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Cardiovascular > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is upstroke?

A

Heading towards a positive membrane potential

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2
Q

What is down-stroke?

A

Heading towards a negative membrane potential

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3
Q

What are regulatory influences of the AP in nodal tissues?

A 
Balance of autonomic input (sympathetic and parasympathetic) 
Stretch
Temperature
Hypoxia
Blood pH 
Thyroid hormones
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4
Q

What is phase 4 and what occurs during it of the nodal AP?

A

Pacemaker potential - Background sodium current inwards, an increased funny current (mediated by HCN channels that conduct Na+ and K+ inwards)
A decreased outward potassium movement

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5
Q

What occurs during phase 0 of the nodal AP?

A

The membrane is depolarised by the opening of T-type Ca 2+ channels

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6
Q

What is phase 3 of the nodal AP?

A

The membrane is repolarised by the opening of potassium channels allowing the efflux of positive potassium ions

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7
Q

What occurs during phase 4 of the AP in atrial and ventricular myocytes of the heart

A

Diastolic potential the resting membrane potential is a steady resting membrane potential
There is potassium conductance allowing potassium to move out of the cell keeping the potential at -90 mV

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8
Q

What occurs during phase 0 of the AP in atrial and ventricular myocytes?

A

The membrane depolarises very quickly due to the opening of sodium channels

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9
Q

What occurs immediately after the peak of action potential in atrial and ventricular myocytes in the heart?

A

There is a period of repolarisation known as phase 1. This is caused by a transient potassium channel that will open briefly causing the brief repolarisation of the membrane

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10
Q

What occurs during phase 2 of the AP in atrial and ventricular myocytes?

A

It is the plateau phase maintained by the opening of L-type Ca 2+ channels and the opening of potassium channels allowing calcium influx and potassium efflux

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11
Q

What is the purpose of the plateau phase?

A

To provide the calcium needed for cardiac contraction - providing the trigger necessary for the release of calcium from the sarcoplasmic reticulum (CICR)
No other action potential can be fired during the plateau phase preventing the heart from beating too quickly

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12
Q

What occurs during phase 3 of the AP in atrial and ventricular cardiac myocytes?

A

The repolarisation of the membrane due to the efflux of potassium bringing the membrane back down to -90 mV

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13
Q

How does the sympathetic stimulation lead to a positive chronotropic effect?

A

B1-adrenoceptors couple to Gs protien on the inside of the cell which once activated increases the enzymatic rate of the membrane bound enzyme adenylyl which converts ATP to cAMP

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14
Q

What does cAMP do in the sympathetic stimulation of cardiac cells?

A

cAMP is a secondary messenger which is vital in the action of B1 adrenoceptor stimulation within the heart. It will cause an increase in heart rate by acting on the SA node.

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15
Q

How does action potential frequency increase in the SA node after sympathetic stimulation?

A

The slope of phase 4 depolarisation (pacemaker potential) will be increased by an enhanced funny current (sodium influx) and calcium influx via T-type Ca 2+ channels. It also causes a reduction in the threshold necessary to initiate an action potential by an increased calcium influx

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16
Q

What effect does sympathetic stimulation have on the heart?

A

Increased heart rate (positive chronotropic effect)
Increase in contractility (positive inotropic effect)
Increased in conduction velocity in AV node (positive dromotropic response)
Increased automaticity
Decrease in the duration of systole (positive lusitropic action)
Increased activity of the Na+/K+-ATPase pump
Increases mass of cardiac muscle

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17
Q

How does sympathetic stimulation create a positive inotropic response?

A

There is an increased number of calcium entering the cell during the plateau phase and therefore there is more calcium to trigger muscle contraction and the troponin becomes more sensitive to calcium making muscle contraction easier and faster

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18
Q

How does sympathetic stimulation create a positive dromotropic response?

A

The rate at which the AP progresses through the AV node to the bundle of his increases due to the enhancement of the funny current and the T-type calcium channels

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19
Q

How does sympathetic stimulation create increased automaticity?

A

During sympathetic stimulation the other nodes in the heart that can fire AP’s being to fire AP’s

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20
Q

How does sympathetic stimulation reduce the duration of systole?

