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Angina Flashcards

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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
Describe the recommendations for nitrate therapy
- 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)
26
State the indication for the use of B-adrenoceptor antagonists and describe how they work
- angina pectoris e.g. propanolol, atenolol | - Antagonise effects of hormones e.g. noradrenaline & adrenaline at B-adrenceptors
27
List the 3 subtypes of B-adrenoceptors
- B1-ARS - heart & kidney - B2-ARS - heart & smooth muscle - B3-ARS
28
Name the 2 classes of B-blockers and give an example for each
- non-selective e.g. propanolol | - B1 - selective - cardioselective e.g. atenolol
29
Describe the classification of b-blockers and give drug examples
- 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
Describe the mechanism of the anti-anginal heamodynamic effects of B-blockers
decreased myocardial O2 demand decreases myocardial contractility decreases HR decreases system BP
31
Describe the mechanism of the anti-anginal ancillary effects of B-blockers
increased diastolic filling time -> increases myocardial perfusion antiarrhythmic activity increases electrical stability antiatherogenic & antithrombotic
32
State the clinical use of B-blockers for angina
First line prophylaxis of chronic stable angina
33
What is the pharmacokinetic difference of B-blockers
Lipid solubility
34
Give an example of a lipid soluble B-blocker
propanolol
35
Describe characteristics of lipid soluble B-blockers
- eliminated via hepatic metabolism - completely absorbed from gut - metabolised in liver - variable bioavailability - short plasma life
36
Describe characteristics of water soluble B-blockers
- eliminated via kidney unchanged - incompletely absorbed from gut - less variable bioavailability - longer plasma life
37
List the adverse effects of B-blockers
- 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
State what CCBs are used to treat
Angina, HPT
39
Describe the pharmacological action of CCBs
Inhibit entry of Ca into cells via voltage-gated Ca channels
40
Describe 2 cardiac effects of CCBs
- Block Ca influx into cardiac muscle cells which decreases cardiac contractility - Block Ca influx into nodal & conducting cells which decreases HR
41
Describe 3 vascular effect of CCBs
- 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
Give 2 examples of CCBs used to treat angina
diltiazem | verapamil
43
Describe the anti anginal effect of reduced myocardial O2 demand (CCBs)
reduced arterial BP, myocardial contractility & HR
44
Describe the anti anginal effect that increases myocardial blood flow (CCBs)
- coronary vasodilation increases coronary blood flow | - spasm reverasl/prevention
45
State 2 types of angina that CCBs manage
First line for chronic stable angina | variant angina
46
List 5 secondary prevention options for a patient being diagnosed with angina
aspirin 75mg daily statin ACEIs (diabetics) BP & diabetic control
47
Name the 4 treatment options for SCAD
Nitrates & nitrites B-blockers CCBs Miscellaneous agents
48
For patients undergoing nitrate therapy for angina, why should they avoid sustained release formulations?
Longer exposure to nitrates speeds up depletion of thiol groups -> tolerance
49
Why are oral nitrates not effective
1st pass metabolism reduces bioavailability
50
Define vasorelaxation
Reduction of vascular tension
51
State a drug (nitrate) used to relieve acute angina attacks
GTN | amyl nitrite
52
State a drug (nitrate) used for prophylaxis of chronic angina
GTN ISMN ISDN
53
Name the 3 groups of miscellaneous agents that treat angina
K channel openers Sinus node inhibitors Late Na current blockers
54
Give 1 example of a K channel opener
Nicorandil
55
Describe the 2 effects of K channel openers
- venodilatation -> decreases preload & MV O2 | - arterial dilatation -> decreases afterload & MV O2
56
Give 1 example of a Sinus node inhibitor
ivabradine
57
Describe the effect of a Sinus node inhibitor
Inhibition of If -> decreases HR & MV O2
58
Give 1 example of a late Na current blocker and describe its effect
Ranolazine | Inhibition of I Na -> anti-ischaemic effects
59
State the 3 treatment options of stable angina
medical PCI CABG
60
State 2 revascularisation procedures
PCI | CABG
61
Describe what revascularisation does
Restore blood flow to artery to increase myocardial O2 supply
62
What are 2 methods of PCI
Ballon angioplasty | Coronary stenting
63
What effect does revascularisation have on myocardial O2 supply and why
increases MV O2 supply due to increased blood flow

PHA222 (7 decks)

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