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BDS2 BAMS > Cardiovascular Epidemiology > Flashcards

Cardiovascular Epidemiology Flashcards

1
Q

what are the 2 types of risk factors for cardiovascular epidemiology?

A
  • reversible

- irreversible

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2
Q

what are irreversible risk factors of cardiovascular epidemiology?

A
  • age
  • sex
  • family history
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3
Q

what are reversible risk factors of cardiovascular epidemiology?

A
  • smoking
  • obesity
  • diet
  • exercise
  • hypertension
  • diabetes
  • stress
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4
Q

what is a key factor to someone getting cardiovascular disease?

A

largely a genetic problem

but can do actions that will make someone more likely to contract

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5
Q

what technique is used to lower a patients risk of cardiovascular disease?

A

patient centred and controlled risk modification

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6
Q

what 4 factors must the patient have for effective risk modification?

A
  • information
  • belief
  • motivation
  • behavioural change
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7
Q

what is healthcare professional in risk modification?

A

assess where patient is in risk modification route and give them appropriate advice and assistance to help them along

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8
Q

what are the 2 classes of prevention for cardiovascular disease?

A

primary

secondary

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9
Q

what is primary prevention?

A

Stop the risk which is going to give you the disease

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10
Q

why is primary prevention hard?

A
  • Hard as people don’t believe they are going to get the disease
  • Not real to them yet - ignorant
  • Motivation to make a change can be difficult if don’t have the awareness
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11
Q

methods of primary prevention?

A
  • Exercise, diet & not smoking
  • Assess total risk
    Medical treatment if high risk
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12
Q

what is secondary prevention?

A

Once contracted how to stop it getting worst

- Motivation to fix the risk factors will be higher

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13
Q

why is secondary prevention easier?

A

Motivation to fix the risk factors will be higher as already contracted the disease

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14
Q

methods of secondary prevention?

A
  • Exercise, diet & not smoking

- medical treatment to reduce risk

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15
Q

how can methods of primary prevention be assessed?

A
  • Family history
  • Diet
  • Smoking
  • Test cholesterol
  • Test blood pressure
  • Test for diabetes (Type 2)
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16
Q

what will the dentist role is primary prevetion?

A

See the dentist as a preventative measure - check up

  • Primary prevention for oral disease is common practice small add on for wider diseases (tend to not see doctor till sick)
  • dentist sees when well and encourage practices to keep them well

Assess areas of risk
- And direct them to appropriate healthcare professional or give advice on diet, cancer screening programmes, BP check

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17
Q

how can someone present with CV disease?

A
  • angine
  • heart attack (myocardial infarction)
  • stroke
  • claudication
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18
Q

what are 4 approaches to prevention of CV disease?

A
  1. lifestyle changes
  2. control total cholesterol
  3. control hypertension
  4. anti-platelet drugs (aspirin)
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19
Q

how can total cholesterol be controlled?

A
  • statin treatment

- reduce cholesterol <5.0mmol/L or 25%

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20
Q

when is hypertension controlled in CV prevention?

A
  • moderate hypertension with evidence of CV disease

- reduce blood pressure to tager of <140/85

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21
Q

when is anti-platelet drugs used in CV disease prevention?

A
  • identified cardiovascular disease

- when high risk with no identified disease

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22
Q

what are the 2 categories of drugs used in CV disease prevention/

A
  • prevent further disease e.g. lower BP

- reduce symptoms of current disease e.g. improve chest pains

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23
Q

what types of drug are used in CV disease to prevent further disease?

A
  • anti platelet drugs
  • lipid lowering drugs
  • anti-arrhythmics
  • anticoagulants
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24
Q

what types of drug are used in CV disease to reduce symptoms of current disease?

A
  • anti platelet drugs
  • lipid lowering drugs
  • anti-arrhythmics
  • anticoagulants
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25
Q

3 anti-platelet drugs

A
  • aspirin
  • clopidrogel
  • dipyridamole
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26
Q

how does aspirin work?

A

Inhibits platelet aggregation
- Alter the balance between Throboxane A2 and Prostacycli

Irreversible for the life of the platelet.
(All platelets in blood at that time will not work; Platelet life is 7-10days; aspirin every day stops new ones being made)

75mg to prevent platelet function (lower than painkiller/analgesia dose)

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27
Q

how does clopidogrel work?

A

inhibits ADP induced platelet aggregation

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28
Q

how does dipyridamole work?

A

inhibits platelet phophodiesterase

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29
Q

what does using drugs in combination cause?

