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Pharmacology > Cardiac-related pharmacology > Flashcards

Cardiac-related pharmacology Flashcards

1
Q

What are the two most important types of arrhythmia?

A

Supraventricular

Ventricular

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2
Q

What does the QRS complex refer to?

A

The electrical activity of the heart

Nothing to do with the mechanical activity of the heart

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3
Q

What does the P wave of the QRS complex represent?

A

Atrial depolarisation

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4
Q

What does the QRS complex represent?

A

Ventricular depolarisation

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5
Q

What does the T wave of the QRS complex represent?

A

Ventricular repolarisation

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6
Q

What does the PR interval represent?

A

The beginning of atrial depolarisation to the onset of ventricular depolarisation

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7
Q

Why is atrial repolarisation not shown in the QRS complex?

A

Hidden by the wave caused by ventricular depolarisation

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8
Q

What is the most common form of arrhythmia?

A

Atrial fibrillation

Occurs in 5-10% of patients over 65 years of age

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9
Q

What are the characteristics of atrial fibrillation?

A

Chaotic atrial activity

All atrial cells become independent pacemakers that fire at different times

Causing small areas to contract at the same time

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10
Q

What are the causes of atrial fibrillation?

A

Chronic distention of atria

Systemic inflammation

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11
Q

How does chronic distention of atria cause atrial fibrillation?

A

Mechanical pressure causes fibrosis, causing changes to the electrical connectivity

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12
Q

How is atrial fibrillation spotted?

A

Lack of a P wave

Palpitations - chance findings

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13
Q

How are is fibrillation normally discovered?

A

Through chance discoveries

Secondary morbidities like hypertension and CHF are normally the reason AF is detected

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14
Q

What is the reason atrial fibrillation is so dangerous?

A

Thromboembolism

Stroke

Blot clot formation in the atria

Due to the stasis of blood

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15
Q

Why do strokes develop in atrial fibrillation?

A

The irregular contraction of atria means the rate of successful contractions is decreased, and not enough force is created to move the clot

However, if the rhythm becomes normal and synchronised for a short period of time, the clot can travel and cause deadly consequnces

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16
Q

What are the two main ways to inhibit blood clot formation?

A

Anticoagulants

Antiplatelets

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17
Q

What is the primary anticoagulant used for inhibition of clot formation?

A

Heparin

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18
Q

Where is heparin found?

A

Endogenously

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19
Q

What is the primary anticoagulant used for inhibition of clot formation?

A

Warfarin

Vitamin K inhibitor

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20
Q

Where is Warfarin found?

A

In nature

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21
Q

When are wafarin and heparin respectively used?

A

Warfarin acts slow, and is used for long term monitoring of blood clots

Heparin is fast acting and is used in a thromboembolism crisis

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22
Q

What is the major side effect of clot inhibitors?

A

Bleeding

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23
Q

Why is there no natural receptor for warfarin in the body?

A

It is not endogenously produced

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24
Q

How do we treat a warfarin overdose?

A

Injection of fresh frozen plasma

Contains all the coagulation factors you need

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25
Q

Why is it not advised to inject vitamin K upon warfarin overdose?

A

Takes a long time before the effect is observed

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26
Q

How do we treat heparin overdose?

A

Protamine, a positively charged nuclear protein, binds to the negatively charged heparin

Forms a complex which inhibits it from entering the circulation

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27
Q

How was the importance of platelets discovered?

A

Hiroshima victims presented with spontaneous bleeding without having low coagulation factors

Low platelet counts however

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28
Q

What is an important antiplatelet agent?

A

Aspirin

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29
Q

How does aspirin work?

A

Inhibits platelet aggregation

Blocks COX through irreversibly binding to it

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30
Q

Aspirin works at high concentrations more effectively than low concentrations

TRUE or FALSE

A

FALSE

Aspirin only works effectively in low concentration

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31
Q

Why does aspirin only work at low concentration?

