heart drugs Flashcards

1
Q

what consitutes to congestive heart failure?

A

cardiac output is below normal range due to biochemical defect or related underlying cause such as hypertension

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2
Q

what are symptoms of congestive heart failure

A

decrease exercise tolerance, tachycardia, oedema, shortness of breath, cardiomegaly and failure to pass urine

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3
Q

what type of drugs are used to treat congestive heart failure? and what is main drug used and what is brief mechanism of action of the others

A

inotropes: increase intracellular calcium

cardiac glycosides

beta 1 agonists

type 3 phosphodiesterase inhibitors; increase cAMP in heart, thus increasing strength of contraction

dopamine: D1 receptors cause renal arterial vasodilation, reducing blood pressure, presynaptic D2 receptors inhibit noradrenaline release
diuretics: reduce pre load (venous pressure) causing more efficient contractions

main drug: cardiac glycosides

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4
Q

what is the effect of cardiac glycosides

A

increase cardiac output, decrease heart rate, decrease cardiac area, decrease body weight, urine output increases, increase of atrioventricular conduction time

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5
Q

give an example of 2 cardiac glycosides and what is their mechanism of action

A

ouabain: leads to greater increase in intracellular sodium concentration in response to membrane potential, thus causing greater contraction
digoxin: inhibits sodium/potassium ATPase pump, causing increase in intracellular calcium:

in heart there is sodium/calcium pump which pumps calcium out and sodium in, due to inhibition of ATPase pump there is increase of sodium concentration and so less calcium concentration is pumped out, increasing intracellular calcium

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6
Q

how does body potassium effect digoxin?

A

hypokalaemia increases digoxins actions, hyperkalaemia decreases it

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7
Q

what are unwanted effects of cardiac glycosides?

A

atrioventricular block, ectopic beats, anorexia, nausea, vomiting
has low therapeutic index

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8
Q

what are symptoms of angina pectoris and why is it caused?

A

ischaemic chest pain

cause: imbalance between oxygen supply and output, can be brought on by exercise

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9
Q

what is the treatment for angina pectoris?

A

reduce metabolic demand, improve myocardial perfusion

drugs: organic nitrates/ites, calcium channel antagonists, beta adrenoceptor antagonists (to reduce metabolic demand)
surgery: bypass stents

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10
Q

name some organic nitrates/ites used for treatment and what is their action on body

A

nitrites: amyl nitrite
nitrates: glyceryl trinitrate (nitroglycerin), isosobide dinitrate

action: relaxation of smooth muscle, causing dilation of large veins, reduce preload

redistribution of coronary flow to ischaemic areas

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11
Q

what is action of beta adrenoceptor antagonists in treatment of angina pectoris, and how does it affect exercise tolerance

A

reduction in heart rate, blood pressure and contractility of cardiac muscle (reduces oxygen demand)

increases exercise tolerance in angina patients, decreases tolerance in normals

increased time in diastole, causing increase in myocardial perfusion as well as increase in left ventricular left diastolic volume

are co-administered with nitrates

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12
Q

what are side affects of organic nitrates/nitrites

A

reflex tachycardia due to lowered blood pressure

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13
Q

what is mechanism for calcium channel antagonists in angina, give examples and their difference

A

inhibitors of L type voltage gated calcium channels in heart

inhibit calcium entry and so reduce coronary after load

verapamil; selective for cardiac muscle, nifedipine; selective for smooth muscle (reduces after load)

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14
Q

what are unwanted effects of calcium channel blockers

A

supress cardiac contractility, and slow conduction

bradycardia
high degree of AV block

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15
Q

what drugs are used in treatment of coronary heart disease and what is their mechanism

A

drugs have prognostic benefit

aspirin: anti-platelet agent, alters balance between thromboxane A2 and PGI2, low doses of aspiring has prophylactic effect against thrombosis
statins: inhibit enzyme HMG-CoA reductase, the rate limiting step in cholesterol synthesis , aimed at treating underlying atheromatous disease

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