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Y1 Cardiovascular > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

B1-adrenoceptor couples to the g-protein….

A

Gs

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2
Q

The sympathetic nervous system releases noradrenaline as a __________ _____________ and adrenaline as a ___________ ___________

A

Post-ganglionic transmitter

Adrenomedullary hormone

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3
Q

B1-adrenoceptors are activated in which locations? (2)

A

Nodal cells

Myocardial cells

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4
Q

Activations of b1-adrecopteors NASA positive/negative chronotropic force

A

Positive

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5
Q

Chronotropic is an increase in

A

Rate

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6
Q

Ionotropic is…

A

Force

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7
Q

Increase in heart rate in presence of noradrenaline is due to what?

A

Increase in slope of phase 4 of action potential

Reduction in threshold for AP initiation due to enhanced Ica

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8
Q

Increase in contractility in the presence of noradrenaline is due to?

A

Increased in phase 2 of AP

Sensitisation of contractile proteins to calcium

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9
Q

The duration of systole is ______in the presence of noradrenaline

A

Decreased - this is a positive lusitropic reaction

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10
Q

Noradrenaline causes a ______ in the efficiency of the heart muscle

A

Decrease - heart starts to use oxygen less efficiently

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11
Q

Effect of noradrenaline on the Na-K-ATPase

A

Increases activity which is important for the normal balance of ions across the membrane

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12
Q

Parasympathetic system releases ___ to the cardiac muscle

A

ACh

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13
Q

In the heart, ACh acts on ____ muscarinic cholinoceptors largely in the ______ cells

A

M2

Nodal

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14
Q

The M2 receptor couples to the ____ g-protein

A

Gi

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15
Q

Coupling through Gi decreases the activity of ______ _______ thus reducing _______. The ________ potassium channel is opened causing a hyperpolarisation mediated by _________

A

Adenylate cyclase, cAMP.

GIRK, G-by subunits

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16
Q

Parasympathetic action of the cardiac muscle is…. (3)

A

Decreased chronotropic effect
Slight decrease in contractility
Decreased conduction in AV node

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17
Q

Why does the parasympathetic stimulation of the heart have little/no effect on ventricular contractility?

A

There is no parasympathetic stimulation on the ventricles

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18
Q

Parasympathetic stimulation of the heart may cause ….

A

Arrhythmias to occur in the atria

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19
Q

Vagal manoeuvres can can be used to…

A

Suppress atrial tachycardia

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20
Q

The funny current is mediated by channels that are activated by….(2)

A

hyperpolarisation and cAMP

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21
Q

other name for funny current channels

A

HCN

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22
Q

Blocking HCN channels causes what?

A

decrease of slope of pacemaker potential and reduces HR

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23
Q

Drug used to block HCN channels

A

Ivabradine

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24
Q

Ivabradine

A

Selectively blocks HCN Channels - slows HR in angina and reduces cardiac O2 consumption

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25
Q

cAMP is converted to 5’AMP by …

A

PDE - phosphodiesterase

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26
Q

Inhibition of PDE has a positive/negative inotropic

A

positive

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27
Q

Drug which inhibit PDE in acute heart failure

A

milrinone

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28
Q

Catecholamines that act as b-adrenoceptor agonists (3)

A

dobutamine, adrenaline, noradrenaline

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29
Q

Actions of b-adrenoceptor agonists

A

increase rate, force and CO and O2 consumption

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30
Q

Medical situations for use of adrenaline

A

Cardiac arrest; anaphylactic shock

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31
Q

Dobutamine is used in what medical situation?

A

acute but potentially reversible Heart Failure

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32
Q

Adrenaline is administered…

A

IC, IM, SC or IV infusion

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33
Q

Dobutamine is administered…

A

as an IV infusion

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34
Q

Advantage of dobutamine

A

causes less tachycardia than other b1 agonists

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35
Q

Examples of b-adrenoceptor antagonists

A

Propanolol, atenolol, bisoprolol, metoprolol

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36
Q

non-selective and partial agonist b-adrenoceptor drug

A

alprenolol

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37
Q

Effects of b-blockers at rest

A

little effect

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38
Q

Effect of b-blockers during exercise

A

cardiac stress, rate, force, CO are significantly reduced

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39
Q

Disadvantage of b-blockers during exercise

A

can reduce maximal exercise tolerance

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40
Q

Use of b-blockers in medical situations (4)

A

Disturbance of cardiac rhythm; treatment of angina; treatment of HF; treatment of HBP

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41
Q

How do b-blockers act in A-fib and SVT

A

delay conduction through the AV node

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42
Q

Use of b-blockers in angina

A

Alternative to calcium entry blockers

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43
Q

Treatment of HF with b-blockers

A

must be low-dose to prevent cardiac death

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44
Q

Another suggested drug in HF

A

carvedilol

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45
Q

Carvedilol is…

A

a1 - antagonist, b-blocker

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46
Q

Adverse effects of b-blockers (6)

A

Bronchospasm; Aggravation of HF; Bradycardia/Heart Block; Hypoglycaemia; Fatigue; Cold extremities

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47
Q

What is atropine?

