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Cardio Revision > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Atropine

A

Muscarinic antagonist

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2
Q

Tubocurarine

A

Nicotinic antagonist

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3
Q

Edrophonium

A

Anticholinesterase

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4
Q

Neostigmine/pyridostigmine

A

Anticholinesterase

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5
Q

Donepezil

A

Anticholinesterase

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6
Q

Clinical use of edrophonium

A

Diagnosis of myaesthenia gravis (short duration)

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7
Q

Clinical uses of neostigmine

A

Reversal of non-depolarising neuromuscular blockers

Treatment of myaesthenia gravis

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8
Q

What is the Tensilon test?

A

Used for diagnosis of myaesthenia gravis (involves administration of edrophonium)

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9
Q

Clinical use of donepezil

A

Treatment of AD (enters CNS well)

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10
Q

Varenicline

A

Partial agonist of nicotinic receptors

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11
Q

Nm type nicotinic receptor

A

Somatic nicotinic receptor

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12
Q

Nn type nicotinic receptor

A

Ganglion nicotinic receptor (both branches of ANS)

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13
Q

Clinical uses of tubocurarine/vecuronium

A

Pre-surgical skeletal muscle relaxant (non-depolarising)

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14
Q

Mechanism of action of non-depolarising block

A

Competitive antagonist at motor end plate nicotinic receptors

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15
Q

Mechanism of action of depolarising block

A

Stage I: depolarisation of motor end plate (muscle fasciculations)
Stage II: drug resistant to breakdown by cholinesterases, causes loss of sensitivity to ACh

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16
Q

Hexamethonium

A

Ganglion nicotinic receptor blocker

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17
Q

Side effects of muscarinic agonists

A 
Salivation
Lacrimation
Urination
Defecation
Sweating
Bradycardia
Bronchoconstriction
Vasodilation (non-neural)
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18
Q

Pilocarpine

A

Muscarinic agonist

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19
Q

Clinical use of pilocarpine

A

Glaucoma

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20
Q

Clinical uses of atropine

A

Anaesthesia (for bronchodilation and reduced secretions)
Bradycardia
Pupil dilation in eye examination
AChE-inhibitor poisoning (e.g. organophosphate)

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21
Q

Clinical use of hyoscine

A

Motion sickness

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22
Q

Clinical use of ipratropium

A

Inhaled for COPD

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23
Q

Ipratropium

A

Anti-muscarinic

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24
Q

Hyoscine

A

Anti-muscarinic

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25
Q

Isoprenaline

A

B1 and B2 agonist

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26
Q

Propanolol

A

B1 and B2 antagonist

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27
Q

Dobutamine

A

B1 agonist

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28
Q

Atenolol

A

B2 antagonist

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29
Q

Clinical use of dobutamine

A

Short term support in acute HF (increased HR and contractility)

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30
Q

Clinical use of atenolol

A

Hypertension (reduced HR and contractility)

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31
Q

Salbutomol

A

B2 agonist

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32
Q

Clinical use of salbutomol

A

Asthma (bronchodilation)

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33
Q

Phentolamine

A

a1 and a2 antagonist

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34
Q

Phenylephrine

A

a1 agonist

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35
Q

Clinical use of phenylephrine

A

Nasal decongestant (vasoconstriction)

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36
Q

Prazosin

A

a1 antagonist

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37
Q

Clinical use of prazosin

A

Hypertension (vasodilation)

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38
Q

What is the “triple response” of histamine?

