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Master YLL Pharmacology > Renal - Diuretics > Flashcards

Renal - Diuretics Flashcards

1
Q

What is the nephron?

A

The smallest functional unit in the kidney.

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2
Q

How many nephrons are in each kidney of a healthy adult?

A

Approximately 1.2-1.4 million.

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3
Q

List the structures of a nephron.

A

Bowman’s Capsule, Proximal Convoluted Tubule, Loop of Henle, Distal Convoluted Tubule, Collecting Tubules & Ducts.

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4
Q

What is the function of the nephron?

A

Filtering blood, reabsorbing substances, secreting waste, and regulating pH.

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5
Q

What does the glomerulus do?

A

Filters blood and allows small molecular weight substances into Bowman’s Capsule.

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6
Q

What substances does the proximal convoluted tubule reabsorb?

A

Water, Na+, Cl-, H+.

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7
Q

What is the primary function of the Loop of Henle?

A

Controls the concentration of urine.

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8
Q

How does the distal convoluted tubule contribute to urine formation?

A

By reabsorbing Na+ and Cl- but not water, making the filtrate more dilute.

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9
Q

What hormone increases water permeability in the collecting tubules?

A

Vasopressin (ADH).

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10
Q

How do diuretic drugs generally work?

A

By decreasing Na+ reabsorption, increasing Na+ in the tubule, leading to increased urine production.

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11
Q

Name the major classes of diuretic drugs.

A

Loop diuretics, Thiazide diuretics, Potassium-sparing diuretics, Osmotic diuretics, Carbonic anhydrase inhibitors.

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12
Q

What is the mechanism of action of loop diuretics?

A

Inhibit the Na+/K+/2Cl- cotransporter in the thick ascending limb of the Loop of Henle.

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13
Q

Give two examples of loop diuretics.

A

Furosemide, Bumetanide.

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14
Q

What are the clinical indications for loop diuretics?

A

Acute pulmonary/peripheral edema, hypertension in renal failure, acute hyperkalemia, acute hypercalcemia.

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15
Q

List three side effects of loop diuretics.

A

Hypovolemia, hypokalemia, hyperglycemia.

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16
Q

What are the contraindications for loop diuretics?

A

Severe hypovolemia, severe hyponatremia, hypersensitivity to sulfonamides, anuria.

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17
Q

What is the mechanism of action of thiazide diuretics?

A

Inhibit the Na+/Cl- symporter in the distal convoluted tubules.

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18
Q

Give two examples of thiazide diuretics.

A

Hydrochlorothiazide, Chlorthalidone.

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19
Q

What are the clinical indications for thiazide diuretics?

A

Hypertension, edema, nephrogenic diabetes insipidus.

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20
Q

List three side effects of thiazide diuretics.

A

Hypokalemia, hypercalcemia, hyperglycemia.

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21
Q

What are the contraindications for thiazide diuretics?

A

Hypersensitivity to sulfonamides, anuria.

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22
Q

What is the mechanism of action of potassium-sparing diuretics?

A

Inhibit epithelial Na+ channels or block aldosterone receptors in the collecting tubules.

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23
Q

Give two examples of potassium-sparing diuretics.

A

Spironolactone, Amiloride.

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24
Q

What are the clinical indications for potassium-sparing diuretics?

A

Heart failure, hypertension, primary hyperaldosteronism.

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25
Q

List two side effects of potassium-sparing diuretics.

A

Hyperkalemia, metabolic acidosis.

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26
Q

What are the contraindications for potassium-sparing diuretics?

A

Hyperkalemia, patients taking ACE inhibitors or ARBs, patients taking potassium supplements.

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27
Q

What is the mechanism of action of osmotic diuretics?

A

Increase the osmotic pressure in the nephron, preventing water reabsorption.

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28
Q

Give an example of an osmotic diuretic.

A

Mannitol.

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29
Q

What are the clinical indications for osmotic diuretics?

