hllj/quesmed huggingface dataset:
Which drug from the list below induces diuresis via opposing afferent arteriole vasoconstriction leading to a raised GFR?

Options:
explanation: This is incorrect. Acetazolamide is a carbonic anhydrase inhibitor which works by preventing the reabsorption of bicarbonate, Na+ and hence water.
name: Acetazolamide
label: e
answer: no
explanation: This is incorrect. Spironolactone is a potassium-sparing diuretic which works by inhibiting aldosterone and hence preventing Na+ reabsorption.
name: Spironolactone
label: d
answer: no
explanation: This is incorrect. Indapamide is a thiazide-like diuretic which works by inhibiting the Na+/Cl- cotransporter and hence reducing Na+ reabsorption in the distal convoluted tubule.
name: Indapamide
label: c
answer: no
explanation: Caffeine acts as a diuretic primarily by increasing the GFR and hence increasing urine output. It does this by preventing afferent arteriole vasoconstriction and so keeping the pressure across the glomerulus high. It also has a secondary mechanism by inhibiting Na+ reabsorption in the proximal convoluted tubule
name: Caffeine
label: a
answer: yes
explanation: This is incorrect. Furosemide is a loop diuretic which works by inhibiting the NKCC2 transporter in the loop of Henle.
name: Furosemide
label: b
answer: no

Correct answer: a
What is the mechanism through which furosemide can cause cardiac arrhythmias?

Options:
explanation: This is incorrect. Furosemide is a loop diuretic and so blocks the Na-K-Cl cotransporter (NKCC2) in the loop of Henle. This can lead to excess K+ loss in the urine, causing hypokalaemia. Hypokalaemia can disrupt the cardiac membrane potential resulting in arrhythmias.
name: Blocks Na+/Cl- cotransporter leading to hypernatraemia
label: d
answer: no
explanation: This is incorrect. Furosemide is a loop diuretic and so blocks the Na-K-Cl cotransporter (NKCC2) in the loop of Henle. This can lead to excess K+ loss in the urine, causing hypokalaemia. Hypokalaemia can disrupt the cardiac membrane potential resulting in arrhythmias.
name: Blocks Na+/Cl- cotransporter leading to hyponatraemia
label: c
answer: no
explanation: This is correct. Furosemide is a loop diuretic and so blocks the Na-K-Cl cotransporter (NKCC2) in the loop of Henle. This can lead to excess K+ loss in the urine, causing hypokalaemia. Hypokalaemia can disrupt the cardiac membrane potential resulting in arrhythmias.
name: Blocks NKCC2 leading to hypokalaemia
label: a
answer: yes
explanation: This is incorrect. Whilst furosemide does block NKCC2, this causes hypokalaemia, not hyperkalaemia. Blocking NKCC2 means less K+ is reabsorbed so more is lost in the urine, reducing serum K+ levels.
name: Blocks NKCC2 leading to hyperkalaemia
label: b
answer: no
explanation: This is incorrect. This describes the mechanism of action of spironolactone. Furosemide is a loop diuretic and so blocks the Na-K-Cl cotransporter (NKCC2) in the loop of Henle. This can lead to excess K+ loss in the urine, causing hypokalaemia. Hypokalaemia can disrupt the cardiac membrane potential resulting in arrhythmias.
name: Inhibits aldosterone leading to hyperkalaemia
label: e
answer: no

Correct answer: a
Which ion transporter in the nephron is inhibited by indapamide?

Options:
explanation: This is incorrect. AQP1 is not targeted by indapamide. Indapamide is a thiazide-like diuretic which works by inhibiting the Na+/Cl+ cotransporter, preventing Na+ reabsorption and hence increasing Na+ and water excretion.
name: AQP1
label: d
answer: no
explanation: This is incorrect. NKCC2 is the transporter targeted by loop diuretics such as furosemide. Indapamide is a thiazide-like diuretic which works by inhibiting the Na+/Cl+ cotransporter, preventing Na+ reabsorption and hence increasing Na+ and water excretion.
name: NKCC2
label: b
answer: no
explanation: This is correct. Indapamide is a thiazide-like diuretic which works by inhibiting the Na+/Cl+ cotransporter, preventing Na+ reabsorption and hence increasing Na+ and water excretion.
name: Na+/Cl- cotransporter
label: a
answer: yes
explanation: This is incorrect. SGLT2 is the transporter targeted by drugs such as canagliflozin. Indapamide is a thiazide-like diuretic which works by inhibiting the Na+/Cl+ cotransporter, preventing Na+ reabsorption and hence increasing Na+ and water excretion.
name: SGLT2
label: c
answer: no
explanation: his is incorrect. The Na+/H+ exchanger is not targeted by indapamide. Indapamide is a thiazide-like diuretic which works by inhibiting the Na+/Cl+ cotransporter, preventing Na+ reabsorption and hence increasing Na+ and water excretion.
name: Na+/H+ exchanger
label: e
answer: no

Correct answer: a
Which of the following correctly identifies the site of synthesis, release, and action of ADH?

