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3rd Year Drugs > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

1
Q

Name loop diuretics

A

Furosemide, bumetanide

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2
Q

When to use loop diuretics

A

1) Acute pulm. oedema
2) Chornic heart failure
3) Symptomatic fluid overload

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3
Q

How do loop diuretics work?

A

Inhibits the Na+/K+/2CL- transporter in the ascending loop of Henle
Also dilate capicatance veins –> reduces preload and improves contractile function of heart in acute heart failure

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4
Q

Side effects of loop diureits

A

Dehydration + hypotension
Increased loss of sodium and potassium –> also indirectly causes the excretion of Mg, Ca and H+
Hearing loss and tinnitus at high doses –> this is because there is a similar transporter in the ear

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5
Q

Contraindications of loop diuretics

A

Severe kypokalaeamia

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6
Q

Caution of loop diuretics

A

Hepatic encephalopathy ( as low potassium can cause/worse coma)
Hypokalaemia/natraemia
Gout (as they inhibit the excretion of uric acid)

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7
Q

Interactions of loop diurectics

A

1) Lithium increased (due to reduced excretion)
2) Increased risk of digoxin toxicity due to possible hypokalaemia
3) Increased risk of ototoxicity and nephrotoxicity with aminoglycosides!

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8
Q

Name potassium sparing diuretics

A

Amiloride

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9
Q

How does amiloride work

A

Weak dirutetic alone
Inhibits Na reabsorption via ENaC channels in the distal convoluted tubule
Causes sodium and water excretion

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10
Q

How is amiloride normally prescribed

A

As combination e.g.

Co-amilofruse or co-amilozide

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11
Q

Adverse effects of amiloride

A

GI Upset

Hypotension and urinary symptoms

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12
Q

Contrainidcations of amiloride

A

Severe renal impairment

Hyperkaelaemia

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13
Q

Do not start amiloride if??

A

Hypokalaemia as effects on potassium are unpredictable

Severe volume depretion

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14
Q

What drugs do most diuretics effect

A

Most diuretics effect the renal clearance of digoxin and lithium increasing there dose so monitor this!!

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15
Q

Name an aldosterone antagonist

A

Spirinolactone, eplerone (only for heart failure)

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16
Q

Indications for aldosterone antagonists

A

1) Ascites and oedema due to liver cirrhosis –> first line
2) Chronic heart failure: usually with ACEi and beta blocekr
3) Primary hyperaldosteronism

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17
Q

How does aldosterone antagonists work

A

Normally aldosterone produced by the adrenal cortex –> Increase ENaC activity causing Na and water reabsorption
BUT these block this

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18
Q

Adverse effects of aldosterone antagonists

A

Gynacomastia
Hyperkalaemia –> muscle weakness, arrhytmias
Liver impairment and jauncide
Steven Johnsons Syndrome

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19
Q

Contraindications of aldosterone antagonists

A 
Severe renal impairment and hyperkalaemia
Addisons disease (aldosterone deficient)
Avoid in pregnant or lactating women
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20
Q

Interactions of aldosterone antagonists

A

1) Other potassium elevating drugs e.g. ACEi and ARB)

Don’t combine with potassium supplements

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21
Q

Name Beta blockers

A

Bisoprolol, atenolol, metoprolol (beta 1 selective)

Propanolol (non-selective)

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22
Q

Indications of beta blockers

A

1) IHD –> 1st line to improve angina & ACS
2) CHD –> 1st line to improve prognosis
3) AF –> 1st line to ventricular rate and in paroxysmal AF to maintain sinus rhythm
4) SVT –> 1st line
5) Hypertension –> not for initial therapy, use 4th line; after ACEi, ARBs, Ca2+ channel blockers, thiazide diuretics

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23
Q

Where are the different types of beta receptors

A

B1 receptors - mainly heart

B2 receptors - smooth muscle in vessels and airways

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24
Q

How do beta blocker work

A

Via B1 receptors reduce the force of contraction and speed of condution in the heart

This decreases oxygen demand to relieve ischaemia and increase myocardial perfusion
Also protects the heart from chronic sympathetic stimulation

Prolongs the refractory period of the AV node
Breaks self-perpetuating circuits of SVT
Reduce renin secretion from the kidney –> as this is mediated by B1 receptors

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25
Q

Adverse effects of beta blockers

A 
Fatigue
Cold extremities
Headache
GI disturbance
Impotence
Sleep distrubance
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26
Q

Contradindications of beta blockers

A

Asthma
Heart failure –> can use but start slow dose as initially decreases cardiac function
Haemodynamic instability
Hear block
Avoid with verapamil and diltiazem (non-DHP calcium channel blockers ) –> can cause HF, bradycardia and asystole!

