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Cardiovascular > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what are the regulatory influences on the action potential of the nodal tissue of the heart

A

autonomic input (para and symp), stretch, temp, hypoxia, blood pH, thyroid hormones

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2
Q

what phase is the upstroke of the action potential in nodal tissue and describe it

A

phase 0, increased ICal (long calcium current)

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3
Q

what phases are missing from the action potential of nodal tissue that are present in cardiac myocytes

A

phases 1 and 2

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4
Q

describe phase 3 of the action potential in nodal tissue

A

downstroke of AP, repolarisation, increased Ik (delayed rectifier potassium current) (outward)

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5
Q

describe phase 4 of the action potential in nodal tissue

A

pacemaker potential; Ib (background sodium channel (inward)), increase If (funny channel), ICaL (long calcium current (inward)) and decreased IK (delayed rectifier potassium current outward)

Ib, ^IF, ICal, -Ik

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6
Q

what is funny current (If)

A

mediated by hyperpolarisation-activated and cyclic neucleotide gated (HCN) channels that conduct Na+ and K+ (inward)

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7
Q

what determines the upstroke of the action potential

A

opening of voltage gated calcium channels (L-type channels)

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8
Q

why are they called calcium long channels

A

as produce a long calcium current by staying open for a long period of time

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9
Q

during phase 0 what is the inward movement is calcium being opposed by

A

outward movement of positive charge (hyperpolarisation) via back currents and V activated potassium channels (slow to open) why mem potential only reaches +10mV

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10
Q

what causes the down stroke of a membrane potential in nodal tissue

A

opening of V activated potassium channels (delayed rectifier)

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11
Q

how do potassium channels cause repolarisation

A

as move positive charged potassium ions out of cell making inside membrane potential negative

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12
Q

what state are the calcium channel in during repolarisation of AP in nodal tissue

A

inactivated

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13
Q

what give rise to the pacemaker potential

A

net movement of pos charge into the cell by different types of ion channel (e.g. sodium selective channels background)

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14
Q

what is the role of the transient calcium channel ICaT

A

opens very briefly during pacemaker potential to give final kick to reach threshold and initiate opening of L type channels

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15
Q

when do Ik channels open

A

during downstroke of AP

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16
Q

when are Ik channels closed

A

during pacemaker potential to speed up depolarisation

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17
Q

what activates funny channels

A

neg mem potentials (v neg= hyperpolarisation)

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18
Q

what current is active during phase 1 of myocyte AP

A

Ito- transient outward potassium current

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19
Q

what current is active during phase 0 of myocyte AP

A

sodium current (inward)

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20
Q

what is phase 4 of myocyte AP

A

diastolic potential, resting potential, steady

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21
Q

what is phase 4 in normal tissue similar to

A

pacemaker potential

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22
Q

what maintains the steadiness diastolic potential

A

potassium’s ability to move out of the cell and maintain potential

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23
Q

what opens V activated sodium channels in cardiac myocyte AP

A

AP form SA node at ventricular muscle

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24
Q

what is the upstroke of the AP in cardiac myocytes regulated by

A

sodium channels

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25
Q

what upstroke AP’s do calcium channels mediate

A

normal and PM

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26
Q

is the upstroke of a cardiac myocyte or PM quicker

A

cardiac myocyte

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27
Q

what stops the depolarised membrane potential from reaching +100mV

A

competing conductance

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28
Q

describe phase 1 of a cardiac myocyte AP

A

brief stage of repolarisation caused by transient outward current due to potassium channel that opens very briefly

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29
Q

what is Ik1 current

A

inward rectifier potassium current

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30
Q

what happens to calcium channels during the upstroke of a cardiac myocyte AP

A

opened- slightly delayed, opened for long period of time

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31
Q

what currents are present during the plateau phase

A

ICal (increased) and INal

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32
Q

why does the membrane potential not change greatly during the plateau phase

A

a calcium ions are moving out of the cell

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33
Q

what enters muscle cells to dribe contraction

A

calcium

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34
Q

can another action potential be fired during the plateau phase, why

A

no, because of v activated sodium channels being activated (only conduct or a millisecond but long plateau period permits calcium entry over a long period of time)

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35
Q

what provides small current to the plateau but could also disrupt rhythm of the heart

A

late sodium current INaL

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36
Q

in phase three what are the two currents that activate and reduce membrane potential to the resting pot of -90mV

A

Ik and Ik1

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37
Q

what direction is sodium channelled

A

inward

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38
Q

what direction is potassium channelled… except in?

