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36 Cards in this Set
- Front
- Back
ACE Inhibitors MOA |
Inhibit ACE - occupy the active site region of ACE, usually taken by angiotensin I's proline. The -COOH groups block the catalytic activity of the Zn2+ ions on the active site. This reduces angiotensin II and aldosterone levels and increases bradykinin levels. This causes vasodilatation --> reduction in peripheral resistance. There is little change in heart rate and cardiac output and reduced sodium retention. |
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ACE Inhibitors examples |
-pril Catopril, enalapril, lisinopril, ramipril. |
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ACE Inhibitors administration, indications and contraindications |
Oral Hypertension, heart failure & renal dysfunction (esp. in diabetes) Pregnancy, reno-vascular disease, aortic stenosis. |
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ACE Inhibitors adverse effects |
A - Angio-oedema C - Cough E - Electrolyte imbalance First dose hypotension, diarrhoea, muscle cramps, dizziness and headache. NSAIDs + ACE Inhibitors = hypotension. |
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Angiotensin-II receptor antagonist/blockers (ARBs) MOA |
Inhibit angiotensin-II receptor - highly selective for AT1R and can shift the balance of which receptors A-II bind to. If AT1R are occupied by ARBs, then A-II can bind to AT2R receptors instead. Activation of AT2R receptors tends to cause opposing effects to the activation of AT1R receptors. This results in vasodilatation --> reduction in peripheral resistance. |
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ARBs examples |
-sartan Losartan, valsartan |
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ARBs administration, indications and contraindications |
Oral Hypertension & heart failure Pregnancy, breastfeeding. Caution in renal artery stenosis and aortic stenosis. |
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ARBs adverse effects |
Cough (less common than ACE), orthostatic hypotension, dizziness, headache & fatigue, hyperkalaemia & rash. |
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Beta-blockers MOA |
Limits sympathetic activity. Cario-selective antagonist of B1-adrenoreceptors. Reduces the slope of Phase 4 potential and reduces Ca2+ entry to myocytes. This causes a fall in systolic BP, in cardiac contractile activity and in myocardial O2 demand. Decreases BP by reducing cardiac output, also reduces renin release in the kidneys. |
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Beta-blockers examples |
-olol Non-selective: propanolol, B1 selective: atenolol, bisprolol & metoprolol |
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Beta-blockers administration, indications, contraindications |
Oral, IV Angina, most MI, arrhythmias, hypertension, thyrotoxicosis, glaucoma, anxiety. Non-selective B-blockers should not be given to asthmatic patients. At high doses, B1-adrenoreceptor antagonists lose their selectivity and should be used in caution in those with asthma. |
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Beta-blockers adverse effects |
Bronchospasm, fatigue & insomnia, dizziness, cold extremities (B2) effect, bradycardia, heart block, hypotension & decreased glucose tolerance in diabetic patients. |
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Hydralazine MOA |
Effects are unclear, appears to interfere with the action of inositol trisphosphate in vascular smooth muscle, reducing peripheral resistance and BP. |
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Hydralazine administration, indications and contraindications |
Oral, IV Moderate to severe hypertension. Can be used in conjunction with B-blockers and thiazides in hypertensive emergencies and in hypertensive pregnant women. Idiopathic systemic lupus, erythematosus, severe tachycardia. |
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Hydralazine adverse effects |
Tachycardia, fluid retention, N&V, headache. |
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Cardiac Glycosides MOA |
They have a positive inotropic effect. Normally Ca2+ regulates muscle contraction (and is taken out of the cell by a Na+/Ca2+ exchanger), in heart failure more Ca2+ is needed. CG's inhibit the membrane Na+/K+ APTase pump, raising intracellular [Na+] causing the Na+/Ca2+ exchanger to change direction meaning more Ca2+ is trafficked into the cell. Increased [Ca2+] in the cell --> force of contraction is increased. |
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Cardiac glycosides MOA altering electrical activity of the heart |
Stimulate vagal activity (useful in atrial fibrillation), slowing AV conductance and shortening the atrial AP. Direct effects mainly due to loss of intracellular potassium. Resting membrane is reduced, causing enhanced automaticity, slowed cardiac conduction, increased AVN refractory period. |