A

COX inhibitors cause different effects in two different cells

In platelet cells, aspirin blocks the formation of TXA2, a molecule which stimulates platelet aggregation and vasoconstriction

In epithelial cells, aspirin blocks the formation of PGI2, a molecule which inhibits platelet aggregation and causes vasoconstriction

In high concentration of aspirin, the epithelial cells cannot replenish COX and less PGI2 is produced. Therefore, even though the harmful TXA2 from platelets is inhibited, the positive effect of PGI2 is also, so the aspirin is not beneficial

In low concentrations of aspirin, the epithelial cells can produce new COX which produces more PGI2. The beneficial effect of PGI2 complements the effect of aspirin in platelets

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32
Q

What is the role of COX in epithelial cells?

A

Catalyses the formation of PGI2

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33
Q

What is the role of COX in platelets?

A

Catalyses the formation of TXA2

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34
Q

How does clopidrogel inhibit platelet aggregation?

A

Platelets release ADP to stimulate other platelet cells around them in a positive feedback loop

Clopidrogels inhibits these ADP molecules and prevent them from working effectively

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35
Q

How does Clopidrogel mimic the effect of endothelial cells?

A

Endothelial cells also inhibit the positive feedback loop between platelets by transforming ADP into AMP

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36
Q

What did George Mines discover?

A

Vulnerable period in the action potential of the heart

Where electrical stimulation at this point can cause ventricular fibrillation

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37
Q

What is ventricular fibrillation?

A

Desynchronisation of ventricular myocytes

Very rapid and irregular ventricular activation leads to no cardiac output

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38
Q

What is the most lethal arrhythmia?

A

Ventricular fibrillation

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39
Q

What are triggers of ventricular fibrillation?

A

Myocardial ischaemia

Some drugs

Electrical imbalance

Genetic predisposition

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40
Q

What are the two main ways in which ventricular fibrillation is treated?

A

Pharmacological approach

Cardioversion

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41
Q

Describe the pharmacological approach of ventricular fibrillation

A

Inhibits phase O

Through sodium channel antagonists

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42
Q

Describe how cardioversion treats ventricular fibrillation

A

DC shock synchronises the heart

During P wave or QRS complex

AED makes sure it is not firing during the vulnerable period

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43
Q

What is the funny current?

A

The unique current seen in pacemaker cells

Responsible for propagating diastole

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44
Q

Describe the funny current

A
  1. Sodium channels open upon diastole
  2. Sodium enters and changes the voltage to -40mV
  3. This is the threshold for voltage-gated calcium channels
  4. Calcium enters and at +10mV, the calcium channels close
  5. Potassium channels open and decrease the voltage of the cell
  6. Sodium channels open again and the diastolic voltage is returned
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45
Q

What is the characteristic feature of funny currents?

A

They have no resting potential

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46
Q

What is after-depolarisation?

A

Pathological wave were ventricular myocytes become spontaneously active

Phase 2/3 = early afterdepolarisation

Phase 4 = delayed afterdepolarisation

Early after-depolarisation requires pacemaker cells, late after-depolarisation occurs in non-pacemaker cells

Repolarisation is delayed and the action potential is abnormally long

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47
Q

What is extrasystole?

A

After-depolarisation in a small area

Normal

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48
Q

What is ventricular tachycardia?

A

Premature beats are one after the other and rapid

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49
Q

What is ventricular fibrillation?

A

Premature beats happen in all myocytes

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50
Q

What is a characteristic of ventricular action potentials?

A

Prolonged calcium influx

Allows the heart to contract well

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51
Q

What are arhythmias?

A

Disorders of the heart rate and rhythm

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52
Q

What is the cause and importance of the refractory period?

A

Caused by the prolonged opening of calcium channels

Induced prolonged contraction required for effective ejection of blood during systole

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53
Q

What are the two clinically important arrhythmia?

A

Tachycardia

Bradycardia

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54
Q

What are the types of atrial tachycardia?

A

Supraventricular tachycardia

Paroxysmal tachycardia

Atrial fibrillation

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55
Q

What are the types of ventricular tachycardia?

