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BAMS > Cardiovascular Epidemiology > Flashcards

Cardiovascular Epidemiology Flashcards

1
Q

what are 2 types of risk factors?

A

irreversible - age , sex, family history
reversible (patient) - diet, smoking cessation, exercise
reversible (medical) : treat hypertension and hyperlipidaemia, diabetes

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2
Q

what is hyperlipidaemia?

A

high concentration of fats or lipids in the blood

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3
Q

what are the types of prevention ?

A

Primary prevention: upon examination
o Assess total risk
o Check exercise, diet, not smoking
Secondary prevention: after event has taken place
o All the above information is given
o Medical treatment to reduce risk

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4
Q

what is the approach to prevention?

A

Approach to prevention
1. Lifestyle changes: walking to work, exercise
2. Control total cholesterol: statin treatment, reduce cholesterol: 25%
3. Control hypertension: reduce blood pressure to target of <140/85
4. Anti-platelet drugs (aspirin)

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5
Q

why is primary prevention hard?

A

because patients don’t believe they will get the disease
no motivation to make a change

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6
Q

why is secondary prevention easier?

A

patient has motivation to fix the factors are higher as the patient has had the disease

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7
Q

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

A

-patient has the information
-has the belief
-has the motivation
-makes the behavioural change

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8
Q

what is the dentists role in primary prevention?

A

-dentists see ‘well’ patients regularly. doctors only see you occasionally when you are sick

  • and they can give general health education messages as well as oral health education messages
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9
Q

how can someone present with CV disease?

A
  • myocardial infarction
  • stroke
  • peripheral vascular disease
  • claudication
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10
Q

what are the 2 categories of used in CV disease prevention?

A
  • prevent further disease
  • reduce symptoms of current disease
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11
Q

what are the drugs used to prevent further disease?

A
  • Anti platelet drugs
  • Anticoagulants (NOAC)
  • Lipid lowering drugs – statins
  • Anti-arrhythmic – beta-adrenergic blockers
  • Diuretics
  • Ace-inhibitors
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12
Q

what are the drugs used to reduce symptoms of current disease?

A
  • Diuretics
  • Anti-arrhythmic
  • Nitrates
  • Calcium channel blockers
  • Ace-inhibitors
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13
Q

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

A

when the patient has an identified cardiovascular disease

OR

when high risk with no identified disease

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14
Q

what are 3 anti-platelet drugs?

A

-aspirin
-clopidogrel
-dipyridamole

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15
Q

how does aspirin work?

A

o Prevents platelet aggregation by altering the balance of thromboxane A2 which initiates platelet aggregation and clotting factors
o Inhibiting platelet aggregation reduces blood clots forming
o Aspirins action is irreversible and can last 7-10 days until a new platelet is formed

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16
Q

how does clopidogrel work?

A

o Inhibits platelet aggregation – reduces ability to stick together and form blood clots
o Commonly used with aspirin in patients with high CVE risk – previously had a heart attack or stroke
o Needs to be activated in the liver

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17
Q

what is given to a patient if they have mild anti-platelet action?

A

a single anti-platelet drug

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18
Q

what is given to a patient if they have an intense anti-platelet action?

A

combinations of drugs can be used together

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19
Q

what does using drugs in combination cause? the advantages and disadvantages

A
  • Used in combination to increase the effect
  • Significantly reduces the chances of a heart attack or stroke
  • Prolongs bleeding time following a dental extraction
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20
Q

what is a negative of anti-platelet drugs?

A

o Drug combinations increase the risk of prolonged bleeding
o Patients taking aspirin or clopidogrel will have more of a bleeding problem compared to patients that are taking the drugs separately

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21
Q

what are new antiplatelet drugs?

A
  • New antiplatelet drugs – prasugrel, ticagrelor
    o Only prescribed in conjunction with aspirin
    o Prescribed by hospital specialist for acute coronary syndromes
    o But there is a poor evidence of bleeding risk in dentistry
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22
Q

what are oral anti-coagulants?