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27
Q

Name thiazide diuretics

A

Bendroflumethiazide

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28
Q

Indications of thiazide diuretics

A

1) Alternative 1st line for hypertension (where Ca blockers otherwise unsuitable e.g. oedema or features of heart failure)
2) Add on tratment for hypertension –> in patients who bp isnt controlled by ACEi or Ca channel blockers

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29
Q

How do thiazide diuretics work

A

Inhibit the Na+/Cl- transported in the distal convoluted tubulue
Diuresis causes fall in extracellular volume –> overtime compensatory changes this (due to RAS activation)

Long term anti-hypertesnive effect is due to vascodilatation

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30
Q

Adverse of effects of thiazide diurtetics

A

Hyponatraemia
Hypokalaemia (as increase Na delivery to distal tubulae, is exchanged for K+)
Increased glucsoe –> may unmask type 2 DM
Increase LDL triglycerids
Impotence in men

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31
Q

Contraindications of thiazide diuretics

A

Hypokalaemia
Hyponatraemia
Gout (decreases uric acid excretion_

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32
Q

Interactions of thiazide diurietics

A

NSAIDS –> reduce their efffect

Avoid combo with other drugs that lower potassium

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33
Q

Name cardiac glycosides

A

Digoxin

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34
Q

Indications for digoxin

A

1) AF or atrial flutter –> 3rd line

2) Severe HF –> 3rd line after ACEi and beta blocker

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35
Q

Actions of digoxin

A

Negatively chronotropic and positively inotropic (decreaeses HR and increases force of contraction)

Increaese parasympathetic tone –> slow conduction at the AV node

Inhibits the Na/K ATPase pump –> sodium accumulates in the cell

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36
Q

Adverse effects of digoxin

A 
Bradycardia
GI disturbance
Dizziness
Visual distubance
Rash
Proarrhythmic --> Low therapeutic index
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37
Q

Contraindications of digoxin

A

2nd degree heart block

ventricular arrhytmias

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38
Q

Caution of digoxin in

A

Renal failure –> as eliminated by kidneys
Electrolyte disturbance –> potassim is the most important as digoxin competes with K+ at the Na/K pump, hence low potassium enhance the effects of digoxin

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39
Q

Interactions of digoxin

A

Loop and thiazide diuretics –> these decrease potassium

Amiodarone, calicum channel blockers, spirinolactone, quinine –> all increase the risk of digoxin toxicity

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40
Q

Name an anti-dysrhythmic

A

Amiadorane

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41
Q

How does amiodarone work?

A

Blockade of the Na, Ca and K channels
Antagonism of the alpha and beta adrenergic receptors –> this reduces spontaneous depoaliration, slows conduction velocity, increases refractoriness, affects the AV node
Breaks the self-perpetuating circle in SVT
Treats VT and refractoy VF by suppressing spontaneous depolaristations

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42
Q

Indications for amiodaroneq

A

Wide range of tachyarrhytmias

e.g. SVT, AF, refractory VF, ventricular tachycardia

43
Q

Adverse effects of amiodarone

A

Hypotension if IV
Chronic side effects: pneumonitis, hepatitis, bradycardia, skin photosensitivity and grey discolouration, thyroid abnormalaties

44
Q

Why does amiodarone cause thyroid abnormalities

A

As it has a similar structural similarties to thyroid hormones

45
Q

Warnings of using amiodarone

A

Avoid in severe hypotension
Heart block
Active thyroid disease

46
Q

Incteractions of amiodarone

A

Increases the plasma conc of digoxin, dilitazem and verpalmil
This may incrases the risk of bradycardia, AV block and heart fialure therefore doses of these drugs should be halved if amiodarone is started

