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Angina Flashcards

1
Q

Define angina

A

Chronic/acute ischaemic heart disease associated with transient chest discomfort/pain due to reduced blood flow to heart

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2
Q

Angina is characterised by reversible/irreversible mismatch between myocardial O2 supply & demand

A

reversible

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3
Q

List the 3 types of angina

A

Classic angina
Variant angina
Microvascular angina

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4
Q

Describe classic angina and its effect on myocardial O2

A

Atherosclerotic plaque partially obstructs coronary arteries, so myocardial O2 demand increases and the supply cannot match it

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5
Q

When does classic angina normally occur

A

Exercise/stress induced

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6
Q

Describe variant angina and its effect on myocardial O2 supply

A

Spasm of coronary arteries due to a decrease in myocardial O2 supply

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7
Q

When does variant angina normally occur?

A

Rest/asleep

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8
Q

Describe microvascular angina

A

Primary dysfunction of small coronary arteries due to a functional/structural defect resulting in chest pain at rest or on exertion

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9
Q

Name the 2 clinical subtypes of angina

A

Angina with obstructive CAD

Angina without obstructive CAD

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10
Q

Describe the features of angina with obstructive CAD

A
  • effort induced, chest pain on exertion
  • fixed obstructive CAD = atherosclerotic plaque
  • ST-segment DEPRESSION
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11
Q

Describe the features of angina without obstructive CAD

A
  • pain at rest/night
  • spontaneous coronary artery spasm
  • ST-segment ELEVATION
  • Arrhythmias
  • Variant angina - angiospastic
  • microvascular angina - syndrome X
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12
Q

What is the result of a positive stress test for microvascular angina during exercise

A

ST-segment depression

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13
Q

List the 3 clinical features of angina

A

haemodynamic
metabolic
electrocardiographic

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14
Q

State why angina causes breathlessness & dizziness

A

Due to ischaemia-induced transient LV dysfunction

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15
Q

Describe the metabolic effects of angina

A

Increased myocardial lactate breakdown & net ATP breakdown due to anaerobic metabolism

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16
Q

What does an ECG machine show for a person with angina

A

ST-segment depression OR elevation

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17
Q

What is the aim on clinical management of angina?

A

Control symptoms
Prevent/reduce frequency of anginal episodes
Slow progression
Prolong survival

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18
Q

Describe 3 features of the multi-faceted approach to manage angina

A
  • lifestyle & risk factor modification
  • pharmacological therapy for symptomatic control
  • myocardial revascularisation
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19
Q

State how does pharmacological/anti-viral drug therapy work to treat angina

A

Improves myocardial O2 supply and reduces demand

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20
Q

Describe the pharmacological action of nitrates & nitrites

A

Directly acts on blood vessels by reducing vascular r

tension (vasorelaxation) -> systemic vasodilation ( decreases SVR & increases BF)

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21
Q

Describe the cellular mechanism of vasorelaxation

A

In vivo conversion to NO
Activation of guanalyte cyclase which increases cGMP
Activation of PKG -> vasorelaxation

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22
Q

Describe the mechanisms of the anti anginal effect of nitrates

A
  • peripheral venodilation decreases preload -> decreases MV O2
  • peripheral arterial & arteriolar dilation decreases afterload -> de creases MV O2
  • coronary vasodilation reverses & prevents spasm
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23
Q

Describe the process of nitrate action to decrease preload

A 
Peripheral venodilation
peripheral pooling of blood
decreases venous return
decreases ventricular volume & intraventricular pressue
decreases CO
decreases myocardial O2 demand
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24
Q

List adverse effects of the clinical use of nitrate treatment for angina

A
  • flushing
  • headaches (throbbing)
  • postural hypotension
  • reflex tachycardia
  • increases myocardial contractility
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25
Q

Describe the recommendations for nitrate therapy

A
  • begin with a small dose & establish dose threshold
  • use the smallest amount possible that gives symptomatic relief
  • nitrate interval of 8-10hrs (split doses to 8am & 2pm)
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26
Q

State the indication for the use of B-adrenoceptor antagonists and describe how they work

A
  • angina pectoris e.g. propanolol, atenolol

- Antagonise effects of hormones e.g. noradrenaline & adrenaline at B-adrenceptors

27
Q

List the 3 subtypes of B-adrenoceptors

A
  • B1-ARS - heart & kidney
  • B2-ARS - heart & smooth muscle
  • B3-ARS
28
Q

Name the 2 classes of B-blockers and give an example for each

A
  • non-selective e.g. propanolol

- B1 - selective - cardioselective e.g. atenolol

29
Q

Describe the classification of b-blockers and give drug examples

A
  • 1st generation
    non-selective without vasodilation
    e.g. propanolol, timolol
  • 2nd generation
    B1 selective without vasodilation e.g. atenolol, bisoprolol
    B1 selective with vasodilation e.g. nebivolol
  • 3rd generation
    non-selective with vasodilation e.g. carvedilol
30
Q

