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year 1 > CARDIO DRUGS > Flashcards

CARDIO DRUGS Flashcards

1
Q

what effect do nitrates have

A

venorelaxation - reduced preload
arteriolar relaxation - reduced afterload
increased coronary blood flow - dilates collateral vessels redirecting blood towards ischaemic areas

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2
Q

what is the pharmacology of nitrates

A

interact with SH groups in smooth muscle cells to liberate NO
NO activated guanylate cyclase causing increased cAMP which activates protein kinase G —> relaxation

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3
Q

what are 3 side effects of nitrates

A

postural hypotension/collapse
headaches
tolerance - 8hr free day

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4
Q

what is GTN used for

A

angina ST

+ aspirin in ACS prophylactically

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5
Q

how is GTN administered

A

sublingual spray or tablet

transdermal patch

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6
Q

what is isosorbide mononitrate used for

A

angina for sustained effect

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7
Q

how is isosorbide mononitrate administered

A

oral

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8
Q

what is the pharmacology of CCBs

A

prevent opening of L-type Ca2+ channels in heart and smooth muscle to cause decreased Ca2+ entry
this slows conduction through AV node (upstroke in SA node AP) and causes negative inotropic effect (less Ca2+ in plateau phase of ventricular AP - phase 2)

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9
Q

what effect do CCBs have

A

vasodilation

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10
Q

amlodipine
nifedipine
felodipine
are examples of what

A

dihydropyridines - CCBs

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11
Q

what are some side effects of dihydropyridines

A 
ankle oedema
dizziness
flushing
headaches
tachycardia and palpitation
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12
Q

what are dihydropyridines used for

A

hypertension

angina

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13
Q

name 2 rate limiting CCBs

A

verapamil

diltiazem

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14
Q

what are rate limiting CCBs used for

A

hypertension
post MI
Angina (diltiazem)
Verapamil (SVT arrhythmias e.g. AF)

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15
Q

what are some side effects of rate limiting CCBs

A

head ache
constipation (verapamil)
risk of heart block

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16
Q

why is amlodipine preferred for hypertension, especially in heart failure/heart block

A

smooth muscle selective - minimised unwanted cardiac effects

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17
Q

why should verapamil be avoided in HF

A

cardiac selective

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18
Q

what is the pharmacology of beta blockers

A 
block b1 +/- b2 adrenoreceptors
prevents coupling of NA through Gs proteins
decreases cAMP
decreases PKA
decreases CICR via RyR2 proteins
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19
Q

what is the effect of beta blockers

A

negative chronotropic effect
negative inotropic effect
decreased O2 demand/workload

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20
Q

why are B1 selective preferred

A

B2 adrenoreceptors cause vasodilation of coronary arteries so if blocked opposite will occur

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21
Q

atenolol
bisoprolol
metoprolol
are examples of what

A

b1 selective

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22
Q

when are b1 selectives used

A

Chronic HF
MI treatment LT and ST (metoprolol for immediate)
angina (unstable)
hypertension (no longer 1st line - reduces MAP and renin release from kidneys)

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23
Q

what are some side effects of beta blockers

A

tiredness
cold peripheries
bradycardia/heart block

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24
Q

why can BBs worsen HF in short term

A

person may rely on sympathetic stimulation to maintain adequate perfusion of body tissues

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25
Q

give an example of a non-selective BB

A

propranolol

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26
Q

what are non-selective BBs used for

A

anti-arrhythmic

thyrotoxicosis

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27
Q

what are side effects of non-selective BBs

A 
worsening of claudication - stops vasodilation in skeletal muscle vessels
bronchospasm in asthmatics
tiredness
cold peripheries
bradycardia/heart block
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28
Q

why should you be cautious with BB and insulin dependent diabetics

A

BBs may mask hypoglycaemia as sympathetic nervous system suppressed

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29
Q

why can BB cause tiredness

A

cardiac output (B1) and skeletal muscle perfusion (B2) in exercise are regulated by B adrenoreceptors

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30
Q

Give an example of a drug that selectively blocks HCN channels to slow down funny current and therefore reduce heart rate and oxygen demand

A

ivabradine

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31
Q

when are HCN channel blockers used

A

angina as an alternative to BBs

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32
Q

what are some side effects of ivabradine

A 
head aches
blurred vision
dizziness
tiredness
weakness
hypotension
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33
Q

give 2 examples of a K channel agonist

A

nicorandil

minoxidil

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34
Q

how do K channel agonists work

A

open Katp channels in vascular smooth muscle and antagonise ATP causing hyper polarisation
this switches off L-type Ca2+ channels
resulting in relaxation

