Pharmacology Chapter 29: Diuretics and Transporters
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Questions and Answers

What is the primary action of thiazide diuretics in the kidneys?

  • They increase Mg2+ reabsorption.
  • They block K+ reabsorption.
  • They promote Na+ and K+ wasting.
  • They inhibit reabsorption of Na+ and Cl−. (correct)

Thiazide diuretics can decrease calcium reabsorption in the kidneys.

False (B)

Name two conditions for which thiazide diuretics are commonly used.

high blood pressure, congestive heart failure

Thiazide diuretics are ____ sensitive Na+-Cl− symporter inhibitors.

<p>thiazide</p> Signup and view all the answers

Match the following diuretics to their respective characteristics:

<p>Loop diuretics = Inhibit Na+ reabsorption at the thick ascending limb Thiazide diuretics = Inhibit Na+ and Cl− reabsorption at the distal convoluted tubule Furosemide = Example of loop diuretic Hydrochlorothiazide = Example of thiazide diuretic</p> Signup and view all the answers

Which diuretic acts primarily on the Loop of Henle?

<p>Loop diuretics (A)</p> Signup and view all the answers

Thiazide diuretics act on the collecting duct of the nephron.

<p>False (B)</p> Signup and view all the answers

What is the mechanism of action for loop diuretics?

<p>Inhibition of Na+/K+/2Cl- co-transporter (NKCC2)</p> Signup and view all the answers

Loop diuretics primarily increase the concentration of ions in the ______.

<p>tubule</p> Signup and view all the answers

Match each type of diuretic with its site of action:

<p>Osmotic diuretics = Proximal tubules Loop diuretics = Loop of Henle Thiazide diuretics = Early distal tubule Potassium-sparing diuretics = Late distal tubule</p> Signup and view all the answers

What percentage of the filtered load of Na+ is reabsorbed in the thick ascending limb (TAL)?

<p>25% (C)</p> Signup and view all the answers

Carbonic anhydrase inhibitors act on the Loop of Henle.

<p>False (B)</p> Signup and view all the answers

Name a common loop diuretic.

<p>Furosemide</p> Signup and view all the answers

What ion loss is associated with alkalosis in compensatory actions?

<p>Cl- (C)</p> Signup and view all the answers

Digoxin toxicity can result in increased intracellular calcium concentration.

<p>True (A)</p> Signup and view all the answers

Which plant is the source of Digoxin?

<p>Foxglove</p> Signup and view all the answers

Digoxin acts as an inhibitor of the Na+/K+ _____ pump.

<p>ATPase</p> Signup and view all the answers

Which condition can potentiate the effect of Digoxin and increase the risk of cardiac arrhythmias?

<p>Hypokalaemia (C)</p> Signup and view all the answers

Match the following components with their respective functions:

<p>Na+/K+ ATPase pump = Maintains Na+ and K+ gradients Na+/Ca2+ exchanger = Regulates intracellular calcium levels Aldosterone = Increases Na+ reabsorption Aldosterone antagonists = Reduce Na+ reabsorption</p> Signup and view all the answers

Aldosterone receptor antagonists promote Na+ reabsorption.

<p>False (B)</p> Signup and view all the answers

What is the therapeutic window for Digoxin in µg/L?

<p>0.6-1.2</p> Signup and view all the answers

What mechanism do thiazides primarily affect in the kidneys?

<p>Na+/Ca2+ antiporter (D)</p> Signup and view all the answers

Thiazides increase the clearance of uric acid in patients with gout.

<p>False (B)</p> Signup and view all the answers

What condition is NOT listed as a contraindication for thiazide diuretics?

<p>Dehydration</p> Signup and view all the answers

Thiazides cause __________ potassium levels while conserving blood calcium.

<p>low</p> Signup and view all the answers

Match the following conditions with their effects of thiazide diuretics:

<p>Hypotension = Contraindication Gout = Increased uric acid levels Hyperglycemia = Associated with chronic administration Hyperkalemia = Not caused by thiazides</p> Signup and view all the answers

Increased aldosterone activity due to thiazide use primarily leads to:

<p>Potassium loss (D)</p> Signup and view all the answers

Thiazides directly inhibit the Na+/Ca2+ antiporter in the distal convoluted tubule.

<p>False (B)</p> Signup and view all the answers

What effect do thiazides have on blood calcium levels?

<p>Conserve or increase</p> Signup and view all the answers

What adverse effect is primarily associated with potassium-sparing diuretics?

<p>Hyperkalaemia (B)</p> Signup and view all the answers

Potassium supplements can be safely prescribed alongside potassium-sparing diuretics.

<p>False (B)</p> Signup and view all the answers

Which diuretic type is often used in combination with loop diuretics and thiazides to reduce potassium loss?

<p>Potassium-sparing diuretics</p> Signup and view all the answers

Hyperkalaemia can lead to cardiac ______.

