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Cardiovascular > Pharmacology (Cardiovascular) > Flashcards

Pharmacology (Cardiovascular) Flashcards

1
Q

What are the regulatory influences on the heart rate?

A

Balance of autonomic input, stretch, temp, hypoxia, blood pH, thyroid hormones.

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2
Q

What are phase 4, 0 and 3 of the action potential of a pacemaker cell?

A

4 - pacemaker potential (increases steadily to threshold). 0 - Rapid depolarisation. 3 - repolarisation.

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3
Q

What currents cause the pacemaker potential (phase 4)?

A

Background sodium current inward (Ib), funny current inward (If), transient calcium current inward (IcaT), delayed rectifier potassium current outward (Ik).

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4
Q

What current causes phase 0 and phase 3 of the action potential of a pacemaker cell?

A

0 - long calcium current inward (IcaL). 3 - delayed rectifier potassium current (outward).

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5
Q

How does noradrenaline/adrenaline binding to an adrenoceptor in nodal and myocardial cells increase the heart rate?

A

Adrenoceptor coupled to a Gs protein which activates adenylyl cyclase to convert ATP into cAMP which increases [cAMP]i. This causes an increase in heart rate (positive chronotropic effect).

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6
Q

What effect does sympathetic stimulation have on the action potential of pacemaker cells?

A

It increases the slope of the pacemaker potential and decreases the threshold for AP initiation.

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7
Q

Describe the 2 effects of sympathetic stimulation on the cardiac myocytes that causes an increase in contractility?

A

It increases phase 2 (plateau phase) of the cardiac action potential in atrial and ventricular myocytes by enhanced Ca2+ influx and sensitises contractile proteins to Ca2+.

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8
Q

What do they terms chronotropic, inotropic, dromotropic and lusitropic mean?

A

Chronotropic - affects heart rate. Inotropic - affects contractility. Dromotropic - affects AV node conduction velocity. Lusitropic - affects duration of systole.

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9
Q

List all of the effects of sympathetic stimulation in the heart.

A

Increases heart rate, increases contractility, increases conduction velocity in AV node, increases automaticity, decreases duration of systole, increases activity of Na/KATPase and increases mass of cardiac muscle.

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10
Q

How does sympathetic stimulation cause an increase in conduction velocity in the AV node?

A

Due to enhancement of funny current and calcium current.

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11
Q

What is automaticity?

A

The tendency for non-nodal regions to acquire spontaneous activity.

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12
Q

How does sympathetic stimulation decrease the duration of systole?

A

Due to increase uptake of calcium into the sarcoplasmic reticulum.

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13
Q

Describe on the molecular level how parasympathetic stimulation affects heart rate.

A

ACh binds to M2 receptor, activates Gi protein which both decreases the activity of adenylate cyclase and reduces [cAMP]i and opens potassium channels (GIRK) to cause hyperpolarisation of SA node (mediated by betagamma subunits).

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14
Q

Why does the parasympathetic nervous system decrease the heart rate (negative chronotropic effect)?

A

Due to decreased slope of pacemaker potential caused by reduced If and ICa, hyperpolarisation caused by the opening of GIRK channels and increase in threshold for AP initiation caused by reduced ICa.

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15
Q

What effects does parasympathetic stimulation have on the heart?

A

Decreases heart rate, decreases contractility (atria only), decreases conduction in the AV node, and may cause atrial arrhythmias.

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16
Q

How does parasympathetic stimulation decrease contractility and where does it do this?

A

Due to decrease in phase 2 of cardiac AP and decreased Ca2+ entry.

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17
Q

How does parasympathetic stimulation decrease conduction in the AV node?

A

Due to decreased activity of voltage-dependent Ca2+ channels and hyperpolarisation via opening of K+ channels.

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18
Q

What are HCN channels?

A

Hyperpolarisation-activated cyclic nucleotide gated channels.

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19
Q

What current are HCN channels involved in?

