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Cardiovascular > PHARMACOLOGY > Flashcards

PHARMACOLOGY Flashcards

1
Q

mechanism of ivabradine

A

selective blocker of HCN channels

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2
Q

effect of ivabradine on the pacemaker potential

A

reduces the slope

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3
Q

ivabradine effect

A

slows HR

reduces oxygen consumption

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4
Q

ivabradine uses

A

angina
tachycardia
mild to moderate chronic heart failure

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5
Q

side effects of ivabradine

A

arrhythmias

hypotension

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6
Q

name B-adrenoreceptor agonists

A

dobutamine
adrenaline
noradrenaline

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7
Q

which channels is dobutamine selective for?

A

B1

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8
Q

mechanisms of B-adrenoreceptor agonists

A

results in stimulation of adenylyl cyclase and production of cAMP which generates protein kinase A
phosphorylation increases Ca++ influx and release of Ca++ from the SR

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9
Q

effect of B-adrenoreceptor agonists

A

increase contractility, force and rate

decrease cardiac efficiency

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10
Q

use of B-adrenoreceptor ligands

A 
infarction
cardiogenic shock 
cardiomyopathies 
inotropic support 
heart failure (dobutamine) 
asthma emergency (adrenaline)
anaphylactic shock
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11
Q

side effects of B-adrenoreceptor agonists

A

arrhythmias

acute MI

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12
Q

name B blockers

A

propranolol
metoprolol
atenolol

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13
Q

which of the B blockers is non selective?

A

propranolol

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14
Q

which of the B blockers are selective for B1?

A

metoprolol

atenolol

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15
Q

effect of B blockers

A

decrease in heart rate, contractility, MAP and O2 consumption

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16
Q

use of B blockers

A

angina
hypertension
heart failure

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17
Q

side effects of B blockers

A 
asthma 
fatigue 
cold peripheries 
heart failure 
bradycardia (heart block) 
hypoglycaemia
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18
Q

which patients could have heart failure as a side effect of beta blockers?

A

in patients who rely on sympathetic drive to maintain CO

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19
Q

name the muscarinic antagonist which is non selective for M2 receptors

A

atropine

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20
Q

effect of atropine (muscarinic antagonist)

A

increase in heart rate

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21
Q

use of atropine (muscarinic antagonist)

A

reverse bradycardia following an MI

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22
Q

side effects of atropine

A

arrhythmias
hallucinations
confusion

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23
Q

name the cardiac glycoside

A

digoxin

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24
Q

mechanism of action of digoxin

A

competes with K+ and at alpha subunit blocks the Na/K ATPase pump

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25
Q

effect of digoxin

A

increase in contractility, force and CO
indirect- increased vagal discharge and slows SA node discharge
shortens action potential and refractory period

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26
Q

when are the effects of digoxin dangerously enhanced?

A

hypokalaemia

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27
Q

use of digoxin

A

heart failure

atrial fibrillation

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28
Q

side effects of digoxin

A

heart block
dysrhythmias
myocarditis

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29
Q

name the calcium sensitiser

A

levosimendan

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30
Q

mechanism of levosimendan

A

binds to troponin C in myocytes, sensitising them to Ca2+

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31
Q

effect of levosimendan

A

increase in contractility

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32
Q

use of levosimendan

A

acutely decompensated congestive heart failure

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33
Q

side effects of levosimendan

A

headaches
arrhythmias
hypokalaemia

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34
Q

class I anti arrhythmic drug

A 
A = disopyramide 
B = lignocaine 
C = flecainide
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35
Q

mechanism of class I

A

voltage activated Na+ channels

reduces Na+ channel current

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36
Q

use of class I

A

rhythm control

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37
Q

side effects of class I

A

negative inotropic effects

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38
Q

class II anti arhythmic drug

A

B-blockers eg propranolol

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39
Q

use of class II

A

rate control

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40
Q

class III anti arhythmic drug

A

amiodaron sotalol

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41
Q

mechanism of amiodaron sotalol

A

voltage activated K+ channels

action potential prolongation

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42
Q

use of amiodaron sotalol

A

rhythm control

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43
Q

class IV anti arrhythmic drug

A

Ca2+ channel antagonist eg verapamil

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44
Q

use of class IV

A

rate control

45
Q

name nitrates

A

isosobide mononitrate

GTN spray

46
Q

mechanism of nitrates

A 
mimic the effect of endothelium 
produce nitric oxide 
NO causes efflux of Ca++ producing hyperpolarisation and relaxation 
cGMP is also produced which regulates protein kinase G activity causing relaxation 
endothelin is also produced 
venorelaxation
arteriolar dilatation 
increase in coronary blood flow
47
Q

name ACE inhibitors

A

prills eg ramipril

48
Q

mechanism of ACE inhibitors

A

block the conversion of angiotensin I to angiotensin II so aldosterone and ADH are not stimulated

49
Q

effect of ACE inhibitors

A

vasodilation and arterial dilation

50
Q

use of ACEis

A

hypertension

heart failure

51
Q

side effects of ACEis

A

renal dysfunction
oedema
dry cough

52
Q

when are ACEi and ARBs contraindicated?