A

There is an increased uptake of Ca 2+ from the cytoplasm into the SR and therefore less muscle contraction can occur. When HR increases, if the duration of systole stayed the same then there would be an insufficient diastole for the ventricle and therefore the stroke volume would decrease

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21
Q

Why does sympathetic stimulation increase the activity of the Na/K ATPase pump?

A

To maintain a steady membrane potential and to repolarise the membrane

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22
Q

What is the cellular effect of parasympathetic stimulation on heart cells?

A

ACh will act upon M2 receptors which is coupled to a Gi protein that has the opposite effect to Gs and will reduce the effect of adenylyl cyclase and reduce the concentration of cAMP
When the beta and gamma subunits of the Gi G-protein are liberated, they will act upon a potassium channel (GIRK) to hyperpolarise the cell making the heart tissue less excitable and therefore making it harder to initiate an action potential

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23
Q

How does parasympathetic stimulation create a negative chronotropic effect?

A

The pacemaker potential decreases due to a reduced funny current and calcium ion influx.
It will also increased the threshold for AP caused by a reduced affinity for Ca 2+ channels and the efflux of K+ from the cell via GIRK
This will occur in SA and AV nodes

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24
Q

What is the effect of parasympathetic stimulation on the heart?

A

Negative chronotropic effect
Negative inotropic effect
Reduced conduction in the AV node - negative dromotropic effect
Parasympathetic stimulation may cause arrhythmia’s to occur in the atria

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25
Q

How does parasympathetic stimulation create a negative inotropic effect?

A

The force of atrial contraction is reduced by the force of ventricular contraction is largely unaffected as the ventricles are not well innervated by the parasympathetic nerves. There is reduced Ca 2+ entry during the plateau phase and therefore less release of Ca 2+ from the SR and less muscle contraction

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26
Q

How does parasympathetic stimulation create a negative dromotropic effect?

A

There is a decrease in activity of Ca 2+ channels and the opening of KIRK K+ channels. This can cause arrhythmia’s due to a reduction in AP duration which reduces the refractory period and could allow for re-entrant arrhytmia’s

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27
Q

What is the pacemaker current modulated by?

A

A depolarising current - the funny current

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28
Q

What activated the funny current?

A

Hyperpolarisation and cyclic AMP - HCN channels
Hyperpolarisation following the action potential activates positive ions that are selective to HCN channels in the SA node which facilitates a slow depolarisation (pacemaker potential)
The blockage of HCN channels decreases the slope of the pacemaker potential and reduces heart rate

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29
Q

What is an example of a drug that blocks the HCN channels?

A

Ivabradine is a selective blocker that can be used to slow heart rate in angina which is a condition in which there is a reduced blood supply to the cardiac muscle and therefore a slower heart rate will reduce the oxygen consumption

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30
Q

What initiates contraction of cardiac muscle?

A

The phase 2 plateau phase where calcium enters the cell via L-type Ca 2+ channels. Calcium will bind to ryanodine type 2 channels and induce CICR. Ca 2+ will now bind to troponin moving it out of the way allowing cross bridges to form and muscle contraction to occur

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31
Q

How does the cardiac muscle relax?

A

There is repolarisation of the membrane and the L-type Ca 2+ channels close ceasing calcium influx. Ca 2+ efflux will be initated by the NXC1 membrane pumping 1 Ca ion out of the cell and 3 Na+ ions into the cell. Calcium is also sequestered back into the SR by Ca 2+ ATPase

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32
Q

What enyme does cAMP active?

A

Protein kinase A

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33
Q

What does protein kinase A do?

A

It will phosphorylate phospholamban which will increase the pumping of calcium into the SR by modulating the activity of Ca 2+ ATPase, therefore reducing systole duration
It will phosphorylate the L-type Ca 2+ channel increasing calcium influx allowing increased CICR
It will also phosphorylate some of the proteins in the contractile machinery making them more sensitive to calcium

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34
Q

How is cAMP turned off?

A

By phosphodiesterase enzymes (PDE) breaking down cAMP to the inactive form inactive 5’AMP

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35
Q

What are dobutamine, adrenaline, noradrenaline and dopamine all?

A

They are agonist catecholamines

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36
Q

What do agonist catecholamines do?