A

outward, funny channel

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39
Q

what direction is calcium channelled

A

inward

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40
Q

what is noradrenaline

A

post-ganglionic transmitter

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41
Q

what is adrenaline

A

adrenomedullary hormone

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42
Q

what do adrenaline and noradrenaline activate

A

B1 adrenoceptors in nodal and myocardial cells

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43
Q

what does the activation of B1 adrenoceptors by the sympathetic system activate and via what mechanism

A

activates adenylyl cyclase in increase cAMP concentration. By coupling through Gs protein

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44
Q

what mechanisms cause the positive chronotropic effect of sympathetic stimulation in terms of the pacemaker potential

A

increase in slope of pacemaker potential caused by enhanced If and ICa

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45
Q

changes in what current cause a decrease in the AP threshold

A

increased ICa

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46
Q

generally which beta receptors are present where in the body

A

beta 1 heart, beta 2 airways

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47
Q

what are increases in heart rate mediated by

A

action on SA node

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48
Q

what is a positive inotropic effect

A

increased contractility

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49
Q

changes in what part of the cardiac action potential in atrial and ventricular myocytes cause increased contractility

A

increase in phase 2

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50
Q

changes in which current cause increase contractility

A

enhanced Ca2+ influx

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51
Q

sensitisation of what to what causes increased contractility

A

sensitisation of contractile proteins to Ca2+

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52
Q

what is a positive dromotropic response

A

increase in conduction in AV node

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53
Q

what changes in current increase conduction in the AV and SA node

A

increased If and ICa

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54
Q

what is automaticity

A

tendency for non nodal regions to acquire spontaneous activity

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55
Q

what is a positive Lusitropic action

A

decreasing the duration of systole

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56
Q

what cause a decrease in the duration of systole

A

increased uptake of Ca2+ into the sarcoplasmic reticulum

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57
Q

what effect does sympathetic stimulation have on the activity of the Na+/K+ ATPase

A

increases it

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58
Q

what effect does sympathetic stimulation have on mass of cardiac muscle

A

increases it (cardiac hypertrophy)

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59
Q

how is the frank staling curve affected by sympathetic stimulation

A

curve elevated

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60
Q

what happens at any end diastolic pressure during symp stimulation

A

stroke volume increased

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61
Q

why is contractility increased during sympathetic stimulation

A

as more calcium enters cell during plateau phase

proteins in the contractile apparatus become more sensitive to calcium

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62
Q

what affect does symp stim have on systole and why

A

reduces it so heart has more time to refill (if not would reduce stroke volume)

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63
Q

what is acetylcholine

A

post-ganglionic transmitter for the parasympathetic system

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64
Q

what does acetylcholine activate

A

M2 muscarinic cholinoceptors, largely in nodal cells

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65
Q

what effect does coupling of activated M2 muscarinic cholinoceptors with Gi protein do

A

1- decreases activity of adenylate cyclase and reduces [cAMP]I

2- opens potassium channels (GIRK) to cause hyperpolarization of SA node

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66
Q

what effect does the parasympathetic system have on heart rate

A

reduces it

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67
Q

what effect does the parasympathetic system have on slope of pacemaker potential and how

A

reduces it by reducing If and ICa

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68
Q

what effect does the parasympathetic system have on the threshold for AP and how

A

increases it via reducing ICa channels

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69
Q

what happens when GIRK channels are opened

A

potassium leaves cell, hyper polarising it and making it less excitable

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70
Q

what inotropic effect does para stim have and why

A

(negative) decreases contractility (in atria only) as decrease in phase 2 of cardiac action potential and decreased Ca2+ entry

