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P1: Card System > Pharmacology of CVS - Angina > Flashcards

Pharmacology of CVS - Angina Flashcards

1
Q

What is angina?

A

→ Angina is chest pain or pressure when there is a build up of lactic acid during anaerobic respiration
→ due to not enough blood flow to the heart muscle.
Signal via cardiac nerves and upper posterior nerve roots

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2
Q

What are the symptoms of angina pectoris?

A

→crushing chest pain, also in the jaw, shoulders, arms, etc.
→shortness of breath
→sweating
→ nausea

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3
Q

How many people suffer from angina pectoris in the UK and what is the prevelance?

A

→2 million sufferers in the UK

2-4% of Western countries

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4
Q

What are the symptoms of typical angina?

A

→ typical angina
→ substernal chest discomfort of characteristic quality + duration
→provoked by exertion or emotional stress
→symptoms attributed to myocardial ischemia
→short duration radiation to left arm, neck, jaw. Lasts 2-5 minutes

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5
Q

How can typical angina be relieved?

A

→ rest + medications

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6
Q

Why is stable angina classified as predictable?

A

→ recurrent episodes have a similar onset pattern, duration + intensity

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7
Q

What does a coronary spasm lead to? (Prinzmetal angina)

A

Caused by drugs like cocaine.

→ Critical reduction in blood flow so oxygen supply is inadequate

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8
Q

What is supply ischaemia?

A

→ When there is decreased coronary blood flow due to vasospasm or a thrombus / blockage

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9
Q

What is demand ischaemia?

A

→Increased demand for oxygen in the heart muscle

→ Due to fixed stenosis

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10
Q

What are precipitating factors for angina?

A

→ Increased sympathetic activity
→ Increased contractility - exercise, emotion or stress
→ Increased vasoconstriction

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11
Q

What are the three ways to treat angina?

A

→ Improving perfusion
→ Reducing metabolic demand
→ Prevention

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12
Q

How do you improve perfusion with angina?

A

→ Increase oxygen delivery by improving coronary blood flow

→ coronary vasodilators

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13
Q

How do you reduce metabolic demand with angina?

A

→ Decrease cardiac work
→ Using vasodilators ( reduce afterload + preload)
→ Using cardiac depressants ( reduce HR + contractility)

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14
Q

How do you prevent angina?

A 
→ Prophylactic to reduce risk of episodes
→ lipid lowering
→ anti-coagulants
→ Fibrinolytic
→anti-platelet
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15
Q

What does clot formation lead to? (unstable angina)

A

→ Occludes the artery

→ There is a critical reduction in blood flow so oxygen supply is inadequate even at rest

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16
Q

What does a narrowed coronary artery lumen lead to? (stable angina)

A

→ Restricted blood flow to area of the myocardium it supplies
→ Oxygen is receives is insufficient when the heart has to work harder
→ Anaerobic respiration
→Pain

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17
Q

How is preload reduced by giving nitrates?

A

→ Peripheral venodilation
→ Decreases intraventricular pressure
→ Cardiac preload decreases
→reduced oxygen demand by decreasing the work of the heart

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18
Q

How is afterload reduced by giving nitrates?

A

→ Arterial dilation
→ Decreases total TPR
→ Reduces afterload
→reduced oxygen demand

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19
Q

What are adverse effects of nitrates and why?

A

→ Headache, flushing, syncope ( arterial dilation)
→ Postural hypotension ( venodilation)
→ Reflex tachycardia ( sympathetic outflow)

20
Q

How does nitric oxide work?

A

→NO synthase makes NO from L-arginine
→ NO activates guanylyl cyclase
→ It activates cGMP
→ Activates protein kinase G

→cGMP converted to GMP by phosphodiesterase type 5

21
Q

How does PKG reduce smooth muscle tone?

A

→ Increase uptake of Ca2+
→ Myosin light chain dephosphorylation
→ Activates K+ channels causing hyperpolarization + closing VGCC

22
Q

What do organic nitrates mimic?

A

→ Mimic the effects of endogenous nitric oxide

23
Q

How do beta blockers reduce CO and lower blood pressure?

A

→ Inhibit funny current in the SA node
→ Reduce the force of cardiac contractions- improves exercise tolerance

act on beta 1 receptors in SA node and ventricular myocytes

24
Q

How do beta blockers slow heart rate?

A

→ Lengthens diastole and gives more time for coronary perfusion
→ Improves myocardial oxygen supply

25
Q

What are the contraindications and adverse side effects of beta blockers?

