Drugs and Membrane Transporters

Thiazide diuretics cause loss of Na+ and inhibit Cl- reabsorption.

Loop diuretics promote significant loss of K+ in addition to Na+, resulting in hypokalaemia.

Digoxin inhibits the Na+/K+ ATPase pump, increasing intracellular Na+, which subsequently raises intracellular Ca2+.

<p>Aldosterone promotes the expression of Na+/K+ ATPase and ENaC, enhancing Na+ reabsorption.</p> Signup and view all the answers

<p>Digoxin's therapeutic range is between 0.6 to 1.2 µg/L, where doses above this can lead to toxicity.</p> Signup and view all the answers

<p>Na+ channel inhibitors block ENaC, reducing Na+ reabsorption and subsequently decreasing K+ secretion.</p> Signup and view all the answers

<p>The body may retain bicarbonate or increase reabsorption of other ions to correct the alkalosis.</p> Signup and view all the answers

<p>Increased intracellular Na+ and Ca2+ from digoxin can disturb cardiac rhythm, especially at high doses.</p> Signup and view all the answers

<p>Thiazide diuretics increase the activity of the Na+/Ca2+ antiporter by lowering sodium concentration in epithelial cells.</p> Signup and view all the answers

<p>Thiazide diuretics are contraindicated in patients with hypotension, gout, renal failure, lithium therapy, hypokalemia, and may worsen diabetes.</p> Signup and view all the answers

<p>Thiazide diuretics induce potassium loss primarily by increasing aldosterone activity, which promotes sodium reabsorption at the expense of potassium.</p> Signup and view all the answers

<p>Thiazide diuretics raise the levels of uric acid by reducing its clearance as they compete for the same transporter in the kidneys.</p> Signup and view all the answers

<p>Thiazide diuretics cause loss of potassium while conserving calcium, leading to hypokalemia and potential hypercalcemia.</p> Signup and view all the answers

<p>Hypochloraemic alkalosis occurs due to chloride loss as a result of thiazide diuretic action, which also contributes to increased potassium loss.</p> Signup and view all the answers

<p>Thiazide diuretics primarily act in the early portion of the distal convoluted tubule (DCT).</p> Signup and view all the answers

<p>Chronic thiazide diuretic use may lead to hyperglycemia due to metabolic changes induced by prolonged sodium and potassium imbalances.</p> Signup and view all the answers

<p>They help to reduce potassium loss, thereby mitigating the risk of hypokalaemia.</p> Signup and view all the answers

<p>The primary adverse effect is hyperkalaemia, which can lead to cardiac arrythmias.</p> Signup and view all the answers

<p>Aldosterone increases Na+/K+ ATPase activity and ENaC expression, promoting sodium reabsorption and potassium secretion.</p> Signup and view all the answers

<p>Both can increase potassium levels, raising the risk of hyperkalaemia and potential cardiac complications.</p> Signup and view all the answers

<p>They block ENaC, reducing sodium reabsorption from the tubular lumen and consequently decreasing blood sodium levels.</p> Signup and view all the answers

<p>Thiazide resistance develops due to increased aldosterone secretion in response to low blood sodium levels, leading to potassium retention.</p> Signup and view all the answers

<p>They promote retention of potassium in the urine, leading to lower urinary potassium excretion.</p> Signup and view all the answers

<p>Aldosterone is secreted primarily in response to hyponatremia or low sodium levels in the blood.</p> Signup and view all the answers