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Cardiac glycoside example |
Digoxin |
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Cardiac glycoside administration, indications and contraindications |
Oral Heart failure, supra-ventricular arrhythmias Heart block, hypokalaemia associated with diuretics |
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Cardiac glycoside adverse effects and therapeutic notes |
Arrhythmias, anorexia, N&V, visual disturbances, abdominal pain and diarrhoea. V. narrow therapeutic window - common toxicity. |
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Loop diuretics MOA |
Inhibit the Na+/K+/CL- symporter (spec. Cl- transporter) on the thick ascending loop of Henle. Increases sodium reaching the collecting duct --> increases K+ and H+ secretion. Calcium and magnesium reabsorption is also inhibited (decrease in potential difference across the ell normally generated from the recycling of potassium). Also vasodilate |
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Loop diuretics examples |
Furosemide, bumentaide, torsemide |
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Loop diuretics administration, indications, contraindications |
Oral, IV, IM Acute pulmonary oedema, oliguria due to acute renal failure, resistant CCF, hypertension Severe renal impairment. Cardiac glycosides (hypokalaemia potentiates action & increases the risk of cardiac-glycoside-induced arrhythmias), aminoglycoside antibiotics (increase the risk of ototoxicity and hearing loss). |
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Loop diuretics adverse effects |
Hypokalemia, hyponatraemia, hyperuricemia, hypotension, hypovolemia. Metabolic alkalosis (increased H+ secretion). [Hypocalcaemia and hypomagnesaemia.] |
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Potassium-sparing diuretics MOA |
Act on late distal tubule and collecting duct. Two classes: 1. Sodium-channel blockers - reduce potential difference across the cell and reduce K+ secretion. Secretion of H+ from the intercalated cells is also decreased. 2. Aldosterone antagonists - Outcompetes aldosterone for the mineral-corticoid receptor, reducing Na+ reabsorption and therefore H+ and K+ secretion. Degree of diuresis depend son aldosterone levels. |
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Potassium-sparing diuretics examples |
Sodium channel blockers - amiloride & triamterene. Aldosterone antagonists - spironolactone |
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Potassium-sparing diuretics administration, indications, contraindications |
Oral Heart failure, hypotension whilst maintaining normal serum potassium levels. Aldosterone antagonists used to treat hypoeraldosteronism (primary = Conn's, secondary CCF). Interact with ACE inhibitors, increasing risk of hyperkalaemia. Renal failure. |
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Potassium-sparing diuretics adverse effects |
Hyperkalemia, GI disturbances, hyponatremia, gynaecomastia, menstrual disorders, male sexual dysfunction. |
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Thiazide diuretics MOA |
Increase the excretion of Na+ and Cl- by inhibiting the Na+/Cl- co-transporter. Increases the reabsorption of Ca2+ (may involve stimulation of Na+/Ca2+ counter-transport due to an increase in the concentration gradient for Na+ across the basolateral membrane. |
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Thiazide diuretics example |
Bendroflumethiazide |
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Thiazide diuretics indications and contraindications |
Hypertension and oedema Hypotension, allergy to sulphur-containing medications, gout, renal failure, lithium therapy, hypokalemia, may worsen diabetes |
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Thiazide diuretics adverse effects |
Hypokalemia, increase in blood sugar, GI disturbances, hypotension, impotence. |
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Osmotic Diuretics MOA |
Acts on the tubular segments that are water permeable (proximal tubule, descending loop of Henle, collecting ducts) Freely filtered at the glomerulus, only partially reabsorbed (if at all). Passive water reabsorption is reduced by the presence of this non- reabsorb-able solute within the tubule lumen. Net effect is increased water loss, with relatively smaller loss of sodium. |
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Osmotic Diuretics example |
Mannitol |
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Osmotic diuretics administration, indications, contraindications |
IV Raised intracranial pressure (& intra-ocular pressure) CCF, pulmonary oedema |
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Osmotic diuretics adverse effects & therapeutic notes |
Chills & Fever Seldom used in HF as expansion of blood volume can be > than degree of diuresis produced. |