Options:
explanation: This is incorrect. Antidiuretic hormone (ADH) is a hormone that is synthesised in the hypothalamus but secreted from the posterior pituitary gland. It travels to the kidney where it acts at the collecting duct of the nephron. Here, it increases the insertion of AQP2 channels to promote water reabsorption from the urinary filtrate.
name: Posterior pituitary gland, hypothalamus, collecting duct of the nephron
label: c
answer: no
explanation: This is incorrect. Antidiuretic hormone (ADH) is a hormone that is synthesised in the hypothalamus but secreted from the posterior pituitary gland. It travels to the kidney where it acts at the collecting duct of the nephron. Here, it increases the insertion of AQP2 channels to promote water reabsorption from the urinary filtrate.
name: Hypothalamus, anterior pituitary gland, distal convoluted tubule of the nephron
label: d
answer: no
explanation: This is correct. Antidiuretic hormone (ADH) is a hormone that is synthesised in the hypothalamus but secreted from the posterior pituitary gland. It travels to the kidney where it acts at the collecting duct of the nephron. Here, it increases the insertion of AQP2 channels to promote water reabsorption from the urinary filtrate.
name: Hypothalamus, posterior pituitary gland, collecting duct of the nephron
label: a
answer: yes
explanation: This is incorrect. Antidiuretic hormone (ADH) is a hormone that is synthesised in the hypothalamus but secreted from the posterior pituitary gland. It travels to the kidney where it acts at the collecting duct of the nephron. Here, it increases the insertion of AQP2 channels to promote water reabsorption from the urinary filtrate.
name: Posterior pituitary gland, hypothalamus, distal convoluted tubule of the nephron
label: e
answer: no
explanation: This is incorrect. Antidiuretic hormone (ADH) is a hormone that is synthesised in the hypothalamus but secreted from the posterior pituitary gland. It travels to the kidney where it acts at the collecting duct of the nephron. Here, it increases the insertion of AQP2 channels to promote water reabsorption from the urinary filtrate.
name: Hypothalamus, anterior pituitary gland, collecting duct of the nephron
label: b
answer: no

Correct answer: a
Which of the following correctly describes the pathophysiology of nephrogenic diabetes insipidus?

Options:
explanation: This is incorrect. This describes Conn's syndrome whereby a loss of aldosterone release suppression leads to abnormally high levels of aldosterone and hence increased sodium (and water) reabsorption. Nephrogenic diabetes insipidus is a form of diabetes insipidus whereby the kidney loses its sensitivity to ADH. This means ADH no longer exerts its function to reabsorb water leading to inappropriately high levels of water loss in the urine.
name: An inability to suppress aldosterone release
label: d
answer: no
explanation: This incorrect. Nephrogenic diabetes insipidus does not affect aldosterone. Nephrogenic diabetes insipidus is a form of diabetes insipidus whereby the kidney loses its sensitivity to ADH. This means ADH no longer exerts its function to reabsorb water leading to inappropriately high levels of water loss in the urine.
name: A loss of aldosterone release
label: e
answer: no
explanation: This is incorrect. This describes the pathophysiology of SIADH whereby the loss of ADH release suppression leads to inappropriately high levels of ADH causing excess water reabsorption. Nephrogenic diabetes insipidus is a form of diabetes insipidus whereby the kidney loses its sensitivity to ADH. This means ADH no longer exerts its function to reabsorb water leading to inappropriately high levels of water loss in the urine.
name: An inability to suppress ADH release
label: c
answer: no
explanation: This is correct. Nephrogenic diabetes insipidus is a form of diabetes insipidus whereby the kidney loses its sensitivity to ADH. This means ADH no longer exerts its function to reabsorb water leading to inappropriately high levels of water loss in the urine.
name: Loss of sensitivity of the kidneys to ADH
label: a
answer: yes
explanation: This is incorrect. This describes central diabetes insipidus whereby there is defective ADH secretion from the posterior pituitary. Nephrogenic diabetes insipidus is a form of diabetes insipidus whereby the kidney loses its sensitivity to ADH. This means ADH no longer exerts its function to reabsorb water leading to inappropriately high levels of water loss in the urine.
name: Loss of ADH secretion from the posterior pituitary
label: b
answer: no

Correct answer: a
Which part of the nephron is primarily responsible for detecting changes in Na+ concentration as part of tubuloglomerular feedback?

