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BDS2 BAMS Cardiovascular > Cardiovascular Medicine > Flashcards

Cardiovascular Medicine Flashcards

1
Q

what are the irreversible risk factors for cardiovascular disease

A

age
sex
family history

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2
Q

what are there reversible risk factors for CV disease

A

smoking
obesity
diet
exercise

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3
Q

what are the reversible cardiovascular diseases

A

hypertension
hyperlipidaemia
diabetes
stress

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4
Q

how do we modify risks?

A

it is patient centered and controlled

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5
Q

what influences patients to modify their risks

A

information so they know why they should change t
belief
motivation
behavioral change

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6
Q

what is primary prevention

A

preventative measures that prevent the onset of illness or injury before the disease process begins

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7
Q

what do we do in primary prevention

A

exercise, diet and not smoking

we assess the total risk and give medical treatment if there is a high risk

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8
Q

what is secondary prevention

A

the disease has already occurred so we are reducing trying to prevent the disease getting worse

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9
Q

what do we do in secondary prevention

A

all the correct lifestyle changes as well as medical treatment to reduce risk

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10
Q

why is motivation for secondary prevention greater than that of first

A

before we knew the risk but we did not see this risk applying to us

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11
Q

why is primary prevention difficult

A

it is opportunistic - doctors do not see their patients as a preventative measure to be able to screen for risk factors

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12
Q

how can dentists help in primary prevention

A

we see our patients regularly so we can look out for risk factors such as family history, smoking and diet and direct them to the correct health professional to get screened for any illnesses e.g cholesterol, hypertension, diabetes etc

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13
Q

what are examples of common cardiovascular diseases where we would start secondary prevention

A

angina
heart attack
stroke
claudication

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14
Q

what are the approaches to prevention

A

We look at the risk factors

  1. lifestyle changes
  2. control total cholesterol
  3. control hypertension
  4. anti platelet drugs
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15
Q

how do we control total cholesterol

A

through statin treatment

we reduce the cholesterol to lower than 25%

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16
Q

when do we control hypertension

A

when there is moderate hypertension

when there is mild hypertension with evidence of CV disease

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17
Q

what do we want to reduce hypertension to

A

140/85

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18
Q

when do we use anti platelet drugs (aspirin)

A

when we have identified Cv disease

when there is high risk with no identified disease

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19
Q

what is the function of drugs used in the CV system

A

prevent further disease

reduce symptoms of current disease

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20
Q

what are the drugs that prevent further disease

A

anti-platelet drugs
lipid lowering drugs
anti-arrhythmic drugs
anticoagulants

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21
Q

what drugs reduce symptoms of current disease

A 
diuretics 
anti-arrhythmics 
nitrates
calcium channel blockers
ace inhibitors
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22
Q

what are examples of anti platelet drugs

A

aspirin

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23
Q

what are the antiplatalet drugs

A

aspirin
clopidogrel
dipyridamole

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24
Q

how does aspirin work

A

inhibits platelet aggregation by altering the balance between thromboxane A2 and prostacyclin

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25
Q

what does prostacyclin do

A

potent inhibitor of platelet aggregation

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26
Q

what does thromboxane A2 do

A

produced by platelets and it stimulates activation of new platelets as well as increasing platelet aggregation

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27
Q

what effect does aspirin have on platelets

A

an irreversible one
it makes a permanent change
needs to be taken everyday for it to work effectively

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28
Q

what does clopodogrel do

A

inhibits ADP induced platelet aggregation

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29
Q

what does dipyridamole do

A

inhibits platelet phosphodiesterase

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30
Q

what are the new anti platelet drugs

A

prasugrel
ticagrelor
only prescribed in conjunction with aspirin and only liscenced for acute coronary syndromes

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31
Q

what is atherosclerosis

A

everyone has it
attracts platelets to stick to the artery and possibly block it
can limit blood flow and oxygen supply
can be controlled with anitplatelet drug

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32
Q

what is the difference between an anti platelet drug and an anticoagulant

A

antiplatalet stops platelets sticking to the walls and each other
anticoagulants stop the clotting cascade

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33
Q

what are the oral anticoagulants

A

warfarin
rivaroxiban
apixaban
dabigatran

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34
Q

which is the most common oral antigcouaglant

A

warfarin

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35
Q

why is warfarin monitored

A

it is individually tailored to the patient so blood needs to be taken regularly to ensure warfarin level is effective
it can have drug and food interactions which can effect plasma protein binding and liver metabolism

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36
Q

what is warfarin

A

coumarin based anticoagulant

37
Q

what does warfarin do

A

inhibits synthesis of vitamin K dependent clotting factors

38
Q

what clotting factors does warfarin inhibit the synthesis of

A

2, 7, 9, 10

slow - takes 2 days to have an effect as we have clotting factors in the blood already

39
Q

what are the proteins that warfarin inhibits

A

protein C, protein S

quick effect

40
Q

what effect does warfarin have initially

A

hyper coagulation
anticoagulation effect takes 2-3 days
often heparin is sued concurrently initially

