward movement of potassium ions with the inward movement of calcium ions through L-type calcium channels.
name: Balanced sodium influx and potassium efflux
label: b
answer: no
explanation: Rapid depolarisation is first brought about by sodium influx. sodium channels are then inactivated and initial repolarisation begins to occur due to potassium efflux. At the same time, calcium influx occurs through L-type calcium channels. This potassium efflux and calcium influx are balanced, giving a plateau phase and prolonging the action potential. The L-type calcium channels are eventually inactivated, giving unopposed potassium efflux and hence repolarisation of the cell.
name: Balanced calcium influx and potassium efflux
label: a
answer: yes
explanation: This is incorrect as this describes the ion movement during the rapid depolarisation phase. Once the cell has depolarised, sodium channels are deactivated so sodium influx stops. The plateau phase is caused by the balanced outward movement of potassium ions with the inward movement of calcium ions through L-type calcium channels.
name: Sodium influx
label: d
answer: no

Correct answer: a
Which of the following is the correct sequence of events in left ventricular systole?

Options:
explanation: This is incorrect as isovolumetric contraction must occur before the aortic valve opens. If the aortic valve opened first, the pressure would still be higher in the aorta than the ventricle and so blood would pass back down from the aorta into the left ventricle. Instead, isovolumetric contraction occurs first to raise the left ventricular pressure above that of the aorta to open the aortic valve.
name: Bicuspid valve closure, aortic valve opening, isovolumetric contraction, ventricular ejection
label: d
answer: no
explanation: This is the correct order of events. Initially, the left ventricle begins to contract, raising its pressure above that of the left atrium so that the bicuspid valve closes. There is then the period of isovolumetric contraction whereby the ventricular pressure rises rapidly. Once this exceeds the pressure in the aorta, the aortic valve opens and ventricular ejection occurs.
name: Bicuspid valve closure, isovolumetric contraction, aortic valve opening, ventricular ejection
label: a
answer: yes
explanation: This is incorrect as bicuspid valve closure must occur before isovolumetric contraction. Isovolumetric contraction is the period when both bicuspid and aortic valves are closed, such that the ventricle contracts, raising the pressure very rapidly. This allows the ventricular pressure to increase above that of the aorta so that the aortic valve can open. If isovolumetric contraction occurred before bicuspid valve closure, blood would be forced back up into the left atrium.
name: Isovolumetric contraction, bicuspid valve closure, aortic valve opening, ventricular ejection
label: c
answer: no
explanation: Although the order of events is correct, the question refers specifically to the left ventricle and so it is the bicuspid valve that initially closes, not the tricuspid valve.
name: Tricuspid valve closure, isovolumetric contraction, aortic valve opening, ventricular ejection
label: b
answer: no
explanation: This answer is incorrect for two reasons. Firstly, the question refers specifically to the left ventricle and so it is the bicuspid valve that initially closes, not the tricuspid valve. Secondly, it is isovolumetric contraction, not relaxation, that occurs in systole to raise the ventricular pressure.
name: Tricuspid valve closure, isovolumetric relaxation, aortic valve opening, ventricular ejection
label: e
answer: no

Correct answer: a
Which of the following statements is correct regarding excitation-contraction coupling in cardiomyocytes?

Options:
explanation: This is incorrect. The T-tubule system describes the invaginations of cell membranes deep into the centre of cardiomyocytes, allowing rapid transmission of the action potential. This, therefore, helps with the initial depolarization of the cell but is not the site of calcium release. calcium is released from the sarcoplasmic reticulum.
name: Calcium, released from the T-tubule system, binds to troponin-C, causing a conformation change and allowing actin and myosin to form cross-bridges, shortening the sarcomere
label: c
answer: no
explanation: This is incorrect. Whilst the sequence of events is otherwise correct, the process of myosin and actin filaments sliding past each other results in the shortening, not lengthening of the sarcomere. This is the basis of cardiomyocyte contraction.
name: Calcium, released from the sarcoplasmic reticulum, binds to troponin-C, causing a conformation change and allowing actin and myosin to form cross-bridges, lengthening the sarcomere
label: b
answer: no
explanation: This is incorrect. calcium binds to troponin-C, not troponin-I. Troponin-I is the inhibitory form, preventing actin-myosin cross-bridge formation.
name: Calcium, released from the sarcoplasmic reticulum, binds to troponin-I, causing a conformation change and allowing actin and myosin to form cross-bridges, lengthening the sarcomere
label: e
answer: no
explanation: This option is incorrect for two reasons. Firstly, the T-tubule system describes the invaginations of cell membranes deep into the centre of cardiomyocytes, allowing rapid transmission of the action potential. This, therefore, helps with the initial depolarization of the cell but is not the site of calcium release. calcium is released from the sarcoplasmic reticulum. Secondly, calcium binds to troponin-C, not troponin-I. Troponin-I is the inhibitory form, preventing actin-myosin cross-bridge formation.
name: Calcium, released from the T-tubule system, binds to troponin-I, causing a conformation change and allowing actin and myosin to form cross-bridges, shortening the sarcomere
label: d
answer: no
explanation: This is correct. Calcium is released from the sarcoplasmic reticulum during calcium-induced calcium release. This binds to troponin-C which causes a conformational change, moving troponin-C and exposing binding sites on the actin molecule. This allows myosin heads to bind. As the myosin and actin filaments slide past each other, the sarcomere is shortened.
name: Calcium, released from the sarcoplasmic reticulum, binds to troponin-C, causing a conformation change and allowing actin and myosin to form cross-bridges, shortening the sarcomere
label: a
answer: yes

Correct answer: a