Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SGUL - Physiology 1 > Pharmacology of the CVS - Angina > Flashcards

Pharmacology of the CVS - Angina Flashcards

1
Q

What are the 3 main symptoms of angina?

A
  • Feeling of cramping in the chest
  • Referred pain- shoulders, neck and arms
  • May be associated with shortness of breath, sweating, and nausea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is angina?

A

Chest pain due to insufficient blood flow to heart muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does anginal pain form?

A
  • Ischaemia causes build-up of lactic acid during anaerobic respiration of cardiomyocytes.
  • Activates myocardial pain receptors which sends signals via sensory neurones to the brain. These signals trigger pain.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

FPATH RECAP

What is the purpose of pain?

A
  • Protective response
  • Warning to stop person doing whatever they are about to do
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How was angina traditionally classified?

A
  • Typical angina
  • Atypical angina
  • Non-anginal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the three characteristics of typical angina?

A
  • substernal chest discomfort of characteristic quality + duration
  • provoked by exertion or emotional stress
  • relived by rest and/or nitrates within minutes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do atypical and non-anginal pain have in common with typical angina?

Focus on the three characteristic of typical angina

A

ATYPICAL - shares at least two of the characteristics
NON-ANGINAL -presentation of one or none of the characteristic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the new classification of angina?

A
  • Stable Angina
  • Unstable Angina
  • Prinzmetal Angina
  • Microvascular Angina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is stable angina commonly attributed to?

A
  • Myocardial ischaemia
  • Coronary artery disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is unstable angina commonly attributed to?

A
  • Stable angina complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is prinzmetal angina attributed to?

A
  • Cyclical coronary spasms commonly induced by cocaine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is unique about microvascular angina?

A
  • Angina symptoms but no signs or evidence of coronary heart disease
  • Coronary angiograms will present as normal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Outline the aetiology of stable angina.

A
  • Narrowed coronary artery lumen
  • Restricted blood flow to myocardium so reduced oxygen delivery
  • Oxygen received is insufficient when the heart has to work harder
  • Leads to anaerobic respiration which forms lactic acid - leads to pain.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the characteristics of stable angina? PART 1

A
  • Follow a set pattern and so are predictable. They have recurring episodes that have similar initial pattern, duration and intensity
  • Last a short duration and radiate from the left arm, neck, jaw or back
  • Caused by exertion or increased O2 demand
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the characteristics of stable angina? PART 2

A
  • Not life-threatening but can act as a warning for serious cardiovascular events (e.g. heart attacks)
  • Relieved by rest or taking medication
  • Symptoms are attributed to myocardial ischemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Outline the aetiology of unstable angina

A
  • Clot formation occludes artery (following plaque rupture)
  • Leads to reduction in blood flow so reduced oxygen delivery to myocardium
  • Oxygen supply is inadequate even at rest
  • Anaerobic respiration occurs forming lactic acid - causes pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the characteristics of unstable angina? PART 1

A
  • Unpredictable
  • Pain symptoms are more severe and last longer
  • Happens at rest with little exertion
  • May not have a trigger
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the characteristics of unstable angina? PART 2

A
  • Not usually relived by medications
  • Progression from stable angina – not possible to predict who will progress
  • Serious, regarded as emergency - requires hospital admission
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Outline the aetiology of prinzmetal angina

A
  • Coronary Spasm (induced by drugs)
  • Reduced blood flow so reduced oxygen delivery
  • Oxygen supply is inadequate even at rest
  • Anaerobic respiration occurs forming lactic acid - causes pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the characteristics of prinzmetal angina. PART 1

A
  • Usually occurs while resting at night or early morning
  • Episodes tend to last 5-15 mins (and sometimes longer)
  • Rare
  • Typically found in younger patients
  • Attacks are very severe and painful
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the characteristics of prinzmetal angina. PART 2

A
  • Symptoms include heart burn, nausea, sweating, dizziness and Raynaud’s phenomenon
  • It is usually caused by spasms in the coronary arteries and comes in cycles
  • Cocaine is the leading cause
  • Relieved by medication
22
Q

Outline the aetiology of microvascular angina.