A

pregnancy

53
Q

name the ARBs

A

tans eg losartan

54
Q

mechanism of ARBs

A

blocks angiotensin II receptors

55
Q

use of ARBs

A

hypertension
heart failure
intolerance of dry cough of ACEi

56
Q

side effects of ARBs

A

renal dysfunction

oedema

57
Q

name calcium antagonists

A

amlodipine
verapamil
diltiazem

58
Q

mechanism of calcium antagonists

A

decrease conduction at SA and AV node

59
Q

effect of calcium antagonists

A

decrease in heart rate

60
Q

use of calcium antagonists

A

hypertension
angina
supraventricular arrhythmias

61
Q

side effects of calcium antagonists

A

ankle oedema

bradycardia (caution when using beta blockers)

62
Q

name the main alpha blocker

A

doxazosin

63
Q

mechanism of alpha blockers

A

block alpha adrenoreceptors to cause vasodilation

64
Q

use of alpha blockers

A

hypertension

prostatic hypertrophy

65
Q

side effect of alpha blockers

A

postural hypertension

66
Q

name potassium channel openers

A

DILS
minoxidil
nicroandil

67
Q

mechanism of potassium channel openers

A

causes hyper polarisation which switches off calcium channels
mediated by ATP

68
Q

effect of potassium channel openers

A

relaxation of vascular smooth muscle

69
Q

use of potassium channel openers

A

severe hypertension

angina

70
Q

side effects of potassium channel openers

A

tachycardia

salt and water retention

71
Q

name a thiazide diuretic

A

bendrofluazide

72
Q

name a loop diuretic

A

furosemide

73
Q

mechanism of thiazide diuretics

A

inhibit NaCl reabsorption in distal tubules by blocking NaCl co-transporter

74
Q

mechanism of loop diuretics

A

inhibit NaCl reabsorption in the thick ascending limb of the loop of henle

75
Q

use of diuretics

A

hypertension

heart failure

76
Q

effect of diuretics

A

increase in excretion of Na, Cl and water

77
Q

side effects of diuretics

A 
hypokalaemia
arrhythmias 
fatigue 
hyperglycaemia 
increase in uric acid = gout
78
Q

name statins

A

simvastatin

atorvastatin

79
Q

mechanism of statins

A

blocks HMG coA reductase which inhibits the formation of cholesterol

80
Q

effect of statins

A

decrease in LDL and total cholesterol inflammation

stabilised atherosclerotic plaque and decreases thrombosis

81
Q

use of statins

A

hypercholesterolemia

82
Q

side effects of statins

A

used in caution with hypothyroidism and history of liver disease
myalgia, myopathy, myositis

83
Q

name fibrates

A

bezafibrate

gemfibrozil

84
Q

mechanism of action of fibrates

A

agonist of nuclear receptors which enhances transcription of lipoprotein lipase which hydrolyses triglycerides to fatty acids and glycerol

85
Q

use of fibrates

A

high triglyceride levels

86
Q

side effect of fibrates

A

myositis

87
Q

name bile acid binding resins

A

colestyramine
colestipol
colsevelam

88
Q

mechanism of bile acid binding resins

A

cause the excretion of bile salts resulting in more cholesterol to be converted to bile salts
bile resins bind bile in the intestine so it is not absorbed in the duodenum
liver uses metabolises cholesterol to compensate for its lost

89
Q

use of bile acid binding resins

A

decreased absorption of triglycerides

increased LDL receptor expression

90
Q

side effect of bile acid binding resins

A

GI tract irritation

91
Q

mechanism of action of ezetimibe

A

inhibits transport proteins and reduces absorption of cholesterol

92
Q

use of ezetimibe

A

to lower LDL cholesterol

93
Q

side effects of ezetimibe

A

diarrhoea
abdominal pain
headache

94
Q

when is ezetimibe contraindicated?

A

in breast feeding

95
Q

name anticoagulants

A

warfarin
heparin
LMWH
orally active inhibitors

96
Q

mechanism of action of warfarin

A

acts as a vitamin K antagonist which prevents production of mature coagulation factors

97
Q

use of anticoagulants

A

DVT
PE
NSTEMI
AF

98
Q

side effect of warfarin

A

haemorrhage anywhere

reversed by vitamin K

99
Q

mechanism of action of anticoagulants (except warfarin)

A

binds to antithrombin III, increasing its affinity for serine proteases to greatly increase their rate of inactivation

100
Q

side effects of anticoagulants

A

haemorrhage
osteoporosis
hypoaldosteronism
hypersensitivity reactions

101
Q

name anti platelets

A

aspirin

clopidogrel

102
Q

mechanism of action of anti platelets

A

prevent new thrombosis
blocks COX, inhibiting formation of TXA2 which causes cross linking of platelets
blocks ADP from binding to P2Y12 receptor and formation of fibrin

103
Q

use of anti platelets

A

angina
acute MI
cerebral vascular incident (CVA) and TIA
patients at risk of above

104
Q

side effects of anti platelets

A

haemorrhage
peptic ulcer
aspirin sensitivity -> asthma

105
Q

name fibrinolytic drugs

A

streptokinase
tissue plasminogen activator
alteplase duteplase

106
Q

mechanism of fibrinolytic drugs

A

fibrinolytic cascade opposes coagulation cascade

activate formation of plasmin from plasminogen which lysis fibrin into fibrin fragments causing lysis of the clot

107
Q

use of fibrinolytics

A

STEMI
PE
stroke
reopen acclude arteries

108
Q

side effect of fibrinolytics

A

haemorrhage risk (controlled by tranexamic acid which inhibits plasminogen activation)

Cardiovascular (31 decks)

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