47
Q

Name calcium antagonists

A

Amlodipine, nifedipine

Verapamil, diltiazem

48
Q

Indications of calcium antagonsis

A

1) Hypertension –> 1st line
2) stable angina –> use all calcium channel blockers
3) Supraventricular arrhytmias -> use diltiazem and verapamil

49
Q

Action of calcium antagnosis

A

Decreases Ca2+ entry into vasculr and cardiac cells
Causes relaxation and dilatation of arterial smooth mucle
reduces myocardial contractility
Suppresses cardiac conduction –> particularly across the AV node

50
Q

What are the 2 classes of calcium antagonists

A

1) Dihydropyridines: Amlodipine and nifedipine –> relatively selective for vessels
2) Non-DHP: Verampil and diltiazem. Relatively cardioselective, diltiazem some action on vessels

51
Q

Side effects of calcium antagonists

A

Dihydropyridies: Ankle swelling, flushing, headaches, palpitations

Non- DHP: Constiption, bradycardias, hert block, F

52
Q

Contraindications of calicum antagonists

A

Poor LV function
Avoid in AV nodal delay
Unstable angina –> as vasodilatation causes reflex increase in contractility and tachycardia increases o2 demand
Severe aortic stenosis

53
Q

Interactions of calcium antagonists

A

Avoid non-DHP and beta blockers unless close supervision:

Both drugs are -vely chronotropic and negatively inotropic –> together might cause HF, bradycardia and even asytole

54
Q

Name nitrates

A

GLyceryl trinatrate

Isosorbine mononitrate

55
Q

Indications of nitrates

A

1) acute angina/ACS
2) angina prohylaxis
3) Pulm oedema –> with O2 and furosemide

56
Q

How do nitrates work

A

Converted to NO–> increases intracellular cGMP and decreases intracellular calcium

Causes venous and arterial vasodilatation (arterial lesser)

Relaxation of cappacitance veins –> decreases preload and LVF filling –> this reduces cardiac work and myocardial demand hence relieving angina and AF

IT IS REDUCING PRELOAD THAT RPEVENT MOST ANDINA

It also relieves coronary vasospasm and dilates collateral vessels to increase coronary perfusion

57
Q

Adverse effets of nitrates

A

Vasodilatory effects: headache, flushing, light-headedness, hypotension
Sustained use can cause tolerance

58
Q

Contraindications of nitrates

A

Severe aortic stenosis
Haemodynamic instability
Hypotension

59
Q

Interactions of nitrates

A

1) DO NOT USE WITH PHOSPHODIESTERASE INHIBITOS –> these enhance and prolong the effects of nitrates
2) Caution with anti0-hypertensives

60
Q

Name some statins

A

Simvastatin, atorvastatin, rosuvastatin, pravastatin

61
Q

Indications for statins

A

1) Primary preventin of CV Disease
2) Secondary prevention of CV disease
3) Primary hyperlipidaemia

62
Q

Action of statins

A

Inhibit HMG CoA Reductase –> Decreases cholesterol production by the liver and also increases clearance of LDL cholesterol
Indirectly also reduces triglycerides and slightly increases HDL levels

63
Q

Adverse effects of statins

A

Headaches and GI disturbances
Sumple aches to more serious myopathy and rhabdomyolysis
Can cause a rise in liver enzymes (ALT)

64
Q

Contraindications of statins

A

Pregnancy

Breastfeeding

65
Q

Caution of statins in

A

Heptic

Renal impairment

66
Q

What should you avoid grapefruit juice when taking?

A

Statins

As grapfruit juive is a CP450 inhibitor, enzymes whcih eliminate simvastatin and atorvastatin

67
Q

Interactions of statins

A

Metabolism reduced by CP450 inhibitos

Amlodipine –> has a similar interaction to CP450 inhibitors

68
Q

Name some CP450 inhibitors

A

Amiodarome, diltiazem, itraconazide, macrolides, protease inhibtors, grapefruit juice

69
Q

When should you take statins

A

at night as they have greater effect when dietary intake is at its lowest

70
Q

Uses of heparins

A

1) VTE
2) ACS –> use LMWH and fondaparinux as first line to impve revascularisation and prevent intracoronary trombus progression

71
Q

How does UFH work

A

Activates antithrombin –> inturn inactivates FXa and thrombin

72
Q

How does LMWH work?