A

Non-selective muscarinic ACh receptor antagonist

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48
Q

When is atropine used first line?

A

In severe or symptomatic bradycardia, particularly following MI. Also used in anticholinesterase poisoning

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49
Q

What type of drug is digoxin?

A

cardiac glycoside

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50
Q

What does digoxin bind?

A

a-subunit of Na-K ATPase

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51
Q

What is the end effect of digoxin binding the Na-K ATPase?

A

Increases the Calcium in the cell and thus the calcium uptake into the sarcoplasmic reticulum and increase CICR

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52
Q

Where should digoxin be used with caution?

A

In those with hypokalaemia or on diuretics

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53
Q

Half life of digoxin

A

40 hours

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54
Q

Digoxin is a chronotropic agent - True or False?

A

False - it is an inotropic agent - it increases contractility by increasing calcium available for CICR

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55
Q

Direct effects of digoxin on the heart (2)

A

shortens the AP and refractory period.

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56
Q

Indirect effects of digoxin on the heart

A
  • increased vagal activity
  • slows SAN discharge
  • increased refractory period
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57
Q

Adverse effects of digoxin on the heart? (2)

A

excessive depression of AV node conduction - heart block

Propensity to cause arrhythmias

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58
Q

Non-cardiac adverse effects of digoxin (4)

A

nausea
vomiting
diarrhoea
disturbance of colour vision

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59
Q

Calcium sensitiser

A

Levosimendan

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60
Q

Mechanism of action of levosimendan

A

binds to troponin C and increases sensitivity to calcium

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61
Q

where is levosimendan used?

A

in acute decompensated heart failure

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62
Q

Amrinone and Milrinone act to…

A

inhibit PDE in cardiac and smooth muscle cells and hence increase cAMP

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63
Q

Why is it suspected that amrinone and milrinone decrease survival?

A

Increase arrhythmias

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64
Q

Where are amrinone and milrinone used?

A

limited to acute heart failure

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65
Q

Which molecule is important in the activation of PKG to cause VSM relaxation?

A

cGMP

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66
Q

___ stimulates the production of cGMP

A

Nitric Oxide - NO

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67
Q

Substances that activate the production of NO (3)

A

bradykinin, ADP, 5-HT

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68
Q

3 effects of organic nitrates

A

Venorelaxation; arteriolar dilation; increased coronary blood flow

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69
Q

When are organic nitrates used?

A

in stable angina and ACS

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70
Q

Benefits in angina from using GTNs (3)

A

decreased preload, decreased afterload and improved perfusion

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71
Q

common organic nitrates used

A

GTN

isosorbide mononitrate

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72
Q

longer acting organic nitrate

A

isosorbide mononitrate

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73
Q

GTN sprays do not undergo first pass metabolism - true or false?

A

false - they undergo first pass metabolism, ISMN does not undergo first pass metabolism

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74
Q

Drug used orally for prophylaxis of angina

A

ISMN

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75
Q

Adverse effects of organic nitrates

A

postural hypotension;

headaches; formation of methaemoglobin; tolerance

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76
Q

Molecules that stimulate endothelin production

A

Adrenaline
AngII
ADH

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77
Q

situations where renin is released (3)

A

decreased renal perfusion pressure; increased renal sympathetic activity; decreased glomerular filtration

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78
Q

where is angiotensinogen produced?

A

liver

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79
Q

The AT1 receptor causes smooth muscle relaxation - true or false

A

false - it causes smooth muscle contraction

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80
Q

the RAAS overall contributes to a(n) _______ in MABP and blood volume

A

increase

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81
Q

Where does aldosterone originate?

