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drugs y3 > Cardiac > Flashcards

Cardiac Flashcards

1
Q

what type of drug is aspirin

A

anti-platelet

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2
Q

how does aspirin work

A
  • decreases platelet accumulation and inhibits thromboxane, decreasing platelet aggregation
  • inhibits cyclooxygenase 2, decreasing prostaglandins, decreasing pain and inflammation
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3
Q

when is aspirin used

A

ACS, secondary prevention for CV syndromes, AF, angina

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4
Q

contraindications for aspirin

A
  • children under 16 - Reyes Syndrome
  • Haemophilia
  • Peptic ulcers
  • NSAID hypersensitivity
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5
Q

side effects of aspirin

A

GI disturbance, GI ulcers, bleeds, bronchospasm

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6
Q

possible interactions with aspirin

A

alcohol - GI bleeds
ibuprofen - reverses anti-platelet effects
corticosteroids - decreases aspirin concentration

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7
Q

what type of drug is clopidogrel

A

anti-platelet

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8
Q

when is clopidogrel used

A

prevention of atherosclerosis for people with PAD, ACS, secondary prevention, prevents stunts from occluding, AF, when aspirin is contraindicated

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9
Q

contraindications for clopidogrel

A

active bleeding

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10
Q

side effects of clopidogrel

A

GI disturbance, GI / intracranial bleeds

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11
Q

possible interactions for clopidogrel

A

antifungals/virals/bacterials/depressants/epileptics - decrease clop effect
analgesics increase risk of bleeding
anticoags - increases effect

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12
Q

how is clopidogrel eliminated

A

liver

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13
Q

how does clopidogrel work

A

decreases platelet aggregation and thrombus formation in arterial circulation

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14
Q

example of thrombolytic

A

alteplase / streptokinase

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15
Q

how does streptokinase works

A

dissolves clots

- activates plasminogen to form plasmin, decreases fibrin and breaks down thrombi

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16
Q

when is streptokinase used?

A

acute MI, DVT, PE

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17
Q

contraindications for streptokinase

A

haemorrhage, trauma or recent surgery

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18
Q

side effects of streptokinase

A

N&V, bleeding

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19
Q

possible interactions for streptokinase

A

antiplatelet/anti-coags - bleeding complications

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20
Q

how is streptokinase eliminated

A

hepatic

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21
Q

what type of drug is heparin

A

Anti-coag

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22
Q

examples of heparin

A

enoxaparin / fondaparinux

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23
Q

how does heparin / enoxaparin work

A

binds to and accelerates the activity of antithrombin III, decreasing co-factor 5a, decreasing prothrombin, decreasing thrombin, decreasing fibrin clot formation

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24
Q

when is enoxaparin used

A

DVT, PE, ACS - unstable angina to decrease clot progression

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25
Q

when is enoxaparin contraindicated

A

bleeding / clotting disorders, severe hypertension, renal failure, surgery or trauma

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26
Q

side effects of enoxaparin

A

haemorrhage, hyperkalaemia, heparin induced thrombocytopenia (HIT

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27
Q

possible interactions of enoxaparin

A

antiplatelets increase effect, ACEi increase risk of hyperkalaemia

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28
Q

how is heparin eliminated

A

renal

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29
Q

what type of drug is warfarin

A

oral anti-coag

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30
Q

how does warfarin work

A

inhibits vitamin K dependent clotting factors

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31
Q

when is warfarin used

A

VTE, AF to prevent PE, prosthetic valves

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32
Q

contraindications for warfarin

A

pregnancy (teratogenic), patients at risk of bleeding

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33
Q

side effects of warfarin

A

bleeding / haemorrhage

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34
Q

possible interactions of warfarin

A

NSAIS / aspirin increases bleeding risk, abx increase effect, hypothyroid decreases effect and hyperthyroid increases effect

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35
Q

target INR for patients taking warfarin

A

2-3

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36
Q

what is INR

A

international normalised ratio

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37
Q

examples of statins

A

simvastatin, atorvastatin

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38
Q

how do statins work

A

HMG-CoA reductive inhibits - these are enzymes which help to produce cholesterol (decreases LDL and increases HDL)

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39
Q

when are statins used

A
  • primary prevention of CVS events in patients >40 with >10% Q-risk off stroke
  • secondary prevention on CVS events
  • hyperlipidaemia
  • hypercholesterolaemia
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40
Q

contraindications for statins

A
  • liver disease
  • renal impairment
  • pregnancy
  • hypersensitivity
  • breastfeeding
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41
Q

side effects of statins

A
  • dizziness and headaches
  • GI disturbance
  • muscle problems (myopathy, rhabdomyolysis, myalgia)
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42
Q

possible interactions of statins

A
  • cytochrome P450 inhibitors such as amiodarone as these decrease the metabolism of statins
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43
Q

example of loop diuretics

A

furosemide

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44
Q

how does furosemide work

A

inhibits the Na+/K+/2Cl channel in the ascending loop of Henle, leading to decreased water reabsorption