A

They produce a sympathetic like effect - increase force, rate, cardiac output and oxygen consumption
They will however reduce cardiac efficiency - more oxygen is needed making the amount of oxygen required disproportionate to the work of the heart

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37
Q

What is the function of adrenaline in the heart?

A

It is a mixed agonist and so will act against alpha and beta adrenoceptors. It has a very short plasma half life and is removed from the plasma via tissues such as nerves. It has a positive inotropic and chronotropic effect (B1). It redistributes blood flow to the heart (A1) and dilates coronary arteries (B2)

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38
Q

How should adrenaline be administered in anaphylactic shock?

A

IM NOT IV (only IV if cardiac arrest occurs)

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39
Q

What is the action of dobutamine?

A

It is selective for beta-adrenoceptors and is given as an IV infusion
It has an acute but reversible effect for heart failure.
Dobutamine only has an effect in acute heart failure not chronic heart failure

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40
Q

What are the clinical uses of beta-adrenoceptors?

A

Treatement of arrhythimas
Treatment of angina
Treatment of compensated heart failure
Treatment of hypertension

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41
Q

What does the action of beta blockers depend on?

A

The degree to which the sympathetic nervous system has been activated

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42
Q

What is an example of a non-selective beta-adrenoceptor?

A

Propanolol

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43
Q

What are some examples of a selective B1 beta blocker?

A

Atenolol, bisoprolol and metoprolol in a commpetitve manner

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44
Q

What is the pharmacodynamic effect of a non-selective blocker?

A

During exercise/stress - rate, force and CO is depressed and therefore there is a reduction in maximal exercise tolerance. Coronary vessel diameter is marginally reeduced but myocardial oxygen requirement falls and thus there is better oxygenation of the myocardium

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45
Q

How do beta blockers treat arrhythmias?

A

Excessive sympathetic drive caused by stress, emotion or disease can lead to tachycardia or spontaneous activation of latent cardiac pacemakers outside of the nodal tissue and therefore beta blockers are helpful as they decrease excessive sympathetic drive and help to restore normal sinus rhythm. They can also be used to treat AF or SVT because they delay the conduction through the AV node to help restore sinus rhythm

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46
Q

How are beta blockers used to treat angina?

A

They can be used first line as an alternative to calcium entry blockers

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47
Q

How are beta blockers used to treat compensated heart failure?

A

Low dose beta blockers improve morbidity and mortality by reducing excessive sympathetic drive.

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48
Q

What is an example of a beta blocker used to treat compensated heart failure?

A

Carvediol - pure beta blocker which antagonises alpha 1 receptors reducing the SVR and therefore reduces afterload of the heart

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49
Q

What is compensated heart failure?

A

The patient is stable and is managed by many other drugs

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50
Q

What are adverse effects of beta blockers?

A

Bronchospasm (don’t give beta blockers to severe asthmatics)
Aggravation of cardiac failure
Bradychardia
Hypoglycaemia - poorly controlled diabetes the release of glucose from liver is controlled by Bw adrenoceptors
Fatigue - CO and skeletal muscle perfusion
Cold extremites - loss of beta adrenoceptor mediated vasodilatation in cutaneous vessels

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51
Q

How many of these side effects be reduced?

A

Less risk associated with B1 selective agents - atenolol, bisoprolol, metoprolol

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52
Q

What are the pharmocodynamic effects of atropine?

A

Increases HR - more pronounced in athletes

No effect on BP - resistance vessels lack parasympathetic innervation

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53
Q

When is atropine used?

A

First line in management of severe bradycardia, particularly following MI (vagal tone elevated)
First IV bolus of atropine give 300-600 micrograms

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54
Q

How does atropine work?

A

It is a non-selective muscarninic ACh receptor antagonist

Blocks parasympathetic innervation in the heart

55
Q

What is digoxin?

A

A cardiac glycoside that increases heart force

56
Q

When is digoxin used?

A

In heart failure - with patients that have an insufficient CO to provide adequate tissue perfusion

57
Q

What effect does digoxin have on the frank-starling curve?

