Cardiovascular Medicine Flashcards
what are the irreversible risk factors for cardiovascular disease
age
sex
family history
what are there reversible risk factors for CV disease
smoking
obesity
diet
exercise
what are the reversible cardiovascular diseases
hypertension
hyperlipidaemia
diabetes
stress
how do we modify risks?
it is patient centered and controlled
what influences patients to modify their risks
information so they know why they should change t
belief
motivation
behavioral change
what is primary prevention
preventative measures that prevent the onset of illness or injury before the disease process begins
what do we do in primary prevention
exercise, diet and not smoking
we assess the total risk and give medical treatment if there is a high risk
what is secondary prevention
the disease has already occurred so we are reducing trying to prevent the disease getting worse
what do we do in secondary prevention
all the correct lifestyle changes as well as medical treatment to reduce risk
why is motivation for secondary prevention greater than that of first
before we knew the risk but we did not see this risk applying to us
why is primary prevention difficult
it is opportunistic - doctors do not see their patients as a preventative measure to be able to screen for risk factors
how can dentists help in primary prevention
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
what are examples of common cardiovascular diseases where we would start secondary prevention
angina
heart attack
stroke
claudication
what are the approaches to prevention
We look at the risk factors
- lifestyle changes
- control total cholesterol
- control hypertension
- anti platelet drugs
how do we control total cholesterol
through statin treatment
we reduce the cholesterol to lower than 25%
when do we control hypertension
when there is moderate hypertension
when there is mild hypertension with evidence of CV disease
what do we want to reduce hypertension to
140/85
when do we use anti platelet drugs (aspirin)
when we have identified Cv disease
when there is high risk with no identified disease
what is the function of drugs used in the CV system
prevent further disease
reduce symptoms of current disease
what are the drugs that prevent further disease
anti-platelet drugs
lipid lowering drugs
anti-arrhythmic drugs
anticoagulants
what drugs reduce symptoms of current disease
diuretics anti-arrhythmics nitrates calcium channel blockers ace inhibitors
what are examples of anti platelet drugs
aspirin
what are the antiplatalet drugs
aspirin
clopidogrel
dipyridamole
how does aspirin work
inhibits platelet aggregation by altering the balance between thromboxane A2 and prostacyclin
what does prostacyclin do
potent inhibitor of platelet aggregation
what does thromboxane A2 do
produced by platelets and it stimulates activation of new platelets as well as increasing platelet aggregation
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
what does clopodogrel do
inhibits ADP induced platelet aggregation
what does dipyridamole do
inhibits platelet phosphodiesterase
what are the new anti platelet drugs
prasugrel
ticagrelor
only prescribed in conjunction with aspirin and only liscenced for acute coronary syndromes
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
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
what are the oral anticoagulants
warfarin
rivaroxiban
apixaban
dabigatran
which is the most common oral antigcouaglant
warfarin
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
what is warfarin
coumarin based anticoagulant
what does warfarin do
inhibits synthesis of vitamin K dependent clotting factors
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
what are the proteins that warfarin inhibits
protein C, protein S
quick effect
what effect does warfarin have initially
hyper coagulation
anticoagulation effect takes 2-3 days
often heparin is sued concurrently initially
how long does it take warfarin to lose its effect
2-3 days
how is warfarin monitored
with INR test tells us whether patient is adequately anti coagulated
what is the INR
international standard for the PT
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
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
how does warfarin effect our drug prescribing
we should get the INR tested the day after prescribing
what common dental drugs interact with warfarin
amoxycillin
metronidazole
erythromycin
NSAIDs
what are the new anticoagulants
rivaroxiban
apixaban
dabigatran
what is an example of an activated factor 10 inhibitor
rivaroxaban
what are the features of new oral anticoagulants
have a short half life
bioavailibity is predictable so there is no anticoagulant test used
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
what are the macrolides
erythromycin and clarithromycin
what are the other drugs preventing disease
statins beta-adrenergic blockers diuretics calcium channel blockers ACE inhibitors
what are the lipid lowering drugs also known as
HMG coA reductase inhibitors
STATINS
what are the main statins
simvastatin (prodrug)
atorvastatin
what do statins do
inhibit cholesterol synthesis in the liver
reduce total cholesterol and LDL cholesterol
what are the side effects of statins
possible myositis with some drug interactions - includes antifungals
what do statins interact with
fluconazole - they omit the statin during anti fungal treatment
why is it okay to stop taking statin for a week or two
has an effect in the long run
what are the beta-adrenergic blockers
atenolol
propranolol
many others ending in olol
what is atenolol
selective - beta 1 only
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
what is it that kills during a heart attack
arrhythmia
what do beta blockers do
they stop arrhythmia leading to cardiac arrest
reduces heart muscle excitation
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
what are diuretics used for
antihypertensive and for heart failure
what are the 2 types of diuretics
thiazide diuretics
loop diuretics
what is an example of thiazide diuretics
bendroflumethiazide
what do diuretics do
they increase salt and water LOSS
reduce plasma volume
reduce cardiac workload
what are the side effects of diuretics
can lead to a Na/K imbalance if not monitored carefully
dry mouth in elderly
what are short acting nitrates
glyceryl trinitrate (GTN)
used for emergency management of angina pectoris
sprayed under tongue
how can GTN be used to distinguish a HA and angina
HA - pain does not go away
angina - pain goes away
what are long acting nitrates
isosorbide mononitrate
used in prevention of angina pectoris
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
why are nitrates used sublingually/transfermally/intravenously
they are inactivated by first pass metabolism
what is these side effects of nitrates
headaches
what are calcium channel blockers used for
hypertension
what do calcium channel blockers do
block calcium channels in smooth muscle
what do nifedipine and amlodipine do
CALCIUM CHANNEL BLOCKERS
more active on peripheral blood vessels
cause relaxation and vasodilation
what does verapamil do
more active on heart muscle
slow conduction of pacing impulses
what do calcium channel blockers have a side effect of
gingival hyperplasia
linked with how well it is kept clean
what are examples of ACE inhibitors
enalapril
ramapril
lisinopril
what do ACE inhibitors do
inhibit conversion of angiotensin I to angiotensin II
prevents aldosterone dependent reabsorption of salt and water
what is the effect of ace inhibitors
reduce blood pressure
reduce excess salt and water retention
what are the side effects of ace inhibitors
cough, hypotension
what are angiotensin II blockers
inhibit the same system but by a different mechanism
losartan and others ending in -artan
what are oral reactions to ACE inhibitors
angio-odema
lichenoid reaction
Give an example of a loop diuretic
frusemide
