ACS drugs Flashcards

1
Q

main targets for CAD management (4)

A

supply - coronary blood flow, arterial oxygen content;
demand - HR, force of contraction

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2
Q

main drug classes in CAD (6)

A

reduce cardiac workload (decrease myocardial O2 demand) - B-blockers, CCBs, other channel inhibitors, BP lowering (indirectly, effect afterload);
coronary vasodilators - nitrates, K+ channels openers (e.g.nicorandil)

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3
Q

where are L-type Ca2+ Channels present and what is the effect of blocking them (3)

A
  1. arterial smooth muscle - vasodilation
  2. cardiac muscle - reduced force of contraction
  3. cardiac pacemaker tissue - reduced heart rate/AVN block
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4
Q

how does Ca2+ cause muscle contraction (mech)

A
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5
Q

what are the 2 types of CCBs and examples

A
  1. non-dihydropiridine (negative ionotropic), useful for arrythmias and angina, veramapil/ diltiazem
  2. dihydropiridine (non-ionotropic), acts on smooth muscle to reduce BP - used for hypertension, little/no cardiac effect, amolodipine, nifedipine
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6
Q

common adverse affects of CCBs (6)

A

negative ionotropic - slow HR, reduced contraction (may worsen heart failure);
non-ionotropic - headache (due to increased flood flow), flushing, peripheral oedema, reflex tachy (to counteract increased blood flow)

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7
Q

what does ionotropic mean (in terms of the heart)

A

contractility - positive inotropy is an increase in contractility (contract with more force)

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8
Q

verapamil vs diltiazem

A

verapamil - mainly cardiac affects; diltiazem - cardiac and vascular effects; choose appropriate drug depending on the action required

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9
Q

high levels of what NTs (2) result in high mortality levels from heart disease

A

NA; adrenaline

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10
Q

what does increased NA/adrenaline cause (cardiac + resp)

A

activates beta-receptors which act on cardiac tissue and pacemaker cells to increase force and rate of contractions (B1); acts of bronchial smooth muscle to dilate airways (B2)

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11
Q

what is the effect of BBlockers

A

block beta-receptors so they cannot be stimulated by NA/adrenaline release -> stops increase in HR/contraction force; new BBs try to focus on just blocking B1 receptors so that lung function is not affected, otherwise it could be danger out to people with asthma

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12
Q

commonly used BBs

A

non-specific: propanolol (worsens asthma);
cardioselective: atenolol, bisoprolol, metoprolol;
vasodilator activity: carvedilol, labetelol (alpha blocking properties, causes vasodilation)

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13
Q

what conditions have BBs demonstrated a reduction in mortality in

A

ACS; MI; chronic heart failure; angina; AF; resistant HTN (small roll in HTN alone)

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14
Q

adverse effects of BBs (4)

A

cardiac: bradycardia, HF initially worsens (start a low dose);
sympathetic blockade: bronchoconstriction, fatigue/feeling cold (due to decreased adrenaline)

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15
Q

MOA of nitrates

A

nitrates -> increased nitric oxide -> increased cGMP -> increased dephosphorylation of myosin light chain, decreased Ca2+ influx into cell -> relaxation of vascular smooth muscle (vasodilation)

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16
Q

effects of nitrates (3)

A

arterial dilation: improves coronary supply by vasodilating coronary artery to reduce BP;
venous dilation: decreased preload and stretching of the heart (decreased venous return to heart), Decreased pressure in ventricles (Especially diastolic wall pressure)

17
Q

adverse effects of nitrates (4)

A

hypotension, reflex tachy, headaches, flushing

18
Q

what are nitrates used for

A

symptom relief in ischaemic chest pain; relief of acute heart failure (high dose IV required)

19
Q

commonly used nitrates (2)

A

glyceryl trinitrate (GTN) - sublingual or spray usually (oral is broken down by liver), rapid relief but short acting;
isosorbide mononitrate - oral, OD, prevention of angina pain

20
Q

specialist drugs for angina treatment (3)

A

nicorandil (K+ channel opener, nitrate action); ranolazine (late Na+ current inhibitor); ivabradine (sinus node inhibitor, slows HR, blocks conduction)

21
Q

when to use CCBs

A

uncontrolled hypertension; vasoplastic/mixed angina, MI without HF

22
Q

when to use BBs

A

previous MI or HF

23
Q

what are the key targets for hypertension

A

cardiac output (decrease - slow pumping); vascular resistance (vasodilation to reduce resistance, vol of blood is reduced)

24
Q

main drug targets in hypertension (and drug types)

A

intravascular volume - diuretics, thiazides;
sympathetic tone - alpha and B-blockers;
peripheral arteries - CCBs (vasodilation);
neuroendocrine mediators of BP (block) - ACEi, ARBs, renin inhibitors

25
Q

renin-angiotensin-aldosterone system pathway

A

angiotensin – (rennin, causes Na+ depletion, decreaded BP and increased B1 adrenogenic symp stimulation)–> angiotensin I –(ACE)–> angiotensin II, causes vasoconstriction, ADH release, increased symp stimualtion —-> aldosterone release, causes salt and water retention

26
Q

examples of ACE inhibitors

A

ramipril, captopril, enalapril

27
Q

when to use ACE inhibitors

A

first line for hypertension UNLESS >55yro or african heritage

28
Q

what should be given to those who cannot take ACE inhibitors (>55yro, african heritage)

A

CCBs, Angiotensin II blockers (2nd line)

29
Q

physiological effects (+side effects) of starting an ACE inhibitor + how to ensure safety (4)

A

drops BP (give small dose, check not too volume depleted); worsens renal function (check U&Es after a week); retains K+ (stop K+ supplements or K+ sparing diuretics); causes cough and other allergies

30
Q

examples of angiotensin II blockers

A

lostartan; irbestartan

31
Q

types of diuretics (4)

A

loop; thiazides; thiazide-like-diuretics; potassium-sparing

32
Q

loop diuretics - use, effectiveness, examples

A

heart failure; high efficacy, 25% of sodium load can be excreted (used in renal impairement), IV works within 30 min - 1h, Used orally for long term 1/day in morning; Furosemide, bumetanide

33
Q

thiazide diuretics - use, examples

A

hypertension; Bendroflumethiazide

34
Q

thiazide-like- diuretics - use, effectiveness, examples

A

hypertension; Only excrete 5-10% of sodium load, Ineffective if GFR is under 30 and should be avoided; indapamide

35
Q

K+ sparing diuretics - use, effectiveness, examples

A

heart failure, hypertension; <5% sodium load excreted
Used in combination with more effective diuretics; spironolactone

36
Q

side effects of diuretics and how to ensure safety

A

Hypovolaemia, dehydration, hypotension (affects renal function); Electrolyte imbalance - Low K+, High urea;
Monitor BP, urine output, body weight; Check electrolytes regularly if on high dose

37
Q

HTN treatment plan (4)

A
  1. ACEi/CCB (if not tolerated)
  2. ACEi + CCB
  3. ACEi + CCB + thiazide like diuretic
  4. resistant hyper tension, continue as above + consider further diuretic + seek specialist help
38
Q

contraindications for ACEi

A

pregnancy (affects growth); african heritage; >55yro; HOCM; renal impairment