A

Drugs that are taken to inhibit the clotting cascade these do not affect platelets:

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23
Q

what are some names of oral anti-coagulants?

A

warfarin
rivaroxaban
apixaban
dabigatran

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24
Q

what is warfarin’s action?

A
  • Inhibit the function of vitamin K
  • Vitamin K is essential to produce several clotting factors in the blood – inhibits the synthesis
    o 2, 7, 9, 10
    o Protein C, Protein S
  • Reduces the ability for blood to clot, reduce the amount of fibrin formed and therefore clots stability
  • Platelets will function as normal: unless there is a platelet inhibitor
  • Will have post bleeding after a few hours after a procedure
  • Once stabilised it would take 2-3 days to lose effect if drug stopped
  • Must be monitored regularly
  • Monitored with an INR test
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25
Q

how long does it take for warfarin to take effect?

A

2-3 days

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26
Q

how long does it take for warfarin to lose its effects?

A

2-3 days

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27
Q

why must warfarin’s effects be monitotred?

A

-drug and food interactions
-liver metabolism

28
Q

how do you monitor warfarin?

A

o International Normalised Ratio
o How long it takes for blood to clot
o INR is a standardised prothrombin time (PT)
o Therapeutic range would be 2-4

29
Q

what is therapeutic range of an INR?

A

2-4

30
Q

how do you carry out an INR test?

A

-compare results from one lab to another lab
-whether patient is adequately anti-coagulated or not
-ratio compared to control sample

31
Q

what must be done if there is a higher risk of bleeding prior to a dental care procedure?

A

o if there is a higher risk of bleeding following a dental care procedure (extraction) then local haemostatic measures must be used to help with bleeding such as:
 fibrinogen activator
 suture
 LA – a vasoconstrictor which slows blood flow to that area

32
Q

what happens if an INR is within range>

A

perform procedure safely

33
Q

what happens if an INR is too high?

A

risk for catastrophic bleeding

34
Q

what happens if an INR is too low high?

A

can produce unwanted clots as don’t have the protection offered by the drug

35
Q

what should be assumed when prescribing a drug to a patient?

A

o Get INR tested day after prescribing antibiotics. Avoid NSAID analgesics.
o LA is safe

36
Q

what is initial hypercoagulation?

A

Hypercoagulation is a condition in which the blood has an increased tendency to form clots. This can lead to the formation of blood clots within the veins or arteries, which can cause serious health problems such as deep vein thrombosis (DVT), pulmonary embolism (PE), stroke, and heart attack.

37
Q

what happens during initial coagulation?

A

o action of anticoagulation takes 2-3 days
o need something to thin the blood straightaway
o HEPARIN (intravenous injections) – works straight away
o Given along with warfarin or another anticoagulant so that it can start to work

38
Q

what are new oral anti coagulants?

A
  • Rivaroxaban
  • Apixaban
  • Dabigatran
39
Q

what happens if the patient taking NOACs have a low bleeding risk for dental procedures?

A

treat without interrupting medication

40
Q

what happens if the patient taking NOACs have a high bleeding risk for dental procedures?

A

advise patient to miss/delay morning dose before treatment as that is when the effect of the blood will be at its lowest

41
Q

what are the properties of NOACs?

A

Short half-life – effect is rapidly lost – drug is eliminated from the body rapidly
- helpful if you want to do an extraction just before the dose of the drug is due when the effect of the blood will be at its lowest.
- this will allow maximum chance of a blood clot to form and after this has occurred the next dose of the drug can be taken

May only be a short course – leads to DVT
- postpone extraction until stopped
- leave the tooth at present until discontinuation of the oral anti-coagulant before carrying out the extraction

No significant drug interactions in dentistry

42
Q

what do lipid lowering drugs do?

A

HMG-coA reductase inhibitors which reduce the level of cholesterol that are circulating in the blood

Inhibit cholesterol synthesis in the liver and reduce the total cholesterol and LDL-cholesterol

43
Q

what are a type of lipid lowering drugs?