A

The funny current (depolarising current in pacemaker potential).

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20
Q

What are HCN channels in the SA node activated by?

A

Hyperpolarisation following the action potential.

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21
Q

What happens to HCN channels which decreases the slope of the pacemaker potential and reduces heart rate?

A

They are blocked.

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22
Q

Give an example of a selective blocker of HCN channels and what disease is it used in?

A

Ivabradine and angina.

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23
Q

What does calcium released from the sarcoplasmic reticulum bind to and how does this cause cardiac muscle contraction?

A

Troponin C, shifts tropomyosin out of actin cleft and causes cross bridge formation.

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24
Q

What are the 6 steps in cardiac muscle relaxation?

A
  1. Repolarisation in phase 3 to phase 4.
  2. Voltage-activated L-type Ca2+ channels close.
  3. Ca2+ influx ceases. Ca2+ efflux occurs by the Na+/Ca+ exchanger 1 (NCX1).
  4. Ca2+ release from the sarcoplasmic reticulum ceases. Active sequestration via Ca2+-ATPase (SERCA) of Ca2+ now dominates.
  5. Ca2+ dissociates from troponin C. 6. Cross bridges between actin and myosin break.
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25
Q

What does SERCA stand for and what does it do?

A

Sarco-endoplasmic reticulum Ca2+ ATPase, it transports calcium into the sarcoplasmic reticulum.

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26
Q

What enzyme does cAMP activate?

A

Protein kinase A.

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27
Q

What does protein kinase A do in cardiac muscle cells?

A
  1. It phosphorylates L-type voltage-activated Ca2+ channel which increases the Ca2+ influx.
  2. It increases muscle fibre sensitivity to Ca2+ which increases contractility. 3. Causes phosphorylation of phospholamban which increases pumping of Ca2+ and rate of relaxation.
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28
Q

What are the pharmacodynamic effects of B2 agonists on the heart?

A
  1. Increase force, rate (cardiac output) and O2 consumption. 2. Decreases cardiac efficiency (O2 consumption increase more than cardiac work).
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29
Q

Why is adrenaline used in cardiac arrests?

A

Has positive inotropic and chronotropic actions (B1), redistributes blood flow to the heart (constricts blood vessels in skin, mucosa and abdomen, a1), dilates the coronary arteries (B2).

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30
Q

What adrenoceptor is dobutamine selective for, how is it given and when is it used?

A

B2 adrenoceptors, given IV, acute but potentially reversible heart failure.

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31
Q

What do the physiological effects of B-blockers depend on?

A

The degree to which the sympathetic nervous system is activated.

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32
Q

Give an example of a non-selective beta-blocker and 3 examples of beta-1 selective ones.

A

Non-selective: propranolol. Selective: atenolol, bisoprolol, metoprolol.

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33
Q

Give an example of a beta-blocker that is non-selective and a partial agonist.

A

Alprenolol.

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34
Q

How do non-selective blockers reduce maximal exercise tolerance?

A

They reduce rate, force and CO significantly.

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35
Q

What effect do non-selective beta-blockers have on coronary vessel diameter and myocardial oxygen requirement?

A

Reduced coronary vessel diameter marginally, myocardial O2 requirement falls so better oxygenation of the myocardium.

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36
Q

How do beta-blockers help in atrial fibrillation and supraventricular tachycardia?

A

Delay conduction through AV node and help restore sinus rhythm.

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37
Q

What are B-blockers used to treat?

A

Arrhythmias, angina, heart failure (compensated, carvedilol has additional a1 antagonist activity causing vasodilation), hypertension (no longer first-line unless co-morbidities are present).

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38
Q

What are the adverse effects of beta-blockers?

A

Bronchospasm, aggravation of cardiac failure, bradycardia, hypoglycaemia (in patients with poorly controlled diabetes), fatigue

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39
Q

What adverse effects of beta-blockers are removed by using B1-selective agents?