41
Q

how long does it take warfarin to lose its effect

A

2-3 days

42
Q

how is warfarin monitored

A

with INR test tells us whether patient is adequately anti coagulated

43
Q

what is the INR

A

international standard for the PT

44
Q

what kind of range are we looking for with the INR test for warfarin

A

2-4
less than 2 then risk of clot
more than 4 then risk of bleed

45
Q

what do we do if the therapeutic iNR range is out of range

A

we need to refer for medical advice before proceeding with dental care

46
Q

how does warfarin effect our drug prescribing

A

we should get the INR tested the day after prescribing

47
Q

what common dental drugs interact with warfarin

A

amoxycillin
metronidazole
erythromycin
NSAIDs

48
Q

what are the new anticoagulants

A

rivaroxiban
apixaban
dabigatran

49
Q

what is an example of an activated factor 10 inhibitor

A

rivaroxaban

50
Q

what are the features of new oral anticoagulants

A

have a short half life

bioavailibity is predictable so there is no anticoagulant test used

51
Q

what are the NOAC dental drug interactions

A

safe with dental antibiotics EXCEPT MACROLIDES
safe with antifungals - topical and fluconazole
safe with LA
safe with antivirals
AVOID NSAIDS - will prolong action and inhibit platelets

52
Q

what are the macrolides

A

erythromycin and clarithromycin

53
Q

what are the other drugs preventing disease

A 
statins
beta-adrenergic blockers
diuretics
calcium channel blockers
ACE inhibitors
54
Q

what are the lipid lowering drugs also known as

A

HMG coA reductase inhibitors

STATINS

55
Q

what are the main statins

A

simvastatin (prodrug)

atorvastatin

56
Q

what do statins do

A

inhibit cholesterol synthesis in the liver

reduce total cholesterol and LDL cholesterol

57
Q

what are the side effects of statins

A

possible myositis with some drug interactions - includes antifungals

58
Q

what do statins interact with

A

fluconazole - they omit the statin during anti fungal treatment

59
Q

why is it okay to stop taking statin for a week or two

A

has an effect in the long run

60
Q

what are the beta-adrenergic blockers

A

atenolol
propranolol
many others ending in olol

61
Q

what is atenolol

A

selective - beta 1 only

62
Q

what is propranolol

A

non-selective - beta 1 and beta 2

generallyy not used for CV disease as it has too wide a range of effects

63
Q

what is it that kills during a heart attack

A

arrhythmia

64
Q

what do beta blockers do

A

they stop arrhythmia leading to cardiac arrest

reduces heart muscle excitation

65
Q

what are considerations with beta blockers

A

they prevent an increase in heart rate which can cause postural hypotension
reduce heart efficiency so can make heart failure worse
block beta receptors in the lung so can make asthma worse

66
Q

what are diuretics used for

A

antihypertensive and for heart failure

67
Q

what are the 2 types of diuretics

A

thiazide diuretics

loop diuretics

68
Q

what is an example of thiazide diuretics

A

bendroflumethiazide

69
Q

what do diuretics do

A

they increase salt and water LOSS
reduce plasma volume
reduce cardiac workload

70
Q

what are the side effects of diuretics

A

can lead to a Na/K imbalance if not monitored carefully

dry mouth in elderly

71
Q

what are short acting nitrates

A

glyceryl trinitrate (GTN)
used for emergency management of angina pectoris
sprayed under tongue

72
Q

how can GTN be used to distinguish a HA and angina

A

HA - pain does not go away

angina - pain goes away

73
Q

what are long acting nitrates

A

isosorbide mononitrate

used in prevention of angina pectoris

74
Q

what do nitrates do

A

dilate veins to reduce preload
dilate resistance arteries to reduce after load and reduce cardiac oxygen consumption
dilate collateral coronar artery supply to reduce anginas pain

75
Q

why are nitrates used sublingually/transfermally/intravenously

A

they are inactivated by first pass metabolism

76
Q

what is these side effects of nitrates

A

headaches

77
Q

what are calcium channel blockers used for

A

hypertension

78
Q

what do calcium channel blockers do

A

block calcium channels in smooth muscle

79
Q

what do nifedipine and amlodipine do

A

CALCIUM CHANNEL BLOCKERS
more active on peripheral blood vessels
cause relaxation and vasodilation

80
Q

what does verapamil do

A

more active on heart muscle

slow conduction of pacing impulses

81
Q

what do calcium channel blockers have a side effect of

A

gingival hyperplasia

linked with how well it is kept clean

82
Q

what are examples of ACE inhibitors

A

enalapril
ramapril
lisinopril

83
Q

what do ACE inhibitors do

A

inhibit conversion of angiotensin I to angiotensin II

prevents aldosterone dependent reabsorption of salt and water

84
Q

what is the effect of ace inhibitors

A

reduce blood pressure

reduce excess salt and water retention

85
Q

what are the side effects of ace inhibitors

A

cough, hypotension

86
Q

what are angiotensin II blockers

A

inhibit the same system but by a different mechanism

losartan and others ending in -artan

87
Q

what are oral reactions to ACE inhibitors

A

angio-odema

lichenoid reaction

88
Q

Give an example of a loop diuretic

A

frusemide

BDS2 BAMS Cardiovascular (6 decks)

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