A

statins

44
Q

what is a negative of lipid lowering drugs?

A
  • if plasma levels of these drugs get too high then this can cause inflammation in the muscles: myositis
  • fluconazole interaction
    o Omit statin during antifungal treatment.
    o stop statin for antifungal treatment and restart once treatment is done
45
Q

what are anti-arrhythmic drugs?

A

Beta- adrenergic blockers – treat or prevent arrhythmias by regulating the electrical impulses that control that heartbeat. Block the effect of adrenaline on the heart

46
Q

what are types of anti-arrhythmic drugs?

A

drugs ending in -lol

47
Q

where is beta 2?

A

brain and lungs
-can be used for anxiety by blocking receptors in the brain

48
Q

what are a result of anti-arrhythmic drugs work?

A

o prevent an increase in heart rate
 postural hypotension: getting out of the dental chair
 prevent unusual heart rhythms which can lead to heart attacks

o reduce heart efficiency
 heart failure worse

o block beta receptors in the lungs
 make asthma worse or difficult to treat
 leads to constriction of the airways

49
Q

what do diuretics do and what are they used for?

A

drugs remove salt and water from the body

used for heart failure

50
Q

what happens when you take diuretics?

A
  • result of reduced salt and water levels we get
    o reduced plasma volume
    o reduce cardiac workload
51
Q

what are the side effects of taking diuretics?

A

lead to a Na+/K+ imbalance if not monitored carefully, dry mouth, dehydration

52
Q

what age groups are diuretics more effective on?

A

elderly

53
Q

what are nitrates used for?

A

Used to treat emergency management of including angina (chest pain) or long-term prevention of angina

54
Q

how do nitrates work?

A

They work by dilating or widening the blood vessels which improves blood flow and reduces the workload on the heart

-dilating vein: reducing preload to the heart
-Dilate resistance arteries: reduce cardiac workload and therefore reduce cardiac oxygen consumption
-Dilate collateral coronary artery supply: reduce anginal pain

55
Q

what are the types of nitrates you can get?

A

short acting - GTN spray (acts quickly)
long acting - Isosorbide Mononitrate (acts for many hours)

56
Q

what are the methods of administration for nitrates?

A

short acting: sublingually
spray under the tongue to relieve chest pain, this causes the blood vessels in the body to relax

long acting: dermal transcutaneous patch

57
Q

what are the side effects of nitrates?

A

headache, hypotension

58
Q

when do you use calcium channel blockers?

A

Drugs used in the management of hypotension, migraine, and some pain conditions

59
Q

what are some types of calcium channel blockers?

A

drugs ending in -pine

60
Q

how do calcium channel blockers work?

A
  • Calcium channel blockers work by blocking calcium ions into the smooth muscle cells that line the blood vessels and the heart muscle cells
  • By reducing the number of calcium that enters, this causes the blood vessels to relax and widen which improve blood flow and reduces workload on the heart
61
Q

what is a side effect of calcium channel blockers?

A

o Can lead to gingival hyperplasia in some – need to keep good OH

62
Q

what do ace inhibitors do?

A
  • Blocks the action of an enzyme called angiotensin converting enzyme
  • This enzyme is involved in the production of the hormone called angiotensin II
  • Angiotensin II is a potent vasoconstrictor: which means it narrow blood vessels and increases blood pressure
  • By blocking production of angiotensin II: help to relax and widen the blood vessels which improve blood flow and reduce blood pressure
63
Q

what are some types of ace inhibitors?

A

Drugs ending in -pril

64
Q

what are some side effects of ace inhibitors?

A

cough
hypotension
angio-odema : swelling of lips and tongue caused by the accumulation of fluid in tissues due to inhibition of the complement cascade by ACE enzyme
lichenoid reaction: are of ulceration, white change. found in patients taking ace inhibitors as well as beta blockers

65
Q

what are angiotensin II blockers?

A

they do not stop the production the just prevent the effect
same effect as ACE inhibitors but different mechanism

end in -artan

BAMS (1 decks)

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