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35
Q

what type of vessels do K channel agonists primarily vasodilate

A

arteries

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36
Q

what are some side effects of K channel agonists

A 
headache
flushing
dizziness
reflex tachycardia (give alongside BB)
salt and water retention (give alongside loop diuretic)
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37
Q

true/false

Minoxidil also has NO donor activity to bring about venorelaxation

A

false

Nicorandil does

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38
Q

what is nicorandil used for

A

Angina - if still symptomatic despite optimal treatment with other drugs

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39
Q

what is used if HR still fast after a BB

A

+ ivabradine

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40
Q

why do BBs have little effect at rest

A

sympathetic stimulation not very active during rest

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41
Q

give an example of a selective B1 agonist

A

dobutamine

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42
Q

give an example of an alpha and beta agonist

A

Adrenaline

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43
Q

what is the pharmacology of B-adrenoreceptor agonists

A

activate b-adrenoreceptors to enhance coupling of NA through Gs proteins
increases [cAMP]
positive chronotropic and positive inotropic effect
increased CO and increased O2 demand of heart

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44
Q

what are some side effects of BBs

A

hypertension
tachycardia
arrhythmia

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45
Q

when are B agonists used

A

cardiac arrest (adrenaline IV)
emergency asthma/anaphylactic shock (adrenaline IM)
acute HF/cardiogenic shock (Dobutamine, IV)
post cardiac surgery

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46
Q

how does adrenaline redirect blood flow to heart

A

constricts BVs in skin, mucosa and abdomen

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47
Q

why are B agonists considered toxic

A

LT stimulation of sympathetic system causes HF

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48
Q

what kind of drugs are Prazosin and Doxazosin

A

alpha-1 adrenoreceptor antagonists

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49
Q

what is the pharmacology of a-1 adrenoreceptor antagonists

A

block sympathetic/hormonal effect on alpha receptors causing reduced sympathetic drive
vasodilation, reduced MAP and TPR

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50
Q

what are some side effects of alpha-1 antagonists

A 
postural hypotension
flushing
tachycardia
nasal congestion
impotence
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51
Q

when are alpha adrenoreceptor antagonists used

A

hypertension with prostatic hypertrophy

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52
Q

what kind of drugs are atropine and hyoscine

A

Muscarinic receptor antagonists

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53
Q

how do muscarinic receptor antagonists work

A

reduction of vagal tone by competing with ACh - reduces parasympathetic drive to the heart –> increased HR

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54
Q

what are some side effects of atropine

A

dry mouth
urinary retention
blurred vision

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55
Q

when are muscarinic receptors used

A

bradycardia (e.g. following MI where vagal tone raised)
anaesthesia adjunct
antispasmodic
anti cholinesterase poisoning

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56
Q

when is isoprenaline used

A

heart block

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57
Q

when are calcium/magnesium chlorides used

A

VT due to hyperkalaemia
VF
digoxin toxicity

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58
Q

name a drug that inhibits PDE in cardiac and smooth muscle causing increased cAMP and therefore increased contractility

A

amrinone

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59
Q

how do ACEIs work

A

inhibit conversion of AT I to AT II by inhibiting ACE
reduces BP secondary to vasodilation
prevents degradation of bradykinin - potent vasodilator
increased fluid excretion due to decreased aldosterone

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60
Q

where is the greatest vasodilation effect of ACEIs and therefore improved perfusion

A

kidney
heart
brain

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61
Q

what do all ACEIs end in

A

-pril

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62
Q

when are ACEIs used

A 
hypertension
HF - reduced afterload
LV dysfunction
post MI
stroke prevention
diabetic nephropathy
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63
Q

what are some side effects of ACEIs

A 
dry irritant cough
taste disturbance
angioneurotic oedema
hyperkalaemia due to potassium retention - reduced aldosterone
renal dysfunction
hypotension
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64
Q

when are ACEIs/ARBs contraindicated

A

renal artery stenosis

pregnancy/child bearing potential

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65
Q

what should be used in pregnancy induced hypertension

A

BB or CCB

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66
Q

true / false

angioneurotic oedema is more common in black people

A

true

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67
Q

what do all ARBs end in

A

-sartan

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68
Q

how do ARBs work

A

competitively block agonist action of angiotensin II at AT1 receptors
preventing vasoconstriction, aldosterone release and sympathetic activation
reduced BP secondary to vasodilation