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71
Q

what dromotropic effect does para symp have and how

A

(negative) decreases conduction in AV node- decreases activity of voltage dependent Ca+ channels and hyper polarisation via opening of K channels

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72
Q

what may para stim cause in the atria and why

A

arrhythmias as AP duration is reduced and so too the refractory period

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73
Q

what do vagal manoeuvres do

A

increase parasympathetic output

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74
Q

when may vagal manoeuvres be employed

A

in atrial tachycardia, atrial flutter, or atrial fibrillation to suppress impulse conduction through the AV node

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75
Q

what is the valsalva manoeuvre used to do

A

activates aortic baroreceptors (popping your ears)

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76
Q

what does massage of the bifurcation of the carotid artery do and why is it not recommended

A

stimulates baroreceptors in the carotid sinus- could dislodge deposit causing thrombis= stroke

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77
Q

what current mediates pacemaker potential

A

funny current (If)

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78
Q

what are the channels that mediated funny current activated by

A

(gated HCN channels)

hyperpolarisation

cyclic AMP

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79
Q

what does hyperpolarisation follow action potential do to HCN channels

A

activates HCN channels in the SA node

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80
Q

what does activation of CHN channels in the SA node cause

A

a slow phase 4 (pacemaker potential) depolarisation

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81
Q

what does block of HCN channels do to the slope of pacemaker potential and therefore heart rate

A

decreases slope and heart rate

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82
Q

what increases the activation of HCN channels

A

cAMP

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83
Q

what drug can be used as a selective blocker of HCN channels

A

ivabradine

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84
Q

what is ivabradine used to treat, how

A

angina as slow HR and reduces O2 consumption

angina is a coronary artery disease which reduces the blood supply to the cardiac muscle

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85
Q

what is RyR2

A

the major mediator for sarcoplasmic release of stored calcium ions

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86
Q

what activate RyR2

A

Ca2+ influx during muscle contraction

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87
Q

what plasma membrane ATPase allows calcium efflux during muscle relaxation

A

Na+/Ca2+ exchanger 1 (NCX1)

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88
Q

only when what happens can muscle relaxation occur

A

when calcium has been removed from the cytoplasm

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89
Q

what ion rato does NCX1 move in/out of cardiac muscle cells

A

1 calcium out 3 sodium in

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90
Q

how is Ca put back into the SR

A

via Ca2+ATPase (SERCA), (sequesters calcium back into SR)

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91
Q

summarise how B1 adrenoceptor activation modulates cardiac contractility

(sympathetic stimulation)

A

B1 adreno activated= make cAMP

cAMP activate protein kinase A= phosphorylation reactions

L type Ca channels phosphorylated= opens= calcium influx= increased force of contraction

PKA also phosphorylates proteins in contractile machinery= more sensitive to calcium= pro-contractility

phospholamban phosphorylated by PKA= increase activity of CaATPase= increased pumping of Ca2+ into SR= increased rate of relaxation

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92
Q

how is cardiac force affected when you prevent the breakdown of cAMP

A

increase cardiac force

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93
Q

what are three agonists that act on B adrenoceptor

A

dobutamine, adrenaline and noradrenaline

94
Q

what class of drugs do dobutamine, adrenaline and noradrenaline belong to

A

catecholamines

95
Q

what are the pharmacodynamic effects of of B-adrenoceptor ligands

A

increase force, rate, CO and O2 consumption

decrease cardiac efficiency (O2 consumption less than cardiac work)

can cause disturbances in cardiac rhythm

96
Q

what is adrenaline used to treat

A

cardiac arrest (IV), anaphylatic shock (IM)

97
Q

what is dobutamine used to treat

A

acute (but potentially reversible heart failure)