A

Reddening (vasodilation)
Wheal (increased vascular permeability)
Flare (spreading response through sensory fibres)

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39
Q

3 classes of H1 blockers and characteristics of each

A

Sedative
Non-sedative: poor entry to CNS, reduced anti-muscarinic activity, can cause rare ventricular arrhythmias (withdrawn)
Newer non-sedative: reduced risk of cardiac effects

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40
Q

Chlorpheniramine

A

Sedative H1 blocker

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41
Q

Promethazine

A

Sedative H1 blocker

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42
Q

Terfenadine

A

Non-sedative H1 blocker

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43
Q

Astemizole

A

Non-sedative H1 blocker

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44
Q

Cetirizine

A

Newer non-sedative H1 blocker

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45
Q

Loratidine

A

Newer non-sedative H1 blocker

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46
Q

Cimetidine

A

H2 blocker

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47
Q

Ranitidine

A

H2 blocker

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48
Q

Clinical use of H2 blockers

A

Peptic ulcer

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49
Q

Bradykinin

A

Local peptide mediator of pain and inflammation

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50
Q

Kininase II/ACE

A

Degrades bradykinin

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51
Q

Side effects of ACEI mediated by increased bradykinin

A

Cough (bronchoconstriction)
Angioedema and/or rash
Hypotension
Inflammation-related pain

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52
Q

Actions of bradykinin

A

Vascular: dilate arterioles and venules (via PGs/NO), increased permeability
Neural: stimulate sensory nerve endings (pain)
Contracts uterus, airway and gut
Stimulates epithelial secretion in airways and gut

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53
Q

Icatibant

A

BK2 antagonist

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54
Q

Clinical use of icatibant

A

Limited (hereditary angioedema)

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55
Q

Cause of hereditary angioedema

A

C1esterase inhibitor deficiency

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56
Q

C1esterase inhibitor

A

Inhibits kallikrein to reduce bradykinin production

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57
Q

Effect of ACh on endothelium vs vascular smooth muscle

A

Endothelium: stimulates release of NO (EDRF)

Vascular smooth muscle: contracts at high enough concentration

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58
Q

L-NAME (N-nitro-L-arginine methyl ester)

A

NOS inhibitor (causes vasoconstriction, hypertension)

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59
Q

Physiological roles of NO

A

“Flow-dependent” vasodilation
Inhibits platelet adhesion and aggregation
Neurotransmitter

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60
Q

What stimulates NO release?

A

ACh or bradykinin acting on receptor of endothelial (or other) cell

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61
Q

Constitutive COX

A

COX-1

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62
Q

Inducible COX

A

COX-2 (inflammatory stimuli e.g. IL-1)

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63
Q

Effects of PGE2

A 
Vasodilation
Natriuretic
Hyperalgesic
Pyrogenic
Angiogenic
Stimulates mucus secretion
Reduces gastric acid secretion
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64
Q

Effects of PGF2

A

Bronchoconstrictor

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65
Q

Effects of PGD2

A

Bronchoconstrictor

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66
Q

Mechanism of action of stable prostaglandins

A 
Act locally (do not circulate) at site of production
Degraded by endothelial cells of pulmonary capillaries
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67
Q

Mechanism of IL-1 induced hyperalgesia

A

Increases BK1 receptors

Increases COX-2 and PLA2

68
Q

How do NSAIDs cause gastric ulcers?

A

Decreased mucosal blood flow and angiogenesis
Decreased mucus secretion
Increased gastric acid secretion

69
Q

Which cells produce prostacyclin (PG12)?

A

Endothelial

70
Q

Which cells produce thromboxane A2 (TXA2)?

A

Platelets

71
Q

Actions of PGI2

A

Vasodilation

Reduces platelet activation

72
Q

Actions of TXA2

A

Vasconstriction

Increases platelet activation

73
Q

How does aspirin provide vascular protection?