A

Inotropes (digoxin, dobutamine) cause an upward and leftward shift of the ventricular function curve, such that SV increases at any given EDP

58
Q

What effect does digoxin have on ion concentrations within the cell?

A

It blocks the NA+/K+ ATPase pump increasing the concentration of Na+ within the cell, decreasing the resting potential of the cell. There will therefore be less of a drive to pump sodium into the cell via the Na+/Ca2+ pump as there is a higher sodium conc within the cell and so more calcium will stay in the cell. There will also be an increased storage of calcium within the SR and an increased CICR and ultimately heart contractility

59
Q

How can digoxin be dangerous?

A

It competes with potassium for binding to ATPase and therefore is there is less potassium in the plasma due to hypoolalaemia then digoxin will bind to ATPase and the effect will be dangerously enhanced. Therefore in patients treated with diuretics there will be potassium loss and treatment with digoxin is dangerous

60
Q

What are the parmacodynamics of digoxin?

A

Indirectly - increases vagal activity (slows SA nodal discharge and AV nodal conduction )
Directly - shortens AP and refractory period in atrial and ventricular myocytes

61
Q

What route is digoxin given?

A

IV in acute heart failure with patients who are still symptomatic after optimal use of other drugs (ACE inhibitors, diuretics)

62
Q

What are some adverse effects of digoxin?

A 
Excessive depression of AV nodal conduction (heart block) 
Arrhythmias 
Nausea
Vomiting
Diarrhoea
Disturbances in colour vision
63
Q

What is the action of levosimendan?

A

Binds to troponin C in cardiac muscle sensitizing it to the action of calcium. It also opens K-ATP channels in vascular smooth muscle causing vasodilation (reducing afterload)

64
Q

When is levoseimendan used?

A

IV in acute decompensated heart failure

65
Q

What type of drugs are amrinone and milrinone?

A

Inodilators

66
Q

What is the action of milrinone and amrinone?

A

Inhibit PDE in cardiac and smooth muscle cells and hence increased cAMP. This increases cardiac contraction and decreases peripheral resistance

67
Q

What drugs are used to treat hypertension?

A

Thiazide dieuretics
Beta blockers
Vasodilators: Calcium antagonists, alpha blockers, ACE inhibitors, angiotensin receptor blockers

68
Q

What drugs are used to treat angina?

A 
Beta blockers
Calcium antagonists 
Nitrates
Nicorandil 
Ivabradine 
Ranolazine
69
Q

What drugs are used to treat thrombolysis?

A

Antiplatelet drugs - aspirin, clopidogrel, prasugrel, ticagrelor
Anticoagulants - warfarin, rivaroxaban, dabigatran
Fibrinolytics - streptokinase

70
Q

What drugs are used to treat high cholesterol?

A

Statins

Fibrates

71
Q

What is the action of diuretics?

A

They make you pass more sodium and water in the urine by preventing the sodium reabsorption in the kidneys

72
Q

What type of diuretic is used in hypertension?

A

Thiazide dieuretic - bendrofluazide which is a mild diuretic

73
Q

What type of diuretic is used in heart failure?

A

Loop diuretics - furosemide which is a strong diuretic

74
Q

What are the side effects of diuretics?

A

Hypokalaemia - making you tired and predisposing you to arrhythmias
Hyperglycaemia - high sugar causing diabetes
Increased uric acid which can cause gout (accumulation of uric acid crystals in joints)
Impotence - inability to sustain an erection

75
Q

What are the two types of beta blockers?

A

Cardioselective (only B1 receptors blocked)

Non selective beta blockers (block B1 and B2)

76
Q

When are cardioselective beta blockers used?

A

In angina, hypertension and heart failure

Atenolol

77
Q

When are non selective beta blockers used?

A 
In thryotoxicosis (overactive thyroid) 
Propanolol
78
Q

What are the side effects of beta blockers?

A

Asthma - always check if the patient has asthma when prescribing beta blockers
Tired
Heart failure - only if used in short term, small doses built up is the way to prescribe
Cold peripheries

79
Q

What are the two types of calcium antagonists?

A

Dihydropyridines

Rate limiting calcium antagonists (vasodilator and AV nodal conduction block)

80
Q

When are dihydropyridines used?