98
Q

how is adrenaline a mixed antagonist

A

as acts on both alpha and beta adrenoceptors

99
Q

why does adrenaline have a short half life

A

as rapidly metabolised and removed from plasma by uptake systems of many tissues and nerves

100
Q

what effect does adrenaline have on blood supply to organs

A

causes constriction of vessels around organs not essential at the time which reduces blood flow and redirects it to the heart

101
Q

what type of beta receptor is present in cardiac muscle

A

B1

102
Q

what type of beta receptor is present in respiratory smooth muscle

A

B2

103
Q

how does adrenaline affect the coronary artery

A

dilates it to improve blood supply to the heart

104
Q

what is a beta blocker

A

beta adrenoceptor antagonist

105
Q

what do the physiological effects of B-adrenoceptor blockade depend upon

A

the degree to which the sympathetic nervous system is activated

106
Q

name a non-selective beta blocker

A

propanolol

107
Q

name 3 selective beta blockers

A

atenolol, bisoprolol, metoprolol

108
Q

name a non selective and partial agonist

A

alprenolol

109
Q

what are the pharmacodynamic effects of non-selective blockers

A

little effect at rest, during exercise; HR, force and CO significant depressed, O2 requirement and coronary vessel diameter reduced too

110
Q

what is meant when a beta blocker has mixed activity

A

mildly stimulates heart and acts as antagonist to block agonist behaviour)

111
Q

what are the clincal uses of a B-adrenoceptor antagonist

A

arrhythmias (tachycardia,atrial fibrillation or supraventricular tachycardia), angina, heart failure (compensated), hypertension

112
Q

how do beta blockers treat excessive sympathetic activity (arrhythmias)

A

-blockers decrease excessive sympathetic drive and help restore normal sinus rhythm

113
Q

how do beta blocker treat Atrial fibrillation (AF) and supraventricular tachycardia (SVT)

A

delay conduction through the AV node and help restore sinus rhythm

114
Q

how do beta blockers treat angina

A

calcium entry blockers, help reduce O2 consumption and pain

115
Q

what are stress induced arrhythmias

A

Increased delivery of noradrenaline and adrenaline causes emergence of latent pacemakers-stress induced arrhythmias

116
Q

what is heart failure

A

when heart is giving insufficient cardiac output to provide adequate tissue perfusion

117
Q

what is compensated heart failure

A

patient is stable and managed by drugs

118
Q

what list the adverse effects of beta blockers

A

bronchospasm, aggravation of cardiac failure, bradycardia, hypoglycaemia, fatigue, cold extremities

119
Q

why do beta blockers cause bronchospasma

A

block of airway smooth muscle B2-adrenoceptors (can be severe in asthmatics)

120
Q

why do beta blockers cause aggravation of cardiac failure

A

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

121
Q

why do beta blockers cause bradycardia

A

heart block – in patients with coronary disease; B-adrenoceptors facilitate nodal conduction

122
Q

why do beta blockers cause hypoglycaemia

A

in patients with poorly controlled diabetes – the release of glucose from the liver is controlled by B2-adrenoceptors

123
Q

why do beta blockers cause fatigue

A

CO (β1) and skeletal muscle perfusion (β2) in exercise are regulated by adrenoceptors

124
Q

why do beta blockers cause cold extremities

A

loss of B2-adrenoceptor mediated vasodilatation in cutaneous vessels

125
Q

what adverse effects are at less of a risk with B1-selective agents

A

bronchospasm and hypoglycaemia

126
Q

why do beta blockers pose an extra risk in hypoglycaemia

A

as hypo warning mechanisms (anxious, tremor, HR and force increases) could be suppressed by beta blocker

127
Q

what is atropine

A

a non selective competitive antagonist of Muscarinic ACh Receptor

128
Q

what are the pharmacodynamic effects of atropine

A

increase HR (more pronounced in athletes), no effect on arterial BP (as resistance vessels lack para innervation), no effect on response to exercise

