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supporting life > pharmacolgy of angina > Flashcards

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
Q

rank dhp verapamil and ditiazem which is the best vasodialator

A

dhp then diltiazem then verapamil

26
Q

rank calcium channel blockers in order of the best for negative iontropy to the worst

A

verapamil, diltaziem and then dhp

27
Q

dhp act mainly by vasodilation how does this help angina

A

reduces afterload , therefore lowers cardiac work

28
Q

why are calcium channel blockers useful for mixed angina and prinzmetal’s angina sometimes

A

because they dilate the coronary arteries to helping restore coronary flow reserve

29
Q

Other potentially beneficial actions of CCB that can be overlooked(hint left ventricle, endothelial)

A

↓ reperfusion injury (cardiac damage occurring after ischaemia)
endothelial ‘protection’
↓ atheroma progression
reduction of left ventricular hypertrophy

30
Q

describe the dual action of nicorandil

A

opens atp sensitive k channels in vascular smooth muscle

stimulates guanine cyclase, increasing cyclic gmp

31
Q

how does increase cGMP and atp sensitive k channels opening in smooth muscles help angina

A

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
Q

give an example of an organic nitrate

A

GTN

33
Q

how is GTN taken

A

sublingual (rapid effect)

34
Q

what is the haemodynamic mechanism of GTN

A

reduce preload and cvp, increase coronary blood flow vasodilation

35
Q

why are people taking long acting organic nitrates such as isosorbide dinitrate) advised to have 8 hr free drug periods usually when sleeping

A

body can become tolerant to drug after around 12 hours

36
Q

do nitrates dilate arteries or veins more

A

veins

37
Q

lower CVP reduce cardiac work how?(major action)

A

lower central venous pressure,

and thus less cardiac wall tension

lower cardiac O2 demand

38
Q

what are the minor actions of nitrates

A

Dilate larger coronary arteries, increasing blood flow through coronary
collaterals

lowers TPR and afterload, therefore lower O2 demand
(affects arteries less than veins)

39
Q

What are the side effects of haemodynamic nitrates

A

headache, facial flushing
low BP, reflex increase HR
Due to vasodilatation

40
Q

how does ranolazine work

A

Acts by inhibiting the ‘late Na+ current’ in

myocytes:

41
Q

how does ivabradine work

A

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
Q

what is the mechanism of action for statins

A

statins block HMG-CoA

reductase, so you cant produce as much cholesterol

43
Q

what type of indivdual would you give statins to

A

Used long term in those with elevated LDL cholesterol levels to reduce
risk of developing coronary heart disease.

44
Q

what is coronary atery bypass grafting

A 
uses piece(s) of saphenous
vein or diverted internal
mammary artery. More invasive than PCI but better outcomes and improves survival
45
Q

what is PCI

A

percutaneous coronary intervention (PCI), stenosis baloon used to inflate atery mechanically. however restenosis often occurs which is treated with a stent

supporting life (20 decks)

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