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Pharmacology > Cardiovascular Disease > Flashcards

Cardiovascular Disease Flashcards

Cardiovascular conditions; CVD risk factors; ACS diagnosis; MI; Antiplatelets; Beta blockers; Statins; Renin angiotensin system; ACE inhibitors; ARBs; Angina; Nitrates; CCBs; Anticoagulants; Parental anticoagulants; Oral anticoagulants; Direct oral anticoagulants.

1
Q

9 CVD conditions

A 
Angina 
MI 
Heart valve disease 
Vascular disease 
Arrythmias 
Cardiomyopathy 
Congenital heart failure 
Heart failure 
Pericardial disease
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2
Q

10 risk factors for CVD

A 
Smoking 
Obesity 
Family history 
Diabetes 
Hypertension 
Inactive lifestyle 
Drugs 
Electrolyte imbalance 
Hyperlipidaemia
Increased age
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3
Q

Process of ACS diagnosis

onset of what symptom, type of MI or painful condition called…based on what feature of ECG + test result

A

Pt admitted with chest pain
Diagnosed with ACS
Continuing ST elevation = STEMI
Abnormal ST/T wave with increased/decreased troponin levels = NSTEMI or Unstable angina
Normal ECG with increased/decreased troponin = Stable angina

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4
Q

What occurs in myocardial infarction?

what tissue, lack of what leading to what

A

Myocardial/cardiac muscle ischaemia leading to necrosis of myocardium

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5
Q

What leads to MI?

pathophysiology of clot formation

A

Rupture or erosion of artherosclerotic plaque within tunica intima layer of artery.
Dislodged plaque results in thrombus formation.
Thrombus partially or fully occludes artery decreasing or cutting off blood supply to myocardium.

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6
Q

What 3 generic tests are carried out to diagnose MI?

3 blood tests for diagnosis

A

ECG
Blood chemistry: U&Es, FBC, Troponin
Chest X-ray

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7
Q

What 4 groups of drugs should patients following MI be prescribed?

A 
BARS: 
Beta blocker 
Anti-platelet 
Renin angiotensin system blocker
Statin
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8
Q

What are the 2 types of MI and describe their cause, what they occlude?
(thrombus)

A

NSTEMI - Atheromatous plaque with partially occluding thrombus, may cause occlusion of small coronary arteries due to platelet aggregation.
STEMI - artheromatous plaque that completely occludes coronary artery.

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9
Q

Which 2 hormones are involved in the mechanism of platelets and do they stimulate/inhibit aggregation?

A

Thromboxane - activates platelet aggregation

Prostacyclins - inhibits platelet aggregation

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10
Q

Name 4 mechanisms of platelets in clotting

A

Adhesion
Shape change
Secretion
Aggregation

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11
Q

What is a drug interaction and ADR of all anti-platelets?

A

Interaction - SSRIs as seritonin is involved in platelet formation
ADR - GIT bleeds

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12
Q

What is the function/mechanism of asprin?

enzyme, hormone, inhibits ? in regards to platelets

A

Non-selective COX1 inhibitor

Inhibits production of thromboxane thus preventing platelet aggregation

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13
Q

What is an ADR of asprin and how is it caused?

A

GIT irritation
Caused by inhibition of cytoprotective prostaglandins resulting in decreased stomach acid secretion and unregulated blood flow. Increasing risk of GIT ulcer formation.

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14
Q

5 contraindications of asprin use

A 
Dyspepsia 
Active GIT ulcer 
Under 16 yrs 
Hypersensitivity 
Severe hepatic impairment
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15
Q

2 drug interactions of asprin

A

Anticoagulants

NSAIDs

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16
Q

Name 3 anti platelet drugs

A

Asprin
Clopidogrel
Ticagrelor

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17
Q

What is the function/mechanism of clopidogrel?

binds to what preventing what

A

Inhibits platelet aggregation

Acts as a ADP receptor antagonist preventing the binding of fibrin with platelets = no aggregation.

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18
Q

What organ is clopidogrel metabolised by?

A

Liver

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19
Q

5 ADRs of clopidogrel

A 
Nausea/vomiting 
GIT discomfort 
Rash 
Thrombocytopenia (low thrombocyte count <150000 mc/L) 
GIT bleeds
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20
Q

3 drug interactions of clopidogrel

A

NSAIDs
Anticoagulants
PPIs

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21
Q

3 contraindications for the use of clopidogrel

A

Hypersensitivity
Active bleed
Severe hepatic impairment

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22
Q

How does ticagrelor work?

A

Inhibits platelet aggregation

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23
Q

What does ticagrelor do to liver enzymes?

A

Reversibly inhibits liver enzymes

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24
Q

Which one of the 3 antiplatelet medications requires a loading dose of 180mg before BD doses?