129
Q

how does atropine act

A

blocks effect of parasympathetic stimulation on the heart

130
Q

why does atropine increase HR in athletes more

A

as have increased vagal tone and HR is much lower

131
Q

what are the clinical uses for atropine

A

first line for severe bradycardia, particularly following MI (IV) and in anticholinesterase poisoning

132
Q

why must you give a dose of a least 300-600 micrograms of atropine to treat bradycardia after an MI

A

as low doses will decrease HR

133
Q

what is digoxin

A

A aardiac glycoside that increases contractility of the heart

134
Q

how does Digoxin Increases Contractility

A

by Blocking the Sarcolemma ATPase

135
Q

what does the Na+/Ca2+ exchanger move in and out

A

3 na out 2 k in

136
Q

what are the by Sarcolemma ATPase

A

sodium potassium pump, Na+/Ca2+ exchangerm L-type Ca2+ channel

137
Q

what part of Na+/K+ ATPase

A

alpha subunit

138
Q

what can dangerously enhance the effect of digoxin and how

A

low plasma K+ as in competition with this to bind

139
Q

what are the indirect electrical effects of digoxin

A

increased vagal activity, slows SA node discharge, slows AV node conduction (increases refractory period)

140
Q

what are the direct electrical effects of digoxin

A

shortens action potential and refractory period in atrial and ventricular myocytes

141
Q

does digoxin increase or decrease parasympathetic drive

A

increases it

142
Q

what is oscillatory afterpotentials and what causes it

A

because of Ca2+ overload, ‘delayed after depolarisation’, id reaches threshold for AP then could cause self propagating AP= ventricular arrhythmia= tachy cardia= ventricle fibrillation

143
Q

what are the clinical uses of digoxin

A

Iv in acute heart failure, orally in chronic heart failure

144
Q

how does digoxin help in heart failure with atrial fibrillation

A

increase in AV node refractory period is beneficial, helps to prevent spreading of the arrhythmia to the ventricles

145
Q

what causes the most severe adverse affects of digoxin

A

suppression of both nodes

146
Q

what are the severe adverse effects of digoxin (2)

A

excessive depression of AV node conduction (heart block)

propensity to cause arrhythmias

147
Q

what are the extracardiac effects of digoxin

A 
(all involving Na/K ATPase)
nausea
vomiting
diarrhoea
disturbances of colour vision
148
Q

what is Levosimendan

A

inotropic drug and calcium sensitiser

149
Q

what does Levosimendan do

A

Binds to troponin C in cardiac muscle sensitizing it to the action of Ca2+

opens KATP channels in vascular smooth muscle causing vasodilation (reduces afterload and cardiac work)

150
Q

name two inodilator drugs

A

amrinone and milrinone

151
Q

how do inodilators act

A

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

152
Q

what effect to inodilators cause

A

Increase myocardial contractility, decrease peripheral resistance (haemodynamic indices are improved), but worsen survival – perhaps due to increased incidence of arrhythmias

153
Q

what is the use of inodilators limited to

A

IV administration in acute heart failure

154
Q

what are three common types of anti hypertensive drugs

A

Thiazide Diuretics
Beta Blockers
Vasodilators

155
Q

what are 4 types of vasodilator drugs commonly used to treat hypertension

A

Calcium Antagonists

Alpha Blockers

ACE Inhibitors (ACEI)
		Angiotensin Receptor Blockers (ARB)
156
Q

what are 6 types of anti anginal drugs

A 
Beta Blockers
Calcium Antagonists
Nitrates
Nicorandil
Ivabradine
Ranolazine
157
Q

what are the three types of anti thrombotic drugs

A

antiplatelet, anticoagulants, fibrinolytics

158
Q

what do antiplatelet drugs do and name 4

A

prevent platelets from forming; Aspirin, Clopidogrel, Prasugrel, Ticagrelor

159
Q

what do anticoagulant drugs do and name 3

A

attack clotting factors; Warfarin, Rivaroxaban, Dabigatran

160
Q

what do fibrinolytic drugs do and name 2

A

streptokinase, tPA

161
Q

what are two types of anti cholesterol drugs

A

statins, fibrates

162
Q

what do diuretics do

A

block Na reabsorbtion in the kidneys (makes you pee out more sodium)