A

Torsades de pointes

Ventrical fibrillation

56
Q

What is another name for bradycardia?

A

Heart block

57
Q

What are the features of heart block?

A

Ventricles beat slower and irregularly

Caused by damage to the AVN

Driven by pacemaker activity in the ventricular conducting tissue

Pacemaker required rather than drug therapy

58
Q

What is meant by abnormal pacemaker activity?

A

Pacemaker activity that is initiated at an ectopic focus in the atria and ventricles

59
Q

What is re-entry?

A

The refractory period normally prevents the action potential re-invading the tissue

In re-entry there is unidirectional propagation of action potentials

Provides abnormal site for cardiac excitation

More likely to happen in calcium channels due to longer refractory periods

60
Q

What drugs van be used to target arrhythmias?

A

Class I - IV antiarrhythmic drugs

61
Q

What are class I drugs?

A

Bind to Na+ channels

Block is more pronounced at rates above normal or in depolarised tissues

62
Q

Why should calcium channel blockers be avoided in heart failure patients?

A

Reduce contractility

63
Q

Which patient population should not use class II drugs?

A

Asthmatic patients

Exacerbate bronchoconstriction

64
Q

What do class II drugs do?

A

B-adrenoceptor antagonism

65
Q

What do class III drugs do?

A

K+ channel block

66
Q

What do class IV drugs do?

A

Ca2+ channel block

67
Q

What is the main driving force for the flow of blood through the systemic circulation?

A

Arterial blood pressure

68
Q

What are the principle homeostatic factors controlling arterial pressure?

A

Arterioles

Cardiac output

Kidneys

Vasoconstriction

Vasodilation

69
Q

Describe the importance of arterioles in controlling arterial pressure

A

Major role in controlling peripheral resistance

Regulate the relative blood flow through individual organs

70
Q

Describe the importance of cardiac output in controlling arterial pressure

A

CO = SV X HR

Main factors affecting SV are plasma volume and venous return

Main factors affecting HR is sympathetic and parasympathetic innervation

71
Q

How is vasocontriction controlled?

A

Increase in intracellular calcium

Through noradrenaline released by sympathetic acting on a1-adrenoceptors

72
Q

How is vasodilation controlled?

A

Increase in cAMP

Brought by adrenaline acting on B2-adrenoceptors

73
Q

What are causes of hypertension?

A

Renal disease

Endocrine disorders

Pheochromocytoma

74
Q

What is essential hypertension?

A

Cases of hypertension with no known cause

75
Q

What are the main antihypertensive drugs?

A

Agents affecting the renin-angiotensin system

Thiazide diuretics

Calcium antagonists

B-adrenoceptor antagonists

76
Q

What are the main antihypertensive drugs?

A

Agents affecting the renin-angiotensin system

77
Q

Which system is preferrably targetted in young patients with hypertension?

A

Renin-angiotensin system

78
Q

Which system is preferrably targeted in older patients with hypertension?

A

Thiazides

Calcium antagonists

79
Q

How do thiazide diuretics work?

A

Increase salt and water excretion

Decrease cardiac output through reduced plasma volume

Reduce peripheral resistance

Decrease renin release

80
Q

What stimulates renin release?

A

Decreased blood flow to the kidneys

Reduced Na+ concentration in the distal tubule

B-adrenoceptor agonist

81
Q

Which drugs decrease the effect of the renin-angiotensin system?

A

ACE inhibitors

AT1 receptor antagonists

82
Q

How do AT1 receptor antagonists work?

A

Antagonise the effect of angiotensin II on the AT1 receptor

83
Q

How do calcium antagonists relieve hypertension?

A

Block calcium entry

Inhibit depolarisation-induced calcium entry into cardiac and vascular smooth muscle

Reduces arterial pressure

84
Q

How do B1-receptor antagonists alleviate hypertension?