A

the zona glomerulosa of the adrenal cortex

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82
Q

Aldosterone causes the tubular _______ of Na

A

reabsorption

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83
Q

Aldosterona production leads to a(n) _______ in blood volume and MABP

A

increase

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84
Q

Example of an ACE inhibitor

A

lisonopril

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85
Q

ACE converts AngI to AngII - true or false

A

true

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86
Q

example of an AT1 receptor blocker

A

losartan

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87
Q

ACE acts to … (2)

A

inactivate bradykinin

convert AngI to AngII

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88
Q

ACE inhibitors have an effect on cardiac contractility - true or false?

A

false - the mechanism of action means that ACEIs will cause venodilation and vasodilation - this reduces the strain on the heart but does not affect the heart contractility

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89
Q

Where is the greatest effects of ACEIs?

A

Brain, kidneys, heart

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90
Q

Main adverse effects of ACEIs

A

hypotension

dry cough

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91
Q

ARBs are useful in patients who…

A

find the ACEIs dry cough intolerable

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92
Q

ACEIs and ARBS are contraindicated in which two groups?

A

Pregnancy

Bilateral renal artery stenosis

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93
Q

3 clinical uses of ACEIs and ARBs

A

Hypertension
Cardiac Failure
Following MI

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94
Q

a1-adrenoceptors act to…

A

constrict vascular smooth muscle

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95
Q

b1-adrenoceptors act to…

A

increased cardiac rate, force and AV node conduction velocity

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96
Q

b2-adrenoceptors act to…

A

relaxes bronchial and vascular smooth muscle

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97
Q

b1- adrenoceptor antagonists can be used in the treatment of (3)

A

Angina pectors; hypertension; heart failure

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98
Q

action of b-blockers in angina pectoris?

A

decreases O2 requirements; counter-elevated sympathetic activity; increase the amount of time spent in diastole

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99
Q

Action of b-blockers in hypertension?

A

reduce CO; reduce renin release from kidney; a CNS action that reduces sympathetic outflow

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100
Q

Arrhythmias can be formed from defects in which two ways?

A

defects in impulse conduction or impulse formation

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101
Q

Types of defects in impulse formation (2)

A

Altered Automaticity

Triggered Activity

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102
Q

Pathological reasons for altered automaticity

A

SAN firing frequency is pathologically low (escape beats); latent pacemaker fires faster than the SAN (ectopic beats)

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103
Q

Causes of ectopic rhythms

A

ischaemia, hypokalaemia, increased sympathetic activity

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104
Q

Triggered Activity can be either of…?

A

EAD

DAD

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105
Q

Where do EADs come from?

A 
Phase 2 (Ca) and Phase 3 (Na);
associated with prolonged AP and drugs prolonging the QT interval
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106
Q

Where do DADs appear?

A

after complete repolarisation

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107
Q

Where do EADs appear?

A

during the inciting AP

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108
Q

What is DAD associated with?

A

Ca overload provoked by catecholamines, digoxin, heart failure

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109
Q

What are the 3 defects in impulse conduction?

A

Re-entry; conduction block; Accessory tract pathways

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110
Q

What are re-entry arrhythmias?

A

self-sustaining electrical circuit where action potentials can create a self-sustaining loop

111
Q

Types of partial block?

A

Mobitz type I

Mobitz type II

112
Q

Mobitz type I conduction block

A

PR interval gradually increases from cycle to cycle until a beat is missed

113
Q

Mobitz type II conduction block

A

PR interval is constant but every n-th beat is mossed

114
Q

Complete block is…

A

when the atria and ventricles beat independently

115
Q

Example accessory tract

A

Bundle of Kent

116
Q

What do accessory tracts predispose patients to?

A

tachyarrhythmias

117
Q

Class I agents are what?

A

Sodium channel blockers

118
Q

Class II agents are what?

A

b-adrenoceptor antagonists

119
Q

Class III act on?

A

Voltage gated K+ channels

120
Q

Class IV agents act on?

A

Calcium channel

121
Q

How do Class I agents work?

A

they act on the SAN in a use dependent manner; there are varying degrees of block from short acting to long acting

122
Q

Action of adenosine?

A

activates A1-adenosine receptors coupled to Gi/o - opens ACh sensitive K channels

123
Q

When is Adenosine used?

A

to terminate paroxysmal SVT - atrial firing of 140-250bpm

124
Q

Action of Digoxin?

A

stimulates vagal activity; slows conduction and prolongs refractory period in AV node

125
Q

What is digoxin used to treat?

A

used to treat AF

126
Q

What is the action of Verapamil?

A

type IV agents - blocks LTCC; slows conduction and prolongs refractory period in AV node and bundle of His

127
Q

When is verapamil used to treat?

