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Pharmacology of Chronic Kidney Disease Questions 10 SBAs and 1 SAQ 1. Which section of the nephron does dapagliflozin act? D A B C E a. A b. B c. C d. D e. E 2. Which of the following best describes how trimethoprim affects the kidneys? a. Competitive inhibition of creatinine secretion from the bloodstream into the renal tubule, decreasing serum creatinine b. Non-competitive inhibition of creatinine secretion from the renal tubule into the bloodstream, decreasing serum creatinine c. Competitive inhibition of creatinine secretion from the bloodstream into the renal tubule, increasing serum creatinine d. Non-competitive inhibition of creatinine secretion from the bloodstream into the renal tubule, increasing serum creatinine e. Competitive inhibition of creatinine secretion from the renal tubule into the bloodstream, increasing serum creatinine3. Lily, a 67-year-old female, is diagnosed with acute diverticulitis. As part of her treatment, she receives gentamicin. Which of the following most accurately describes its action on the kidneys? a. It targets epithelial cells in the distal convoluted tubule, inhibiting protein synthesis in these cells, causing acute tubular necrosis b. It targets epithelial cells in the proximal convoluted tubule, inhibiting the sodium-glucose co-transporter 2, reducing glucose and sodium reabsorption c. It targets epithelial cells in the proximal convoluted tubule, inhibiting protein synthesis in these cells, causing acute tubular necrosis d. It targets epithelial cells in the distal convoluted tubule, inhibiting the sodium- glucose co-transporter 2, reducing glucose and sodium reabsorption e. It binds to the bacterial 30S ribosomal subunit, disturbing the translation of mRNA leading to the formation of dysfunctional proteins 4. How does aspirin reduce cardiovascular risk? a. It inhibits the COX-2 enzyme, preventing oxidation of arachidonic acid to produce prostaglandins, reducing inflammation b. It inhibits the COX-1 enzyme, preventing oxidation of arachidonic acid to produce prostaglandins, reducing inflammation c. It reduces the amount of atheroma deposits in your arteries and stops any further atheroma deposition d. It inhibits the generation of thromboxane A2, reducing platelet aggregation e. It increases the generation of thromboxane A2, reducing platelet aggregation 5. Which of the following statements most accurately represents how ACE inhibitors and ARBs affect renal vasculature? a. Dilates the afferent and efferent arterioles equally b. Dilates the afferent and constricts the efferent arteriole c. Constricts the afferent and dilates the efferent arteriole d. Dilates the afferent more than the efferent arteriole e. Dilates the efferent more than the afferent arteriole 6. Ted, a 58 year-old male, is diagnosed with chronic kidney disease caused by hypertension. Which of the following statements most accurately describes the mechanism of his CKD? a. Decreased glomerular pressure causing decreased GFR and increased eGFR b. Increased glomerular pressure causing increased GFR and increased eGFR c. Increased glomerular pressure causing decreased GFR and increased eGFR d. Increased glomerular pressure causing increased GFR and decreased eGFR e. Increased glomerular pressure causing decreased GFR and decreased eGFR 7. What is the mechanism by which ACE inhibitors cause hyperkalaemia? + a. Inhibits angiotensin I production → inhibits aldosterone → decreased K excretion b. Inhibits angiotensin II production → inhibits aldosterone → decreased K + excretion + c. Inhibits angiotensin I production → increased aldosterone → decreased K excretion d. Inhibits angiotensin II production → increased aldosterone → decreased K + excretion e. Inhibits angiotensin I production → inhibits aldosterone → increased K + excretion 8. Which of the following statements is true? a. ARBs inhibit the conversion of angiotensin I to angiotensin II b. CCBs inhibit vasodilation of peripheral vasculature c. Renin inhibits the conversion of angiotensinogen into angiotensin I d. ACE inhibitors act on the AT-1 receptors in the kidneys and the vasculature e. Dapagliflozin increases natriuresis 9. Which compounds do the kidneys secrete? a. EPO, renin, calcitriol b. EPO, ADH, calcitriol c. Renin, ADH, creatinine d. Renin, creatinine, calcitriol e. EPO, ADH, creatinine 10. Which of the following statements most accurately describes the difference between acute kidney injury (AKI) and chronic kidney disease (CKD)? a. AKI → slow deterioration, CKD → fast deterioration b. AKI → normal sized kidneys, CKD → small kidneys c. AKI → small kidneys, CKD → normal sized kidneys d. AKI and CKD → fast deterioration e. AKI → small kidneys, CKD → large kidneys 1 SAQ 