<p>arrhythmias</p> Signup and view all the answers

Match the following components with their associated actions:

<p>Aldosterone = Increases Na+/K+ ATPase expression Spironolactone = Blocks aldosterone receptor ENaC = Facilitates sodium transport K+ sparing diuretics = Prevent potassium loss</p> Signup and view all the answers

Which of the following statements is true regarding ENaC?

<p>Blocking ENaC reduces Na+ transport. (B)</p> Signup and view all the answers

Aldosterone is secreted in response to hyponatremia.

<p>True (A)</p> Signup and view all the answers

What effect does spironolactone have on sodium and potassium levels?

<p>Decreases sodium and increases potassium levels</p> Signup and view all the answers

Flashcards

Thick Ascending Limb

Part of the nephron responsible for active transport of Na+, K+, and Cl- out of the lumen and into the interstitium, making the interstitium more positive.

NKCC2

Sodium-potassium-2 chloride cotransporter, a protein in the thick ascending limb that pumps sodium, potassium, and chloride out of the lumen.

Loop diuretics

Medications (e.g., furosemide) that block NKCC2, leading to increased urine output by preventing reabsorption of electrolytes.

Thiazide diuretics

Medications (e.g., hydrochlorothiazide) that block Na+-Cl- symporter in the distal convoluted tubule, increasing urine output and potentially increasing calcium reabsorption.

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Role of Diuretics in High blood pressure & Edema

Diuretics reduce blood volume by increasing urine output, thus lowering blood pressure and reducing swelling (edema).

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Loop Diuretics Site of Action

Loop diuretics such as furosemide act on the thick ascending loop of Henle.

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Loop Diuretics Mechanism

Loop diuretics block the Na+/K+/2Cl- co-transporter (NKCC2), reducing Na+ and Cl- reabsorption in the thick ascending loop of Henle.

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Loop Diuretics Effect on Na+ and Cl-

Loop diuretics decrease sodium and chloride reabsorption, leading to increased excretion of these ions in urine.

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Loop Diuretic Diuretic Action

Loop diuretics significantly increase urine output due to their effect on sodium and chloride reabsorption.

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Thiazide Diuretics Site of Action

Thiazide diuretics affect the early distal tubule.

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Thiazide Diuretics Mechanism

Thiazide diuretics inhibit sodium and chloride co-transport, reducing their reabsorption.

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Osmotic Diuretics Site of Action

Osmotic diuretics affect the proximal tubules, loop of Henle, and collecting duct.

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Osmotic Diuretics Mechanism

Osmotic diuretics prevent water reabsorption due to their osmotic effect, increasing urine output.

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Thiazide diuretic action

Thiazides decrease sodium in epithelial cells, boosting Na+/Ca2+ antiporter activity.

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Thiazide effect on uric acid

Thiazides compete with uric acid for transporters, raising blood uric acid levels.

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Thiazide-induced hyperglycemia

Chronic thiazide use can lead to elevated blood sugar levels.

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Thiazide potassium loss

Thiazides cause potassium loss due to increased aldosterone activity and chloride loss.

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Thiazide contraindications

Conditions like hypotension, gout, renal failure, and lithium therapy are contraindications for thiazide use.

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Aldosterone's role with thiazides

Increased aldosterone activity contributes to potassium loss through sodium-potassium exchange.

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Mechanism of potassium loss with thiazides

Thiazides, by decreasing sodium reabsorption, trigger a compensatory increase in aldosterone, causing potassium loss by the kidney.

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Hypotension contraindication for Thiazides

Low blood pressure is a reason to be cautious when taking thiazides.

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K+ sparing diuretics

Medications (e.g., spironolactone) that block aldosterone receptors in the collecting tubules, reducing sodium reabsorption and potassium excretion, leading to increased blood potassium levels.

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Adverse Effects of K+ sparing diuretics

The main side effect is hyperkalemia (high blood potassium levels). This can be dangerous because it can lead to cardiac arrhythmias (irregular heartbeat).

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Interaction with ACE inhibitors

Co-administration with ACE inhibitors (which also increase blood potassium) can significantly increase the risk of hyperkalemia.

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ENaC

Epithelial sodium channel, a protein in the collecting tubules that plays a key role in sodium reabsorption and potassium secretion.

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Aldosterone's Role in Sodium Reabsorption

Aldosterone, a hormone, increases the expression and activity of Na+/K+ ATPase and ENaC, promoting sodium reabsorption and potassium excretion.

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Spironolactone's Mechanism

Spironolactone, a K+ sparing diuretic, blocks aldosterone receptors, decreasing ENaC and Na+/K+ ATPase activity, leading to reduced sodium reabsorption and potassium excretion.

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Spironolactone's Impact on Potassium

Spironolactone's effect on aldosterone leads to a decrease in urinary potassium excretion, resulting in an increase in blood potassium levels.