Options:
explanation: This is incorrect. Tubuloglomerular feedback is the mechanism by which the nephron alters the GFR according to changing Na+ concentration. A high Na+ concentration is detected by the macula densa in the distal convoluted tubule which stimulates the release of adenosine. This results in afferent arterial constriction to drop the GFR.
name: Bowman's capsule
label: e
answer: no
explanation: This is incorrect. Tubuloglomerular feedback is the mechanism by which the nephron alters the GFR according to changing Na+ concentration. A high Na+ concentration is detected by the macula densa in the distal convoluted tubule which stimulates the release of adenosine. This results in afferent arterial constriction to drop the GFR.
name: Collecting duct
label: c
answer: no
explanation: This is correct. Tubuloglomerular feedback is the mechanism by which the nephron alters the GFR according to changing Na+ concentration. A high Na+ concentration is detected by the macula densa in the distal convoluted tubule which stimulates the release of adenosine. This results in afferent arterial constriction to drop the GFR.
name: Distal convoluted tubule
label: a
answer: yes
explanation: This is incorrect. Tubuloglomerular feedback is the mechanism by which the nephron alters the GFR according to changing Na+ concentration. A high Na+ concentration is detected by the macula densa in the distal convoluted tubule which stimulates the release of adenosine. This results in afferent arterial constriction to drop the GFR.
name: Glomerulus
label: d
answer: no
explanation: This is incorrect. Tubuloglomerular feedback is the mechanism by which the nephron alters the GFR according to changing Na+ concentration. A high Na+ concentration is detected by the macula densa in the distal convoluted tubule which stimulates the release of adenosine. This results in afferent arterial constriction to drop the GFR.
name: Proximal convoluted tubule
label: b
answer: no

Correct answer: a
Which of the following is an intrinsic cause of an acute kidney injury (AKI)?

Options:
explanation: This is incorrect. AKI causes can be split into pre-renal, renal (or intrinsic), and post-renal. A pre-renal AKI is caused by reduced blood flow to the kidney. A renal/intrinsic AKI is caused by direct damage to the nephron. A post-renal AKI is caused by an obstruction in the urinary tract distal to the kidney. Dehydration is therefore an example of a pre-renal AKI cause as it results in reduced blood flow to the kidney. The only renal cause on the list was glomerulonephritis.
name: Dehydration
label: c
answer: no
explanation: This is incorrect. AKI causes can be split into pre-renal, renal (or intrinsic), and post-renal. A pre-renal AKI is caused by reduced blood flow to the kidney. A renal/intrinsic AKI is caused by direct damage to the nephron. A post-renal AKI is caused by an obstruction in the urinary tract distal to the kidney. Renal artery stenosis is therefore an example of a pre-renal AKI cause as it results in reduced blood flow to the kidney. The only renal cause on the list was glomerulonephritis.
name: Renal artery stenosis
label: b
answer: no
explanation: This is correct. AKI causes can be split into pre-renal, renal (or intrinsic), and post-renal. A pre-renal AKI is caused by reduced blood flow to the kidney. A renal/intrinsic AKI is caused by direct damage to the nephron. A post-renal AKI is caused by an obstruction in the urinary tract distal to the kidney. The only renal cause on the list was glomerulonephritis.
name: Glomerulonephritis
label: a
answer: yes
explanation: This is incorrect. AKI causes can be split into pre-renal, renal (or intrinsic), and post-renal. A pre-renal AKI is caused by reduced blood flow to the kidney. A renal/intrinsic AKI is caused by direct damage to the nephron. A post-renal AKI is caused by an obstruction in the urinary tract distal to the kidney. Benign prostatic hypertrophy is therefore an example of a post-renal AKI cause as it obstructs the urinary tract such that fluid backs up to the kidney, causing damage. The only renal cause on the list was glomerulonephritis.
name: Benign prostatic hypertrophy
label: e
answer: no
explanation: This is incorrect. AKI causes can be split into pre-renal, renal (or intrinsic), and post-renal. A pre-renal AKI is caused by reduced blood flow to the kidney. A renal/intrinsic AKI is caused by direct damage to the nephron. A post-renal AKI is caused by an obstruction in the urinary tract distal to the kidney. A renal calculus is therefore an example of a post-renal AKI cause as it obstructs the urinary tract such that fluid backs up to the kidney, causing damage. The only renal cause on the list was glomerulonephritis.
name: Renal calculus
label: d
answer: no

Correct answer: a
James, a 76-year-old gentleman, is seen at the GP surgery for a routine blood test to monitor the progression of his CKD. His eGFR was found to be 27 mL/min/1.73 m².

