Pharmacology Final Exam Lecture 9 Slide 25

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  1. Hypertension - Diuretics
    • Thiazide e.g. Hydrochlorothiazide
    • Thiazide-like e.g. Chlorthalidone
    • Loop e.g. Frusemide
    • Selective Aldosterone Blocker e.g. Eplererone
    • Potassium sparing e.g. Spironolactone
  2. Hypertension - Diuretics - MOA
    • - increase sodium excretion, ␣reduction in plasma volume and cardiac output.
    • - reduction in peripheral resistance, (mechanism is unclear)
  3. Hypertension - Thiazide and Thiazide-like diuretics
    • - Inhibit absorption of sodium and chloride in the proximal segment of the distal convoluted tubule by binding to the chloride-binding site of the Na+-Cl-
    • - Promote renal excretion of water, sodium, chloride, potassium and magnesium
    • - Decrease excretion of uric acid and calcium
    • - Thiazides are less potent than loop diuretics and have a longer half-life
  4. Thiazide-like Indapamide
    • - Often regarded as belonging to the thiazide diuretics class as it acts at the same place in the renal tubules and has a similar effect, although they have different chemical structures.
    • o Indapamide is often used as a first-line treatment of mild to moderate essential hypertension.
    • o At low doses, it appears to decrease vasoconstriction mediated through adrenaline and noradrenaline which leads to decreased total peripheral resistance (TPR) ␣ decreased BP.
    • o At high doses, it works on the proximal part of the distal tubule in the kidney, inhibiting the inc Na+/Cl- (as well as Cl- & water) (much like a thiazide diuretic). This leads to decreased cardiac output resulting in decreased BP.
  5. Thiazides & thiazide-like diuretics - interactions
    • - Can aggravate digoxin toxicity
    • - Can aggravate lithium toxicity
    • - Increases hyperglycaemic effect of corticosteroids
    • - NSAIDs (decreased natriuresis and reduced
    • antihypertensive effect)
  6. Indapamide (thiazide-like) - care exercised if taking
    • - digoxin (increase toxicity in presence of abnormal plasma K+),
    • - lithium (decrease renal clearance and create Li- toxicity),
    • - or if patient has gout (decreased uric acid clearance by kidney).
  7. Hypertension Loop diuretics
    E.g. Frusemide
    • - Loop Diuretic is actively secreted into the lumen of the nephron proximal tubule cells (PCT)
    • - In the ascending Loop of Henle they inhibit the Na+-K+- 2Cl- transporter thus preventing reabsorption of sodium and chloride
    • - Loss of fluid volume from the blood␣spontaneous feedback to increase release of aldosterone (hormone that normally further increases activity of Na+/K+ ATPase pump, resulting in even more loss of K+
    • - Also decreases uric acid excretion & increases serum uric acid.
  8. Loop diuretics - Indications
    • - Oedema (peripheral and pulmonary) associated with chronic renal failure, chronic liver cirrhosis and hypertension (usually associated with renal or cardiac failure)
    • ␣ Used for Syndrome of inappropriate ADH secretion (SIADH)
    • ␣ Loop diuretics enhance excretion of calcium and magnesium by interfering with reabsorption ␣ thus can be used for hypercalcaemia
  9. Loop diuretics - Cautions and Warnings
    • - Loop diuretics should be used with caution in patients with possible electrolyte disturbances, prostatic hypertrophy or pregnancy (Category C).
    • ␣Co-Administration of a K+ sparing diuretic can help to prevent development of hypokalaemia in vulnerable patients. Diuretics are not potent enough to be used as monotherapy in CCF (Congestive Cardiac Failure).
    • ␣Hypokalaemia or hyperkalaemia can aggravate digoxin toxicity (many patients requiring diuretics, especially loop diuretics, may be on
    • Digoxin® concurrently).
  10. Potassium-sparing diuretics Aldactone - MOA
    • - Aldosterone Antagonists - competitive antagonists to Aldosterone for the distal renal collecting tubule/duct receptors ␣ decreased Na+ reabsorption in renal collecting tubules/ ducts, and increased retention (decreased excretion) of K+.
    • - weak diuretics, so work best as an adjunctive therapy.
  11. Potassium-sparing diuretics - e.g. spironolactone - Indications
    • - Used to treat hyperaldosteronism, liver cirrhosis (because aldosterone is not being metabolized), and may be combined with a loop or thiazide diuretic in treating hypertension or CCF in patients losing K+.
    • - Prevention and treatment of diuretic-induced hypokalaemia

    • Main adverse effect
    • ␣ Hyperkalaemia.
  12. Beta - Blockers
    Atenolol - cardioselective
    Carvedilol - only one used in CCF (CHF)
    • - blockers inhibit the binding of catecholamines (e.g adrenaline, noradrenaline, dopamine) at the Beta 1
    • adrenoreceptor site in the heart
    • o Pharmacologically, blockade of Beta 1 receptors decreases rate, conduction velocity, myocardial contractility and cardiac output
    • o Anti-hypertensive effect results from decreased cardiac output without a reflex increase in peripheral vascular resistance;
    • - diminished sympathetic outflow from the vasomotor centre in the brain to the peripheral blood vessels; reduced renin release by the kidney
    • o They also have direct effect on the heart itself (blocking the ␣1adrenoceptor-mediated increase in rate (chronotropicity) and force (inotropicity) of cardiac contractions).
    • o ␣1-blockade can also decrease conduction velocity within the heart, therefore some ␣-blockers such as sotalol can be prescribed for certain tachyarrhythmias.

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Pharmacology Final Exam Lecture 9 Slide 25
2011-06-05 12:32:11
Pharmacology hypertension

ECNH Pharmacology end of semester 1 exam
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