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CV Drugs > Cardiovascular drugs all > Flashcards

Cardiovascular drugs all Flashcards

1
Q

Lisinopril

A

ACE inhibitor

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2
Q

action of lisinopril

A

blocks ACE preventing the conversion of angiotensin I to angiotensin II. alderstrone is not stimulated and vasodilation occurs

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3
Q

what are ACE Inhibitors used to treat

A 
hypertension (under 55, caucasian) 
heart failure (lengthens prognosis)
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4
Q

side effects of ACE Inhibitors

A

dry cough
renal dysfunction
angioneurmtic oedema
foetal abnormalities if used in pregnancy

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5
Q

losartan

A

ARB- Angiotensin II receptor blocker.

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6
Q

action of ARB’s

A

Angiotensin II is a vasoconstrictor so blocking it leads to vasodilation

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7
Q

Amlodipine

A

non-rating limiting calcium channel blocker

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8
Q

Nifedipine

A

non-rating limiting calcium channel blocker

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9
Q

Verapamil

A

rate limiting calcium channel blocker

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10
Q

Diltiazem

A

rate limiting calcium channel blocker

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11
Q

dihydropridine

A

non-rate limiting Calcium channel blocker

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12
Q

mechanism of calcium channel blockers

A

inhibit L type channels
stops calcium entering the cell
causes relaxation of arteriolar smooth muscle

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13
Q

when are calcium channel blockers used

A

Hypertension (older than 55, not caucasian)
angina (rate limiting)
supra ventricular arrhythmias (rate limiting)

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14
Q

bendrofluazide

A

thiazide diuretic

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15
Q

mechanism of thiazide diuretics

A

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

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16
Q

when are thiazide diuretics used

A

Hypertension

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17
Q

side effects of thiazide diuretics

A

Hypokalaemia
Gout (↑ uric acid)
Hyperglycaemia
Sexual dysfunction

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18
Q

Furosemide

A

loop diuretic

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19
Q

mechanism of loop diuretics

A

Inhibit NaCl reabsorption in the thick ascending loop of Henle

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20
Q

when are loop diuretics used

A

heart failure

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21
Q

side effects of loop diuretics

A

Hypokalaemia

Hypotension

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22
Q

Spironolactone

A

potassium sparing diuretic

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23
Q

mechanism of potassium sparing diuretic

A

Reduce Na+ absorption by antagonising aldosterone

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24
Q

when are potassium sparing diuretics used

A

Ascites/oedema from liver cirrhosis

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25
Q

side effect of potassium sparing diuretic

A

Gynecomastia

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26
Q

Doxazosin

A

alpha blocker

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27
Q

prazosin

A

alpha blocker

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28
Q

mechanism of alpha blockers

A

Block α-adrenoreceptors to cause vasodilation

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29
Q

when are alpha blockers used

A

hypertension

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30
Q

side effect of alpha blockers

A

Postural hypotension

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31
Q

propanolol

A

non selective beta blocker

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32
Q

atenolol

A

B1 selective beta blocker

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33
Q

metoprolol

A

B1 selective beta blocker

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34
Q

bisoprolol

A

B1 selective beta blocker

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35
Q

action of B1 receptor stimulation

A

increased force, rate and AV node conduction speed

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36
Q

action of B2 receptor stimulation

A

relaxation of vasculature and bronchial smooth muscle

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37
Q

mechanism of beta blockers

A

block B1 (B2) receptors which decreases force, rate and AV node stimulation. decreases oxygen consumption heart rate, contractility and MABP

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38
Q

when are beta blockers used

A

arrhythmias
angina
heart failure
hypertension (if comorbidities)

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39
Q

side effects of beta blockers

A 
bronchospasm 
cold peripheries 
worsening of heart failure 
hypoglycaemia 
bradycardia 
fatigue
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40
Q

when should beta blockers not be used

A

Raynaud’s

asthmatic patients

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41
Q

GTN spray

A

Nitrate

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42
Q

Isosorbide mononitrate

A

Nitrate

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43
Q

mechanism of nitrates

A

metabolised to NO which causes efflux of calcium resulting in relaxation of smooth muscle

cGMP is produced which regulation Protein kinase G causing relaxation

endothelin is produced

decreases preload, decreases afterolad, decreases oxygen requirement and increases perfusion to ischameic area

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44
Q

do nitrates causes increase in MABP

A

nitrates cause NO change in MABP due to reflex increase in HR to maintain CO

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45
Q

when are nitrates used

A

angina

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46
Q

side effects of nitrates

A

repeated use = tolerance
hypotension
headache

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47
Q

nicrorandil

A

potassium channel opener

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48
Q

Minoxidil

A

potassium channel openers

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49
Q

mechanism of potassium channel openers

A

causes hyperpolarisation which switched off calcium channels and results in relaxation of vascular smooth muscle and coronary vasodilation

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50
Q

when are potassium channel openers used

A 
stable angina (work when nitrates don't)
last resort in hypertension
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51
Q

side effects of potassium channel openers

A

reflex tachycardia
salt and water retention
Minoxidil- hair growth

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52
Q

mechanism of ivabradine

A

selective blocker of HCN channels. reduced the slope of pacemaker potential. decreases HR and oxygen consumption.