A

increased effect

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30
Q

what does anti-platelet drugs (used alone or in combination do)

A

significantly reduce the chance of a heart attack or stroke
- Only in an ‘at risk’ population

(the 2 main diseases of platelets sticking onto to BV walls)

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31
Q

what is a negative of anti-platelet drugs?

A

Prolong the bleeding time following dental extraction

  • Not a significant problem individually
  • Drug combinations increase the risk
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32
Q

what are new anti-platelet drugs?

A
  • Prasugrel
  • Ticagrelor

Only prescribed in conjunction with aspirin
Only licenced for Acute Coronary Syndromes
- Small use in population currently
Poor evidence of bleeding risk in dentistry

33
Q

what can happen if atherosclerosis occurs?

A

Plug platelets will narrow and block artery
- Can suddenly get with split ruptures platelet adhere quickly big blockage in artery

anti-platelet drug can help this

34
Q

what is the prevalence of atherosclerosis?

A

Everyone has but can limit how bad it comes:

  • By takin aspirin
  • Having a good diet and exercise regime

Present in healthy and young increases with age
- Genetic related problem depends upon your genes and Chemical factors in body

35
Q

what are 4 oral anticoagulants?

A
  • warfarin
  • rivaroxiban
  • apixaban
  • dabigatran
36
Q

what are the benefits and negatives of warfarin?

A
  • Cheapest and most common
  • Need to monitor how effective - too much poison too little ineffective
  • Individual tailored dose - blood tests regularly
37
Q

how does warfarin work?

A

Coumarin based anitcoagulant

Inhibits synthesis of Vitamin K dependent clotting factors

  • 2, 7, 9,10 (slow – 2 days)
  • Protein C, Protein S (quick)

Some already in blood so once used already in blood then clotting factors levels will drop

If you want them to not clot now not very good drug
- Initial Hypercoagulation

Anticoagulation takes 2-3 days
- Often HEPARIN used concurrently initially

38
Q

how long does it take for warfarin to cause an effect?

A

2-3 days

39
Q

how long does it take for warfain’s effect to be lost?

A

2-3 days

40
Q

why must warfarin’s effect be monitored?

A

very easily upset and displaced

  • drug and food interactions
  • plasma protein binding
  • liver metabolism

can change warfarin’s metabolism and effectiveness

41
Q

how to monitor warfain?

A 
INR test (internationalised normalised ratio)
- standardised prothrombin time (PT)
42
Q

what is INR test

A

internationalised normalised ratio

  • Compare results from one lab to another lab
  • Whether patient is adequately anti coagulated or not
  • Ratio compared to control sample
43
Q

what is the therapeutic INR range?

A

2-4

44
Q

what happens if warfarin INR is less than 2?

A

risk of clot

45
Q

what happens if warfarin INR is more than 4?

A

risk of bleed

46
Q

what should you assume when prescribing a drug to a patient on warfarin?

A

all drugs will interact with warfarin

- Get INR tested day after prescribing – can effect protein binding and metabolism

47
Q

what are new oral anticoagulants? (NOACs)

A
  • Rivaroxaban x1 daily – (aXi)
  • Apixaban x2 daily – (aXi)
  • Dabigatran x2 daily – (dTi)

(aXi) activated factor X
(dTi) direct thrombin inhibitors

48
Q

what are properties of new oral anticoagulants? (4)

A

Short half life

No ‘anticoagulant test’ used
- Bioavailability predictable

May only be a short course – DVT
- Postpone extraction until stopped

Rapidly lost
- Unlike warfarin 2 days to start 2 days to lost
Effect more predictable and controllable

49
Q

New oral anticoagulant dental drug interactions

A

mainly safe so able to treat patients safely with less worry of interactions

Safe with ‘Dental’ Antibiotics (except Macrolides- Erythromycin and Clarithromycin)

Safe with Antifungals – topical and fluconazole

Safe with Local Anaesthetics

Safe with Antivirals

NSAID will prolong action and inhibit platelets – avoid

50
Q

what others drugs are used in combination to prevent CV disease (target most problems?

A
  • statins
  • beta-adrenergic blockers
  • diuretics
  • calcium channel blockers
  • ACE inhibitos
51
Q

what do lipid lowering drugs do?

A

inhibit cholesterol synthesis in liver

- reduce total cholesterol and LDL

52
Q

what are lipid lowering drugs?