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69
Q

why is there no dry cough with ARBs

A

no effect on bradykinin metabolism

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70
Q

what are some side effects of ARBs

A

dizziness
syncope
hyperkalaemia
renal dysfunction

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71
Q

where do thiazide diuretics inhibit reabsorption

A

distal tubule

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72
Q

where do loop diuretics inhibit reabsorption

A

ascending loop of henle

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73
Q

what are some side effects of diuretics

A 
hypokalaemia
hyponatraemia
thirst
headaches
dizziness
arrhythmia
impotence
ankle oedema
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74
Q

when are diuretics contraindicated

A

diabetics - hyperglycaemia

history of gout - increased uric acid

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75
Q

what kind of diuretic is bendroflumethiazide

A

thiazide-like

76
Q

what kind of diuretic is furosemide

A

loop

77
Q

when would a thiazide diuretic be used

A

hypertension (mild diuresis)
HF (mild or congestive)
severe resistant oedema (with a loop agent)

78
Q

when would a loop diuretic be used

A

hypertension (strong diuresis)
acute pulmonary oedema
chronic HF or congestive

79
Q

how can hypokalaemia be avoided

A

potassium sparing diuretic e.g. spironolactone

K+ supplements

80
Q

when and how are statins given

A

oral at night

81
Q

how do statins work

A

competitively inhibit HMG CoA reductase to decrease hepatic cholesterol synthesis
decreased cholesterol conc in hepatocytes
results in increase in LDL receptor expression
enhanced LDL clearance

82
Q

give 4 effects of statins

A

decrease inflammation
decrease thrombosis
reversal of endothelial dysfunction
stabilisation of atherosclerotic plaque

83
Q

what are some side effects of statins

A

myopathy
Rhabdomyolysis renal failure
GI disturbance
Insomnia

84
Q

when are statins used

A 
hypercholesterolaemia
MI long term
primary and secondary prevention of CVD events
Angina/TIA
diabetes
85
Q

when are statins contraindicated

A

pregnancy

homozygous familial hypercholesterolaemia - LDL receptors lacking - no effect

86
Q

What kind of drugs are
Bezafibrate
Gemfibrozil

A

fibrates

87
Q

when are fibrates used

A

1st line treatment in low HDL cholesterol - hypertriglyceridaemia

88
Q

how do fibrates work

A

decrease triglyceride levels by increasing rate of removal
slight decrease in LDL and HDL by decreasing liver production of particle that carried them in blood
agonists of PPAR-alpha to enhance transcription of gene encoding LPL

89
Q

what is a possible side effect of fibrates

A

hyositis - combine with statin

90
Q

aspirin tirofiban and clopidogrel are examples of what

A

antiplatelets

91
Q

do anti platelets break down clots that are already formed?

A

no

92
Q

how does aspirin work

A

irreversibly blocks COX-1 enzyme in platelets to inhibit production of TXA2 - mediator for platelet aggregation and clot formation
therefore prevents aggregation and cross linking (adhesion)

93
Q

when is aspirin used

A 
immediate MI treatment
post PCI/post CABG
stroke/TIA
prevention of athero-thrombotic events
MI longterm
94
Q

what are some side effects of aspirin

A

bronchospasm (aspirin sensitivity)
GI irritation
Haemorrhage

95
Q

when should you be cautious with aspirin

A

asthma

uncontrolled hypertension

96
Q

how does clopidogrel work

A

blocks P2Y12 receptors on platelets
to prevent ADP binding to receptor
prevents platelet aggregation and cross linking

97
Q

when is clopidogrel used

A

immediate MI

prevention of atherothrombotic events

98
Q

how does tirofiban work

A

blocks GP IIA/IIB receptors on platelets to prevent fibrinogen binding
inhibits conversion to fibrin

99
Q

when is tirofiban used

A

preventative of MI in unstable angina patients - IV short term + aspirin + heparin

100
Q

give an example of a fibrinolytic drug

A

streptokinase

101
Q

when should streptokinase not be given

A 
post streptococcal infection
recent haemorrhage
trauma
severe diabetic retinopathy
ulcers
bleeding tendencies
102
Q

how do fibrinolytics work

A

activate plasminogen to form plasmin - a protein which promotes fibrin degradation - opposes coagulation cascade

103
Q

can streptokinase reopen occluded arteries/dissolve formed clots

A

yes

104
Q

how does digoxin work

A

blocks sarcolemma Na/K ATPase by binding to alpha subunit so calcium unable to leave cell so more goes into SR - increased contractility

105
Q

what is an indirect action of digoxin

A

stimulates vagal activity on the heart - slows conduction through AV node and prolongs AV node refractory period - decreased heart rate