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53
Q

when is Ivabradine used

A

sinus tachycardia
Angina
Mild to moderate chronic heart failure

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54
Q

side effects of ivadradine

A

arrhythmias

hypotension

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55
Q

atropine

A

muscarnic antagonists

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56
Q

mechanism of atropine

A

increases heart rate

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57
Q

when is atropine used

A

severe bradycardia

reverse bradycardia post MI

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58
Q

side effects fo atropine

A

dry mouth

blurred vision

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59
Q

what dose much atropine always be given at

A

greater than 600mg as less than 300mg can transiently lower HR

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60
Q

mechanism of digoxin

A

blocks AV conduction, increases AV delay blocks ATPase.

increases calcium causes increase in force of contraction

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61
Q

when is digoxin used

A

heart failure

atrial fibrillation

62
Q

side effects of digoxin

A

heart block
bradycardia
dysrhythmias

63
Q

what drug should digoxin not be given with

A

diuretics - effects can be dangerously increased by hypoalaemia

64
Q

Levosimendon

A

calcium sensitizer

65
Q

action of levosimendan

A

bind to troponin C in myocytes , sensitising them to calcium

66
Q

when are calicum sensitisers used

A

acute compensated heart failure

67
Q

dobutamine

A

B adrenorecpetor agonists

68
Q

Adrenaline

A

B-adrenoreceptor agonists

69
Q

Noradrenaline

A

B-adrenoreceptor agonists

70
Q

mechanism of B-adrenoreceptor agonists

A

stimulate B-adrenorecpeotrs which activate adenyl cyclase, producing cAMP, PKA is generated which increases contractility force and rate

71
Q

when is dobutamine used

A

acute heart failure

72
Q

when is adrenaline used

A 
anaphylactic shock (IM)
cardiac arrest (IV)
73
Q

flecanide

A

Sodium channel blocker

74
Q

what class are sodium channel blockers

A

class I

75
Q

which drugs are used in rate control

A

B-blockers

calcium channel blockers

76
Q

which drugs are used in rhythm control

A

sodium channel blockers

potassium channel blockers

77
Q

what phase do sodium channel blockers act on

A

phase 0

78
Q

metoprolol

A

B blocker (Class II drugs)

79
Q

what class of drug are beta blockers

A

II

80
Q

what class of drug are potassium channel blockers

A

III

81
Q

what class of drug as calcium channel blockers

A

IV

82
Q

amiodarone

A

potassium channel blocker

83
Q

verapamil

A

calcium channel blocker

84
Q

diltiazem

A

calcium channel blocker

85
Q

mechanism of class III drugs

A

block potassium channels

slow depolarisation and prolong AP and refractory period in cardiac tissue

86
Q

when are potassium channel blockers used

A

VT, VF, wide complex tachycardia
AF and paroxysmal SVT
rhythm control

87
Q

mechanism of class II drugs

A

decrease rate of depolarisation
control SVT
suppress sympathetic drive that may trigger VT

88
Q

what phase do beta blockers act on

A

phase 4

89
Q

mechanism of class IV drugs

A

block L type calcium channels
decrease AV node conduction
shorten plateau
decrease contractility

90
Q

what phase do calcium channel blockers act on

A

phase 2

91
Q

what phase do potassium channel blockers act on

A

3

92
Q

aspirin

A

anti-platelet

93
Q

clopidogrel

A

antiplatlet

94
Q

ticagrelor

A

antiplatlet

95
Q

when are antiplatelets used

A

angina
acute MI
CVA/ TIA

96
Q

side effects of anti platelets

A

haemorrage elsewhere
peptic ulcer leads to haemorrhage
aspirin sensitivity leads to asthma