163
Q

describe thiazide diuretics (strength, use and an example)

A

mild, used in hypertension, Bendrofluazide

164
Q

describe loop diuretics (strength, use and an example)

A

stronger than thiazidem used in heart failure, furosemide

165
Q

what are the side effects of diuretics

A

hypokalaemia (low potassium) = tired, arrhythmias

hyperglycaemia= diabetes

increased uric acid= gout

impotence

166
Q

what beta adrenoceptor do cardioselective B blockers act on

A

B1 receptors

167
Q

what are cardioselective beta blockers use in and give an example of one

A

used in angina, hypertension and heart failure; atenolol

168
Q

what beta adrenoceptor do non selective B blockers act on

A

B1 and B2

169
Q

give and example of a non selective beta blocker and what it is used in

A

propanolol, used less in cardiology, more in thyrotoxicosis (hyperactive thyroid as B2 involved with these symptoms)

170
Q

what are the side effects of a beta blocker

A

never use in asthma= bronchospasm

tiredness

heart failure (can worsen is short term, good in long/medium term)

cold peripheries

171
Q

what are the two types of calcium agonist

A

Dihydropyridines, Rate limiting calcium antagonists

172
Q

describe rate limiting calcium antagonists (use, what to avoid and 2 examples)

A

used in hypertension, angina and supraventricular arrhythmias (AF, SVF), avoid use with beta blockers, Verapamil, Diltiazem

173
Q

describe Dihydropyridines (use, side effects and an example of one)

A

used in hypertension and angina, can cause ankle oedema, amlodipine

174
Q

why do you avoid the use of rate limiting calcium antagonists with a beta blocker

A

as they block AV node in heart and use with beta blocker would suppress conduction in the heart why too much- heart block

175
Q

what do alpha blockers do

A

Block aplha adrenoceptors to cause vasodilatation

176
Q

what are alpha blockers used in

A

hypertension and prostatic hypertrophy

177
Q

give an example of an alpha blocker

A

doxazosin

178
Q

what are the side effects of alpha blockers

A

postural hypotension

179
Q

what do Angiotensin Converting Enzyme Inhibitors do

A

Block angiotensin I becoming angiotensin II

180
Q

what are ACE inhibitors used in

A

hypertensio, heart failure

181
Q

give an example of an ACE inhibitor

A

lisinopril

182
Q

how do ACE inhibitors affect the kidneys

A

most neutral but…

Good for kidneys in diabetic nephropathy

Bad for kidneys in renal artery stenosis

183
Q

what are the side effects of ACE inhibitors

A

cough (irritating and dry), renal dysfunction, Angioneurotic oedema

184
Q

what is Angioneurotic oedema

A

life threatening response, if causes larynx to swell which could obstruct breathing. If patient had this reaction in the past never give ace inhibitor

185
Q

what should you never use ACE inhibitors in and why

A

pregnancy induced hypertension and damages fetus

186
Q

what do angiotensin receptor blockers do

A

block angiotensin II receptors

187
Q

give an example of an angiotensin receptor blocker and their side effects

A

losartan, renal dysfunction

188
Q

how do Angiotensin receptor blockers affect the kidneys

A

Good for kidneys in diabetic nephropathy

Bad for kidneys in renal a stenosis

189
Q

what do all angiotensin blocker drugs name end in

A

artan

190
Q

why would you swap an ACE inhibitor for an Angiotensin Receptor Blocker

A

if patient has dry irritating cough or ankle oedema

191
Q

can you use an Angiotensin Receptor Blockers in pregnancy induced hypertension

A

no

192
Q

what do nitrates do and give an example of one

A

Venodilators

e.g. Isosorbide monoritrate

193
Q

what are nitrates used in

A

angina and acute heart failure

194
Q

what are the side effects of nitrates

A

headache and hypotension/collapse

195
Q

tolerance in nitrates is common how is it avoided

A

have 8 hours a day nitrate free

196
Q

what are antiplatelet agents used in

A

angina acute MI, CVA(cerebralcasvualr accident (stroke))/TIA (transient ischaemic attack), patients at high risk of MI and CVA

