Cardiovascular Medicine Flashcards

(88 cards)

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
what does prostacyclin do
potent inhibitor of platelet aggregation
26
what does thromboxane A2 do
produced by platelets and it stimulates activation of new platelets as well as increasing platelet aggregation
27
what effect does aspirin have on platelets
an irreversible one it makes a permanent change needs to be taken everyday for it to work effectively
28
what does clopodogrel do
inhibits ADP induced platelet aggregation
29
what does dipyridamole do
inhibits platelet phosphodiesterase
30
what are the new anti platelet drugs
prasugrel ticagrelor only prescribed in conjunction with aspirin and only liscenced for acute coronary syndromes
31
what is atherosclerosis
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
32
what is the difference between an anti platelet drug and an anticoagulant
antiplatalet stops platelets sticking to the walls and each other anticoagulants stop the clotting cascade
33
what are the oral anticoagulants
warfarin rivaroxiban apixaban dabigatran
34
which is the most common oral antigcouaglant
warfarin
35
why is warfarin monitored
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
36
what is warfarin
coumarin based anticoagulant
37
what does warfarin do
inhibits synthesis of vitamin K dependent clotting factors
38
what clotting factors does warfarin inhibit the synthesis of
2, 7, 9, 10 | slow - takes 2 days to have an effect as we have clotting factors in the blood already
39
what are the proteins that warfarin inhibits
protein C, protein S | quick effect
40
what effect does warfarin have initially
hyper coagulation anticoagulation effect takes 2-3 days often heparin is sued concurrently initially
41
how long does it take warfarin to lose its effect
2-3 days
42
how is warfarin monitored
with INR test tells us whether patient is adequately anti coagulated
43
what is the INR
international standard for the PT
44
what kind of range are we looking for with the INR test for warfarin
2-4 less than 2 then risk of clot more than 4 then risk of bleed
45
what do we do if the therapeutic iNR range is out of range
we need to refer for medical advice before proceeding with dental care
46
how does warfarin effect our drug prescribing
we should get the INR tested the day after prescribing
47
what common dental drugs interact with warfarin
amoxycillin metronidazole erythromycin NSAIDs
48
what are the new anticoagulants
rivaroxiban apixaban dabigatran
49
what is an example of an activated factor 10 inhibitor
rivaroxaban
50
what are the features of new oral anticoagulants
have a short half life | bioavailibity is predictable so there is no anticoagulant test used
51
what are the NOAC dental drug interactions
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
what are the macrolides
erythromycin and clarithromycin
53
what are the other drugs preventing disease
``` statins beta-adrenergic blockers diuretics calcium channel blockers ACE inhibitors ```
54
what are the lipid lowering drugs also known as
HMG coA reductase inhibitors | STATINS
55
what are the main statins
simvastatin (prodrug) | atorvastatin
56
what do statins do
inhibit cholesterol synthesis in the liver | reduce total cholesterol and LDL cholesterol
57
what are the side effects of statins
possible myositis with some drug interactions - includes antifungals
58
what do statins interact with
fluconazole - they omit the statin during anti fungal treatment
59
why is it okay to stop taking statin for a week or two
has an effect in the long run
60
what are the beta-adrenergic blockers
atenolol propranolol many others ending in olol
61
what is atenolol
selective - beta 1 only
62
what is propranolol
non-selective - beta 1 and beta 2 | generallyy not used for CV disease as it has too wide a range of effects
63
what is it that kills during a heart attack
arrhythmia
64
what do beta blockers do
they stop arrhythmia leading to cardiac arrest | reduces heart muscle excitation
65
what are considerations with beta blockers
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
what are diuretics used for
antihypertensive and for heart failure
67
what are the 2 types of diuretics
thiazide diuretics | loop diuretics
68
what is an example of thiazide diuretics
bendroflumethiazide
69
what do diuretics do
they increase salt and water LOSS reduce plasma volume reduce cardiac workload
70
what are the side effects of diuretics
can lead to a Na/K imbalance if not monitored carefully | dry mouth in elderly
71
what are short acting nitrates
glyceryl trinitrate (GTN) used for emergency management of angina pectoris sprayed under tongue
72
how can GTN be used to distinguish a HA and angina
HA - pain does not go away | angina - pain goes away
73
what are long acting nitrates
isosorbide mononitrate | used in prevention of angina pectoris
74
what do nitrates do
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
why are nitrates used sublingually/transfermally/intravenously
they are inactivated by first pass metabolism
76
what is these side effects of nitrates
headaches
77
what are calcium channel blockers used for
hypertension
78
what do calcium channel blockers do
block calcium channels in smooth muscle
79
what do nifedipine and amlodipine do
CALCIUM CHANNEL BLOCKERS more active on peripheral blood vessels cause relaxation and vasodilation
80
what does verapamil do
more active on heart muscle | slow conduction of pacing impulses
81
what do calcium channel blockers have a side effect of
gingival hyperplasia | linked with how well it is kept clean
82
what are examples of ACE inhibitors
enalapril ramapril lisinopril
83
what do ACE inhibitors do
inhibit conversion of angiotensin I to angiotensin II | prevents aldosterone dependent reabsorption of salt and water
84
what is the effect of ace inhibitors
reduce blood pressure | reduce excess salt and water retention
85
what are the side effects of ace inhibitors
cough, hypotension
86
what are angiotensin II blockers
inhibit the same system but by a different mechanism | losartan and others ending in -artan
87
what are oral reactions to ACE inhibitors
angio-odema | lichenoid reaction
88
Give an example of a loop diuretic
frusemide