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Pharmacology > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

1
Q

Who are statins indicated for primary prevention

A

Individuals >40y with a QRISK2 score of >10%

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2
Q

What is the MOA of statins

A

Inhibits HMG coA reductase

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3
Q

What are the 2 most common side effects of statins

A

Headache

GI disturbances

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4
Q

What are 3 serious side effects of statins

A

Myopathy
Rhabdomyolysis
Increase in ALT

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5
Q

Why should statins not be prescribed to pregnant and breastfeeding women

A

as cholesterol is required for foetal development

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6
Q

What drugs may lead to increased statin in the body

A

CYP450 inhibitors

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7
Q

What dose is used for primary prevention with a statin

A

40mg simvastatin

20mg atorvastatin

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8
Q

What time of day should statins be taken and why

A

Evening - as cholesterol synthesis is greatest in the morning

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9
Q

What monitoring is required with a statin

A

Check liver enzymes at 3 and 12 months

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10
Q

Explain the MOA of clopidogrel

A

Binds to ADP receptors on platelets and prevents aggregation preventing arterial occlusion

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11
Q

What is the most common adverse effe ct of clopidogrel

A

Bleeding

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12
Q

What are two other side effects of clopidogrel

A

GI disturbance

Thrombocytopenia

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13
Q

What is an absolute CI of clopidogrel

A

Active bleeding

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14
Q

How long before elective surgery should clopidogrel be with-held

A

7d

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15
Q

What drugs may clopidogrel interact with

A

CYP450 inhibitors - prevent metabolic, leading to increased concentration of clopidogrel

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16
Q

What drugs should clopidogrel be used with caution in

A

Other anti-platelets, increased risk of bleeding

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17
Q

What is the MOA of gabapentin

A

Act via pre-synaptic voltage-gated calcium channels to inhibit neurotransmitter release reducing neuronal excitability

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18
Q

What are 3 main side effects of gabapentin

A

Drowsiness
Dizziness
Ataxia

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19
Q

What is a relative CI of gabapentin

A

Renal impairment - need to reduce dose

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20
Q

What drugs may gabapentin interact with

A

Other sedatives - increases sedating effects.

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21
Q

What is the indication of aspirin

A
  1. Treatment ACS
  2. Treatment of ischaemic stroke
  3. Secondary prevention of cardiovascular events and stroke
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22
Q

What is the mechanism of action of aspirin

A

It is a COX inhibitor. By inhibiting COX, it prevents the production of arachidonic acid from thromboxane A2

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23
Q

How long dose the effect of aspirin last and why

A

during the lifespan of a platelet - this is because a platelet does not have a nucleus and therefore is unable to synthesise new COX

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24
Q

What is the most common side effect of aspirin

A

GI irritation

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25
Q

What side effects may aspirin cause in the gastrointestinal system

A

Peptic Ulcer

Gastric Haemorrhage

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26
Q

What is another side effect of aspirin

A

In high-doses aspirin can cause tinnitus

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27
Q

What are symptoms of aspirin overdose

A
  • Hyperventilation
  • Metabolic acidosis
  • Confusion
  • Convulsions
  • Cardiovascular collapse
  • Respiratory arrest
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28
Q

What are 3 absolute contraindications to aspirin

A
  • 3rd trimester of pregnancy
  • Allergic
  • Children under the age of 16
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29
Q

Why should aspirin not be given to children under the age of 16

A

Due to risk of Reye’s syndrome

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30
Q

What is Reye’s syndrome

A

Rare disorder that causes brain and liver damage

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31
Q

What condition is aspirin not routinely contraindicated in

A

Asthma

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32
Q

Why should aspirin not be given in the third trimester

A

As inhibition of COX causes decreased prostaglandin production that can lead to premature closure of the ductus arteriosus