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45
Q

when is furosemide used

A
  • CCF

- to help breathlessness in pulmonary oedema and oedema due to other things like renal/hepatic impairment

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46
Q

contraindications for furosemide

A
  • hypovolaemia / dehydration
  • AKI (not CKD)
  • hypokalaemia / hyponatraemia
  • hepatic encephalopathy (worsens hypokalaemia which increases risk of coma)
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47
Q

side effects of furosemide

A
  • increase urge to pass urine
  • low electrolytes
  • tinnitus / hearing loss
  • GI disturbance
  • dehydration
  • metabolic alkalosis
48
Q

possible interactions of furosemide

A
  • aminoglycosides, digoxin other drugs excreted by the kidney
49
Q

how is furosemide eliminated

A

kidneys

50
Q

example of thiazide diuretics

A

bendroflumethiazide, indapamide

51
Q

how do thiazide diuretics work

A

inhibit the Na/Cl pump on the convoluted tubule of the nephron, decreasing water reabsorption

52
Q

when are thiazide diuretics used

A

HF, hypertension (either with calcium channel blockers or instead of when they are contraindicated)

53
Q

contraindications for thiazide diuretics

A

hypokalaemia, hypovolaemia, dehydration, hyponatraemia, gout

54
Q

side effects of thiazide diuretics

A

hypokalaemia, hyponatraemia, gout, arrhythmias, impotence, GI disturbance, postural hypotension

55
Q

possible interactions of thiazide diuretics

A

NSAIDS decrease their effectiveness

56
Q

how do potassium sparing diuretics work

A

Inhibits effect aldosterone by competitively binding with the aldosterone receptor, thus increasing sodium and water excretion and increasing potassium retention

57
Q

what type of drug is spironolactone

A

aldosterone antagonist

potassium sparing diuretic

58
Q

when is spironolactone used

A
  • ascites and oedema due to liver cirrhosis
  • chronic heart failure
  • primary hyperaldosteronism
59
Q

contraindications for spironolactone

A

hyperkalaemia, Addison’s disease (low aldosterone), pregnancy, breastfeeding

60
Q

side effects of spironolactone

A
  • hyperkalaemia
  • gynaecomastia
  • liver impairment –> jaundice
61
Q

possible interactions of spironolactone

A

potassium elevating drugs such as ACEi and potassium supplements

62
Q

how is spironolactone eliminated

A

hepatic

63
Q

examples of beta blockers

A

bisoprolol, atenolol, propanolol

64
Q

how do beta blockers work

A
  • blocks beta adrenoreceptors on the heart, leading to decreased conductivity and so decreased contractility, leading to decreased heart rate
  • prolongs refractory period at the AV node
65
Q

when are beta blockers used

A
  • Ischaemic heart disease (angina, ACS)
  • AF
  • hypertension
  • supraventricular tachycardia (SVT)
66
Q

when are beta blockers contraindicated

A
  • asthma
  • COPD (specific B1 blockers like bisoprolol can still be used)
  • heart failure
  • haemodynamic instability
  • hepatic failure
  • heart block
67
Q

side effects of beta blockers

A
  • GI disturbance (nausea)
  • sleep disturbance
  • headache
  • impotence
  • cold extremities
  • bronchospasm / exacerbation of asthma
  • fatigue
68
Q

possible interactions of beta blockers

A

veramapil: non-dihydropyridine calcium channel blocker - this can lead to heart failure, bradycardia and asystole

69
Q

where are B1 receptors located

A

cardiac muscle

70
Q

where are B2 receptors located

A

smooth muscle of blood vessels and airways

71
Q

example of calcium channel blockers

A

amlodipine, verapamil

72
Q

difference between amlodipine and verapamil

A

amlodipine is a dihydropyridine and focusses more on vasculature whilst verapamil is a non-dihydropyridine and focusses more on cardiac function

73
Q

how do calcium channel blockers work

A

block calcium channels, inhibiting calcium influx into the cardiac muscle and vasculature, resulting in relaxation and vasodilation
- causes decreased myocardial contraction, especially at the AV node, decreasing oxygen demand

74
Q

when are calcium channel blockers used

A
  • hypertension
  • supra ventricular arrhythmias
  • angina
75
Q

when are calcium channel blockers contraindicated

A

poor left ventricular function, unstable angina, aortic stenosis AV node delay

76
Q

side effects of calcium channel blockers

A

flushing, ankle oedema, headache, palpitations, bradycardia, constipation, heart block, heart failure, chronic cough

77
Q

possible interactions of calcium blockers

A

beta blockers with non-dihydropyridine calcium channel blockers - this could lead to bradycardia, heart failure or asystole