A

In hypertensino and angina
Amlodipine
Side effect: ankle oedema

81
Q

When are rate limiting calcium antagonists used?

A

Hypertension, angina and supraventricular arrhythmias (AF, SVT)
Verapamil and diltiazem

82
Q

Why should verapimil and diltiazem be avoided with beta blockers?

A

They both slow heart rate and therefore the use of both at the same time could cause bradycardia or complete heart block

83
Q

What is the action of alpha blockers and when are they used?

A

They block the alpha adrenoceptors to cause vasodilation

Used in hypertension and prostatic hypertrophy - doxazosin

84
Q

What is a side effect of alpha blockers?

A

Postural hypotension

85
Q

What is the action of angiotensin converting enzyme inhibitors (ACE)

A

They block angiotensin 1 becoming angiotensin 2

Used in hypertension and heart failure

86
Q

What is the effect of an ACE inhibitor on the kidneys?

A

They have a positive effect on renal function in diabetic nephropathy
They have a negative effect on renal function in renal artery stenosis

87
Q

What are the side effects of ACE inhibitors?

A

Cough
Renal dysfunction
Angioneurotic oedema
NEVER use in pregnancy

88
Q

What is an example of an ACE inhibitor?

A

Lisinopril

89
Q

What is the action of angiotensin receptor blockers?

A

They block the binding of anagiotensin 2 to their receptors

90
Q

When are angiotensin receptor blockers used?

A

Hypertension and heart failure

91
Q

What are the side effects of angiotensin receptor blockers?

A 
Renal dysfunction (good for kidneys in diabetic nephropathy) 
NO cough - if cough present in ACE inhibitors consider switching to an angiotensin receptor antagonist 
NEVER use in pregnancy
92
Q

What is the action of nitrates?

A

Venodilators - isosorbide mononitrate

93
Q

When are nitrates used?

A

Angina and acute heart failure

94
Q

What are the side effects of nitrates?

A

Headache
Hypotension/collapse
Tolerance - leave 8hr a day nitrate free to prevent tolerance

95
Q

What are some examples of anti-platelet agents?

A

Aspirin, clopidogrel, ticagrolor, prasugrel

96
Q

What is the function of anti-platelets?

A

Prevent new thrombis formation

97
Q

When are anti-platelets used?

A

Angina
Acute MI
CVA/TIA
Patients at high risk of MI/CVA

98
Q

What are the side effects of anti-platelet agents?

A

Haemorrhage
Peptic ulcer makes haemorrhage more likely
Aspirin sensitivity can cause asthma

99
Q

What is the action of anticoagulants?

A

Prevent new thrombis - heparin IV only and warfarin oral only
Warfarin blocks clotting factors 2, 7, 9 and 10

100
Q

When are anticoagulants used?

A

DVT
PE
NSTEMI
AF

101
Q

What are the side effects of warfarin?

A

Haemorrhage

INR - monitors how thin the blood is as wararins therapeutic window is very small

102
Q

What can be used to reverse warfarin?

A

Vitamin K (blood clotting factors 2, 7, 9, 10 are all vitamin K dependent)

103
Q

What are some new anticoagulants?

A

Rivaroxaban - factor Xa inhibitor which converts prothrombin 2 to thrombin 2a
Dabigatran - thrombin factor 2a inhibitor

104
Q

What is the function of fibrinolytic drugs?

A

They dissolve formed clots

105
Q

What is an example of fibrinolytic drugs?

A

Stretokinase

Tissue plasminogen activator (tPA)

106
Q

When are fibrinolytic drugs used?

A

STEMI
PE
CVA

107
Q

What are the side effects to fibrinolytic drugs?

A 
Serious haemorrhage 
Avoid in:
Recent haemorrhage (CVA)
Trauma
Bleeding tendencies
Sever diabtetic retinopathy 
Peptic ulcer
108
Q

What are some example of anticholesterol drugs?

A

Statins: simvastatin which blocks HMG CoA reductase

Fibrates - bezafibrate

109
Q

When are statins prescribed?

A 
Hypercholesterolaemia
Diabetes
Angina/MI
CVA/TIA
High risk of MI
110
Q

What are the side effects of statins?

A

Myopathy

Rhabdomyolysis renal failure

111
Q

When are fibrates prescribed?