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Hyperkalemia and Cardiac Arrhythmias

High potassium levels (hyperkalemia) can interfere with normal heart function and lead to dangerous arrhythmias.

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Digoxin

A medication obtained from the foxglove plant, used to treat heart conditions. It inhibits the Na+/K+ ATPase pump, increasing intracellular Na+ and subsequently Ca2+, which strengthens heart contractions.

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Na+/K+ ATPase Pump

A protein pump found in cell membranes that actively transports sodium (Na+) out of and potassium (K+) into the cell, requiring energy. It's crucial for maintaining cell function and potential.

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Digoxin Toxicity

Occurs when digoxin levels in the blood are too high, potentially leading to irregular heartbeat, nausea, and other adverse effects.

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Hypokalaemia

Low potassium levels in the blood, which can be caused by diuretics like loop diuretics and thiazides and worsen digoxin toxicity.

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Aldosterone Antagonists

Medications like spironolactone and eplerenone that block aldosterone's action on the kidneys, reducing both sodium reabsorption and potassium secretion.

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Na+ Channel Inhibitors

Medications like amiloride and triamterene that block sodium channels in the kidneys, reducing sodium reabsorption and potassium secretion.

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Depolarisation

A change in the electrical potential across a cell membrane, which in the heart can be disrupted by high doses of digoxin, leading to arrhythmias.

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Study Notes

Drugs and Membrane Transporters: Renal Transport Systems

  • Renal transport systems are crucial for drug action and excretion.
  • Loop diuretics, thiazide diuretics, and potassium-sparing diuretics affect renal function.

Learning Objectives

  • Students should understand the site of action, mechanism of action, and side effects of loop, thiazide, and potassium-sparing diuretics.

Further Reading

  • Medical Physiology, 3rd Edition, Chapter 35 (Transport of Sodium and Chloride, pp 1111-1116)
  • Rang and Dale's Pharmacology, 10th edition, Chapter 29 (The Kidney and Urinary System, pp 402-412)

Site and Mechanism of Action

  • Diuretic: Site of Action: Mechanism of Action:
  • Osmotic diuretics: Proximal tubules Inhibition of water and Na+ reabsorption
  • Carbonic anhydrase inhibitors: Proximal tubules Inhibition of bicarbonate reabsorption
  • Loop diuretic: Loop of Henle (thick ascending limb) Inhibition of Na+, K+, and Cl− reabsorption
  • Thiazide: Early distal tubule Inhibition of Na+, Cl− co-transport
  • K+ sparing diuretics: Late distal tubule/collecting duct Inhibition of Na+ reabsorption

Loop Diuretics

  • Example drugs: Furosemide, bumetanide
  • Mechanism: Inhibit the Na+/K+/2Cl− co-transporter (NKCC2) in the thick ascending limb of Henle's loop.
  • This reduces Na+ and Cl− reabsorption.
  • 25% of filtered Na+ is normally reabsorbed in this section, so loop diuretics have a significant effect.
  • This leads to a decrease in the concentration of ions in the tubule and reduced hypertonicity in the surrounding interstitium, which impacts water reabsorption.

Thiazide Diuretics

  • Example drugs: Hydrochlorothiazide, chlorothiazide, bendroflumethiazide
  • Mechanism: Block the thiazide-sensitive Na+-Cl− symporter in the early distal convoluted tubule.
  • This inhibits Na+ and Cl− reabsorption.
  • Also increase Ca2+ reabsorption in the distal tubule.

K+ Sparing Diuretics

  • Mechanism: Aldosterone antagonists (e.g., spironolactone, eplerenone) block aldosterone's effect on Na+/K+ATPase and ENaC, reducing Na+ reabsorption and K+ secretion.
  • Na+ channel inhibitors (e.g., amiloride, triamterene) block ENaC, reducing Na+ reabsorption and thus also K+ secretion to a lesser extent.

Contraindications

  • Thiazides: May worsen gout, renal failure, hypokalemia, and may worsen diabetes.
  • K+ Sparing Diuretics: Hyperkalemia, a potential adverse effect, is a concern when used with other drugs that also elevate potassium levels, such as ACE inhibitors

Digoxin Toxicity

  • Digoxin inhibits the Na+/K+ ATPase pump, leading to increased intracellular Na+, reduced Na+/Ca2+ exchange and increased intracellular Ca2+.
  • This can cause cardiac arrhythmias.
  • Loop and thiazide diuretics may increase the risk of digoxin toxicity.

Blood Electrolyte Balance

  • For reference, normal ranges for blood electrolytes (e.g., Na+, K+, Cl-, Ca2+, Mg2+).

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Drugs and Renal Transport Systems PDF

Description

Explore the mechanisms and effects of various diuretics on renal transport systems in this quiz. Understand the action sites and side effects of loop, thiazide, and potassium-sparing diuretics, drawing from the key concepts in medical physiology and pharmacology. Perfect for students aiming to master renal pharmacology.

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