A

Similar action to UFH but preferentially inhibits FXa

73
Q

How does fondaparinux work?

A

It is a synthetic ocmpound that only inhibits FXa

74
Q

Adverse effects of heparins

A

Bleeding
Injection site reactions
Heparin induced thrombocytpenia –> stop drug immediately if this occurs

75
Q

Caution of heparis

A

1) Increased bleeding risk
2) renal impairment –> as can accumulate

3) AVOID AROUND TIME OF INVASIVE PROCEDURES

76
Q

Interactions of heparins

A

Avoid combining with other antithrombotics except

1) when initiating warfarin
2) antiplateletls with fondaparinux/LMWH in ACS

77
Q

What reverses heparin

A

Protamine –> doesnt work for fondaparinux

78
Q

How do we give heparins?

A

SC injection

79
Q

How do we measure UFH effect

A

APTT

80
Q

How do we measure LMWH and fondaprinux’s effect

A

FXa activity –> rarely requires monitoring

81
Q

Name TPAs

A

Alteplase, Reteplase, tenetplase

82
Q

Uses of TPAs

A

1) Acute MI
2) Fibrinolytic treatment of acute ischaemic stroke
3) Acute massive PE with haemodynamic instability

83
Q

How do TPA’s work

A

Convert plasminogen to plasmin

Plasmin then breaks down the clots

84
Q

Adverse effects of TPAs

A

1) Haemorrhages –> intracererbal and haeamatomas are common
2) Hypersensitivity
3) Cardiac disorders –> ischaemia/angina and hypotension and heart failure are common

85
Q

Contrainidications of TPAs

A

1) Hypersensitivity to the drug OR gentamicin

2) High risk of haemorrhage

86
Q

What shoudl we avoid the use of when taking TPAs

A

Rigid catheters

87
Q

Interactions of TPAs

A

1) ACEi –> enhanced risk of anaphylactoid reactions

2) anticoagulants –> enhances risk of haemorrhage

88
Q

What is the short life of TPAs

A

4-5 minutes hence quickly eliminated

89
Q

What are the infications for warfarin?

A

1) VTE –> 3-6 months if single episode, life long if recurrent
2) AF
3) Heart valve replacement –> short term if tissue replacement, lifelong in mechanical

90
Q

What should we not use warfarin to prevent

A

Do not use to prevent arterial thrombosis as they are primarily driven by platelet aggregation

91
Q

How does warfarin work

A

VKOR Inhibitor

This prevents oxidised vitamin K being reactivated which is needed for coagulation factors

92
Q

Adverse effects of warfarin

A

Bleedigin

93
Q

Contraindicatinos fo warfarin

A

1) immediate risk of bleeding

94
Q

Cautions of warfarin

A

1) Liver disease –> less able to metabolise drug and can be over-anticoagulated
2) Avoid in first trimester as teratogenic and avoid in the last trimester as associate with maternal haemorrhage

95
Q

Interactions of warfarin

A

1) CP450 inhibitors can cause increased bleeding risk (e.g. fluconazole, macrolides and protease inhibitors
2) CP450 induces increase the clot risk (e.g. carbamzepine, rifampicin, phenytoin)
3) Antibiotics increase anticoagulation as they kill gut flora that synthesis vitamin K

96
Q

What time shoudl you take warfarin?

A

18:00

97
Q

What is the INR target in AF & VTE

A

2-3

98
Q

Indications of NOACs

A

AF
VTE
DVT + PE (Apixiban only)

99
Q

Mechanisms of NOACs

A

Riovoraxiban and Apixiban = FXa inhibitors

Dabigatran = Direct thrombin inhibitor

100
Q

ADVERSE EFFECTS OF NOACS

A

Bleeding

GI Upset

101
Q

Contraindications of NOACS

A

ACtive pathological bleeding
Hypersensitvity
Mechanical/prosthetic heart valves

102
Q

Interactions of NOACs

A

Antiplatelets/NSAIDS

CP450 Inhibitors –> increases the bleeding risk

103
Q

How are NOACS eliminated

A

Dabigatran –> primarily renally eliinitaed

Rivoroxciban –> 1/3 eliminated by the liver unchanged, the rest is by hepatic CP450 enzymes

3rd Year Drugs (10 decks)

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