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9 Cards in this Set
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Digoxin |
Mechanism: inhibits Na+/K+ATPase pump [prevents K+ entering and Na+ leaving myocyte; increased intracellular Na+ promotes calcium influx at Na+/Ca+ exchanger = increases contractility [inotropic]; stimulates vagus nerve [treats arrythymias] use: symptomatic treatment of chronic heart failure [after ACE inhibitors and diuretics]; antiarrythmic side effects: narrow therapeutic range - digoxin toxicity [hyperkalaemia; arrythmias]; chronic use - concave ST segments on ECG; bradycardia [parasympathetic activity on SA node] |
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ACE Inhibitors [pril suffix] |
Mechanism: ACE is located in vascular endothelium of lungs - converts Angiotensin I to Angiotensin II; Angiotensin II causes vasoconstriction, increases GFR, constricts efferent arteriole, acts at the proximal convoluted tubule to increase sodium bicarb reabsorption, increases aldsterone [a mineralocorticoid] release from the adrenal cortex which acts on the collecting duct to increase Na+ reabsorption at the expense of K+ Mechanism: counteract pressor effects of angiotensin II; decrease sodium bicarb reabsorption at PCT; decrease aldosterone release; dilate efferent tubule - decrease GFR side effects: initial increase in creatinine; hypotension and syncope in patients with high renin levels [heart failure]; increase levels of angiotensin I and renin; hyperkalaemia due to decreased aldosterone levels adverse effects: dry cough [increase in bradykinin] contraindicated: pregnancy; hereditary angioedema [C1 esterase dficiency]; coadministration with NSAIDs can cause AKI; bilateral renal artery stenosis [long HTN plus angina/CAD] Use: first line treatment for heart failure [reduces pre-load; and sympathetic activity on heart via reduction in angiotensin II]; reduces mortality in heart failure and MI; decreases angiotensin II cardiac remodelling; first line treatment in hypertension; slows progression of diabetic nephropathy; patients with albuminuria and BP > 130/80 |
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ARB |
Mechanism: decrease sodium bicarb reabsorption at PCT; decrease aldosterone release; dilate efferent tubule - decrease GFR use: heart failure; HTN; diabetic nephropathy - use to avoid cough side effects: hyperkalaemia [from aldosterone inhibition] |
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Acetazolamide [carbonic anhydrase inhibitor]; Mannitol |
Mechanism: Act on proximal convoluted tubule; inhibits carbonic anhydrase which usually facilitates reabsorption of bicarb - causes bicarb to stay in lumen causing urine alkalization; prevent the reabsorption of sodium [with bicarb] causing natriuresis; side effects: cause a normal anion gap metabolic acidosis - no longer used as a diuretic; hypokalaemia [potassium wasting diuretic]; type 2 renal tubule acidosis; urinary alkalization - promotes calcium phosphate stones [insoluble at high pH] use: decreased production of aqueous humor - glaucoma; decrease production of CSF - idiopathic intracranial hypertension; prevention of mountain sickness |
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Mannitol [osmotic diuretic] |
Mechanism: acts at the PCT and descening loop of henle; draws free water out of the CNS; draws free water out of the eye side effects: pulmonary oedema; exacerbates heart failure; induced free water depletion = hypernatraemia use: reduce elevated intracranial pressure; decreases intraoccular pressure |
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loop diuretics: furosemide |
mechanism: acts on thick ascending limb; selectively blocks the NKCC transporter on the luminal membrane = prevents reabsorption of Na+ = natriuresis = water follows sodium out; reduction of lumen positive potential = excretion of Mg2+ and Ca2+; induce expression of COX = synthesis of prostaglandins = excretion of Na2+ and dilatation of afferent arteriole use: first line for heart failure [symptoms - NOT mortality]; peripheral and pulmonary oedema; ascites in liver failure; adjunctive hypertension side effects: hypokalaemia = potassium wasting diuretics; hypomagnesemia; NSAIDs decrease effect of loop diuretics; ototoxic - reversible; sulphur allergy; interstitial nephritis [blue cells on histology]; hyperuricemia |
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thiazide diuretics |
Mechanism: act on distal convoluted tubule; Na+K+ATPase on basolateral membrane; NaCl cotransporter reabsorbs these ions at apical membrane of DCT - thiazide diuretics inhibit NaCl reabsorption by blocking the NaCl cotransporter causing natriuresis [and hypokalaemia]; enhance calcium reabsorption in DCT use: mild or moderate hypertension; adjunctive [to loop diuretic] symptomatic treatment in heart failure; nephrogenic diabetes insipidus; prevent calcium stones [increased calcium reabsorption causes hypocalciuria]; can help in osteoporosis [increased calcium reabsorption] side effects: hypercalcaemia; hyperlipidaemia; hyperglycaemia; hyperuricaemia [can precipitate gout]; decrease renal clearance of lithium [increase levels]; hypokalaemia [potassium wasting diurectic]; hyponatraemia; metabolic alkalosis [from increased renin production which leads to increase HCO3 absorption] |
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Potassium sparring diuretics: amiloride; spironalactone |
Physiology: ENaCs of Principal cells in collecting duct [reaborption of Na+ creates a negative potential that facilitates K+ excretion] alpha intercalated cells of collecting duct [major site of H+ excretion]; intracellular mineralocorticoid [aldosterone] receptor; aldosterone upregulates ENaCs to increase Na+ reabsorption and therefore potassium secretion; aldosterone upregulates H+ATPase increasing H+ excretion Mechanism: amiloride inhibits Na+ reabsorption and therefore K+ secretion through ENaC = promotes natriuresis; spironolactone antagnosises mineralocorticoid receptor Use: spironolactone used in hyperaldosteronism [HTN and low K+] i.e. Conn syndrome, adrenal tumour etc; heart failure [where diuretics cause K+ wasting]; prevent cardiac remodelling due to high levels of aldosterone amiloride: lithium induced nephrogenic diabetes insipidous; heart failure [where diuretics cause K+ wasting]; side effects: amiloride increases lithium clearance; hyperkalaemia; normal anion gap metabolic acidosis; inhibit effects of aldosterone in collecting duct causing a type 4 renal tubular acidosis |
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calcium channel blockers dihidropyridines: nifedopin, amlodipine non-dihidropyridine: verapamil; diltiazem |
Mechanism: target voltage gated l-type calcium channels; dihidropyridines block l-type calcium channel in smooth muscle; non-dihidropyridines block l-type calcium channel blockers in cardiac muscle [verapamil most cardiac selective] - decrease cardiac contractility; decrease activity in SA and AV nodes use: HTN [IV dihydropridine e.g. clevidipine, nicardipine can treat HTN emergency]; nifedipine is safe in pregnancy; treat stable angina -dihydropiridines [amlodipine] dilate coronary arteries; non-dihyrdropyridines reduces after load; prinzmetal angina; non-dihdropyridines decrease myocardial oxygen demand; dihdropyridines treat Reynaud's syndrome; berry aneurysm/subarachnoid haemorrhage; migraine prophylaxis with verapamil; non-dihdropyridines have anti-arrythmic properties side effects: non-dihdropyridines: bradycardia; verapamil - constipation; gingival hypertrophy; verapamil and diltiazem contraindicated in heart block; dihydropyridines: light headedness; headache; peripheral oedema; reflex tachycardia; nifidepine can exacerbate myocardial ischaemia due to reflex tachycardia - avoid in patients with unstable angina or MI; both dihidropyridines and non-dihydropyridines can worsen heart failure |