What stage of CKD does James have?

Options:
explanation: This is incorrect. The eGFR is used to classify patients with CKD according to their severity. Stage 4 CKD is defined as an eGFR of between 15-29 mL/min/1.73 m² and hence James would belong to this category.
name: 5
label: e
answer: no
explanation: This is correct. The eGFR is used to classify patients with CKD according to their severity. Stage 4 CKD is defined as an eGFR of between 15-29 mL/min/1.73 m² and hence James would belong to this category.
name: 4
label: a
answer: yes
explanation: This is incorrect. The eGFR is used to classify patients with CKD according to their severity. Stage 4 CKD is defined as an eGFR of between 15-29 mL/min/1.73 m² and hence James would belong to this category.
name: 1
label: b
answer: no
explanation: This is incorrect. The eGFR is used to classify patients with CKD according to their severity. Stage 4 CKD is defined as an eGFR of between 15-29 mL/min/1.73 m² and hence James would belong to this category.
name: 2
label: c
answer: no
explanation: This is incorrect. The eGFR is used to classify patients with CKD according to their severity. Stage 4 CKD is defined as an eGFR of between 15-29 mL/min/1.73 m² and hence James would belong to this category.
name: 3
label: d
answer: no

Correct answer: a
A patient suffering from an anxiety attack begins hyperventilating.

Given the likely acid-base disturbance caused by this hyperventilation, how will the kidney respond with respect to bicarbonate reabsorption in the nephron?

Options:
explanation: This is incorrect. Hyperventilation typically results in respiratory alkalosis due to blowing off excess CO2. To compensate, the kidney will reduce the reabsorption of bicarbonate so that there is a lower plasma bicarbonate to buffer the H+ ions, bringing the pH back down. Bicarbonate is primarily reabsorbed at the proximal convoluted tubule.
name: There will be no effect on bicarbonate reabsorption
label: e
answer: no
explanation: This is incorrect. Whilst bicarbonate is primarily reabsorbed through the proximal convoluted tubule, in this case, bicarbonate reabsorption will decrease. Hyperventilation typically results in respiratory alkalosis due to blowing off excess CO2. To compensate, the kidney will reduce the reabsorption of bicarbonate so that there is a lower plasma bicarbonate to buffer the H+ ions, bringing the pH back down.
name: Bicarbonate reabsorption, primarily through the proximal convoluted tubule, will increase
label: b
answer: no
explanation: This is correct. Hyperventilation typically results in respiratory alkalosis due to blowing off excess CO2. To compensate, the kidney will reduce the reabsorption of bicarbonate so that there is a lower plasma bicarbonate to buffer the H+ ions, bringing the pH back down. Bicarbonate is primarily reabsorbed at the proximal convoluted tubule.
name: Bicarbonate reabsorption, primarily through the proximal convoluted tubule, will decrease
label: a
answer: yes
explanation: This is incorrect. Hyperventilation typically results in respiratory alkalosis due to blowing off excess CO2. To compensate, the kidney will reduce the reabsorption of bicarbonate so that there is a lower plasma bicarbonate to buffer the H+ ions, bringing the pH back down. Bicarbonate is primarily reabsorbed at the proximal convoluted tubule.
name: Bicarbonate reabsorption, primarily through the distal convoluted tubule, will increase
label: d
answer: no
explanation: This is incorrect. Whilst bicarbonate reabsorption will decrease to bring the pH down, bicarbonate is primarily reabsorbed at the proximal convoluted tubule, not the distal convoluted tubule.
name: Bicarbonate reabsorption, primarily through the distal convoluted tubule, will decrease
label: c
answer: no

Correct answer: a
Which of the following medications is the only one which does not target the renin-angiotensin-aldosterone system (RAAS)?