106
Q

when is digoxin used

A

isn’t really used anymore
AF
Chronic HF (still symptomatic despite maximal treatment with other drugs)

107
Q

what are the side effects of digoxin toxicity

A 
nausea 
vomiting
yellow vision
bradycardia/heart block 
ventricular arrhythmias - increases ventricular irritability
108
Q

why does hypokalaemia make digoxin toxicity worse

A

binds competitively with K

109
Q

what is digoxin toxicity caused by

A

membrane depolarisation and oscillatory after potentials likely due to Ca2+ overload

110
Q

what is spironolactone

A

potassium sparing diuretic

111
Q

how does spironolactone work

A

aldosterone antagonist - blocks sodium and water reabsorption

112
Q

when is spironolactone used

A

hypertension
chronic HF
oedema

113
Q

what are side effects of spironolactone

A

nausea
postural hypotension
tiredness/fainting
gynaecomastia

114
Q

what is the name of the new drug which is a combination of ARB and Neprilysin

A

Sacubitril-Valsartan

115
Q

what does Sacubitril-Valsartan do

A

blocks NP breakdown and so boosts NP levels (vasodilation)- will replace ACEIs - don’t used in combination with ACEI

116
Q

how does ezetimibe work

A

inhibits NPC1LA transport protein in enterocytes of duodenum reducing absorption of cholesterol
decrease in LDL

117
Q

how is ezetimibe administered

A

oral admin

118
Q

when is ezetimibe used

A

+ statin when statin alone not achieving goal

119
Q

what are some (rare) side effects of ezetimibe

A

diarrhoea
abdominal pain
headaches

120
Q

when is ezetemibe contraindicated

A

breast feeders

121
Q

colestyramine
colestipol
colsevelam
are examples of what

A

bile acid binding resins

122
Q

how do bile acid binding resins work

A

interrupt enterohepatic recycling of cholesterol
non-absorbable so cause excretion of bile salts therefore resulting in more cholesterol being converted to bile salts
- decreased absorption of bile salts and triglycerides
- increased LDL receptor expression

123
Q

what classes control rhythm and what classes control rate

A

1 and 3 - rhythm

2 and 4 - rate

124
Q

what phase do class 1 drugs act on

A

0

125
Q

what phase do class 2 drugs act on

A

4

126
Q

what phase do class 3 drugs act on

A

3

127
Q

what phase do class 4 drugs act on

A

2

128
Q

verapamil is what class of anti arrhythmic drug

A

4

129
Q

atenolol and propranolol are what class of anti arrhythmic drug

A

2

130
Q

lignocaine, flecainide, proprafenone, dysopyramide, hydroquinidine are what class of anti arrhythmic drug

A

1

131
Q

amiodarone, sotalol, dronedarone and bretylium are what class of anti arrhythmic drugs

A

3

132
Q

what do class I AADs do

A

Na channel blockers
with preference to the most active (tachycardia areas)
slow conduction, prolong depolarisation
depress phase 0

133
Q

what are class I AADs used for

A 
paroxysmal AF (+ WPW)
VT / VF
134
Q

what do class II AADs do

A

BBs

135
Q

what are class II AADs used for

A

paroxysmal AF

MI arrhythmias

136
Q

what are class III AADs used for

A

WPW
SVTs
Paroxysmal SVT/VT

137
Q

what do class III AADs do

A

K+ channel blockers

prolong repolarisation

138
Q

what do class IV AADs do

A

CCBs

139
Q

what are class IV AADs used for

A

SVT

AF without WPW

140
Q

what kind of drug is levosimendan

A

calcium sensitiser

141
Q

how does levosimendan work

A

binds to troponin C in cardiac muscle sensitising it to action of Ca2+ - inotropic
also opens Katp channels in vascular smooth muscle causing vasodilation

142
Q

what is levosimendan used for

A

acute decompensated HF

143
Q

what are some side effects of amiodarone

A

phototoxicity
pulmonary fibrosis
thyroid abnormalities (hypo/hyper)

