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BDS2 BAMS Cardiovascular medicine > Cardiovascular epidemiology and drugs > Flashcards

Cardiovascular epidemiology and drugs Flashcards

1
Q

Irreversible risk factors for CVD

A

age
sex
family history

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2
Q

Reversible (by behaviour change) risk factors for CVD

A

smoking
obesity
diet
exercise

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3
Q

Reversible (by pharmacological intervention) risk factors for CVD

A

hypertension
hyperlipidaemia
diabetes
stress

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4
Q

What has to occur in a patients mind for them to have a behavioural change?

A

know the info,
believe the info,
and have a personal motivation to change

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5
Q

What is primary prevention

A

having measures in place to prevent getting a health issue in the first place

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6
Q

What is secondary prevention

A

After presenting with e.g. CVD putting measures in place to not get it again

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7
Q

Why is primary prevention difficult

A 
People don't think they'll get it.
Opportunistic approach
- family history
- diet
- smoking
- test cholesterol
- test bp
- test for type 2 diabetes
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8
Q

Why is secondary prevention easier than primary

A

personal motivation to fix risk factors is much higher

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9
Q

What are the main approaches to preventing CVD

A
  1. lifestyle changes
  2. control total cholesterol
    - statin treatment
    - reduce cholesterol <5.0mmol/L or 25%
  3. control hypertension
    - moderate hypertension
    - mild hypertension with evidence of CVD
    - reduce blood pressure to target of <140/85
  4. Anti platelet drugs - Asprin
    - when identified CVD
    - When high risk with no identified disease
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10
Q

How can drugs be used in the CVS

A

prevent further disease

reduce symptoms of current disease

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11
Q

What drugs are used to prevent further disease

A
  • anti platelet drugs
  • lipid lowering drugs
  • anti-arrhythmics
  • anticoagulants
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12
Q

What drugs are used to reduce symptoms of current disease

A
  • diuretics
  • anti-arrhythmics
  • nitrates
  • Ca channel blockers
  • Ace inhibitors
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13
Q

What do anti-platelet drugs do

A

interfere with platelet aggregation by reversibly or irreversibly inhibiting various steps in the platelet activation required for primary haemastasis

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14
Q

What do anticoagulant drugs do

A

inhibit the production or activity of the factors that are required for the coagulation cascade

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15
Q

What does aspirin do

A

anti-platelet drug

inhibits platelet aggregation

  • after the balance between throboxane A2 and Prostacyclin
  • irreversible for the life of the platelet (but need to take regularly cause newly produced platelets will be unaffected if you don’t)
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16
Q

What does clopidogrel do

A

anti- platelet drug

inhibits ADP induced platelet aggregat

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17
Q

What does dipyridamole do

A

anti-platelet drug

inhibits platelet phosphodiesterase

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18
Q

What are the features of anti-platelet drugs

A
  • used in combination to increase affect
  • significantly reduce chance of a heart attach or stroke
  • prolong the bleeding time following dental extraction
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19
Q

Two new antiplatelet drugs?

A

prasugrel
ticagrelor

  • only prescribed in conjunction with aspririn
  • only licenced for ACS
  • poor evidence of bleeding risk in dentistry
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20
Q

What is it that clots can form over in the arteries leading to CVD

A

atheroma

athrolosclerosis

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21
Q

What does warfarin do

A
  • inhibits synthesis of Vit K dependent clotting factors (2,7,9,10 slow-2 days, Protein C and S quick)
  • initial hypercoagulation. Anticoagulation takes 2-3 days so often heparin used concurrently initially
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22
Q

How is warfarin monitored

A

must be monitored regularly

INR test

  • ratio of patients blood clotting to a control sample
  • a treated person should take 2-4 times as long at clotting
  • under 2 - risk of clot
  • 2-4 fine
  • over 4 risk of bleed

drug and food interaction also important

23
Q

What is it important to consider when treating a patient on warfarin

A

assume all drugs interact with warfarin

  • get INR tested day after prescribing
  • LA safe
  • local haemostatic measures always
24
Q

new oral anticoagulants? (NOAC)

A

rivaroxiban
apixaban
dabigatran

25
Q

activated factor 10 inhibitors?

A

rivaroxaban

26
Q

direct thrombin inhibitors?