Options:
explanation: This is incorrect. Candesartan is an angiotensin receptor blocker (ARB) and works by inhibiting the interaction of angiotensin with its receptor. It therefore has a direct effect on RAAS.
name: Candesartan
label: c
answer: no
explanation: This is incorrect. Spironolactone is a potassium-sparing diuretic that works by inhibiting the action of aldosterone. It therefore has a direct effect on RAAS.
name: Spironolactone
label: d
answer: no
explanation: This is incorrect. Ramipril is an angiotensin-converting enzyme (ACE) inhibitor and works by reducing angiotensin II production. It therefore has a direct effect on RAAS.
name: Ramipril
label: b
answer: no
explanation: This is correct. Indapamide is a thiazide-like diuretic and so inhibits the Na+/Cl- cotransporter in the distal convoluted tubule. This does not involve RAAS.
name: Indapamide
label: a
answer: yes
explanation: This is incorrect. Aliskiren is a drug used for hypertension that works by inhibiting renin and hence reducing the production of angiotensin and aldosterone. It therefore has a direct effect on RAAS.
name: Aliskiren
label: e
answer: no

Correct answer: a
Which of the following is correct regarding the action of atrial natriuretic peptide (ANP)?

Options:
explanation: This is incorrect. Whilst the actions of ANP were correctly described, ANP is released from the atria, not the ventricles.
name: Increased venous return stimulates ANP release from the ventricles. This travels to the kidney to increase the GFR and reduce Na+ reabsorption
label: e
answer: no
explanation: This is incorrect. ANP is released to increase Na+ excretion from the kidney. This is done by increasing the GFR, not decreasing it.
name: Increased venous return stimulates ANP release from the atria. This travels to the kidney to decrease the GFR and reduce Na+ reabsorption
label: b
answer: no
explanation: This is incorrect. ANP is released to increase Na+ excretion from the kidney. This is done via decreasing Na+ reabsorption, not increasing it.
name: Increased venous return stimulates ANP release from the atria. This travels to the kidney to increase the GFR and increase Na+ reabsorption
label: c
answer: no
explanation: This is correct. When the circulating volume is high, the elevated venous return results in increased atrial filling which stimulates ANP release. ANP then acts on the kidney to increase Na+ excretion. This is done by increasing the GFR and reducing Na+ reabsorption.
name: Increased venous return stimulates ANP release from the atria. This travels to the kidney to increase the GFR and reduce Na+ reabsorption
label: a
answer: yes
explanation: This is incorrect. ANP is released to increase Na+ excretion from the kidney. This is done by increasing the GFR and decreasing Na+ reabsorption.
name: Increased venous return stimulates ANP release from the atria. This travels to the kidney to decrease the GFR and increase Na+ reabsorption
label: d
answer: no

Correct answer: a
Which of the following is correct regarding oxybutinin?

Options:
explanation: This is incorrect. Whilst oxybutinin is used in overactive bladder by reducing the parasympathetic activity on the bladder wall, this is achieved via its anti-muscarinic properties, not muscarinic agonism. Since parasympathetic innervation stimulates bladder wall contractility, oxybutynin aims to antagonise this process to treat an overactive bladder.
name: It is a muscarinic agonist used to treat overactive bladder by reducing the parasympathetic activity on the bladder wall
label: e
answer: no
explanation: This is correct. Oxybutinin is an anti-muscarinic medication that works by reducing the parasympathetic activation of the bladder wall. This reduces bladder wall contractility and hence helps to treat an overactive bladder.
name: It is an anti-muscarinic used to treat overactive bladder by reducing the parasympathetic activity on the bladder wall
label: a
answer: yes
explanation: This is incorrect. Whilst oxybutinin does work by reducing parasympathetic activity on the bladder wall, it is used to treat overactive bladder, not overflow incontinence. Reducing parasympathetic activity helps to reduce the bladder wall contractility and hence helps in urge incontinence (a.k.a. an overactive bladder)
name: It is an anti-muscarinic used to treat overflow incontinence by reducing the parasympathetic activity on the bladder wall
label: d
answer: no
explanation: This is incorrect. Oxybutinin is an anti-muscarinic medication that works by reducing the parasympathetic activation of the bladder wall. This reduces bladder wall contractility and hence helps to treat an overactive bladder.
name: It is an anti-muscarinic used to treat overflow incontinence by reducing the sympathetic activity on the bladder wall
label: c
answer: no
explanation: This is incorrect. Whilst oxybutinin is an anti-muscarinic used in overactive bladder, it does this via reducing parasympathetic, not sympathetic activity. Parasympathetic innervation is responsible for bladder wall contraction and hence this needs to be targeted in overactive bladder.
name: It is an anti-muscarinic used to treat overactive bladder by reducing the sympathetic activity on the bladder wall
label: b
answer: no

Correct answer: a