11. Ranjit, a 72-year-old male, presents to the GP with a 6-month history of pruritus, peripheral oedema and muscle cramps. He has a 10-year history of hypertension, to which he has refused treatment for. You suspect chronic kidney disease. a. What investigations are you going to request? (3 marks) b. Your first-line management is ACE inhibitors or ARBs. Compare the similarities and differences between the mechanism of action of these drugs. (4 marks) c. Ranjit then contracts cystitis and is prescribed trimethoprim. Explain the mechanism by which this affects his eGFR. (3 marks)Answers 1. A – SGLT-2 inhibitors act on the renal epithelial cells in the PCT 2. C – Trimethoprim MOA: Competitive inhibition of creatinine secretion from the bloodstream into the renal tubule, increasing serum creatinine 3. C – Gentamicin: It targets epithelial cells in the proximal convoluted tubule, inhibiting protein synthesis in these cells, causing acute tubular necrosis E is not the answer because this describes it’s MOA on bacterial cells but the question was referring to its effect on kidneys. 4. D – Remember that the question is referring to how aspirin reduces cardiovascular risk, not it’s other mechanisms. a. It inhibits the COX-2 enzyme, preventing oxidation of arachidonic acid to produce prostaglandins, reducing inflammation → True but not involved in cardiovascular risk b. It inhibits the COX-1 enzyme, preventing oxidation of arachidonic acid to produce prostaglandins, reducing inflammation → False because COX-2 is the enzyme involved, COX-1 is involved in gastric mucosa protection. This would still be wrong because this mechanism is not involved in cardiovascular risk c. It reduces the amount of atheroma deposits in your arteries and stops any further atheroma deposition → Statins, not aspirin d. It inhibits the generation of thromboxane A2, reducing platelet aggregation e. It increases the generation of thromboxane A2, reducing platelet aggregation → inhibits/ decreases not increases 5. E – ACE inhibitors dilate the efferent more than the afferent arteriole6. D – Increased glomerular pressure causing increased GFR and decreased eGFR Remember that increased glomerular pressure always causes increased GFR, because this is very literally the rate of glomerular filtration. eGFR is a more accurate measure of kidney function because it takes into account serum creatinine, meaning it assesses how well the kidney is able to filter blood. eGFR is lowered because damage to the kidneys from chronic hypertension reduces their ability to excrete creatinine, causing increased serum creatinine. 7. B – ACE inhibitors MOA: Inhibits angiotensin II production → inhibits aldosterone → decreased K+ excretion, causing hyperkalaemia 8. E – a. ARBs inhibit the conversion of angiotensin I to angiotensin II → ACE inhibitors b. CCBs inhibit vasodilation of peripheral vasculature → Vasoconstriction c. Renin inhibits the conversion of angiotensinogen into angiotensin I → Causes d. ACE inhibitors act on the AT-1 receptors in the kidneys and the vasculature → ARBs e. Dapagliflozin increases natriuresis (Natriuresis meaning loss of sodium through the inhibition of sodium reabsorption from the urine into the bloodstream) 9. A – Kidneys secrete EPO, renin and calcitriol 10. B – AKI → normal sized kidneys, CKD → small kidneys AKI → fast deterioration, CKD → slow deterioration 11. a. What investigations are you going to request? (3 marks) i. Bloods → eGFR ii. Urine dipstick → For haematuria iii. Urine test → Albumin:creatinine ratio (ACR) for proteinuria b. Your first-line management is ACE inhibitors or ARBs. Compare the similarities and differences between the mechanism of action of these drugs. (4 marks) i. S: ACE inhibitors and ARBs both act on the renin-angiotensin- aldosterone system (RAAS)/ They both inhibit the production of angiotensin II (1) ii. S: They both lead to decreased blood pressure, both peripherally and in the glomerulus/ They both cause a preferential vasodilation of the efferent arteriole, compared to the afferent arteriole (1) iii. D: ACE inhibitors act on an enzyme (ACE), whereas ARBs act on the AT- 1 receptor on kidneys and vasculature/ The drug target of ACE inhibitors is an enzyme whereas that of ARBs is a receptor. (1) iv. D: ACE inhibitors decrease the amount of angiotensin II produced whereas ARBs do not affect the amount of angiotensin II produced (1) c. Ranjit then contracts cystitis and is prescribed trimethoprim. Explain the mechanism by which this affects his eGFR. (3 marks) i. Trimethoprim is a competitive inhibitor of creatinine secretion from the bloodstream into the renal tubule (1) ii. Increasing serum creatinine (1) iii. Decreasing his eGFR, but this does not signify a deterioration in kidney function (1)