197
Q

what are the side effects of antiplatelet agents

A

haemorrhages, peptic ulcer= haemorrhage

aspirin sensitivity= asthma

198
Q

what is a haemorrhage

A

escape of blood from a damaged vessel

199
Q

what do anticoagulants do

A

prevent new thrombosis via blocking factors 2, 7, 9, 10

200
Q

name two examples of anticoagulants and how they are administered

A

heparin IV, warfarin oral

201
Q

when should anticoagulants be used

A

DVT, pulmonary embolism, NSTEMI, atrial fibrillation

202
Q

what is NSTEMI

A

Non-ST-elevation myocardial infarction

203
Q

what are the side effects of anticoagulants

A

haemorrhage anyway

204
Q

what can the effects of warfarin be overcome with

A

Vitamin K

205
Q

what is rivaroxaban

A

factor X a inhibitor

206
Q

what is dabigatran

A

thrombin factor IIa inhibitor (Xa converts Prothrombin (II) to Thrombin (IIa)

207
Q

what is the dose of anticoagulants controlled by

A

INR- international normalised ratio

208
Q

what do fibrinolytic drugs do

A

dissolve formed clot

209
Q

give two examples of fibrinolytic drugs

A

streptokinase, tissue plasminogen activator (tPA)

210
Q

when should fibrinolytic drugs be used

A

STEMI (selected cases only of pulmonary embolism and CVA)

211
Q

what are the side effects of fibrinolytic drugs

A

haemorrhage

212
Q

when should fibrinolytic drugs be avoided

A

recent haemorrhages (some CVAs), trauma, bleeding tendencies, severe diabetic retinopathy, peptic ulcer

213
Q

what are the two types of anticholesterol drugs

A

statins and fibrates

214
Q

give an example of statins

A

simvastatin

215
Q

what does simvastatin do

A

blocks HMG CoA reductase

216
Q

what are statins used in

A 
hypercholesterolaemia
diabetes
Angina/MI
CVA/TIA
High risk of MI and CVA
217
Q

what are the side effects of statins

A

myopathy and Rhabdomyolysis renal failure

218
Q

give an example of fibrates

A

bezafibrate

219
Q

what are fibrates used in

A

hypertriglyceridaemia,

low HDL cholesterol

220
Q

what do the names of all statins end in

A

statin

221
Q

what anti arrhythmic drugs should be used to treat supra ventricular arrhythmias (SVT)

A

use adenosine in acute phase

222
Q

what does adenosine do

A

creates transient blockage in AV node

223
Q

what anti arrhythmic drugs should be used to treat Ventricular/ Supraventricular Arrhythmias

A

Amiodarone
Beta Blockers
Flecainide

224
Q

what is Amiodarone

A

long acting anti arrhythmic drug

225
Q

what are the side effects of anti arrhythmic drugs

A

Phototoxicity
Pulmonary fibrosis
Thyroid abnormalities
(Hypo or Hyper)

226
Q

what are the two effects of digoxin

A

blocks AV conduction, increases ventricular irritability which produces ventricular arrhythmias

227
Q

what should digoxin be used to treat

A

atrial fibrillation

228
Q

why must the administration of digoxin be carefully monitored

A

as has narrow therapeutic window and can result in digoxin toxicity

229
Q

what are the symptoms of digoxin toxicity

A

Nausea, vomiting

Yellow vision
Bradycardia, Heart Block

Ventricular Arrhythmias

230
Q

when do you not use diuretics

A

gout

231
Q

what does CCF stand for

A

conjested cardiac failure

Cardiovascular (34 decks)

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