pharmacolgy of angina Flashcards

1
Q

State five types of angina

A

angina of effort,

mixed (variable threshold) angina

Microvascular

Vasospastic

Unstable angina

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2
Q

what angina is most common

A

angina of effort

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3
Q

what are the symptoms of angina of effort

A

Symptoms: tightness, squeezing, crushing sensation in the chest

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4
Q

what causes angina of effort

A

exertion/emotion(stress), stenosis in coronary atery means in times of greater oxygen demand, it cannot be delivered, proton bradykinins released causing pain

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5
Q

what receptor do protons and bradykinin act on to cause pain

A

trpv1

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6
Q

during angina of effort what molecule causes vasodilation of coronary arteries

A

substance p

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7
Q

what is vasospastic angina

A

when a spasm of coronary artery occurs when resting often nighttime

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8
Q

what is mixed angina

A

unpredictable, develops at different levels of exercise

probably due to stenosis + vasospasm – thought to be very common. variable threshold

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9
Q

what is unstable angina

A

due to transient formation of a non-occlusive thrombus

an acute coronary syndrome

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10
Q

what is Microvascular (Syndrome X)

A

chest pain, normal coronary angiogram, positive exercise test;
endothelial dysfunction, the microvasculature is constricted.
occurs more commonly in women

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11
Q

what are two aims of drug treatment for angina

A

limit the number and severity of anginal attacks to improve life quality

Prevent against more lethal problems MI and lower risk for athersclerosis progression

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12
Q

what drugs can be used to prevent more lethal ischaemic syndromes

A

aspirin
b-blockers
ACE inhibitors
statins

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13
Q

how can we change lifestyle to protect against risk for ischaemic disease

A

stop smoking, lifestyle measures to lower bp, lower cholesterol intake

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14
Q

what is The main mechanism for the pharmacological treatment of angina of effort

A

to decrease cardiac O2 demand

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15
Q

A secondary mechanism is to increase the O2

supply to the ischaemic zone

A

by

decreasing the heart rate and increasing the blood flow in coronary arteries

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16
Q

for immediate relief/short term prevention of stable angina what would you do

A

Use short acting nitrate for immediate relief/short term prevention

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17
Q

how would you treat angina in the long term (ongoing prophylaxis)

A

b blocker or CCB,

if that does not work B blocker and vascular selective CCB,

if that doesnt work B blocker CCB and long acting nitrate or ivabradine, nicorandil,ranozaline

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18
Q

what can thrombosis lead to

A

STEMI NSTEMI unstable angina, or it can stabilise and become stable angina with loss of coronary flow reserve

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19
Q

what is the mechanism of action for B blockers

A

reduce cardiac contractility, inhibit SNS also decrease renin release which keeps blood pressure down and decrease after load on heart, makes heart work less

20
Q

what is the most common b blocker

A

bisoprolol

21
Q

Why Beta blockers are contraindicated in vasospastic angina?

A

it may worsen such attacks by blocking some β2 receptors that produce vasodilator effects, leaving α-mediated effects unopposed

22
Q

why are beta blockers prescribed after MI

A

reducing the risk of

developing chronic heart failure

23
Q

what hear rate do b blockers aim to keep the heart at during rest and excercise

A

Aim for a resting HR of 55-60 bpm, and an increase of <75% of
the rate causing ischaemia during exercise

24
Q

give an examples of a calcium channel blockers

A

amlodipine (a dihydropyridine, DHP), verapamil, diltiazem

25
rank dhp verapamil and ditiazem which is the best vasodialator
dhp then diltiazem then verapamil
26
rank calcium channel blockers in order of the best for negative iontropy to the worst
verapamil, diltaziem and then dhp
27
dhp act mainly by vasodilation how does this help angina
reduces afterload , therefore lowers cardiac work
28
why are calcium channel blockers useful for mixed angina and prinzmetal's angina sometimes
because they dilate the coronary arteries to helping restore coronary flow reserve
29
Other potentially beneficial actions of CCB that can be overlooked(hint left ventricle, endothelial)
↓ reperfusion injury (cardiac damage occurring after ischaemia) endothelial ‘protection’ ↓ atheroma progression reduction of left ventricular hypertrophy
30
describe the dual action of nicorandil
opens atp sensitive k channels in vascular smooth muscle stimulates guanine cyclase, increasing cyclic gmp
31
how does increase cGMP and atp sensitive k channels opening in smooth muscles help angina
cgmp causes vasodilation removal of calcium from cytoplasm, desensitization , reducing afterload atp sensitive k channels opening causes hyperpolarisation favouring smooth muscle relaxation and vasodilation venous and aterial vasodilation which reduce preload and afterload reducing cardiac work and oxygen demand
32
give an example of an organic nitrate
GTN
33
how is GTN taken
sublingual (rapid effect)
34
what is the haemodynamic mechanism of GTN
reduce preload and cvp, increase coronary blood flow vasodilation
35
why are people taking long acting organic nitrates such as isosorbide dinitrate) advised to have 8 hr free drug periods usually when sleeping
body can become tolerant to drug after around 12 hours
36
do nitrates dilate arteries or veins more
veins
37
lower CVP reduce cardiac work how?(major action)
lower central venous pressure, and thus less cardiac wall tension lower cardiac O2 demand
38
what are the minor actions of nitrates
Dilate larger coronary arteries, increasing blood flow through coronary collaterals lowers TPR and afterload, therefore lower O2 demand (affects arteries less than veins)
39
What are the side effects of haemodynamic nitrates
headache, facial flushing low BP, reflex increase HR Due to vasodilatation
40
how does ranolazine work
Acts by inhibiting the ‘late Na+ current’ in | myocytes:
41
how does ivabradine work
blocks delays funny current, use dependency, so more frequent opening of if channel more ivabradine can bind which slows heart rate a good thing. more time for the blood to perfuse myocardium and lower heart rate means lower afterload
42
what is the mechanism of action for statins
statins block HMG-CoA | reductase, so you cant produce as much cholesterol
43
what type of indivdual would you give statins to
Used long term in those with elevated LDL cholesterol levels to reduce risk of developing coronary heart disease.
44
what is coronary atery bypass grafting
``` uses piece(s) of saphenous vein or diverted internal mammary artery. More invasive than PCI but better outcomes and improves survival ```
45
what is PCI
percutaneous coronary intervention (PCI), stenosis baloon used to inflate atery mechanically. however restenosis often occurs which is treated with a stent