A

Hypertriglyceridaemia

Low HDL cholesterol

112
Q

What are some example of anti-arrhythmic drugs?

A

Adenosine - used in acute phase of SVT
Amiodarone
Beta blockers
Flecainide

113
Q

What are the side effects to amiodarone?

A

Phototoxicity
Pulmonary fibrosis
Thyroid abnormalities (Hypo or Hyper)

114
Q

What are the two effect of digoxin?

A

Blocks atrio-ventricular conduction (good in AF)

Increases ventricular irritability which produces ventricular arrhythmias

115
Q

What are the side effects of digoxin?

A

Nausea, vomiting
Yellow vision
Bradycardia, heart block
Ventricular arrhythmias

116
Q

What are adrenoceptors?

A

G-protein-coupled receptors (GPCRs) that are activated by the aympathetic transmitter noradrenaline and the hormone adrenaline

117
Q

What does alpha 1 adrenoceptors do?

A

Constrict vasculature

118
Q

What does B1 adrenoceptors do?

A

Increase rate, force and AV node conduction velocity

119
Q

What do B2 adrenocptors do?

A

Relax airway smooth muscle and vasculature

120
Q

When are b-adrenoceptor antagonists used?

A

For the treatment of angina pectoris but not variant angina

121
Q

Why are beta blockers useful for the treatment of angina?

A

They decrease myocardial oxygen requirement
Counter elevated sympathetic activity (emotional stress -
anxiety) associated with ischemic pain
Increase the amount of time spent in diastole, improving perfusion of the left ventricle

122
Q

How can beta blockers help to restore normal blood pressure?

A

They reduce the cardiac output

Reduce the amount of renin released from the kidneys

123
Q

What do calcium antagonists do?

A

Prevent the opening of L-type channels in excitabe tissues in response to depolarisation and hence limit the influx of calcium

124
Q

What do L-type channels mediate?

A

Upstroke of the AP in the SA and AV nodes - calcium antagonists can reduce rate and conduction through the AVN
Phase 2 of the ventricular AP - calcium antagonists can reduce force of contraction
Calcium influx is needed for CICR in muscle cells - so calcium antagonists will reduce calcium influx during phase 2 and reduce CICR

125
Q

What are 3 drugs that act as calcium antagonists?

A

Verapamil
Amlodipine - dihydropyridine compound
Diltiazem

126
Q

What are the clinical uses of calcium antagonists?

A

Hypertension - drugs with selectvity for smooth muslce L-type channels (amlodipine) are preferred
Cause coronary vasodilatation and so are particularity helpful in patients with angina and hypertension
Angina - in combo with GTN
They cause arteriolar dilitation (decreased afterload), coronary dilitation

127
Q

What are the adverse effects of calcium antagonists?

A

Excessive vasodiltation - hypotenstion, dizziness, flushing, swollen ankles (ankle oedema)

128
Q

What calcium antagonist is used to treat angina?

A

Amlodipine - little effect on heart and it long acting
Dilitiaem and verapamil - produce negative inotropic effects but offset by activation of baroreceptor reflex in response to vasodilitation and increased symp activity

129
Q

What are potassium channel openers?

A

K+ channels regulated by ATP. ATP will close K-ATP channels, the opening of these channels causes K+ efflux (hyperpolarisation) which will indirectly suppress the opening of L-type Ca 2+ channels.

130
Q

What are some examples of potassium channel openers?

A

Minoxidil - last resort in hypertension but causes reflex tachycardia
Nicorandil - used in angina

131
Q

What is the action of alpha-1 adrenoceptor antagonists?

A

They cause vasodilation by blocking vascular A1-adrenoceptors. A reduced sympathetic transmission results in deccreased MABP

132
Q

What are examples of A1-adrenoceptor antagonists?

A

Prazosin

Doxazosin

133
Q

What is the clinical use of A1-adrenoceptor antagonists?

A

They can provide symptomatic relief in benign prostataic hyperplasia and so are particularity indicated for hypertensive patients with this condition

134
Q

What are the adverse effects of A1-adrenoceptor antagonists?

A

Postural hypotension

Cardiovascular (27 decks)

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