A

Decrease cardiac output

Decrease sympathetic activity

Decrease renin release

85
Q

Give an example of a vasodilator used for antihypertension

A

Minoxidil

K+ channel activator

Relaxes smooth muscle by hyperpolarising the plasma membrane

Prevents Ca2+ influx through voltage-dependent calcium channels

86
Q

What does heart failure mean?

A

Chronic failure of the heart to provide sufficient cardiac output

87
Q

What does congestive mean?

A

Abnormal accumulation of venous blood and oedema

88
Q

What are the two types of congestive heart failure?

A

Fast - rare

Slow - chronic

89
Q

Why is CHF important to tackle?

A

Most common reason for hospitalisation of patients over 65 years of age

90
Q

What are the main causes of CHF?

A

Cardiomyopathy

Excessive afterload

91
Q

What is afterload?

A

Pressure against which the heart muscle must work to eject blood during systole

92
Q

What causes cardiomyopathy?

A

MI

Cardiotoxins

Myocarditis

93
Q

What causes excessive afterload?

A

Hypertension

Valvular heart defects

94
Q

What determines the presentation of CHF?

A

The side of the heart affected by heart failure

95
Q

What is the presentation of left sided heart failure?

A

Positional dyspnea

Due to the build-up of water in the lungs

96
Q

What are possible causes of left sided heart failure?

A

Cor pulmonale

Atherosclerosis

97
Q

How does cor pulmonale/ atherosclerosis cause left sided heart failure?

A

Backflow of blood into the atrium due to narrowed blood vessels

The pressure in the lung vasculature increases

The exchange of fluids in the hydrostatic and oncotic pressure changes

This leads to a build-up of water in the lungs

98
Q

What is the presentation of right-sided heart failure?

A

General venous congestion

Increased venous pressure and peripheral oedema

Prominent jugular vein

99
Q

Describe the pathophysiology of heart failure

A

Low cardiac output causes low perfusion of organs

Compensatory mechanisms come into place to reduce this

100
Q

What compensatory mechanisms are activated upon the decreased CO seen in heart failure?

A

Activation of the renin angiotensin system in the kidneys

Vasoconstriction due to the activation of the sympathetic nervous system

101
Q

Why do the compensatory mechanisms that form as a response of decreased CO worsen the heart failure?

A

Renin angiotensin system is activated, which causes volume retention and vasoconstriction

Sympathetic stimulation causes vasoconstriction

102
Q

How does Laplace’s law relate to CHF?

A

The radius of the heart increases because of the increased afterload

The heart also increases its wall tension because of the increased radius

The heart is therefore working harder and has a higher metabolic and oxygen demand

This leaves the heart more susceptible to things like MI

103
Q

What are the major complications of CHF?

A

Pump failure characterised by tiredness, shortness of breath and oedema

Atrial fibrillation due to the distention of the muscle walls

104
Q

What are the aims of CHF treatment?

A

Reduce congestion

Increase cardiac output

105
Q

Which drugs aim at increasing cardiac output for CHF sufferers?

A

Digoxin - increases vagus activity and inhibits Na+/K+ ATPase

Dobutamine

Beta 1 blockers

Phosphodiesterase inhibitors

106
Q

How does digoxin act on CHF patients?

A

Inhibits the sodium potassium pumps

Increases the Na+ concentration in the cell, so the Na+-Ca2+ pump does not work so effectively

The concentration of calcium inside the cell increases

This leads to increased inotropy = increase the rate of muscular contraction

107
Q

What are the problems of Digoxin in CHF?

A

Narrow TI

Does not reduce mortality

108
Q

How does Dobutamine act on CHF sufferers?

A

Beta-1 agonist

109
Q

How was the use of beta blockers in CHF sufferers revolutionary?

A

Beta blockers work through decreasing heart contractility

Therefore, they were speculated as not being useful for CHF sufferers

However, it was shown that patients on beta blockers had increased survival

This was the birth of evidence medicine

110
Q

How do beta-blockers have a positive impact on CHF sufferers?