A

Atrial flutter, AF

128
Q

Two types of diuretics

A

Loop and thiazide

129
Q

Action of thiazide diuretics

A

block the reabsorption of sodium and chlorine in the distal convoluted tubule

130
Q

Action of loop diuretics

A

block the Na-K-Cl symporter in the ascending loop of henle

131
Q

Potential side effect with Loop diuretics?

A

hypokaleamia

132
Q

Because of the side effects of loop diuretics, which drug should they be used with caution with?

A

Digoxin

133
Q

Diuretics are used in which conditions?

A

hypertension and heart failure

134
Q

Example of a thiazide diuretic

A

Bendrofluazide

135
Q

Example of a loop diuretic

A

Furosemide

136
Q

General side effects of diuretics

A

hypokalaemia, tiredness, arrhythmias, hyperglycaemia in diabetics, gout, impotence

137
Q

Where are cardioselective beta-blockers used?

A

angina, hypertension, heart failure

138
Q

Effect of b-blockers on the heart?

A

increased rate, contractility and decreased O2 efficiency

139
Q

Example of cardioselective b-blockers

A

atenolol, metoprolol, bisoprolol

140
Q

Side effects of b-blockers in general

A

tired, bronchospasm, heart failure, cold peripheries,

141
Q

Two main groups of calcium antagonists

A

dihydropyridines; rate limiting calcium antagonists

142
Q

Action of dihydropyridine CCBs?

A

L-type CC blockers which are more vascular in their action

143
Q

Where are dihydropyridines preferentially used?

A

in hypertension and angina

144
Q

Side effect of dihydropyridines?

A

innocent ankle oedema

145
Q

Example of dihydropyridine CCB

A

amlodipine

146
Q

Where are rate limiting CCBs used?

A

angina, hypertension and supraventricular arrhythmias

147
Q

Where are rate limiting CCBs more selective for?

A

myocardium

148
Q

Why should rate limiting CCBs be avoided with b-blockers?

A

they cause a degree of heart block which would cause bradycardia when combined

149
Q

Examples of rate limiting CCBs?

A

verapamil, diltiazem

150
Q

a-adrenoceptor antagonists cause what?

A

vasodilation

151
Q

Example of an a-adrenoceptor antagonist

A

doxazosin

152
Q

Action of ACE inhibitors

A

blocks conversion of Ang I to Ang II thus preventing vasoconstriction

153
Q

Indications for the use of ACEIs

A

hypertension, heart failure, diabetic nephropathy (hypertension)

154
Q

Contraindications for ACEIs

A

renal artery stenosis

155
Q

Examples of ACEIs

A

lisinopril, Ramipril

156
Q

Side effects of ACEIs

A

cough, renal dysfunction, angioedema

157
Q

Why should ACEIs never be used in pregnancy?

A

causes foetal kidney abnormalities

158
Q

Alternative to ACEIs if they are not tolerated?

A

Angiotensin receptor blockers

159
Q

Example of ARB

A

Losartan

160
Q

Action of nitrates?

A

venodilators and nitric oxide donors

161
Q

When are nitrates used?

A

in angina, acute HF and MI

162
Q

Main side effects of nitrates?

A

headache and hypotension, tolerance is also an issue

163
Q

Examples of nitrates?

A

Isosorbide mononitrate, glyceryl trinitrate

164
Q

Action of anti-platelets?

A

prevent new thrombosis

165
Q

Indications for use of anti-platelets?

A

angina, MI, cerebrovascular attacks, TIA

166
Q

Examples of anti-platelets

A

aspirin, clopidegrel, ticagrlor, prasugrel

167
Q

Main side-effects of anti-platelets

A

haemorrhage, peptic ulcer haemorrhage, aspirin sensitivity in asthma

168
Q

Actions of anti-coagulants

A

prevent new thrombosis

169
Q

Examples of anticoagulants

A

heparin (IV only); Warfarin (oral only); Rivaroxaban; Dabigatran

170
Q

Warfarin blocks which clotting factors?

A

2,5,7,9,10

171
Q

When is warfarin used?

A

DVT, PE, NSTEMI, AF

172
Q

Risks of using warfarin?

A

haemorrhage - needs careful INR monitoring

173
Q

How can warfarin be reversed?

A

Vitamin K

174
Q

Action of rivaroxaban?

A

inhibits factor X

175
Q

Action of dabigatran?

A

thrombin factor IIa inhibitor

176
Q

Action of fibrinolytics

A

dissolve formed clots but not liked due to risk of haemorrhage

177
Q

Where are fibrinolytics used?

