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My cardiac meds

QuestionAnswer
Antiplatelet -agents prevent platelet from clumping and also prevents clots forming and growing
Anticoagulants Slow down clotting, thereby reducing fibrin formation and preventing clots from forming and growing
Aspirin (antiplatelet) -blood thinner Indication=used for risk of CVA,MI and unstable angina. MOA=inhibited cox enzyme which stops the production of thromboxone A2, suppressing platelet aggregation. ADR=GI upset,rash,bleeding,allergy,tinnitus, bronchospasm
Clopidogrel (antiplatelet) *prodrug Indication=used to prevent thrombus formation in IHD or intracoronary stent. MOA=blocks adenosine diphosphate (ADP) from binding to platelet receptors. ADR= bleeding, thrombocytopenia,nausea,fever,headache and rashes.
Ticagrelor (antiplatelet) *not prodrug Indications= MOA=blocks ADP from binding to platelet receptors ADR= bleeding
MOA of which thrombolytic drugs dissolve a blood clot *examples of thrombolytic drugs= streptokinase and urokinase Indications=MI,PE,DVT,ischaemic stroke, restore patency to central venous catheters & chest drains. MOA= converts plasminogen to plasmin
Warfain (anticoagulants) *indications=prevents DVT,PE,AF,prosthetic heart valves *antidote=vitamin K *contraindicated meds= aspirin- both bind to same receptors resulting in to much free warfain in plasma-can result In bleeding MOA= interferes with hepatic synthesis of vitamin K. (Dependant clotting factors).Vitamin k is required for synthesis of clotting factors. ADR= increased risk of blessing & GI upset Nursing responsibilities=not for surgery.-> monitor for bleeding.
Heparin (anticoagulants) -inhibits clotting factor-> stops clots -clexane=smaller version of heparin Indications=acture; PE, surgery, used in dialysis machines Antidotes= protamine MOA=binds with antithrbin to prevent the conversion of prothrombin to thrombin & fibrinogen to fibrin. Stops the clotting cascade. ADR=increases risk of bleeding. Nursinf responsibilities=not for surgery. -if pregnant use clexane as low molecular.
Diuretics *nursing responsibilities when administering diuretics •monitor weight daily especially in heart failure pts •monitor urine colour •start fluid balance •monitor blood pressure
Diuretic meds -diuretic classes & examples *loop diuretic=furosemide, bumetaminde, forsemide,ethacrynic acid. *thiazide diuretic= hydrochlorthiazide *potassium-sparing diuretic= amiloride
Diuretic meds (makes you pee) •indication •General diuretic MOA Indications=HF,HTN,oedema,renal failure MOA=modify renal functions and induce diuretics (peeing) & natriuresis (excretion of sodium chloride).increase in urine volume is achieved by inhibiting reabsorption of NA+ & CL in the nephron. The increase secretio
Nitrates (GTN) *indications= angina MOA=bind to nitrate receptors in vascular smooth muscle relaxing vascular smooth muscle. Causing vasodilation in peripheral veins leading to decr venous return to the heart + oxygen demand. Causes vasodilation of arteries which decr BP,incr myocardium per
Nitrates (GTN) Indications = angina ADR= due to vasodilation, headache,dizziness fainting and postural hypotension, relax tachycardia, N/V, ankle oedema. Be aware of nitrate tolerance
Statins (HMG-COA reductase inhibitor) *statins reduce the risk of coronary heart disease,stroke &death. Eg: atorvastatin,fluvostatin,pravastatin. INDICATION= high cholesterol, prophylaxis of stroke and CVD *HMG-COA is the enzyme necessary for cholesterol biosynthesis
Statins MOA=inhibitors of hmg-coa reductase decr cardiovascular risk by decr cholesterol synthesis by the liver, incr LDL receptors & in turn decr plasma cholesterol levels. Lower plasma LDL means atherosclerotic plaques may not form as readily & therefo or CI will be less likely to occur. Statins enters blood stream through intestinal cells metabolised and eliminated in the liver & kidneys. -> most commonly eliminated by faeces.HMG-COA reductase catalysed the conversions of HMG-COA to mevaloric acid -nee
Beta blockers MOA Indications= Post MI, HF, angina, HTN,arrhythmia **extra- don’t give BB to COPD & asthma pt. - Eg propanol is non-selective would cancel out the effect of the salbutamol interaction is at the B2 receptor. Blocks neurotransmitters adrenaline & noradrenaline from B receptors sites,inhibiting adrenergic activity. -inhibits & decr the affects of the sympathetic NS therefore decr HR, BP, contractability muscle, RR,O2 required for myocardium-> decr heart workloa
Beta blockers ADR Examples of BB= metoprolol, propanolol, labetalol, atenolol, cavedilol Fatigue, depression, bradycardia, hypotension, bronchospasm.
Cardiac Glycosides MOA =digoxin or lanoxin (IV) is the only commonly used digitalis glycoside ** treatment for heart failure & arrhythmia Beware digoxin toxicity. Antidote for digoxin toxicity = digibind MOA= inhibits activity of the sodium potassium pump.this increases intracellular sodium & produces a secondary increase in intracellular calcium which increased cardiac contraction, Overall effect is to reduce cardiac workload & nice output.
Cardiac Glycosides ADR Anorexia + other GI disturbances. CND effects- visual disturbance, confusion, fatigue, arrhythmias. Digoxin toxicity= decrease appetite N+V, abdo pain, bradycardia
ACE inhibitor = eg. Cilazapril, enalapril, quninapril, catropril Indications for ACE inhibitors= hypertension, Post MI, heart failure MOA= completely blocks the angiotensin converting enzyme responsible for the conversion of angiotensin I to angiotensin II. = decr BP. =inhibition of aldosterone release from adrenal cortex. = reduction of sodium & water retention.
ACE inhibitor = eg. Cilazapril, enalapril, quninapril, catropril ADR Effects of vasodilation = angina, CHF,hypotension, headaches, dry persistent tickling cough, GI irritation, rash, renal insufficiency ** people on ACE inhibitors have to be on beta blockers for HF
Created by: Sez123
 

 



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