A 
dabigastran
angatroban
bivalrudin
lepirudin
exceile 1 and 2 (?)
27
Q

features of new oral anticoagulants (NOAC)?

A
  • short half life (effect rapidly lost)
  • no ‘anticoagulant test’ used (bioavaliability predictable)
  • may only be a short course (DVT - postpone extraction until stopped)
28
Q

what dental drugs are NOAC safe with

A
  • dental antibiotics except macrolides
  • antifungals
  • LAs
  • antivirals
29
Q

what dental drugs are NOACs not safe with

A
  • macrolides (antibiotic)

- NSAIDs (will prolong action and inhibit platelets

30
Q

what other drugs prevent CVD

A 
statins
beta adrenergic blockers
diuretics
Ca channel blockers
ACE inhibitors
31
Q

What do statins do

A

Lipid lowering drug

e. g. simvastatin (a prodrug)
e. g. atorvastatin

inhibit cholesterol synthesis in the liver (reduces total cholesterol and LDL cholesterol)

side effects - possible myositis with some drug interactions - includes antifungals

  • interacts with fluconazole
32
Q

what do beta-adrenergic blockers do?

A

Prevent increase in heart rate

  • cause postural hypotension
  • prevent unusual heart rhythms which can lead to heart attacks

Reduce heart efficiency
- make heart failure worse

Block beta receptors in the lungs
- make asthma worse of difficult to treat

can block B1 only (selective) or B1 and B2 (non-selective)

B1 is most common for CVS as it blocks actions of adrenaline on the heart. It slows the heart down (function less well). If someone has a heart attach we want excitability to be less

B2 is in lungs (asthma) and brain (anxiety)

33
Q

if a drug ends in -olol what does that indicate?

A

it’s a beta blocker

34
Q

what are 2 examples of beta blockers

A
  • atenolol (selective B1)

- propanolol (non-selective B1 and B2)

35
Q

What are diuretics used for?

A

hypertension and heart failure

36
Q

2 types of diuretics?

A 
thiazide diuretics (bendroflumethiazide)
loop diuretics (frusemide)
37
Q

How do diuretics work?

A

increase salt and water loss

  • reduce plasma water volume
  • reduce cardiac workload
38
Q

side effects of diuretics?

A

Na/K imbalance if not monitored carefully

dry mouth in elderly

39
Q

2 types of nitrates? examples?

A

short acting - Glyceryl trinitrate (GTN). Used in emergency management of angina pectoris

long acting - Isosorbide mononitrate . Used in prevention of angina pectoris

40
Q

what do nitrates do

A

dilate veins
- reduces preload to heart

dilate resistance arteries

  • reduces cardiac workload (afterload)
  • reduces cardiac oxygen consumption

dilate colateral coronary artery supply
- reduces anginal pain

41
Q

how are nitrates inactivated

A

first pass metabolism

42
Q

how are nitrates applied to work within minutes

A

spray

43
Q

how are nitrates applied to work for hours

A

transdermal patch

44
Q

do nitrates have a short or long shelf life

A

short

45
Q

side effect of nitrates

A

headache

46
Q

What are calcium channel blockers used for

A

hypertension

47
Q

How do calcium channel blockers work

A

Block Ca channels in smooth muscle

  • some more active on peripheral blood vessels (relaxation and vasodilation (-pine e.g. nifedipine))
  • some more active on the heart muscle (slow conduction of pacing impulses e.g verapamil)
48
Q

side effect of ca channel blockers

A

gingival hyperplasia (I think) (make gums grow)

49
Q

3 examples of Angiotensin converting enzyme (ACE) inhibitors

A

Enalapril
Ramapril
Lisinopril

50
Q

What do ACE inhibitors do

A

inhibit the conversion of angiotensin 1 to angiotensin 2
(angiotensin 2 = important vasoconstrictor)

prevent aldosterone dependent reabsobtion of salt and water

51
Q

What results do ACE inhibitors achieve

A

reduce blood pressure

reduce excess salt and water retention

52
Q

side effects of ACE inhibitors

A

cough
hypotension

Dental:
angio-oedema
lichenoid reaction

53
Q

example of ACE inhibitor

A

losartan

BDS2 BAMS Cardiovascular medicine (5 decks)

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