A

STEMI, PE and CVA in selected cases

178
Q

Examples of fibrinolytics

A

Streptokinase, tissue plasminogen activator

179
Q

Anti-cholesterol agents?

A

Statins

Fibrates

180
Q

Action of statins

A

block HMG CoA reductase

181
Q

Where are statins used?

A

hypercholesterolaemia, diabetes, angina, MI, CVA, TIA, high risk of MI or CVA

182
Q

Example of statin

A

simvastatin

183
Q

Side effects of statins?

A

muscle pain, myopathy, rhabdomyolysis

184
Q

Indications for fibrates?

A

hypertriglyceridaemia, low HDL

185
Q

Example of a fibrate

A

benzofibrate

186
Q

Drug used in supraventricular arrhythmias

A

adenosine

187
Q

Drugs used in SV arrhythmias and ventricular arrhythmias

A

amiodarone, beta-blockers, flecainide

188
Q

side effects of amiodarone

A

phototoxicity, pulmonary fibrosis, thyroid abnormalities

189
Q

Two actions of digoxin

A

blocks AV node conduction, increases ventricular irritability

190
Q

What is digoxin useful for treating?

A

atrial fibrillation

191
Q

Side effects of digoxin?

A

nausea, vomiting, yellow vision, bradycardia, heart block, ventricular arrhythmias

192
Q

vascular wall damage exposes (2)

A

collagen and tissue factor

193
Q

primary haemostasis causes what 3 things?

A

local vasoconstriction, platelet adhesion and acitvation, stabilised soft plug

194
Q

Fibrinogen is converted to fibrin by?

A

thrombin

195
Q

activated platelets secrete thromboxane A2 mediated by which enzyme?

A

COX 1

196
Q

Exposed collagen binds the platelet __ ______ _____ to which glycoprotein __ receptors also bind

A

von willibrand factor, Ib

197
Q

Fibrinogen is converted to fibrin by?

A

thrombin

198
Q

vascular wall damage exposes (2)

A

collagen and tissue factor

199
Q

activated platelets secrete ___ which is mediated by the COX 1 enzyme

A

thromboxane A2

200
Q

Exposed collagen binds the platelet __ ______ _____ to which glycoprotein __ receptors also bind

A

von willibrand factor, Ib

201
Q

thrombin is also known as factor__

A

II

202
Q

cells bearing tissue factor are exposed to factor ___ from the plasma to form a complex ____

A

VIIa, VIIa:TF

203
Q

The TF:VIIa complex activates factor __

A

X

204
Q

Factor X works with factor _ to activate prothrombin to thrombin (factor II)

A

factor V, implicated in factor V leiden thrombophilia

205
Q

Factor II activates further platelets and causes the release of ______ _ from platelet granules

A

factor V

206
Q

Factor II liberates factor ___ from von willebrand factor

A

factor VIII - normally bound to vWF

207
Q

Factor XI or TF:VII activate factor

A

IX

208
Q

factor IX forms a complex with factor ___ which powerfully activates factor II

A

VIII

209
Q

Factor VIII activated by thrombin cross-links the fibrin polymer to…

A

form a fibrin fibre network and a solid clot

210
Q

What is a thrombosis?

A

a haematological plug in the absence of bleeding

211
Q

Chances of thrombosis are increased in…

A

virchows triad

212
Q

Virchows triad consists of?

A

injury to vessel wall (atheromatous plaque rupture), abnormal blood flow, increased coagulability of the blood

213
Q

An arterial thrombus is also known as a (white/red) thrombus

A

white

214
Q

Why is an arterial thrombus white?

A

many platelets in a fibrin mesh

215
Q

Where is an arterial embolus likely to travel?

A

artery of brain or other organs depending on site of origin

216
Q

A venous thrombus is also known as a (white/red) thrombus

A

red

217
Q

Where is a venous embolus likely to travel?

A

the lung (PE)

218
Q

How are arterial thrombi usually treated?

A

anti-platelets

219
Q

How are venous thrombi usually treated?

A

anti-coagulants

220
Q

anti-platelets are used to treat which type of thrombus?

A

arterial

221
Q

anti-coagulants are used to treat which type of thrombus?

A

venous

222
Q

A venous thrombus is also known as a (white/red) thrombus

A

Red

223
Q

An arterial thrombus is also known as a (white/red) thrombus

A

white

224
Q

A venous thrombus is rich in…

A

fibrin

225
Q

Warfarin blocks the modification of which 2 factors?