A

Bronchospasm, hypoglycaemia (as B2 adrenoceptors release glucose from the liver).

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40
Q

Why may beta-blockers cause aggravation of cardiac failure?

A

Patients with heart disease may rely on sympathetic drive to maintain an adequate CO.

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41
Q

Why may beta-blockers cause bradycardia?

A

B-adrenoceptors facilitate nodal conduction.

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42
Q

Why may beta-blockers cause fatigue?

A

CO (B1) and skeletal muscle perfusion (B2) in exercise are regulated by adrenoceptors.

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43
Q

Give an example of a non-selective competitive muscarinic antagonist.

A

Atropine

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44
Q

What are the pharmacodynamic effect of atropine?

A

Increase in HR in normal subjects at all but low doses, more pronounced in highly trained athletes (due to increased vagal tone).

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45
Q

What is atropine a first line drug for?

A

Severe or symptomatic bradycardia, particularly post MI (in which vagal tone is elevated).

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46
Q

How is atropine given and why should you not give too little?

A

Low-dose atropine may transiently slow heart rate.

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47
Q

What is an alternative to atropine?

A

Glycopyrronium.

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48
Q

What is the effect on the ventricular function curve in heart failure?

A

It is depressed.

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49
Q

Give 2 examples of drugs that enhance contractility.

A

Digoxin and dobutamine.

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50
Q

What transporter does digoxin block?

A

Na+K+ATPase in the sarcolemma.

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51
Q

Describe how digoxin blocking the sodium-potassium pump leads to greater contractility.

A

Pump blocked -> Increased intracellular sodium and decreased membrane potential -> decreased activity of Na+/Ca+ exchanger so greater intracellular calcium -> greater storage of calcium in sarcoplasmic reticulum -> greater CICR and contractility.

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52
Q

Where does digoxin bind to on the Na+/K+ATPase?

A

The alpha subunit, in competition with K+.

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53
Q

What can dangerously enhance the effects of digoxin and why is this particularly important?

A

Hypokalaemia, digoxin has low therapeutic range.

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54
Q

What are the indirect actions of digoxin on heart electrical activity?

A

Increased vagal activity (slows SA node discharge, slows AV node conduction; increases refractory period).

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55
Q

What are the direct actions of digoxin on heart electrical activity?

A

Shortens action potential and refractory period in myocytes (proarrhythmic). Toxic concentrations cause membrane depolarisation and oscillatory afterpotentials likely due to calcium overload.

56
Q

When would you use digoxin in heart failure?

A

IV in acute heart failure, orally in chronic heart failure in patients remaining symptomatic e.g. ACEIs, diuretics.

57
Q

In what type of heart failure is digoxin particularly indicated in and why?

A

Heart failure with atrial fibrillation (increase in AV node refractory period is beneficial, helps to prevent spread of the arrythmia to the ventricles).

58
Q

What are the most serious cardiac side effects of digoxin?

A

Excessive depression of AV node conduction (heart block). Propensity to cause arrhythmias.

59
Q

What are the extracardiac side effects of digoxin?

A

Nausea, vomiting, diarrhoea, disturbances of colour vision.

60
Q

Give an example of a calcium sensitiser and how does it work?

A

Levosimendan, binds to troponin C in cardiac muscle sensitising it to the action of Ca2+. Also opens K+ channels in vascular smooth muscle causing vasodilation.

61
Q

What is the effect of calcium sensitisers on contractility?

A

Increases contractility (positive inotrope).

62
Q

How is levosimendan administered and what is it used to treat?

A

IV, acute decompensated heart failure.

63
Q

Give 2 examples of inodilators.

A

Amrinone and milrinone.

64
Q

What is the mechanisms of action of inodilators?

A

Inhibit phosphodiesterase (PDE) in cardiac and smooth muscle cells and hence increase [cAMP]i.

65
Q

What effects do inodilators have on the body?

A

Increase myocardial contractility and decrease peripheral resistance.

66
Q

How do inodilators affect survival?