Describe the mechanism of the anti-anginal heamodynamic effects of B-blockers

A

decreased myocardial O2 demand
decreases myocardial contractility
decreases HR
decreases system BP

31
Q

Describe the mechanism of the anti-anginal ancillary effects of B-blockers

A

increased diastolic filling time -> increases myocardial perfusion
antiarrhythmic activity increases electrical stability
antiatherogenic & antithrombotic

32
Q

State the clinical use of B-blockers for angina

A

First line prophylaxis of chronic stable angina

33
Q

What is the pharmacokinetic difference of B-blockers

A

Lipid solubility

34
Q

Give an example of a lipid soluble B-blocker

A

propanolol

35
Q

Describe characteristics of lipid soluble B-blockers

A
  • eliminated via hepatic metabolism
  • completely absorbed from gut
  • metabolised in liver
  • variable bioavailability
  • short plasma life
36
Q

Describe characteristics of water soluble B-blockers

A
  • eliminated via kidney unchanged
  • incompletely absorbed from gut
  • less variable bioavailability
  • longer plasma life
37
Q

List the adverse effects of B-blockers

A
  • cold extremities (peripheral vasoconstriction)
  • increased LV size -> increased MV O2 demand
  • Exacerbation of asthma (bronchospasm)
  • risk of HF (myocardial depression)
  • aggravation of angina (rebound phenomenon)
  • sexual dysfunction - poor patient compliance
  • CNS disturbances (nightmares, depression, confusion)
38
Q

State what CCBs are used to treat

A

Angina, HPT

39
Q

Describe the pharmacological action of CCBs

A

Inhibit entry of Ca into cells via voltage-gated Ca channels

40
Q

Describe 2 cardiac effects of CCBs

A
  • Block Ca influx into cardiac muscle cells which decreases cardiac contractility
  • Block Ca influx into nodal & conducting cells which decreases HR
41
Q

Describe 3 vascular effect of CCBs

A
  • Block of Ca influx into arterioles -> arteriolar dilation
  • peripheral vasodilation decreases SVR & arterial BP
  • Coronary dilation increases coronary blood flow & reverses and prevents spasm
42
Q

Give 2 examples of CCBs used to treat angina

A

diltiazem

verapamil

43
Q

Describe the anti anginal effect of reduced myocardial O2 demand
(CCBs)

A

reduced arterial BP, myocardial contractility & HR

44
Q

Describe the anti anginal effect that increases myocardial blood flow
(CCBs)

A
  • coronary vasodilation increases coronary blood flow

- spasm reverasl/prevention

45
Q

State 2 types of angina that CCBs manage

A

First line for chronic stable angina

variant angina

46
Q

List 5 secondary prevention options for a patient being diagnosed with angina

A

aspirin 75mg daily
statin
ACEIs (diabetics)
BP & diabetic control

47
Q

Name the 4 treatment options for SCAD

A

Nitrates & nitrites
B-blockers
CCBs
Miscellaneous agents

48
Q

For patients undergoing nitrate therapy for angina, why should they avoid sustained release formulations?

A

Longer exposure to nitrates speeds up depletion of thiol groups -> tolerance

49
Q

Why are oral nitrates not effective

A

1st pass metabolism reduces bioavailability

50
Q

Define vasorelaxation

A

Reduction of vascular tension

51
Q

State a drug (nitrate) used to relieve acute angina attacks

A

GTN

amyl nitrite

52
Q

State a drug (nitrate) used for prophylaxis of chronic angina

A

GTN
ISMN
ISDN

53
Q

Name the 3 groups of miscellaneous agents that treat angina

A

K channel openers
Sinus node inhibitors
Late Na current blockers

54
Q

Give 1 example of a K channel opener

A

Nicorandil

55
Q

Describe the 2 effects of K channel openers

A
  • venodilatation -> decreases preload & MV O2

- arterial dilatation -> decreases afterload & MV O2

56
Q

Give 1 example of a Sinus node inhibitor

A

ivabradine

57
Q

Describe the effect of a Sinus node inhibitor

A

Inhibition of If -> decreases HR & MV O2

58
Q

Give 1 example of a late Na current blocker and describe its effect

A

Ranolazine

Inhibition of I Na -> anti-ischaemic effects

59
Q

State the 3 treatment options of stable angina

A

medical
PCI
CABG

60
Q

State 2 revascularisation procedures

61
Q

Describe what revascularisation does

A

Restore blood flow to artery to increase myocardial O2 supply

62
Q

What are 2 methods of PCI

A

Ballon angioplasty

Coronary stenting

63
Q

What effect does revascularisation have on myocardial O2 supply and why

A

increases MV O2 supply due to increased blood flow

PHA222 (7 decks)

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