144
Q

give the name of a drug that is a late sodium channel modulator

A

ranolazine

145
Q

what are the effects of ranolazine

A

improves blood flow so heart works more efficiently

146
Q

what kind of drugs are Bosentan and ambrisentan

A

ETA receptor antagonists

147
Q

what do ETA receptor antagonists do

A

antagonists of ETA receptor which endothelin acts on

vasodilators

148
Q

what are ETARAs used for

A

pulmonary hypertension

149
Q

what is ranolazine used for

A

angina

150
Q

Digoxin
Dobutamine
Levosimendan
have what effect on the force of contraction

A

increased force of contraction - inotropic drugs

151
Q

antiplatelets
anticoagulants
fibrinolytic
are all…

A

antithrombotics

152
Q

give 4 types of anti-anginals

A

nitrates
BBs
CCBs
K channel openers

153
Q

give 4 types of antihypertensives

A

Diuretics (mainly thiazide)
BBs
CCBs
vasodilators (alpha blockers, ACEIs, ARBs)

154
Q

how are the doses of warfarin and heparin controlled

A

INR

155
Q

how is warfarin reversed

A

vitamin K

dietary vitamin K can decrease action

156
Q

how does warfarin work

A

blocks vitamin K reductase
reduces hydroquinone form of Vit K (reduced form)
reduced form is responsible for gamma-carboxylation of glutamate residues of clotting factor precursors II, VII, IX and X (2 7 9 10)
this means the precursors remain inactive and the coagulation cascade is inhibited
clot formation prevented

157
Q

when is warfarin used

same as heparin and LMWH

A 
DVT or PE
NSTEMI
AF
TIA
prophylaxis of embolism e.g. post op
prosthetic valves
158
Q

what are some side effects of warfarin

A 
haemorrhage
black/bloody stools
dizziness
weakness
joint pain
159
Q

what kind of drugs does warfarin interact with

A

hepatic metabolism of warfarin inhibitors
platelet function inhibitors e.g. NSAIDs
Vitamin K availability reducers/inhibitors

160
Q

does warfarin have a high or low therapeutic index

A

low

161
Q

when is warfarin contraindicated

A

liver disease - decreased clotting factors

first few months of pregnancy

162
Q

can heparin be given orally

A

no - only IV

163
Q

can warfarin be given orally

A

yes

164
Q

what kinds of drugs are
fondaparinux
enoxaparin
dalteparin

A

LMWH

165
Q

how does heparin work

A

binds to antithrombin III increasing its affinity for clotting factors to increase rate of inactivation of clotting factors IIa and Xa
inhibits coagulation cascade

166
Q

how do LMWHs work

A

inhibit factor Xa by binding to antithrombin III
factor Xa is upstream to IIa so should indirectly inhibit IIa
(can’t bind to ATIII and IIa at same time)
inhibits coagulation cascade

167
Q

why is heparin preferring to LMWH in renal failure

A

LMWH excreted via renal route

168
Q

what are some side effects of heparin/LMWH

A

haemorrhage
osteoporosis
hypoaldosteronism
hypersensitivity reactions

169
Q

true / false

heparin only needs to bind to ATIII to inhibit Xa

A

true

170
Q

true / false

LMLWH only needs to bind to ATIII to inhibit IIa

A

false

must bind to both ATIII and IIa to inhibit IIa

171
Q

what should be done in the event of haemorrhage due to heparin/LMWH

A

discontinue drug

administer protamine sulfate - inactivated heparin

172
Q

why are rivaroxaban and dabigatran preferred over heparin and LMWH

A

no need for IV and less haemorrhage risk

173
Q

what are rivaroxaban and dabigatran

A

anticoagulants

174
Q

when are rivaroxaban and dabigatran used

A

prophylaxis of venous thromboembolism
PE or DVT
post hip/knee replacement to prevent venous thrombosis

175
Q

what are some side effects of rivaroxaban

A

haemorrhage

renal impairment

176
Q

what are some side effects of dabigatran

A

haemorrhage

anaemia

177
Q

when is rivaroxaban contraindicated

A

liver disease with coagulopathy

178
Q

when is dabigatran contraindicated

A

patients under 50kg

179
Q

how does rivaroxaban work

A

factor Xa inhibitor

180
Q

what does factor Xa do

A

converts prothrombin (II) to thrombin (IIa)

181
Q

how does dabigatran work

A

thrombin inhibitor (IIa inhibitor)

182
Q

what is morphine

A

vasodilator

183
Q

when is morphine used

A

relieve pain, anxiety and tachycardia caused by MI

acute MI treatment + anti-emetic

184
Q

When is adenosine used

A

terminate paroxysmal SVT

SVT in acute phase

185
Q

how does adenosine work

A

activates a1-adenosine receptors
opens ACh-sensitive K+ channels (GIRK channels) causing hyper polarisation of the AV node suppressing impulse conduction - decreases HR

186
Q

true/false

lidocaine can be used for SVT and VT management

A

false - used in VT but ineffective in SVT

year 1 (45 decks)

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