A

Worsen survival - perhaps due to increased incidence of arrhythmias.

67
Q

When are inodilators used?

A

IV administration in acute heart failure.

68
Q

What does binding of vasodilating substances e.g. bradykinin, ADP, 5-HT to endothelial cells cause?

A

Increased intracellular calcium which binds to calmodulin and activates eNOS.

69
Q

What does eNOS combine and what does this form?

A

L-arginine and oxygen. Forms NO and citrulline (byproduct).

70
Q

Once NO is formed in endothelial cells what happens?

A

Diffuses into smooth muscle -> activated guanylate cyclase -> converts GTP to cGMP -> activates protein kinase G leading to relaxation.

71
Q

By what other mechanism can NO cause the cell to relax?

A

It activates calcium dependent potassium channel which causes hyperpolarisation.

72
Q

How do organic nitrates e.g. GTN produced smooth muscle relaxation?

A

They enter the smooth muscle cell and react with enzymes/tissue thiol (SH) groups to produce NO.

73
Q

What do small doses of organic nitrates cause and does this have an affect on MAP?

A

Venorelaxation (decreased CVP (preload) reduces SV, but CO maintained by increased HR so no change in MAP).

74
Q

What do higher doses of organic nitrates cause?

A

Arteriolar dilation (decreases arterial pressure reducing afterload). Large muscular arteries are more sensitive, reduces pulse wave reflection from arterial branches.

75
Q

What is the effect of organic nitrates in the coronary arteries in normal subjects and people with angina?

A

Increased coronary blood flow in normal subjects. In angina, no overall increase but blood is redirected towards the ischaemic zone.

76
Q

What are the 3 ways that organic nitrates decrease myocardial oxygen requirement (good in angina)?

A
  1. Decreased preload. 2. Decreased afterload. 3. Improved perfusion of the ischaemic zone.
77
Q

How do organic nitrates improve blood flow to ischaemic myocardium in angina?

A

Dilates collateral arteries.

78
Q

What are the clinical uses of organic nitrates?

A

In stable angina and acute coronary syndrome.

79
Q

What are 3 examples of organic nitrates?

A

Glyceryltrinitrate (GTN), isosorbide mononitrate (ISMN) and isosorbide dinitrate (less common).

80
Q

How long does GTN act for?

A

30 mins.

81
Q

How is GTN administered and why?

A

As a tablet or spray sublingually (for rapid effect before exertion in stable angina). IV infusion with aspirin in ACS. Sustained effect by transdermal patch. Done parenteral because undergoes first pass metabolism.

82
Q

How long does isosorbide mononitrate last for and is it resistant to first pass metabolism?

A

Half life of 4 hours, and yes.

83
Q

How is it administered and when?

A

Orally for prophylaxis of angina and a more sustained effect.

84
Q

What are the unwanted effects of organic nitrates?

A

May build tolerance (minimised by not using it all the time), postural hypotension, headaches (initially), formation of methaemoglobin (rarely).

85
Q

Describe how endothelin is formed in endothelial cells.

A

If molecules (e.g. adrenaline, angiotensin II, ADH) bind to the endothelial cell it results in more expression of endothelin precursors which are transformed into endothelin I.

86
Q

What ligands decrease the expression of endothelin precursors?

A

NO, natriuretic peptides, shear stress.

87
Q

How does endothelin I cause smooth muscle contraction?

A

Endothelin I binds to ETa receptor on smooth muscle cell -> numerous signallling pathways including Gq/11 -> increased intracellular calcium -> contraction.

88
Q

Give 2 examples of antagonists of the ETa receptor.

A

Bosentan and ambrisentan.

89
Q

What are ETa receptor antagonists used in?

A

The treatment of pulmonary hypertension.

90
Q

What is the mechanism of action of ACE inhibitors?

A

Block the conversion of angiotensin I to angiotensin II. Also prevents ACE from inactivating bradykinin.