A

X and II

226
Q

Rivaroxaban inhibits which factor within prothrombinase

A

Xa

227
Q

prothrombinase is made up of which two factors

A

Xa/Va

228
Q

Heparin, LMWH and fondaparinux inactivate factor Xa via…

A

antithrombin III

229
Q

antithrombin III inactivates…

A

factor Xa

230
Q

Heparin inactivates factor __a via….

A

IIa via antithrombin III

231
Q

Dabigatran directly inhibits

A

IIa

232
Q

Heparin inactivates factor __a via….

A

IIa via antithrombin III

233
Q

Heparin, LMWH and fondaparinux inactivate factor Xa via…

A

antithrombin III

234
Q

prothrombinase is made up of which two factors

A

Xa/Va

235
Q

antithrombin III inactivates…

A

factor Xa

236
Q

Rivaroxaban inhibits which factor within prothrombinase

A

Factor Xa

237
Q

factors dependent on vitamin K

A

II, VII, IX and X

238
Q

warfarin blocks what enzyme essential in recycling vitamin K

A

vitamin K reductase

239
Q

II, VII, IX and X are all factors dependent on…

A

vitamin K

240
Q

vitamin K reductase is inhibited by

A

warfarin

241
Q

anticoagulants can be used to prevent and treat:

A

DVT, post-operative thrombosis, in artificial heart valves, atrial fibrillation

242
Q

Warfarin is an…

A

anti-coagulant

243
Q

The effects of warfarin should be monitored using…

A

the international normalised ration - prothrombin time

244
Q

plasma half-life of warfarin

A

40 hours

245
Q

Factors potentiating the effects of warfarin

A

Liver disease, high metabolic rate, drug interactions (inhibition of platelets)

246
Q

Factors lessing warfarin action

A

pregnancy, hypothyroidism, vitamin K consumption, drug interactions

247
Q

To inhibit factor IIa, heparin needs to bind?

A

Antithrombin III and IIa

248
Q

to inhibit factor Xa, heparin needs to bind?

A

just antithrombin III

249
Q

Examples of LMWHs

A

Exoaparin, Dalteparin

250
Q

LMWHs are administered…

A

subcutaneously

251
Q

fondaparinux is…

A

chemically related to the LMWHs

252
Q

Advantage of elimination of LMWHs

A

first order rather than zero order

253
Q

Heparin is preferred over LMWHs in which situation?

A

renal failure

254
Q

Adverse effects of Heparin and LMWHs

A

Haemorrhage, osteoporosis, hypoaldosteronism, hypersensitivity reactions

255
Q

dabigatran, and rivaroxaban are administered

A

orally

256
Q

Advantages to dabigatran and rivaroxaban are?

A

they have a predictable level of anti-coagulation and a convenient administration route

257
Q

Clopidogrel blocks ADP P2Y receptor irreversibly

A

Clopidogrel blocks ADP P2Y receptor irreversibly

258
Q

Clopidogrel blocks _____receptor irreversibly

A

Clopidogrel blocks ADP P2Y receptor irreversibly

259
Q

Aspirin blocks _____ irreversibly

A

COX -1

260
Q

Tirofiban blocks GPIIb/IIa receptor whose expression is increased by ADP and TXA2

A

Tirofiban blocks GPIIb/IIa receptor whose expression is increased by ADP and TXA2

261
Q

Tirofiban is given IV in short term treatment to prevent MI in high risk patients with unstable angina

A

Tirofiban is given IV in short term treatment to prevent MI in high risk patients with unstable angina

262
Q

Anti-platelet drugs are used in what type of thrombus

A

arterial

263
Q

Examples of the main anti-platelets

A

aspirin, clopidogrel, tirogiban

264
Q

Clopidogrel is given when…

A

patients are intolerant to aspirin

265
Q

Fibrinolytics are used…

A

to reopen occluded arteries in MI or stroke

266
Q

Examples of fibrinolytics

A

Streptokinase, alteplase, duteplase

267
Q

Fibrinolytics act to activate…

A

plasminogen

268
Q

Streptokinase is not…

A

an enzyme

269
Q

Streptokinase shouldnt be given in patients with a recent

A

streptococcal infection

270
Q

Ateplase and Duteplase are…

A

recombinant tissue plasminogen tissue activator

271
Q

Alteplase and duteplase advantages…

A

less allergic reactions, more selective for clots

272
Q

haemorrhage due to fibrinolytics can be controlled by…

A

oral tranexamic acid

273
Q

tranexamic acid inhibits

A

plasminogen activation

Y1 Cardiovascular (12 decks)

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