A
  • Increased vasoconstriction/impaired vasodilation of the coronary arteries
  • Coronary circulation to be impaired
  • Reduced coronary perfusion
  • Myocardium undergoes anaerobic respiration
  • Build up of lactic acid resulting in angina
23
Q

What are the characteristics of microvascular angina. PART 1

A
  • Impaired coronary circulation due to coronary microvascular dysfunction
  • Patients do not have obstructive coronary artery disease
  • Occurs at exertion and at rest but the heart may respond less adequately to nitrates
24
Q

What are the characteristics of microvascular angina. PART 2

A
  • Difficult to diagnose early as coronary microvasculature cannot be directly imaged in vivo
  • Positron emission tomography (PET) or cardiac magnetic resonance (CMR) may be used to asses cardiac microvascular blood flow
25
Q

What are the aims of anginal treatment?

A
  • Enhance quality of life by reducing symptoms
  • Improve prognosis
  • Prevent complications such as myocardial infarctions and premature death
  • Treatment should have minimal side effects
26
Q

How does supply ischemia lead to angina?

A
  • Decreased coronary blood flow
  • Caused by vasospasms (Prizmetal angina) or a thrombus/blockage (unstable angina)
27
Q

How does demand ischaemia lead to angina?

A
  • Increased oxygen requirement
  • Caused by fixed stenosis (chronic/stable angina)
28
Q

What are the three precipitating factors for ischaemia?

A
  • Increased sympathetic activity
  • Increased contractility
  • Increased vasoconstriction
29
Q

Describe how increasing sympathetic activity is a precipitating factor for ischaemia.

A
  • Increases heart rate
  • Reduced diastolic time.
  • The heart is only perfused during diastole as during systole the blood is unable to move.
  • Therefore lower diastolic time means reduced perfusion
30
Q

Describe how increasing contractility is a precipitating factor for ischaemia.

A

Increases oxygen demands

31
Q

Describe how increasing vasoconstriction is a precipitating factor for ischaemia.

A
  • Required to redirect blood flow to areas where there are needed (e.g. after a large meal blood is diverted to the GI tract)
  • Affects coronary circulation
32
Q

How do angina treatments aim to improve perfusion?

A
  • Increasing oxygen delivery by improving coronary blood flow
    EXAMPLE: Coronary vasodilators
33
Q

How do angina treatments aim to reduce metabolic demand?

A
  • Reduce oxygen demands
    EXAMPLES: Vasodilators and coronary depressants
34
Q

How do angina treatments aim to reduce the risk of subsequent anginal episodes?

A
  • Use of prophylactics
  • This is where treatment becomes a form of prevention rather than symptom reduction
    EXAMPLE: Anticoagulants and lipid-lowering drugs
35
Q

RECAP: How does smooth muscle contraction occur?

A
  • Increase in cytoplasmic calcium from interstitial fluid
  • Calcium binds to calmodulin
  • Causes activation of myosin light chain kinase
  • Myosin is phosphorylated
  • Cross bridge formation occurs
36
Q

RECAP: How does cardiac muscle contraction occur?

A
  • Increase in cytoplasmic calcium from SR
  • Calcium binds to troponin C
  • Causes movement of tropomyosin - so myosin binding sites exposed
  • Cross bridge formation occurs
37
Q

How can nitrates be used to treat angina, focussing on its mechanism of action?

A
  • Mimic endogenous NO.
  • Form Guanylyl cyclase - cGMP forms
  • cGMP activates protein kinase G which dephosphorylates the myosin light chain
  • Increases the uptake of Ca2+ by the SR causing a decrease of Ca2+ in the cytoplasm
  • Activate K+ channels causing hyperpolarisation and closing VGCC
38
Q

What are the main effects of nitrates?