A

Ticagrelor

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25
Q

4 ADRs of ticagrelor

A

Dysponea
Nausea/vomiting
Rash
Bruising

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26
Q

4 drug interactions of ticagrelor and the reason for them

A 
Clarythromycin 
Simvastatin 
Digoxin 
Rifampicin 
Caused by drug being metabolised/inhibiting liver enzymes
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27
Q

3 contraindications for ticagrelors use

A

Active bleed
Pregnancy
Moderate-severe hepatic impairment

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28
Q

How do beta blockers work?

A

Reduce oxygen requirement of cardiac muscle cells

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29
Q

True or false, beta blockers require titrating to a max tolerated dose?

A

True

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30
Q

4 mechanisms of how beta blockers work

A

Slow heart rate
Decrease heart contractility
Decrease blood pressure
Improve coronary oxygenation

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31
Q

4 ADRs of beta blockers

A

Fatigue
Bradycardia
Hypotension
Bronchospasm

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32
Q

4 contraindications for beta blockers use

A

Acute heart failure
Symptomatic bradycardia/ hypotension
Severe asthma/ COPD
Hypersensitivity

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33
Q

4 drug interactions with beta blockers

A

Veranapril
NSAIDs
Topical beta blockers
Anti-hypertensives

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34
Q

What is the function of statins?

A

Lower concentration of lipids in circulation

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35
Q

5 mechanisms of statins

A 
Inhibit HMG-CoA enzyme 
Stabilise plaque 
Decrease cholesterol by improving clearance of LDL 
Improve endothelial function 
Prevent thrombus formation
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36
Q

2 ADRs of statins

A

Myopathy (muscle disease)

Hepatoxicity

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37
Q

What 3 interactions occur with statins?

eat, enzyme

A

Grapefruit
Metabolised by CYP enzymes check BNF
Amylodapine

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38
Q

4 management interventions for NSTEMI

A

Angiogram
Angioplasty
Coronary artery bypass grafting (CABG)
Percutaneous coronary intervention (PCI)

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39
Q

2 types of stent

A

Metal stent

Drug emitting

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40
Q

4 functions of renin angiotensin system

A

Regulation of BP and volume, blood sodium and water concentration

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41
Q

Where is renin produced and what does it stimulate where?

A

Kidneys

Stimulates angiotensin production in liver

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42
Q

Where is angiotensin produced and what does it stimulate where?

A

Liver

Stimulates the release of aldosterone from the adrenal cortex

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43
Q

Where is aldoserone produced and what does it stimulate where?

A

Adrenal cortex

Stimulates the uptake of sodium and water in the kidneys

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44
Q

What stimulates the release of atrial natriuretic hormone and what is it’s function?

A

Release stimulated by increased blood volume
Negatively feeds back into RAAS to inhibit aldosterone production causing maintenance of blood water and sodium concentration

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45
Q

2 classes of drugs involved in the renin angiotensin aldosterone system

A

Angiotensin converting enzyme (ACE) inhibitors

Angiotensin receptor blockers (ARBs)

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46
Q

Explain mechanism of ACE inhibitors

system involved in, what stage, which hormone

A

Renin angiotensin aldosterone system

Intercepts at lungs preventing conversion of angiotensin I to angiotensin II

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47
Q

What two things should be monitored when taking ACE inhibitors?

A

Kidney function and BP

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48
Q

Explain the mechanism of ARBs

which system, where by doing what

A

Renin angiotensin system

Acting as competative angiotensin II receptor antagonists

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49
Q

4 ADRS of ACEIs and ARBs

A

Dry cough
Dizziness
Hyperkalaemia
Angiodema

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50
Q

3 drug interactions with ARBs and ACEI

A

NSAIDs
K sparing diuretics
K supplements

51
Q

4 contraindications for ACEI and ARBs use

A

Pregnancy
Renal stenosis
Hereditary angiodemia
Hypersensitivity

52
Q

What 5 drugs may be given to someone with angina?

A 
Asprin 
Angiotensin converting enzyme inhibitors 
Calcium channel blockers 
Statins 
Nitrates
53
Q

What is angina and what is it caused by?

A

Chest pain felt due to ischaemia of coronary arteries reducing oxygen supply to cardiac muscle cells, caused by coronary artery disease

54
Q

What are 2 events that may bring on symptoms of angina?

A

Physical activity

Obstruction of blood flow

55
Q

What do drugs for angina aim to stimulate?

A

Smooth muscle relaxation

56
Q

4 types of angina

A

Stable
Unstable
Variant
Microvascular

57
Q

3 features of stable angina

?expected, trigger, duration, relief with?

A

Predictable, able to be reproduced
Triggered by emotional/physical stress
Short in duration
Relief with rest

58
Q

3 features of unstable angina

?expected, trigger, duration

A

Unexpected, change in stable angina
Spontaneous, can occur at rest
Duration >30mins

59
Q

4 features of variant angina

?expected, trigger, duration, causes what

A

Sudden onset, no warning
No identified trigger, can occur at rest
Duration >15mins
Causes lasting heart damage

60
Q

3 features of microvascular angina

?expected, trigger, duration

A

Unpredictable
No identified trigger
>10-30 mins

61
Q

Explain the mechanism of nitrates for angina

chemical, conversion to which substrate, for which enzyme, to convert to which substance, which stimulates what

A

Convert nitrate ions into nitric oxide
Nitric oxide is the substrate for guanylate cyclase enzyme
Guanylate cyclase converts nitric oxide into guanosine monophosphate cGMP
cGMP stimulates smooth muscle relaxation

62
Q

What is GTN spray used for?

A

Relief of angina chest pain

Secondary prevention for angina related to exercise

63
Q

What does GTN stand for?

A

Glyceryl trinitrate

64
Q

6 ADRs of nitrates

A 
Postural hypotension 
Flushing 
Reflex tachycardia 
Tolerance 
Headache 
Nausea
65
Q

2 drug interactions with nitrates

A

Phosphodiesterase type 5 inhibitors (pulmonary hypotension)

Anti-hypertensives

66
Q

How does GTN work?

A

Stimulates vasodilation, widening lumen of coronary arteries improving blood supply to coronary arteries

67
Q

5 steps f GTN spray use

A 
Chest pain occurs 
Stop, sit, rest 
Spray GTN sublingually - wait 5 mins 
Chest pain persists = spray GTN sublingually again - wait 5 minutes 
Pain persists = call 999
68
Q

4 ADRs of GTN

A

Headache
Dizziness
Nausea/vomiting
Low BP

69
Q

What is the action of nicorandil?

A

Dual action as a nitrate and potassium channel agonist

70
Q

Explain the mechanism of nicorandil

binds to what, stimulates what having what overall effect

A

Binds to potassium channels - indirectly blocking calcium channels + directly stimulating increase in coronary perfusion and vasodilation
Nitrate aspect binds to calcium channels on smooth muscle - lowing ventricular filling pressure and SVR
Both increase blood supply and oxygen to cardiac muscle

71
Q

4 ADRs of nicorandil

A

Headache
Nausea
Diziness
Fatigue

72
Q

2 drug interactions with nicorandil

A

Antihypertensives

Phophodiesterase type 5 inhibitors

73
Q

2 contraindications of nicorandil’s use

A

Low BP/pulmonary oedema

74
Q

How do calcium channel blockers work?

A

Relax smooth muscle and decrease HR

75
Q

What are calcium channel blockers and alternative medication to?

A

Beta blockers

76
Q

Explain mechanism of calcium channel blockers

where is the receptor located, what do they stop, what effect do they have

A

Bind to calcium channels on smooth muscles
Block influx of calcium ions
Results in smooth muscles remaining relaxed

77
Q

Name 3 classes of calcium channel blockers

A

Benzothiazepines
Dihydropyridines
Phenyalkylamines

78
Q

Action of dihydropyridines

selective to what, used for treatment in what, cause what

A

Selective to smooth muscles
Used to treat hypertension
Cause reduction in stroke volume

79
Q

Action of phenylalkylamine

selective to what, cause what

A

Selective to myocardium

Cause vasodilation

80
Q

Action of benziorhiazepines

selective to what, cause what

A

Selective to cardiac muscle

Cause vasodilation

81
Q

5 ADRs of calcium channel blockers

A 
Oedema 
Hypotension 
Bradycardia 
Headache 
Constipation
82
Q

3 drug interactions with calcium channel blockers

A

Amlodipine enzyme inducers/inhibitors
Anti-hypertensives
Verapamil

83
Q

What 2 parts of the clotting cascade to be aware of?

A

Factor Xa

Thrombin

84
Q

What 2 parts of the clotting cascade is factor Xa involved in?

A

Intrinsic and extrinsic pathway

85
Q

What is thrombin what does it produce and what is that required for?
(clotting cascade)

A

Enzyme that produces the protein fibrin required for binding to platelets allowing their aggregation

86
Q

9 ideal features of anticoagulants

A 
Wide therapeutic range
No food or drug ADRs 
Oral administration 
Rapid onset/offset of action 
Predictable effect with weight determined dosing 
No routine monitoring 
Reversible 
Cost effective 
Suitable for pts with renal/hepatic impairment
87
Q

Name two parenteral anticoagulants

A

Heparin

Low molecular weight heparin

88
Q

What is protamine used for?

A

Reversal agent for heparin

89
Q

Explain heparin’s mechanism of action in preventing clotting
(binds to what, inactivates what, preventing what 2 conversions)

A

Binds to antithrombin
Inactivates factor Xa
Prevents conversion of prothrombin to thrombin, fibrogen to fibrin preventing clotting

90
Q

Via what route and method is heparin administered?