91
Q

What is the mechanism of action of AT1 receptor antagonists?

A

Block the agonist action of angiotensin II at AT1 receptors in a competitive manner.

92
Q

What effects do ACEIs have on veins and arteries?

A

Cause venous dilation (decreases preload) and arteriolar dilation (decreases afterload and SVR).

93
Q

What effect do ACEIs have on MAP in normal subjects and hypertensive patients?

A

Causes small fall in MAP of normal subjects, much greater fall in hypertensive patients (esp if renin secretion is enhanced e.g. as a consequence of diuretic therapy).

94
Q

Where do ACEIs have the greatest effect?

A

In angiotensin-sensitive vascular beds (brain, heart, kidney - may help maintain perfusion of critical organs).

95
Q

What are the 2 adverse effects of ACEIs?

A
  1. May initially cause hypotension (esp in patients on diuretics).
  2. Dry cough.
96
Q

What is the one difference in the clinical properties of ACEIs and ARBs?

A

ARBs do not inhibit the metabolism of bradykinin (a vasodilator).

97
Q

When should ACEIs and ARBs not be used?

A

In pregnancy and in bilateral renal artery stenosis (although ACEIs are used in diabetic nephropathy).

98
Q

What are the clinical uses of ACEIs and ARBs?

A

To treat hypertension and cardiac failure, and following myocardial infarction.

99
Q

How do ACEIs/ARBS help in cardiac failure?

A

It is associated with inappropriate RAAS inactivation. ACEIs decrease vascular resistance improving perfusion, increase excretion of salt and water and cause regression of LVH.

100
Q

Give an example of an ACEI and ARB.

A

ACEI - lisinopril.

ARB - losartan. ACEIs end in pril, ARBs end in sartan.

101
Q

Why are beta blockers of value in angina?

A

They: 1. decrease myocardial O2 requirement. 2. Counter elevated sympathetic activity associated with ischaemic pain. 3. Increase the amount of time spent in diastole (decrease heart rate), improving perfusion of the left ventricle.

102
Q

How may beta blockers help in hypertension?

A

Reducing cardiac output, reducing renin release from kidney and a CNS action that reduces sympathetic activity.

103
Q

Which L-type calcium channels do all clinically useful calcium antagonists (calcium channel blockers) interact with?

A

Ones found in the heart, smooth muscle and other locations.

104
Q

In the heart, what can calcium channel blockers do?

A
  1. Can reduce rate and conduction through the AV node (upstroke of AP mediated by L-type calcium channels).
  2. Can reduce force of contraction (as phase 2 of ventricular AP mediated by L-type calcium channels).
105
Q

What is limited by calcium channel blockers preventing the opening of L-type calcium channels?

A

The increase in intracellular calcium concentration.

106
Q

What are the 3 main types of calcium channels and give an example of each?

A
  1. Selective for cardiac L-type channels (verapamil). 2. Dihydropyridine compounds - relatively selective for smooth muscle L-type channels (amlodipine). 3. Intermediate selectivity (diltiazem).
107
Q

What are the clinical uses of calcium channel blockers?

A

In treating hypertension, angina and dysrhythmias.

108
Q

How can calcium channel blockers help hypertension?

A

Reduced calcium entry into vascular smooth muscle cells causes generalised arteriolar dilatation (major effect on arteries/arterioles).

109
Q

What calcium channel blockers are preferred in treating hypertension?

A

Ones with selectivity for smooth muscle L-type channels e.g. amlodipine.

110
Q

Why are calcium antagonists useful in patients suffering from both angina and hypertension?

A

They cause coronary vasodilation.

111
Q

What are the side effects of calcium channel blockers?

A

Mostly result from excessive vasodilation: hypotension, dizziness, flushing and swollen ankles (ankle oedema).

112
Q

When are calcium channel blockers used in angina?

A

As prophylactic treatment often used in combo with GTN if beta-blockers are contraindicated.

113
Q

Why are calcium channel blockers of value in angina?