A

Renal failure, increased intracranial pressure, increased intraocular pressure.

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30
Q

List two side effects of osmotic diuretics.

A

Extracellular volume expansion, dehydration.

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31
Q

What are carbonic anhydrase inhibitors?

A

Diuretics that inhibit the enzyme carbonic anhydrase, decreasing HCO3- reabsorption.

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32
Q

Give an example of a carbonic anhydrase inhibitor.

A

Acetazolamide.

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33
Q

What are the clinical indications for carbonic anhydrase inhibitors?

A

Glaucoma, altitude sickness, metabolic alkalosis.

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34
Q

List two side effects of carbonic anhydrase inhibitors.

A

Metabolic acidosis, hypokalemia.

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35
Q

What is the site of action of loop diuretics?

A

Thick ascending limb of the Loop of Henle.

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36
Q

What is the site of action of thiazide diuretics?

A

Distal convoluted tubule.

37
Q

What is the site of action of potassium-sparing diuretics?

A

Distal tubule and collecting duct.

38
Q

What is the site of action of osmotic diuretics?

A

Proximal tubule and descending loop of Henle.

39
Q

What is the primary transporter inhibited by loop diuretics?

A

Na+/K+/2Cl- cotransporter.

40
Q

What is the primary transporter inhibited by thiazide diuretics?

A

Na+/Cl- symporter.

41
Q

How do potassium-sparing diuretics affect potassium levels in the blood?

A

Increase potassium levels by decreasing secretion into the tubule lumen.

42
Q

How do osmotic diuretics affect urine volume?

A

Increase urine volume by retaining water in the nephron.

43
Q

What is a major side effect of loop diuretics related to the ear?

A

Ototoxicity, which can cause tinnitus and balance problems.

44
Q

What is a benefit of using thiazide diuretics in patients with osteoporosis?

A

Thiazide diuretics increase calcium reabsorption, which can benefit bone health.

45
Q

Why are potassium-sparing diuretics often combined with other diuretics?

A

To counteract the hypokalemic effect of loop and thiazide diuretics.

46
Q

How does the inhibition of the Na+/K+/2Cl- co-transporter by loop diuretics impact the body?

A

Inhibition leads to increased Na+, K+, and Cl- excretion, reducing reabsorption of water, thus increasing urine output and reducing blood volume and pressure.

47
Q

How does the inhibition of the Na+/Cl- symporter by thiazide diuretics impact the body?

A

Inhibition leads to increased Na+ and Cl- excretion, resulting in more water excretion, lowering blood volume and pressure, and reducing edema.

48
Q

How does the inhibition of epithelial Na+ channels by amiloride and triamterene impact the body?

A

Inhibition decreases Na+ reabsorption, reducing water reabsorption, increasing urine output, and conserving K+ by reducing its excretion.

49
Q

How does the blocking of aldosterone receptors by spironolactone and eplerenone impact the body?

A

Blocking aldosterone decreases Na+ reabsorption and water retention, while increasing K+ retention, leading to reduced blood volume and pressure.

50
Q

How does the osmotic gradient created by mannitol impact the body?

A

The gradient leads to water being retained in the renal tubules, increasing urine output, and reducing intracranial and intraocular pressure.

51
Q

How does the inhibition of carbonic anhydrase impact the body?

A

Inhibition reduces bicarbonate reabsorption, leading to increased excretion of bicarbonate, Na+, and water, causing diuresis and reducing intraocular pressure.

52
Q

What are the primary clinical indications for loop diuretics?

A

Loop diuretics are indicated for acute pulmonary and peripheral edema associated with heart failure, liver cirrhosis, nephrotic syndrome, renal failure, and hypertension in patients with renal insufficiency. They are also used for treating acute hyperkalemia and acute hypercalcemia.

53
Q

How are loop diuretics used in the management of acute pulmonary edema?

A

Loop diuretics rapidly reduce fluid overload in the lungs by increasing urine output, which decreases pulmonary congestion and improves breathing.