A

STATINS - HMG coA Reductase inhibitors

  • Simvastatin – (a ‘prodrug’ – metabolised in liver to give an active drug)
    • Atorvastatin
53
Q

what are possible side effects of statins (lipid lowering drugs)

A

possible myositis with some drug interactions (muscle inflammation – some don’t tolerate well)

  • includes antifungals (FLUCONAZOLE interaction)
    Omit statin during antifungal treatment. – then restart – Ok as long term acting drug
54
Q

what are beta-adrenergic blockers?

A

atenolol (selective; beta 1 only)
propranolol (non- selective; beta 1 and 2)

many others; all end in -olol

55
Q

where is beta 2?

A

present in lungs and brain
(involved in anxiety)

  • if block reduce anxiety but more likely to get asthma
56
Q

what are beta-adrenergic blockers role in CV prevention?

A

Stop arrhythmias leading to cardiac arrest (Ventricular fibrillation – VF)

  • Blocks effects of adrenaline on heart
  • Slow it down, less excitability and function less well

Reduces heart muscle excitability

  • Don’t want heart to be over stressed
  • Want electrical excitability to be less

Prevent increase in heart rate

  • Cause postural hypotension (slower when sitting up)
  • Prevent unusual heart rhythms which can lead to heart attacks

Reduce heart efficiency
- Make heart failure worse

57
Q

what are diuretics role in CV prevention?

A

Antihypertensive and for Heart Failure

  • Thiazide diuretics (bendroflumethiazide)
  • Loop diuretics (frusemide)
58
Q

what do diuretics work?

A

Increase salt and water LOSS
o Reduce plasma volume
o Reduce cardiac workload

59
Q

side effects of taking diuretics

A
  • can lead to Na+/K+ imbalance if not monitored carefully (electrolyte imbalance)
  • Can lead to dry mouth in the elderly
60
Q

what age group are diuretics more effective on?

A

elderly than young

61
Q

how can diuretic action be increased?

A

use a combination of diuretics that act on different areas of the renal structure to increase fluid lost

62
Q

what do nitrates do?

A

Dilate VEINS
- Reduce preload to the heart

Dilate resistance arteries

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

Dilate collateral coronary artery supply
- Reduce anginal pain

63
Q

how does nitrates dilating veins do to prevent CV?

A

reduces preload to the heart

64
Q

how does nitrates dilating resistance arteries prevent CV?

A

reduces cardiac workload (afterload)

reduces cardiac oxygen consumption

65
Q

how does nitrates dilating collateral coronary artery supply prevent CV?

A

reduces anginal pain

66
Q

what is a short acting nitrate?

A 
Glyceryl Trinitrate (GTN) 
- Emergency management of angina pectoris

Pain will go away when spray under tongue if angina but if cardiac arrest will not go away

67
Q

what is a long acting nitrate?

A

Isosorbide Mononitrate

- Prevention of angina pectoris

68
Q

methods of administration for nitrates?

A
  • Sublingual - short acting
  • Transdermal - long acting
  • Intravenous

inactivated by first-pass metabolism

69
Q

side effect of nitrates?

A

headache

70
Q

how do calcium channel blockers help prevent CV?

A

hypertension - reduce

71
Q

how do calcium channel blockers act on smooth muscle in peripheral blood vessels?

A
  • Relaxation and vasodilation

Nifedipine, amlodipine (-pine)

72
Q

how do calcium channel blockers act on smooth muscle in heart?

A
  • Slow conduction of pacing impulses

Verapamil

73
Q

what is a risk of taking calcium channel blockers?

A

make gums bigger

- gingival hyperplasia (lumpy fibrous gums)

74
Q

what do angiotensin converting enzyme (ACE) inhibitors do?

A

Inhibit conversion of angiotensin I to angiotensin II (Change angiotensin II production)

  • Angiotensin II is a Vasoconstrictor (Make BP higher)
  • Body compensates as perceived drop in BP by making angiotensin II (as less angiotensin II present)

prevents aldosterone dependent reabsorption of salt and water

75
Q

2 main actions of ACE inhibitors

A
  • reduce blood pressure

- reduce excess salt and water retention

76
Q

side effects of ACE inhibitors

A
  • cough
  • hypertension
  • angio oedema
  • lichenoid reaction
77
Q

ACE inhibitors examples

A
  • Enalapril
  • Ramapril
  • Lisinopril

end in -pril

78
Q

what are angiotensin II blockers?

A

don’t stop production just prevent effect (same effect as ACE inhibitors, different mechanism)

  • losartan

end in -artan

BDS2 BAMS (54 decks)

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