A

Stop the vicious cycle produced by the stimulation of the sympathetic system and the renin-angiotensin system

Decreased the metabolic and oxygen demand of the heart

Give time for the heart stem cells to start the repair process

111
Q

What are the long-term aims of treating heart failure?

A

Reduce mortality

Increase quality of life

112
Q

What are the long-term treatments for CHF?

A

ACE inhibitors

Beta blockers

Low salt diet

113
Q

What is more successful than beta blockers in the treatment of CHF?

A

Combination therapy

Beta 1 blockers and ACE inhibitors

114
Q

Which blood vessels supply blood to the heart muscle?

A

Coronary arteries

115
Q

What affects the blood supply to the heart?

A

Metabolites

Sympathetic nerves

Circulating catecholamines

Mediators from neurons

116
Q

When does blood flow to the heart occur?

A

During diastole

117
Q

What is the main pathological condition of the coronary circulation?

A

Atheroscletosis

118
Q

Describe the development of atherosclerosis

A

Platelets, macrophages and low-density lipoproteins adhere to the damaged endothelium

Macrophages release free radicals causing lipid peroxidation of the LDL, which the macrophages ingest

Macrophages release inflammatory cytokines and growth factors causing proliferation of smooth muscle and fibroblasts

119
Q

What two conditions are caused as a consequence of atherosclerosis?

A

Angina pectoris

Myocardial infarction

120
Q

What causes the pain of angina?

A

Action of nociceptors of chemicals released from the ischaemic muscle

121
Q

What are the three main types of angina?

A

Stable angina - gets better with rest

Unstable angina - does not get better with rest, indication that thrombus has formed in the plaque

Variant angina - caused by coronary artery spasm

122
Q

What is myocardial infarction?

A

Complete block of the coronary artery

123
Q

What are the therapeutic aims of antianginal therapy?

A

Prevent MI

Reduce cardiac work and metabolic demand

Increase perfusion of heart muscle

124
Q

Which drugs prevent MI?

A

Statins

Aspirin

Platelet glycoprotein receptor antagonist

125
Q

How do statins prevent MI?

A

Inhibit plaque formation

126
Q

How does aspirin prevent MI?

A

Reduce possibility of thrombosis

127
Q

Which drugs reduce cardiac work and metabolic demand?

A

Organic nitrates

Calcium antagonists - decreases the excitation of the atrium and ventricles

B-adrenoceptor antagonists - inhibits activity of the sympathetic nervous system

128
Q

Which drugs increase perfusion of the heart muscle?

A

Organic nitrates

Calcium antagonists

129
Q

How do calcium antagonists reduce MI chances?

A

Block voltage-dependent L-type channels in vascular smooth muscle and cardiac muscle

Cause relaxation and vasodilation in blood vessels

Slow the heart rate of the heart by acting on SAN and AVN through inhibiting the inward Ca2+ movement during the plateu phase of the cardiac action potential

130
Q

What are the therapeutic aims of MI?

A

Alleviate the pain

Improve oxygenation of the myocardium

Open the blocked artery by reducing thrombus size

Improve survival

Reduce the possibility of re-infarction

131
Q

Which drugs are used to alleviate pain during MI?

A

Opioids

132
Q

Which drugs are used to open the blocked artery in MI?

A

Thrombolytic drugs

Anticoagulants

Antiplatelets

133
Q

Which drugs improve the survival in MI?

A

Angiotensin-converting enzyme inhibitors

134
Q

Which drugs reduce the possibility of reinfarction?

A

Aspirin

B-antagonists

135
Q

What is a side effect of ACE inhibitors?

A

Dry cough

ACE is involved in the metabolism of bradykinin

Without ACE, bradykinin builds up systemically and causes a cough

136
Q

How do PDE inhibitors increase heart contractility in CHF?

A

Stops the breakdown of cAMP to AMP

Increasing the concentration of cAMP in the heart increases the contractility

137
Q

Why are PDE not used for treatment of heart failure?

A

They increase mortality

Pharmacology (13 decks)

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