54
Q

What role do loop diuretics play in treating hypertension in renal failure?

A

Loop diuretics reduce blood volume and systemic vascular resistance, lowering blood pressure in patients with impaired renal function.

55
Q

How do loop diuretics help in treating hyperkalemia and hypercalcemia?

A

By increasing the excretion of potassium and calcium in the urine, loop diuretics help normalize elevated levels of these electrolytes in the blood.

56
Q

What are the primary clinical indications for thiazide diuretics?

A

Thiazide diuretics are indicated for hypertension, edema due to heart failure, liver cirrhosis, nephrotic syndrome, chronic kidney disease, idiopathic hypercalciuria, and nephrogenic diabetes insipidus.

57
Q

Why are thiazide diuretics commonly used to treat hypertension?

A

Thiazide diuretics reduce blood volume and relax blood vessels, lowering blood pressure effectively, especially in patients with normal renal function.

58
Q

How do thiazide diuretics assist in managing edema?

A

Thiazide diuretics promote the excretion of sodium and water, reducing fluid buildup in tissues and alleviating swelling.

59
Q

How are thiazide diuretics used to prevent kidney stones in idiopathic hypercalciuria?

A

Thiazide diuretics reduce urinary calcium excretion, lowering the risk of calcium stone formation in patients with idiopathic hypercalciuria.

60
Q

What is the application of thiazide diuretics in nephrogenic diabetes insipidus?

A

Thiazide diuretics paradoxically reduce urine volume by decreasing the kidney’s ability to excrete free water, managing symptoms of excessive urination.

61
Q

What are the primary clinical indications for potassium-sparing diuretics (amiloride and triamterene)?

A

Potassium-sparing diuretics like amiloride and triamterene are used to prevent hypokalemia when combined with thiazide or loop diuretics. They are also used in conditions requiring mild diuresis without significant potassium loss.

62
Q

How do amiloride and triamterene prevent hypokalemia in patients on other diuretics?

A

By inhibiting sodium reabsorption in the distal nephron, they reduce the exchange of sodium for potassium, thus conserving potassium and preventing hypokalemia.

63
Q

What are the primary clinical indications for potassium-sparing diuretics (spironolactone and eplerenone)?

A

Spironolactone and eplerenone are used for managing congestive heart failure, resistant hypertension, primary hyperaldosteronism, and conditions with secondary aldosteronism like liver cirrhosis and nephrotic syndrome.

64
Q

How do spironolactone and eplerenone improve outcomes in congestive heart failure?

A

They antagonize aldosterone, reducing sodium retention, myocardial fibrosis, and ventricular remodelling, which improves survival and reduces hospitalizations in heart failure patients.

65
Q

What is the role of spironolactone and eplerenone in treating primary hyperaldosteronism?

A

By blocking aldosterone receptors, they correct hyperaldosteronism, leading to decreased sodium retention, increased potassium retention, and normalization of blood pressure.

66
Q

What are the primary clinical indications for osmotic diuretics?

A

Osmotic diuretics like mannitol are used to manage acute renal failure due to increased solute load, reduce elevated intracranial pressure, decrease intraocular pressure in glaucoma, and promote diuresis in drug toxicity cases.

67
Q

How does mannitol help in reducing intracranial pressure?

A

Mannitol creates an osmotic gradient, drawing water out of the brain tissue into the bloodstream, thereby reducing brain edema and intracranial pressure.

68
Q

What are the primary clinical indications for carbonic anhydrase inhibitors?

A

Carbonic anhydrase inhibitors like acetazolamide are used for glaucoma, altitude sickness, metabolic alkalosis, and as an adjunct in epilepsy treatment.

69
Q

How do carbonic anhydrase inhibitors help in managing glaucoma?

A

They reduce the production of aqueous humor in the eye, lowering intraocular pressure.

70
Q

How are carbonic anhydrase inhibitors used to treat metabolic alkalosis?