A

ASTHMA
→ Blocking beta two can cause constriction + bronchospasm
HEART BLOCK
→ AV conduction is poor can block AV node

→side effects: fatigue, bronchospasm, postural hypotension

26
Q

How do calcium blockers reduce contractility?

A

→ Reduce Ca2+ entry into the myocytes

27
Q

How do calcium blockers cause more coronary blood flow?

A

→ Direct coronary vasodilatation

28
Q

What is the effect of reducing TPR/ BP/ Afterload due to calcium channel blockers?

A

→ Heart works less hard to eject blood

29
Q

How do Ca2+ blockers cause less O2 consumption?

A

→ Reducing the force of contraction

30
Q

What are adverse effects of Ca2+ blockers?

A

→ Lower limb oedema- increased capillary pressure in lower limbs
→ Flushing + headache- excess vasodilation
→ Reflex tachycardia

31
Q

What is a risk of using Ca2+ blockers?

A

→ Blocking Ca2+ channels in the heart can change electrical conduction + contractility

32
Q

What is the mechanism of action of Ca2+ blockers in ventricular myocytes and vascular smooth muscle?

A

→ Reduce Ca2+ influx through voltage gated L-type channels in smooth + cardiac muscle
→In ventricular myocytes, they block the beta 1 receptors- reduced PKA, reduced CICR, reduced contractility
→In vascular smooth muscle, they block alpha 1 receptors, PLC, PKC, Na channels, reduced vasoconstriction

33
Q

What are three drugs given when Ca2+ blockers don’t work?

A

→ Nicorandil, ivabradine and ranolazine

34
Q

What are three prophylactic drugs for angina?

A

→ aspirin - reduces platelet aggregation
→ clopidogrel - reduces platelet aggregation
→ Statins - reduces cholesterol

35
Q

What are the characteristics of unstable angina?

A

→unpredictable
→pain symptoms more severe, and lasts longer
→happens at rest with little exertion or trigger
→not relieved by rest and medications
→serious, emergency

36
Q

Which type of angina is common young people?

A

Prinzmetal angina

→cocaine

37
Q

What are the symptoms and how can atypical angina be relieved?

A

→heart burn, Raynaud’s phenomenon, sweating, dizziness

→medication

38
Q

How does microvascular angina arise?

A

→impaired vasodilation in coronary circulation/ increased constriction
→reduced coronary perfusion
→pain
→patients do not have obstructive coronary artery disease

39
Q

Why is microvascular angina hard to diagnose and how is it done?

A

→because coronary microvasculature cannot be directly imaged in vivo
→positron emission tomography or cardiac magnetic resonance are used to assess coronary microvasculature blood flow

40
Q

What are some prophylactic drugs for angina?

A

→Aspirin- inhibits COX which reduced thromboxane A2, and platelet aggregation(GPIIb/IIa expression)- reduces thrombosis
→Clopidogrel- inhibits ADP receptor on platelets reduces aggregation, reduces thrombosis
→ Statins- HMG Co-a reductase inhibitor- reduced cholesterol levels

41
Q

How does nicorandil work?

A

→K+ channel, hyperpolarisation- VGCC reduced and Ca2+ entry reduced so coronary vasodilation.
Has a nitrate moiety so there’s venodilation via NO generation

42
Q

How does ivabradine work?

A

specific inhibitor of funny cuurent in SA nose- slows heart rate
→decrease pacemaker potential frequency- decreases heart rate to reduce myocardial O2 demand

43
Q

How does ranolazine work?

A

→late Na+ inhibitor- reduces Ca2+ in ischaemic myocardial cells which reduces oxygen demand
→reduce compression of small intramyocardial coronary vessels- improves myocardial perfusion

44
Q

Examples of beta blockers, nitrates and Ca2+ channel blockers

A

BETA BLOCKERS:
→atenolol
→bisoprolol

NITRATES:
→glyceryl trinitrate, isosorbide mononitrate

Ca2+ CHANNEL BLOCKERS:
→dihydropyridines(vascular)- amplodipine, nifedipine
→benzothiazepines(cardiac) - verapamil
→diphenylalkyamines(both)- diltiazem

45
Q

What is the first line of action in symptom control?

A

→ GTN +

→beta blocker or Ca2+ channel blocker

46
Q

What is the second line of treatment in symptom control?

A

→dihydropyridine calcium channel blocker to beta-blocker

→nicorandil, ivabradine, ranolazine

47
Q

What are the primary prevention methods?

A 
→lifestyle advice
→aspirin daily
→lipid lowering therapy
→ACE inhibitor
→angiotensin II receptor agonist

P1: Card System (16 decks)

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