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33
Q

What are two conditions were aspirin is relatively contraindicated

A

Gout - acute flare

History of peptic ulcers

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34
Q

In what drugs does care need to be taken when giving aspirin

A

Other anti-coagulants - increases risk of bleed

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35
Q

What dose of aspirin is given in ACS

A

300mg loading dose and 75mg thereafter

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36
Q

What dose of aspirin is given for acute ischaemic stroke

A

300mg for two weeks

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37
Q

What dose of aspirin is given for long-term prevention of thrombotic events

A

75mg

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38
Q

What should be prescribed with aspirin

A

Omeprazole (20mg) if at risk of peptic ulcer

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39
Q

When should aspirin be taken to minimise gastric complications

A

Following food

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40
Q

What are 4 indications of morphine

A
  1. Treatment of acute severe pain (eg. ACS)
  2. Treatment of chronic pain where other medications are ineffective (WHO analgesia ladder stage 3)
  3. Relieve breathlessness in acute pulmonary oedema
  4. Relieve breathlessness + pain in palliative care patients
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41
Q

Explain the MOA of opioids

A
  • bind to and activate opioid u receptors, which are G protein coupled receptors
  • acts to reduce neuronal excitability and pain
  • in the medulla they blunt the response to hypoxia and hypercapnia, reducing respiratory drive and breathlessness
  • by relieving pain + breathlessness, they reduce sympathetic NS activity
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42
Q

What are the side effects of morphine

A
  • Respiratory depression
  • Constipation
  • Pupil constriction
  • Euphoria
  • CNS depression in high doses
  • Itching, Urticaria
  • Tolerance and dependence
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43
Q

Why do the pupils constrict when using morphine

A

As morphine stimulates u-opioid receptors in the edinger-westphal nucleus

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44
Q

Why do opioids cause constipation

A

As increase smooth muscle tone decreasing motility

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45
Q

Why do opioids cause itching

A

Stimulate degranulation of mast cells and histamine release

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46
Q

When should doses of opioids be reduced

A

Liver Failure
Kidney Failure
Elderly

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47
Q

What is a relative contraindication to opioid use and why

A

Biliary colic. Opioids can cause spasm of the sphincter of Oddi which can worsen pain. Therefore, different analgesia should be used.

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48
Q

What drugs should morphine not be used with

A

Other sedative agents (eg. benzodiazepines)

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49
Q

What dose of morphine is given in ACS

A

2-10mg IV

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50
Q

What are two indications of heparin/ fondaparinux

A
  1. Fondaparinux indicated in ACS treatment

2. Prevention of VTE

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51
Q

What is the role of anti-thrombin

A

Inhibits F2a and F10a of the coagulation cascade

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52
Q

How do heparins and fondaparinux function

A

Enhance action of anti-thrombin to inhibit F2 and F10

53
Q

What is the mechanism of action of unfractioned heparin

A

Inhibits F10 and F2

54
Q

What is the mechanism of action of LMWH

A

Inhibits just F10

55
Q

What is the mechanism of action of fondaparinux

A

Inhibits just F10

56
Q

What is the main risk of heparins

A

Haemorrhage

57
Q

Does LMWH, UFH or Fondaparinux have the lowest risk of haemorrhage

A

Fondaparinux

58
Q

What is another side effect of heparin

A
  • Bruising at injection site

- Hyperkalaemia

59
Q

What is an immune reaction to heparin

A

Heparin induced thrombocytopenia: characterised by low platelet count and thrombosis

60
Q

Is heparin-induced thrombocytopenia less likely to occur with fondaparinux, UFH or LMWH

A
  • It does NOT occur with fondaparinux

- It is less likely to occur with LMWH than UFH

61
Q

What is a relative contraindication of heparin

A

Risk of bleeding:

  • clotting disorders
  • uncontrolled severe HTN
  • recent surgery or trauma
62
Q

What is the heparin regimen surrounding surgery

A

Stop heparin immediately before and after surgery

63
Q

What heparin should be used in renal impairment and why

A

Unfractioned heparin as it is less dependent on the kidneys for metabolism

64
Q

What is used to reverse heparin anticoagulation in major bleeding

A

Protamine

65
Q

What is the effect of protamine on different types of heparin

A

Protamine most effective against UFH, less against LMWH and not at all against fondaparinux.