A

IV via continuous infusion

91
Q

What is the half life of heparin?

A

1-2 hours

92
Q

Via what organ is heparin cleared from the body?

A

Liver

93
Q

What is the name of the monitoring that is required when pt is on heparin?
(aPPT)

A

Activation partial thromboplastin time (aPPT)

94
Q

What is activation partial thromboplastin time a measure of?

A

Time it takes the blood to clot

95
Q

What is a normal activation thromboplastin time?

in secs

A

60-70secs

96
Q

Why is a aPPT activator added to heparin?

A

To narrow the reference range

97
Q

Define ‘the reference range’

heparin

A

Time taken for a pt on heparins blood to clot

98
Q

What is an ideal reference range for someone on heparin?

in secs

A

30-40secs

99
Q

Above how many seconds for aPPT and PPT does spontaneous bleeding occur?

A 
aPPT= >70seconds 
PPT= >100 seconds
100
Q

Explain the mechanism of action of low molecular weight heparin as an anticoagulant
(binds to what, effecting what in the clotting cascade)

A

Binds to antithrombin

Effecting factor Xa

101
Q

Give 7 reasons why low molecular weight heparin is preferred to heparin
(dosing, half life, monitoring- in which pts, clearance, effect on platelets, reduces risk of what)

A

Given OD/ BD
Half life: 5-7 hours
Monitoring: only in certain pts - children with poor renal function/low weight; pts with creatinine clearance <30ml/min
Less inhibition of platelets
Lower risk of heparin induced thrombocytopenia (HIT)

102
Q

What is vitamin K and what is it needed for?

solubility, clotting cascade

A

Fat soluble vitamin

Needed for the production of clotting factors in the clotting cascade

103
Q

What is the mechanism of action of direct oral anticoagulants?
(act on what in clotting cascade)

A

Direct effect on thrombin and factor Xa in clotting cascade

104
Q

Name 4 main direct oral anticoagulants

A

Apixaban
Dabigatran
Endoxaban
Rivaroxaban

105
Q

Which 1 of the 4 direct oral anticoagulants effects thrombin?

A

Dabigatran

106
Q

Which 3 of the 4 oral anticoagulants effect factor Xa?

A

Apixaban
Endoxaban
Rivaroxaban

107
Q

How does dabigatran interfere with the clotting cascade? What type of drug is it?
(clue: what does it require to become active)

A

Interferes with thrombin

It is a prodrug needing first pass metabolism to be activated.

108
Q

What is praxbind the reversal drug for?

A

Dabigatran

109
Q

What is an ADR of dabigatran?

A

Dyspepsia

110
Q

2 interactions of dabigatran

A

ATP inhibitor/inducer

Anti-platelets

111
Q

7 contraindications for dabigatran’s use

A 
Hypersensitivity 
Possit box 
Creatinine clearance <30ml/min 
Active bleed 
Surgery 
Hepatic impairment 
Prosthetic heart valve
112
Q

What is the mechanism of rivaroxaban, apixaban, endoxaban in the clotting cascade?
(inhibits what, interupting what, stopping what)

A

Inhibit factor Xa
Interrupt intrinsic and extrinsic pathway of clotting cascade
Stop formation of thrombin preventing the development of thrombi.

113
Q

What is andexXa a reversal drug for?

A

Factor Xa inhibiting drugs

114
Q

9 ADRs of rivaroxaban, apixaban, endoxaban

A 
Nausea/vomiting 
Diarrhoea 
Jaundice 
Alopecia 
Rash 
Hepatic impairment 
Pyrexia 
Headache 
Haemorrhage
115
Q

5 contraindications for rivaroxaban, apixaban, endoxaban’s use

A 
Hypersensitivity 
Pts with poor adherence 
Bleeding complications 
Creatinine clearance of <15ml/min 
Active bleed
116
Q

What type of anticoagulant is warfarin?

A

Oral anticoagulant

117
Q

What is warfarin’s mechanism of action?

enzyme it effects, vit …

A

Inhibits vitamin K reductase that activates vitamin K

118
Q

Where does warfarin metabolism occur?

A

Liver CYP enzymes

119
Q

True or false the effects of warfarin can last after the end of dose?

A

True

120
Q

What monitoring test is required when a patient is on warfarin?

A

International normalised ratio

121
Q

4 ADRs of warfarin

A

Bleeding
Nausea/vomiting
Liver dysfunction
Jaundice

122
Q

5 contraindications of warfarin

A 
Pregnancy 
Haemorrhagic stroke 
Hypersensitivity 
Active bleed 
Surgery <72 hrs
123
Q

What 2 groups of drugs interact with warfarin?

A

Anti-coagulants

Non-prescription drugs - herbal remedies, vitamins, alternative medicines, OTCs

Pharmacology (10 decks)

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