21 - Systemic drugs 1: cardiovascular Flashcards
modifiable risks of cardiovascular disease
-smoking
- hypertension
-hyperlidaemia
-diet+exercidse
non modifiable risks of CVD
- age
- gender
- genetics
lifestyle measures to reduce risk of CVD
- stop smoking
- normal BMI 20-25
- reduce salt intake to <6g
- limit alcohol consumption <14 a week
- 5 a day
- reduce intake of total and saturated fat
- regular excerie
hypertension is a major risk factor for
- stroke
-myocaridal infarction - heart failure
- chronic kidney disease
- cognitive decline
- premature death
what can untreated hypertension cause
- vascular and renal damage
diagnosing hypertension
if clinic bp higher than 140/90
offer bp monitoring at home to confirm diagnosing
stage 1 HTN
- clinic BP is 140/90 or above and ABPM or HBPM average is 135/85 or above
stage 2 HTN
clinic BP > 60/100
and
ABPM/HBPM > 150/95
stage 3 HTN
- clinic bp is 180 >
or
clinic diastolic bp is >110
why do we treat HTN
- reduces cerebeovascular disease by 40-50%
- reduces myocardial infarction by 16-30%
how do we treat HTN
stepped approach
- low doses of several drugs
minimises adverse events + maximises patient compliance
what is the aim of treatment
- reduce diastolic BP <90
- reduce systolic BP <140
younger 55 and stage 1 - which type of drug
ACE
Over 55 stage 1/ or black patients of any age - which drug
- calcium channel blocker
- diuretic
if px becomes stage 2
do not inrease dose of ACE - it can increase side effects
instead - add low doses of other drugs
suffix of ace inhibitors
PRIL
e.g ramipril
kidney produces renin, what is it and what does it do
an enzyme that converts angiotensin to angiotensin I, catalysing conversion
what is antigensin I the substrate for
angiotensin converting enzyme (ACE)
what does the angiotensin coverting enzyme do
converts angitotensin I to active angiotensin II
what is angiotensin II
- potent vasoconstrictor
- constricts blood vessels: increasing peripheral resistance + increasing blood volume
we want to STOP vasoconstriction as that will increase blood pressure
side effects of ace inhibtors
- persistent dry cough
- taste disturbance
- angiodema
-1st dose hypotension - hyperkalaemia
angiotensin II receptor antagonist
- they completley inhibit the receptor at which angiotensin II acts
-fewer side effects than ACE
Angiotensin II receptor antagonists examples
- candesartan
- losartan
- valsartan
TAN SUFFIX
calcium channel blockers
CCB all inhibit inward movement of calcium ions through the slow L-type calcium channels in active membranes:
—cells of the myocardium
—Cells within the his-purkinje system of the heart
—cells of the vascular smooth muscle
what do CCB affect - and cause as a result
- cardiac contractability
causes vasodilation - cause vasodilation of large and small arteries and also reduce cardiac output
what are calcium channel blockers useful in the treatment of
hypertension and angina
examples of CCB
- Nifedipine,
- Amlodipine
- Verapamil
- Diltiazem
what do diuretics promote
- excretion of water and salt: this is done by increasing urine production and increasing salt consumption
how do diuretics reduce the re uptake of salt
- increase the amount of urine
thereby reducing blood volume - thus lowering blood pressue
3 main classes of diuretics and where do they mainly work
distal convulated tube
- thiazides
- loop diuretic
- potassium sparing
what are thiazides commonly used for
blood pressure
Ignore
how do thiazides work
- inhibit absorbtion of Na in the DCT
- can lead to K deficiency
how do thiazides reduce BP
- vasodilation
- reduction in blood volume
examples of thiazides
bendrofluazide,
Hydrochlorothiazide
Indapamide
what do loop diuretics do
- inhibit absorption of sodium and potassium in TAL of loop of henle
- fast acting
when are loop diuretics used
- renal failure + heart failure
examples of loop diuretcs
Furosemide, Bumetanide
where does potassium sparing act
DCT
What do potassium sparings do
- retain potassium
- used in conjunction with thiazide and loop diuretics
examples of potassium s-paring
- amiloride
- spironolactone
when are beta blockers used
treatment of angina
- increased risk of side effects
examples of beta blockers
- atenolol
- metoprolol
- propanolol
what does the mechanism of beta blockers involve
- reduction of heart rate + force of contraction
- reduction of peripheral resistance
- ihibition of renin release
reduce sympathetic activity
less commonly used in anti-hypertensive agents
used when other drugs are not bringing down blood pressure that easily even with combination drugs. Or if the patient had bad side effects with some drugs.
-Alpha-adrenoceptor antagonists
Doxazosin
-Centrally acting agents
Methyldopa
Moxonidine
-Vasodilators
Hydralazine
Minoxidil
other cardiovascular disease
- ischaemic heart disease
- cardiac failure
- cardiac arrythmias
Ischaemic heart disease: Angina pectoris
-presents with intermittent chest pain on excretion or stress (stable angina)
-caused by insufficient oxygen supplied to cardiac muscle due to narrowing of coronary arteries
how is angina pectoris treated
–>single acute attack (Glyceryl trinitrate-potent vasodilator)
–>Prophylaxis (Sublingual GTN, Aspirin, Beta- blockers, calcium channel blockers). All patients should receive lipid lowering therapy.
stent inserted to widen blood vessel.`
what is atheroma
- Atheroma deposited in the wall of blood vessels
- Atheroma is problematic because it narrows the blood vessels
Also linked to formation of clots
Ischaemic heart disease: Myocardial infarction
-ST elevation on ECG
Immediate:
-Analgesia, Thrombolysis, Aspirin
Prophylaxis:
- Beta blockers
-ACE inhibitors
- Aspirin
- Lipid lowering therapy
Heart failure - due to what
-Usually the result of damage to the myocardium e.g. MI, Myocardiomyopathy, heart valve damage
-results in poor tissue perfusion and eodema of the lungs or peripheral tissue
treatment of heart failure
- Diuretics
- ACE inhibitors
- Nitrates
- Beta blockers
- Ionotropic drugs e.g. Digoxin
Cardiac arrythmias
too long and confusing to write]
Just know causes changes in the cardiac action potential
what is lipid modification
- cholesterol and triglycerdes transported in the blood from the liver in association with lipoproteins
what is low density lipoprotein LDL
bad cholestrol
what is high density lipoprotein HDL
good cholesterol
what is LDL cholesterol associated with
atheroma and cardiovascular disease
what are statins used for
to lower cholesterol
Enzyme: HMG-CoA
rate limiting step in the synthesis of cholestrol in liver
what do statins do to this Enzyme: HMG-CoA
inhibit this enzyme increasing uptake of LDL from blood
statin examples
-Simvastatin
- Atorvastatin
- Pravastatin
by inhibiting cholesterol synthesis in the liver
you get more uptake of LDL cholesterol