A
  1. Cause peripheral arteriolar dilation decreasing afterload and myocardial oxygen requirement.
  2. Produce coronary vasodilation (esp useful in patients with variant angina).
114
Q

What are the specific calcium channel blockers used in angina?

A

Amlodipine (relatively little effect on heart and long acting), diltiazem and verapamil (produce negative inotropic effects but latter offset by activation of baroreceptor reflex in response to vasodilatation and increased sympathetic activity).

115
Q

What calcium channel blocker is used in dysrhythmias?

A

Verapamil (but avoid in heart failure, particularly in combo with a B-blocker).

116
Q

What sort of dysrhythmias does verapamil help and how?

A

Rapid atrial fibrillation - reduces ventricular rate by suppression of conduction through AV node.

117
Q

What channels to potassium channel openers act on and how?

A

ATP-modulated K+ channels in vascular smooth muscle. They antagonise ATP which opens the channel as ATP closes it.

118
Q

What effect do potassium channel openers have on the membrane potential and L-type calcium channels?

A

Cause hyperpolarisation which switches off L-type calcium channels.

119
Q

Where do potassium channel openers act?

A

Arterial smooth muscle.

120
Q

What potassium channel opener is used as a drug of last resort in severe hypertension and what are its side effects?

A

Minoxidil: causes relfex tachycardia (prevented by a B-blocker) and salt and water retention (allieviated by a diuretic).

121
Q

When is the potassium channel opener nicorandil used?

A

In angina resistant to other treatments (also has NO donor activity).

122
Q

How do alpha-1 antagonists work?

A

They cause vasodilation by blocking vascular alpha-1 receptors. Reduced sympathetic transmission results in decreased MABP.

123
Q

Give 2 examples of alpha-1 adrenoceptor antagonists.

A

Prazosin and doxazosin (both competitive antagonists).

124
Q

What other condition do alpha-1 antagonists provide symptomatic relief from?

A

Benign prostatic hyperplasia (abnormally enlarged prostate that compresses the urethra). Use this drug in hypertensive patients with this condition.

125
Q

What is the main adverse effect of alpha-1 antagonists?

A

Postural hypotension.

126
Q

What are the effects of diuretics?

A

Act on the kidney to increase the excretion of Na, Cl and H2O and exert additional relaxant effects on the vasculature.

127
Q

What are the 2 classes of diuretics?

A

Thiazide-like diuretics and loop diuretics.

128
Q

What is the mechanism of action of thiazide-like diuretics?

A

Inhibit NaCl reabsorption in the distal tubule by blocking the Na+/Cl- co-transporter (produce moderate diuresis).

129
Q

What is the mechanism of action of loop diuretics?

A

Inhibit NaCl reabsorption in the thick ascending limb of the loop of Henle by blocking the Na+/K+/2Cl- co-transporter (produce strong diuresis).

130
Q

What is the side effect of diuretics and how is it corrected?

A

Undesirable loss of K+ (occurs through Na+/K+ exchange in the late distal tubule). By co-administration of a potassium sparing diuretic or K+ supplements.

131
Q

Give an example of a thiazide diuretic.

A

Bendroflumethiazide.

132
Q

What are thiazide diuretics used in the treatment of?

A

Widely used: mild heart failure and hypertension. Additionaly in: severe resistant odema (with a loop agent).

133
Q

What effect do thiazide-like diuretics have on blood pressure and how?

A

Reduce MAP. Loss of sodium and water decreases blood volume and CO. When CO returns to normal, MAP remains depressed through lowering of peripheral resistance.

134
Q

Give an example of a loop diuretic.

A

Furosemide.

135
Q

What are loop diuretics used in?

A

Acute pulmonary oedema (IV), chronic heart failure.

136
Q

Why are loop diuretics used for these conditions?

A

Causes reduction of blood volume so ECF contributing to oedema is absorbed into capillaries.

Cardiovascular (32 decks)

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