66
Q

What is an alternative to protamine for reversing heparin

A

adexanet

67
Q

What are 3 indications of fibrinolytic drugs

A
  1. Ischaemic stroke - improves chance of living independently in the long-term if given in the first 24h
  2. ACS
  3. Massive PE w/haemodynamic instability
68
Q

What is the time frame for alteplase in acute ischaemic stroke

A

4.5h

69
Q

What is the time frame for fibrinolytic drug in STEMI

A

12h

70
Q

What is the mechanism of action of fibrinolytic drugs

A

Increases conversion of plasminogen to plasmin which degrades fibrin clots

71
Q

What are 3 common adverse effects of fibrinolytic drugs

A
  1. Hypotension
  2. N+V
  3. Bruising around the injection site
72
Q

What are 4 serious effects that cause fibrinolytic drugs the be stopped

A
  1. Serious bleed
  2. Allergic reaction
  3. Cardiogenic shock
  4. Cardiac arrest
73
Q

What treatment of haemorrhage whilst on fibrinolytic drugs may be given and why is it often not

A

Clotting factors and tranexamic acid - often not given due to short half-life of fibrinolytic drugs

74
Q

What can reperfusion of infarcted brain tissue cause

A

Cerebral oedema

75
Q

What can reperfusion of infarcted cardiac tissue cause

A

Arrhythmias

76
Q

What are 3 CI to fibrinolytic drugs

A
  1. Bleeding
  2. Intracranial haemorrhage
  3. Previous streptokinase use - for streptokinase only
77
Q

Why is previous streptokinase treatment a CI to using streptokinase again

A

as can develop anti-streptokinase antibodies that render the treatment ineffective

78
Q

What drugs increase risk of anaphylactoid reactions with fibrinolytic drugs

A

ACEi

79
Q

Why is the chance of death following fibrinolytic drugs increased for a week

A

due to bleeding

80
Q

What are 4 indications of ACEi

A
  1. HTN
  2. Long-term management after ACS
  3. CKD with proteinuria
  4. Chronic HF
81
Q

What is the action of ACEi

A

Inhibits angiotensin coverting enzyme converting angiotensin I to angiotensin II

82
Q

What is the role of angiotensin II

A

causes vasoconstriction and stimulates aldosterone release

83
Q

What happens if angiotensin II production is blocked

A

causes vasodilation enabling decrease in peripheral vascular resistance

84
Q

How does ACEi work in CKD

A

Inhibits angiotensin II producing causing dilation of the efferent arteriole, reducing hyper filtration and pressure in the glomerulus

85
Q

How does ACEi work in chronic heart failure

A

Decreases aldosterone secretion, reducing reabsorption of sodium and water, therefore reducing pre-load

86
Q

What are 3 common side effects of ACEi

A

Dry Cough
Hyperkalaemia
First-dose hypotension

87
Q

When do ACEi particularly cause hypotension

A

following first-dose

88
Q

Why do ACEI cause a dry persistent cough

A

as ACE normally degrades bradykinin. Dysfunction in ACE causes accumulation of bradykinin

89
Q

What are 2 absolute CIs to ACEi and why

A
  • Renal artery stenosis - as in this circumstance relies on constriction of the efferent to maintain pressure
  • AKI
90
Q

What are two idiosyncratic SE of ACEi

A

Angioedema

Anaphylactoid

91
Q

What are 2 relative CI to ACEi

A

Breast Feeding

Pregnancy

92
Q

What drugs should ACEi be carefully prescribed with and why

A

potassium-sparing drugs (eg. potassium sparing diuretics)