97
Q

warfarin

A

anticoagulant

98
Q

heparin

A

anticoagulant

99
Q

low molecular weight heparin

A

anticoagulant

100
Q

NOAC’s

A

anticoagulant

101
Q

dabigatran

A

NOAC’s

102
Q

rivaroxaban

A

NOAC’s

103
Q

apixaban

A

NOAC’s

104
Q

mechanism of warfarin

A

blocks clotting factors II, VII, IX, X

vitamin K antagonist preventing formation of mature coagulation factors

105
Q

when is warfarin used

A

DVT, PE, NSTEMI, AF

106
Q

side effects of warfarin

A

haemorrhage

reversed by vitamin K

107
Q

how many days could it take for warfarin to be effective

A

up to 3 days

108
Q

mechanism of heparin

A

blocks clotting factors II, factor Xa

109
Q

mechanism of LMWH

A

blocks Xa

110
Q

when are heparin and LMWH used

A

PE

DVT

111
Q

side effects of heparin and LMWH

A

irreversible haemorrhage

112
Q

mechanism of NOAC’s

A

inhibit thrombin and prevent new clot formation

113
Q

when are NOAC’s used

A

DVT, PE, NSTEMI, AF

114
Q

streptokinase

A

fibrinolytic

115
Q

side effect of NOAC

A

haemorrhage

116
Q

mechanism of fibrinolytics

A

dissolve formed clots

117
Q

when are fibrinolytic used

A

STEMI (more than 90 mins to PCI)
PE
CVA

118
Q

when should fibronlytics be avoided

A

recent haemorrhage trauma

bleeding tendencies

119
Q

simvastatin

A

statin

120
Q

atorvastatin

A

statin

121
Q

mechanism of statins

A

block HGM-CoA reductase
reduction of LDL production in liver
increased clearance of LDL in liver

122
Q

when are statins used

A 
hypercholesterolaemia 
diabetes 
Angina/MI
CVA/TIA
high risk of MA and CVA
123
Q

side effects of statins

A

myopathy

rhabomylosis renal failure

124
Q

when should statins not be prescribed

A

pregnancy

125
Q

bezafibrate

A

fibrate

126
Q

Mechanism of fibrates

A

decrease triglyceride levels

slight reduces LDL and HDL levels

127
Q

when are fibrates used

A

hypertriglyceridemia

low HDL cholesterol

128
Q

what are fibrates advised to use in combo with

A

statins

129
Q

colestyramine

A

bile acid binding resins

130
Q

colestipol

A

bile acid binding resins

131
Q

mechanism of bile acid binding resins

A

cause excretion of bile salts resulting in more cholesterol being converted to bile slats by interrupting enterohepatic recycling

reduces absorption of triglycerides
increases LDL receptor expression

132
Q

when are bile acid binding resins used

A

hypercholesterolaemia

133
Q

side effects of bile acid binding resins

A

GI tract irritation

134
Q

mechanism of Ezetimibe

A

inhibits NPC1L1 transport protein in enterocytes of the duodenum, reducing the absorption of cholesterol. causes a decrease in LDL

135
Q

how must warfarin be delivered

A

orally

136
Q

when is ezetimibe used

A

hypercholesterolamiea

137
Q

side effects of ezetimibe

A

diarrhoea
abdominal pain
headaches

138
Q

mechanism of Ranolazine

A

inhibits late or persistent sodium channels causing an increase in intracellular calcium, reduced tension in heart wall and reduces requirements.

139
Q

when is Ranolazine used

A

angina

140
Q

side effects for Ranolazine

A

dizziness

constipation

141
Q

hypertension drugs

A 
ACE inhibitors 
ARB's
CCB
thiazide Diuretics 
alpha blockers 
beta blockers (not first line)
potassium channel openers (last resort)
142
Q

heart failure drugs

A 
ACE inhibitors 
ARBs 
loop diuretics 
beta blockers 
Ivabradine 
Digoxin 
B-adrenoreceptor agonist (Dobutamine)
calcium sensitisers
143
Q

side effects of antiarrythmic drugs

A

photo toxicity
pulmonary fibrosis
thyroid abnormalities

144
Q

when should anti arrhythmic drugs not be used

A

heart failure

145
Q

angina drugs

A 
CCB
Beta blockers 
Nitrates 
potassium channel openers
ivabradine  
antiplatelets 
statins 
Rabolazine
146
Q

supraventrciular drugs

A

CCB
Beta blockers
potassium channel blockers
calcium channel blockers

147
Q

drugs for ascites

A

potassium sparing diuretic

148
Q

drugs for arrhythmias

A 
beta blockers 
ivabradine (sinus tachycardia)
atropine (severe bradycardia)
sodium, calcium potassium channel blockers 
anti coagulants
digoxin
149
Q

DVT and PE drugs

A

anti-coagulants

150
Q

Drugs used in hypercholesterlaemia

A

statins
bile acid binding resins
Ezetimibe

CV Drugs (1 decks)

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