78
Q

example of ACEinhibitor

A

ramipril

79
Q

how do ACEi work

A
  • inhibit angiotensin converting enzyme which prevents angiotensin I from converting into angiotensin II
  • angiotensin II causes vasoconstriction and stimulates aldosterone production
  • blocking angiotensin II stops vasoconstriction so causes a decreases in peripheral vascular resistance
  • also decreased levels of aldosterone increases water and sodium excretion
80
Q

when are ACEi used

A

HTN, CCF, IHD, diabetic nephropathy and CKD

- used as either a treatment of preventor

81
Q

contraindications of ACEi

A
  • aki
  • renal artery stenosis
  • breastfeeding
82
Q

side effects of ACEi

A
  • hyperkalaemia

- persistent dry cough

83
Q

possible interactions of ACEi

A
  • NSAIDS as this can increase risk of renal failure
  • potassium sparing diuretics
  • potassium increasing drugs or supplements
84
Q

examples of angiotensin II receptor antagonist

A

losartan

85
Q

how do AT1 blockers work

A

similar to ACEi

  • inhibit angiotensin II from binding to its receptor
  • inhibiting vasoconstriction - causing vasodilation
  • inhibiting aldosterone production, thus increasing water and sodium excretion
86
Q

when are AT1 blockers used

A

hypertension, CCF, IHD, diabetic nephropathy and CKD

87
Q

contraindications of AT1 blockers

A

aki
renal artery stenosis
breastfeeding

88
Q

side effects of AT1 blockers

A

hyperkalaemia, hypotension, renal failure

89
Q

possible interactions of AT1 blockers

A

NSAIDs, potassium sparing diuretics, potassium enhancing supplements or drugs

90
Q

examples of nitrates

A

isosorbide mononitrate

91
Q

how do nitrates work

A
  • nitrates are converted into nitric oxide
  • nitric oxide increases cGMP synthesis and decreases calcium in smooth muscle
  • causes vasodilation
  • decreases oxygen and cardiac demands
92
Q

when are nitrates used

A
  • angina prophylaxis (long acting)
  • angina relief (short acting like GTN spray)
  • pulmonary oedema (IV)
93
Q

contraindications of nitrates

A

aortic stenosis
hypotension
haemodynamic instability

94
Q

side effects of nitrates

A

causes vasodilation so: flushing, hypotension, headaches

95
Q

possible interactions for nitrates

A

phosphodiesterase inhibitors (sildenafil) as these increase hypotensive effects, viagra

96
Q

what type of drug is digoxin

A

cardiac glycoside

97
Q

how do cardiac glycosides work

A
  • negatively chonotropic (decrease HR) and positively inotropic (increase the force of contractions)
  • inhibits Na+/K+-ATPase pump, increasing intracellular Na
98
Q

when is digoxin used?

A

AF and atrial flutter to decrease HR, 3rd line treatment in HF

99
Q

contraindications of digoxin

A

heart block, renal failure

100
Q

side effects of digoxin

A

bradycardia, GI disturbance, headaches and dizziness, rash, visual disturbances, arrhythmias

101
Q

possible interactions of cardiac glycosides

A

loop and thiazide diuretics (due to increase K+), calcium channel blockers, spironolactone (this increase the plasma concentration)

102
Q

example of anti-dysrhythmics

A

amiodarone

103
Q

how does amiodarone work

A

blocks Na+, Ca2+, K+ channels and causes antagonism of alpha and beta adrenergic receptors - decreases spontaneous depolarisation, slows conduction, decreasing heart rate - overall, restores rhythm

104
Q

when is amiodarone used

A

AF, atrial flutter, SVT, VT, VF

105
Q

contraindications for amiodarone

A

severe hypotension, hyperthyroidism, heart block

106
Q

side effects of amiodarone

A

if used chronically: bradycardia, pneumonitis, hepatitis, hypo/hyperthyroidism, hypotension

107
Q

possible interactions of amiodarone

A

amiodarone increases plasma concentration of certain drugs such as digoxin and verapamil

108
Q

examples of novel anticoags

A

rivaroxiban, dabigatran

109
Q

how do NOACs work

A

inhibit factor Xa, inhibiting thrombin formation

110
Q

when are NOACs used

A
  • similar to wafarin but safer and easier to monitor
  • to prevent recurrence of PE, DVT
  • to prevent complications like stroke in AF
111
Q

contraindications of NOACs

A

haemorrhage risk, surgery

112
Q

side effects of NOACs

A

bleeding - no antidote (in warfarin, vit K can be given)

113
Q

possible interactions of NOACs

A

cytochrome P450 inhibitors

114
Q

how are NOACs eliminates

A

liver

115
Q

what is an anti-coag

A

inhibits clotting factors, thus slowing down the body’s process of making clots

116
Q

what is an anti-platelet

A

inhibits platelets from clumping and forming clots

drugs y3 (10 decks)

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