93
Q

What drugs when prescribed with ACEi are particularly nephrotoxic

A

NSAIDs

94
Q

When are ACEi advised to be taken and why

A

Before bed to reduce risk of hypotension

95
Q

What monitoring should happen on ACEi and why

A

U+E - to check for hyperkalamia

BP

96
Q

What should be checked prior to starting ACEi

A

GFR

97
Q

What are 5 indications of B-blockers

A
  • HTN
  • IHD
  • CHF
  • AF
  • SVT
98
Q

What is the MOA of B-blockers

A

Reduce rate and force of contraction by antagonising B1 adrenoceptors

99
Q

How do B blockers work in AF

A

Slow conduction through the AV node

100
Q

How do B blockers work in HTN

A

Promote renin secretion

101
Q

What are side effects of B blockers

A 
Fatigue 
Cold extremities
Impotence 
Headache
GI disturbance
Sleep disturbance
102
Q

What are 2 absolute CIs to B blockers

A
  • Asthma

- HF

103
Q

What are B blockers absolutely CI in asthma

A

Due to causing bronchoconstriction by acting on B2 receptors

104
Q

What are the B1 selective B-blockers

A

Metoprolol, Bisoprolol

105
Q

What are the non-selective B-blockers

A

Carvediol, Propanolol

106
Q

What drug can B-blockers not be prescribed with and why

A

Non di-hydropyridine calcium channel blockers causes HF, bradycardia and systole.

107
Q

What are two loop diuretics

A
  • Furosemide

- Bumetanide

108
Q

What are 3 main indications for loop diuretics

A
  1. Acute pulmonary oedema
  2. Reduce fluid overload in HF
  3. Reduce fluid overload in other conditions (eg. renal failure)
109
Q

What is the mechanism of action of loop diuretics

A

Inhibit Na+/K+/2Cl- in the ascending loop of henle

110
Q

What are some side effects of loop diuretics

A
  • Hypotension
  • Dehydration
  • Low electrolyte states: hypokalaemia, hyponatremia, hypocholraemia, hypomagnesaemia, hypocalaemia
111
Q

Why may loop diuretics cause tinnitus at high-doses

A

Due to similar Na+/K+/2Cl- channel controlling endolymph in the ear

112
Q

What are two absolute CI of loop diuretics

A

Dehydration

Hypovolaemia

113
Q

What are 4 relative CI of loop diuretics

A

Hepatic encephalopathy
Gout
Hypokalaemia
Hyponatremia

114
Q

Why are loop diuretics relatively CI in gout

A

As they decrease excretion of uric acid and therefore may precipitate acute attacks of gout

115
Q

Why are loop diuretics relative CI in hepatic encephalopathy

A

Hypokalaemia can worsen hepatic encephalopathy

116
Q

What 3 drugs may loop diuretics increase toxicity of

A

Digoxin
Lithium
Aminoglycosides

117
Q

what rate should IV furosemide be administered

A

4mg/ml

118
Q

when should patients be advised to take loop diuretics

A

in the day to avoid nocturia

119
Q

Explain the MOA of nitrates

A
  • Nitrates are converted to NO
  • NO increases cGMP synthesis and reduces intracellular calcium in smooth muscle cells causing relaxation
  • This causes venous and lesser extent arterial dilation. Also causes relaxation of venous capacitance vessels
  • Relaxation of capacitance vessels reduces pre-load and and left-ventricular filling reducing cardiac work and myocardial demand
120
Q

What are 4 common SE of nitrates due to they vasodilatory effects

A

Headache
Flushing
Light-Headedness
Hypotension

121
Q

What can sustained use of nitrates cause

A

Tolerance

122
Q

What are 2 contraindications of nitrates

A

Severe Aortic stenosis

Hypotension

123
Q

Why are nitrates CI in aortic stenosis

A

As the heart cannot increase CO sufficiently through narrowed valve area to maintain pressure in dilated vasculature

124
Q

what drugs must nitrates NOT be used with

A

phosphodiesterase inhibitors

125
Q

give an example of a phosphodiesterase inhibitor

A

sidinefil

126
Q

why can nitrates not be used with sidenifil

A

phosphodiesterase inhibitors prolong hypotensive effects of nitrates

127
Q

What is the half-life of sublingual GTN

A

5min

128
Q

How is GTN given in ACS

A

IV

129
Q

How is GTN given in angina

A

Sublingual

Pharmacology (12 decks)

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