A
  • Cause peripheral venodilation - decreases intravascular pressure to decrease preload
  • Cause arterial dilation - decreases TPR - reduces afterload
  • Lower oxygen demands
39
Q

What are the adverse effects of nitrates?

A
  • Syncope (due to arterial dilation)
  • Postural hypotension (due to venodilation)
  • Reflex tachycardia (due to sympathetic outflow)
40
Q

What is the mechanism of action for beta blockers?

A
  • Reduce sympathetic activity caused by noradrenaline and adrenaline.
  • Reduced activation of adenylate cyclase
  • Intracellular cAMP levels decrease so reduced activation of PKA so reduced phosphorylation and opening of sodium ion channels
  • Reduced sodium ion influx so it takes longer for depolarisation to occur.
  • Harder for voltage-gated calcium channels to open
41
Q

What are the effects of beta-blockers e.g atenolol?

A
  • Inhibits pacemaker current in SAN so heart rate goes down
  • Heart rate decreases - lengthens diastole time, more time for coronary perfusion.
  • Reduced force of cardiac contraction so improved exercise tolerance
  • Myocardial oxygen supply is improved
42
Q

What are the adverse effects of beta-blockers?

A
  • Fatigue
  • Bronchospasm
43
Q

List two contraindications of taking beta-blockers

A

ASTHMA - blocking of the beta receptor causes bronchospasm
HEART BLOCK - blocking of the AVN

44
Q

What is the mechanism of action for calcium channel blockers e.g dihydropyridines - amlodipine?

A
  • Reduced Ca2+ influx into cardiac myocytes and smooth muscle cells
  • Decreased CICR.
  • Overall decrease in intracellular Ca2+
  • Reduced contractility and thus less oxygen consumption
    They also cause coronary vasodilation which causes more coronary blood flow
    They reduce BP/ TPR/ afterload and so the heart works less hard to eject blood
45
Q

What are the effects of calcium channel blockers?

A
  • Cause coronary vasodilation - more coronary blood flow
  • Reduce BP/ TPR/ afterload - the heart works less hard to eject blood
46
Q

What are the adverse effects of calcium channel blockers?

A
  • Lower limb oedema - increased pressure in the capillary in the lower limbs
  • Flushing and headaches - to excessive vasodilation
  • Reflex tachycardia as vasodilation causes increased sympathetic activity (baroreflex) and increases HR and contractility
  • Blocking Ca2+ channels in the heart can alter electrical conductivity and contractility
47
Q

Give examples of prophylactic drugs for angina.

A
  • Aspirin: inhibits COX. As a result, it reduces platelet aggregation
  • Clopidogrel: inhibits ADP receptors on platelets to reduce aggregation
  • Statins: HMG CoA reductase inhibitor - causes decrease in cholesterol levels
48
Q

Aspirin and clopidogrel can be used together. Explain why.

A

Both have different mechanisms

49
Q

Outline the mechanism of action of nicorandil (anti-anginal)

A
  • Potassium channel activator which promotes hyperpolarisation.
  • Inhibits VGCC
  • Reduced calcium influx
  • Coronary vasodilation occurs.
  • Part of its vasodilator action is due to generation of NO
50
Q

Outline the mechanism of action of ivabradine (anti-anginal)

A
  • Inhibitor of the pacemaker current in the SAN.
  • Slows sinus heart rate
  • Decreases the frequency of pacemaker potentials being fired.
  • Decreased heart rate to reduce the myocardial O2 demand
51
Q

Outline the mechanism of action of ranolazine

A
  • Sodium current inhibitor
  • Reduces Ca2+ in ischaemic myocardial cells.
  • Reduces oxygen demand
  • Reduces the compression of small intramyocardial coronary vessels
  • Improves myocardial perfusion

SGUL - Physiology 1 (68 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions