Angina Flashcards

(39 cards)

1
Q

What is the definition of angina and pectoris

A

Angina- from the Latin verb ‘angere’ meaning ‘to choke or throttle’

Pectoris- a reference to the Latin pectus (breast/chest)

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2
Q

What are symptoms of angina pectoris

A

Symptoms:
-feeling of cramping and severe constriction in the chest
-referred pain- jaw, shoulders, neck and arms
-may be associated with shortness of breath, sweating, nausea and heart rate

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3
Q

Explain how angina pectoris pain symptoms occur

A

1) Ischaemia- locally affected myocardium releases a variety of compounds including potassium, lactate, adenosine, bradykinin and prostaglandins

2) Activates myocardial pain receptors

3) Signal sent via sensory neurons to the brain

4) Pain perception

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4
Q

Explain the prevalence of angina pectoris

A

-chronic stable angina pectoris affects 2-4% of the population in western countries

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5
Q

Describe 3 traditional classifications of angina

A

Typical angina:
-substernal chest discomfort of characteristic quality and duration
-provoked by exertion or emotional stress
-relieved by rest and or nitrates within minutes

Atypical angina:
-presentation of two of the above characteristics

Non-anginal:
-presentation of only one or none of the chest pain characteristics

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6
Q

Explain 4 traditional angina (aetiology + chest pain symptoms)

A

Stable angina:
-attributed to myocardial ischemia
-coronary artery disease

Unstable angina:
-due to complications from stable angina

Prinzmetal angin:
-usually due to a spasm in the coronary arteries
-tends to happen in cycles

Microvascular angina:
-patients have angina symptoms but no evidence of coronary artery disease
-normal or near-normal coronary angiogram.

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7
Q

Explain what happens in stable angina:aetiology

A

-narrowed coronary artery lumen
-restricted blood flow to the area of myocardium it supplies
-the oxygen it receives is insufficient when the heart has to work harder
-anaerobic respiration
-pain

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8
Q

Explain characteristics of stable angina (classic, typical)

A

Characteristics of stable angina:
-follows a set pattern/predictable
-short duration radiation to left arm, neck, jaw and back
-precipitated by exertion/cardiac O2 demand
-not life threatening but can be warning sign for something serious (heart attack/stroke)
-relived by rest or taking medications
-symptoms attributed to myocardial ischemia

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9
Q

Explain what happens in unstable angina:aetiology

A

-clot formation occludes artery
-critical reduction in blood flow so that oxygen supply is inadequate at event at rest which causes pain

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10
Q

What are characteristics of unstable angina

A

characteristics of unstable angina:

-unpredictable
-pain symptoms more severe, can persist and last longer
-happens at rest with little exertion
-may not have a trigger
-not usually relieved by rest and medications
-progression from stable angina
-serious, regarded as emergency, patients are advised to go hospital

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11
Q

Explain prinzmetal angina: aetiology

A

-coronary spasm (caused by drugs like cocaine)
-critical reduction in blood flow so that oxygen supply is inadequate so that causes pain

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12
Q

Characteristics of prinzmetal angina (atypical/inversal/variant)

A

Characteristics of prinzmetal angina:

-usually occurs when resting and during the night
-episodes last 5-15 mins
-rare
-younger patients present with this
-attacks are very severe + painful
-pain may spread from chest-head-shoulder or arm
-symptoms: heart burn, nausea, sweating, dizziness, palpation, migraines
-cocaine use is leading cause in coronary vasospasms

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13
Q

Explain microvascular angina: aetiology

A

-impaired coronary circulation
-reduced coronary perfusion which leads to pain

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14
Q

What are characteristics of microvascular angina

A

Characteristics of microvascular angina:

-impaired coronary circulation due to coronary microvascular dysfunction from abnormal vasodilation or increased vasoconstriction
-patients do not have obstructive coronary artery disease
-occurs with exertion and at rest but may respond less but may respond less well to nitrates
-problem diagnosing it early as coronary microvascular cannot be directly imaged in vivo
-PET scans or cardiac magnetic resonance can be used to assess coronary microvascular blood flow
-treatment will vary depending on cause of the microvascular angina

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15
Q

What are treatment aims

A

the Treatment aims are:
-to enhance quality of life through reduction of symptoms
-to improve prognosis and prevent complications such MI and premature death
-well tolerated and cause minimal side effects

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16
Q

Explain what angina is

A

angina is an imbalance between demand and supply of oxygen to the heart

17
Q

Explain how a thrombus can cause angina

A

A thrombus/blockage can cause unstable angina, which can cause vasospasm.
This can cause decreased coronary blood flow so there is supply ischaemia
This causes angina (chest pain)

18
Q

Explain what happens in fixed stenosis to cause angina

A

Fixed stenosis (chronic stable angina)- increased oxygen requirement so there is a demand for ischaemia.
This causes angina (chest pain)

19
Q

Explain precipitating factors for angina (chest pain)

A

Increased sympathetic activity:
-increased heart rate = less diastolic time, less coronary artery perfusion which only occurs in systole

Increased contractility:
-exercise, emotion, stress (greater oxygen demand)

Increased vasoconstriction:
-redistribution of blood flow in cold weather, after a large meal blood diverted to GI (vasoconstriction affects coronary circulation)

20
Q

Explain angina treatment strategy

A

to Improve perfusion:
-increase oxygen delivery by improving coronary blood flow
-coronary vasodilators