A

By promoting bicarbonate excretion, they correct metabolic alkalosis, normalizing blood pH levels.

71
Q

What is renal hypertension?

A

Renal hypertension is high blood pressure caused by kidney disease or narrowing of the arteries that supply the kidneys (renal artery stenosis).

72
Q

How does renal hypertension develop?

A

Renal hypertension develops due to reduced blood flow to the kidneys, which triggers the release of renin and activates the renin-angiotensin-aldosterone system (RAAS), leading to increased blood pressure.

73
Q

What role do ACE inhibitors play in managing renal hypertension?

A

ACE inhibitors block the conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone secretion, thus lowering blood pressure.

74
Q

How do ACE inhibitors affect renal blood flow in patients with renal hypertension?

A

ACE inhibitors improve renal blood flow by dilating the efferent arterioles, which reduces glomerular pressure and helps protect kidney function.

75
Q

What impact do ACE inhibitors have on proteinuria in renal hypertension?

A

ACE inhibitors reduce proteinuria by decreasing glomerular pressure and preventing protein leakage into the urine, thus protecting the kidneys.

76
Q

Why are ACE inhibitors beneficial in patients with diabetic nephropathy?

A

They slow the progression of kidney damage by reducing glomerular hypertension and proteinuria, which are common in diabetic nephropathy.

77
Q

What is the role of ARBs in managing renal hypertension?

A

ARBs block the angiotensin II type 1 (AT1) receptors, preventing the effects of angiotensin II on vasoconstriction and aldosterone secretion, leading to lower blood pressure.

78
Q

How do ARBs improve renal blood flow in renal hypertension?

A

ARBs cause vasodilation of the efferent arterioles, reducing glomerular pressure and improving renal perfusion.

79
Q

What effect do ARBs have on proteinuria in patients with renal hypertension?

A

ARBs reduce proteinuria by lowering intraglomerular pressure, which helps prevent kidney damage and protein leakage.

80
Q

Why might ARBs be preferred over ACE inhibitors in some patients with renal hypertension?

A

ARBs may be preferred in patients who experience side effects like cough or angioedema with ACE inhibitors.

81
Q

How do ACE inhibitors and ARBs protect kidney function in chronic kidney disease (CKD)?

A

Both ACE inhibitors and ARBs reduce proteinuria, lower glomerular pressure, and slow the progression of CKD by inhibiting the RAAS.

82
Q

What is the importance of reducing proteinuria in renal hypertension?

A

Reducing proteinuria helps prevent further kidney damage and slows the progression of renal disease, preserving kidney function.

83
Q

How do ACE inhibitors and ARBs affect aldosterone levels in renal hypertension?

A

Both ACE inhibitors and ARBs reduce aldosterone levels, decreasing sodium and water retention, which lowers blood pressure and reduces stress on the kidneys.

84
Q

Can ACE inhibitors and ARBs be used together in renal hypertension?

A

Generally, ACE inhibitors and ARBs are not used together due to the increased risk of adverse effects like hyperkalemia and renal impairment, but they can be used sequentially or alternately in some cases.

85
Q

What are the common side effects of ACE inhibitors in renal hypertension?

A

Common side effects include dry cough, hyperkalemia, hypotension, and, in rare cases, angioedema.

86
Q

What are the common side effects of ARBs in renal hypertension?

A

Common side effects include hyperkalemia, hypotension, dizziness, and, rarely, angioedema.

87
Q

How do ACE inhibitors and ARBs contribute to cardiovascular protection in patients with renal hypertension?

A

By lowering blood pressure and reducing RAAS activation, they reduce the risk of cardiovascular events such as heart attack and stroke.

88
Q

Why is monitoring renal function important in patients on ACE inhibitors or ARBs?

A

Monitoring is crucial because these medications can affect renal function, especially in patients with pre-existing kidney disease or bilateral renal artery stenosis.

Master YLL Pharmacology (36 decks)

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