To reduce metabolic demand:
-reduce oxygen demand by decreasing cardiac work
-vasodilators
-cardiac depressants

Prevention:
-prophylactic to reduce the risk of subsequent episodes
-lipid lowering drugs
-anti-coagulants
-fibrinolytic
-anti-platelet

21
Q

explain the central role of calcium in smooth muscle contraction

A

Smooth muscle:
1) increase in cytoplasmic Ca2+ (most from interstitial fluid)
2) Ca2+ binding to calmodulin
3) Ca2+ leading to phosphorylation of myosin
4) Cross bridge cycle
5) Contraction by pulling actin along the myosin

22
Q

Explain central role of calcium in heart muscle contraction

A

heart muscle:

1) increase in cytoplasmic Ca2+ all from sarcoplasmic reticulum
2) Ca2+ binding to troponin
3) Ca2+ causes troponin causing tropomyosin to move- exposing the myosin binding site on actin
4) Cross bridge cycle
5) Contraction by pulling actin along the myosin

23
Q

What are examples of anti-anginal nitrates

A

examples:
-glyceryl trinitrate
-isosorbide mononitrate

24
Q

What are effects of anti anginal nitrates

A

effects:
-peripheral venodilation—-> decrease intraventricular pressure —-> decreases cardiac preload
-arterial dilation—-> decrease total peripheral resistance——> reduces afterload
-both these actions lower oxygen demand by decreasing the work of the heart

25
Explain adverse effects of anti anginal nitrates
adverse effects: -throbbing headache, flushing and syncope -postural hypotension -reflex tachycardia
26
Explain the role of NO
NO: -continually produced/released -lipophillic, soluble gas, freely diffusible out of endothelium into surrounding vascular smooth muscle cells
27
Explain how PKG reduces smooth muscle tone
-myosin light chain dephosphorylation -increase uptake of Ca2+ by SR causing a decrease in cytoplasmic levels -activate K+ channels causing hyperpolarisation and closing VGCC (voltage gated calcium channels)
28
Explain examples of anti anginal B-blockers
examples: -atenolol -bisoprolol
29
Explain the effects of anti anginal B-blockers
Effects: -inhibits/ f-pacemaker current in the sinoatrial node (AV conduction)- decrease heart rate. -reduce the force of cardiac contractions—-> improves exercise tolerance -both of these actions reduce cardiac output and lower blood pressure Slower heart rate —> lengthens diastole and gives more time for coronary perfusion, which effectively improves myocardial oxygen supply
30
Explain adverse effects of anti anginal B-blockers
Adverse effects: -bronchospasm, fatigue, postural hypotension
31
Explain contraindication in anti anginal B-blockers
Contraindictation: -asthma-block B2 receptor can cause constriction and bronchospasm -heart block where atrial-ventrical conduction is poor- may block AV node
32
What is the mechanism of action for anti anginal B-blockers
-Reduces the sympathetic activity of noradrenaline and adrenaline on B1 adrenoceptors in heart -SAN: increased funny current increases HR -Ventricular myocytes: increased Ca2+ channel increased force of contraction
33
What are examples of anti anginal Ca2+ channel blocker
Examples: -dihydropyridines (vascular)- amplodipine, nifedipine. -benzothiazepines- Verapamil -Diphenylalkyamines- Diltiazem
34
Explain effects of Anti- anginal Ca2+ channel blocker
Effects: -reduce Ca2+ entry into cardiac myocytes/vascular smooth muscle tone—> reducing contractility -direct coronary vasodilation —-> more coronary blood flow -reduce TPR/ BP/ afterload —-> heart works less hard to eject blood -reduce force of contraction —> less O2 consumption
35
Explain adverse effects of anti anginal Ca2+ channel blocker
Adverse effects: -lower limb oedema (increase capillary pressure in lower limbs) -flushing and headache (excess vasodilation) -reflex tachycardia: vasodilation- increased sympathetic activity causes increased HR/contractility
36
Explain cautions of anti anginal Ca2+ channel blocker
-Blocking Ca2+ channels in the heart may alter electrical conduction and contractility
37
What is a mechanism of action for Ca2+ channel blocker
-to reduce Ca2+ influx through voltage gated L-type Ca2+ channels in smooth and cardiac muscle -drugs which can block VGCC’s and prevent Ca2+ entry reduce force of contraction in ventricular myocytes and cause vasodilation in vascular smooth muscle
38
Explain 3 prophylactic drugs for angina
aspirin- inhibits COX- decreases thromboxane A2 and platelet aggregation Clopidogrel- inhibits ADP receptor on platelets, reduces aggregation Statins- HMG Co-A reductase inhibitor, decreases cholesterol levels
39
Explain 3 other anti anginals
1) Nicrorandil- potassium channel activator, hyperpolarisation—-> Decreases VGCCs and Ca2+ entry, coronary vasodilation. Has nitrate moiety so part of its vasodilator action is via generation of NO 2) Ivabradine- specific inhibitor of the If current in the SAN—-> slow sinus heart rate ——> decreases pacemaker potential frequency—-> decreases heart rate to reduce myocardial O2 demand 3) Ranolazine- late Na+ current inhibitor—> reduces Ca2+ in ischaemic myocardial cells—> reduces oxygen demand, reduce compression of small intramyocardial coronary vessels: improves myocardial perfusion