A

Irreversibly acetylates COX
Platelets traversing the GI circulation are exposed to high [aspirin]; platelets have no nucleus and cannot resynthesise COX for the rest of their lifespan (~8 days)
Lower [aspirin] in systemic circulation causes some inhibition of COX in endothelium, but COX is resynthesised by endothelium within hours
Increased PGI2/TXA2 ratio
Additionally, aspirin-bound COX-2 retains some biological activity and produces aspirin-triggered lipoxins, involved in inflammatory resolution

74
Q

Activation of 5-lipoxygenase

A

By increased IC Ca2+ caused by stimuli produced in inflammation (no known physiological role)

75
Q

Effects of LTA4

A

Bronchoconstrictor
Vasodilation
Increased vascular permeability

76
Q

Effects of LTB4

A

Promotes inflammation by attracting leucocytes

77
Q

Action of class I antidysrhythmics

A

Na+ channel block

78
Q

Action of class II antidysrhythmics

A

B-adrenoceptor antagonists

79
Q

Action of class III antidysrhythmics

A

K+ channel block

80
Q

Action of class IV antidysrhythmics

A

Ca2+ channel block

81
Q

Characteristics and effects of class Ia Na+ channel blockers

A

Moderate Na+ block

Prolong repolarisation and increase ERP

82
Q

Characteristics and effects of class IIa Na+ channel blockers

A

Mild Na+ block

Shorten repolarisation and decrease ERP

83
Q

Characteristics and effects of class IIIa Na+ channel blockers

A

Marked Na+ block

Same repolarisation and ERP

84
Q

Describe the concentration-dependent side effects seen in lignocaine

A

1st side effect noticed is lip and tongue numbness at 4ug/mL

Respiratory arrest and CV depression occurs at >20ug/mL

85
Q

Which class of antidysrhythmics can be used to control aberrant pacemaker activity?

A

Class II

86
Q

What is the effect of class II antidysrhythmics on the Purkinje fibres?

A

Membrane stabilising effects (similar to class I)

87
Q

List 4 adverse effects of class II antidysrhythmics

A

Bradycardia
Hypotension
AV conduction block
Bronchoconstriction

88
Q

Mechanism of action of class III antidysrhythmics

A

Prolong cardiac (myocyte) AP by slowing phase 3 repolarisation

89
Q

Uses of class III antidysrhythmics

A

Decrease incidence of re-entry arrhythmias (but increased risk of triggered events)

90
Q

Amiodarone

A

Class III antidysrhythmic but also blocks Na+, Ca2+ and B adrenoceptors

91
Q

Adverse effects of amiodarone

A

Reversible: photosensitisation, skin discolouration, hypothyroidism
Long term: pulmonary fibrosis

92
Q

Mechanism of action of class IV antidysrhythmics

A

Cardioselective Ca2+ channel blockers (acting preferentially on SA and AV nodal tissue) slow conduction velocity and increase ERP (phase 4)

93
Q

What other drugs/approaches are used to manage dysrhythmias (besides class I, II, III, IV antidysrhythmics)?

A 
Anti-muscarinics
Adenosine
Cardiac glycosides
Electrolyte supplements
DC shock, defibrillators, implantable pacemakers
94
Q

What is the current definition of hypertension?

A

BP >140/90mmHg

95
Q

4 classes of antihypertensives

A 
Angiotensin system inhibitors
B-adrenoceptor antagonists
Ca2+ channel blockers
Diuretics
Others
96
Q

Effects of angiotensin II

A 
Cell growth (including cardiac remodelling)
Vasoconstriction via AT 1 receptors
Aldosterone secretion via AT 1 receptors
97
Q

“Pril”s

A

ACEI (captropril, enalapril, perindopril, ramipril)

98
Q

Effects of ACEIs

A

Blocks angiotensin II production: vasodilation, reduced aldosterone, reduced cardiac hypertrophy
Prevents bradykinin degradation: vasodilation, cardioprotection

99
Q

Adverse effects of ACEIs

A 
First dose hypotension
Dry cough
Ageusia
Itching, rash, angioedema
Hyperkalaemia (use with thiazide diuretic)
ARF
Foetal malformations
100
Q

Contraindications for ACEIs

A

Pregnancy
Bilateral renal stenosis
Angioneurotic oedema

101
Q

“Sartan”s

A

AT receptor antagonists (losartan, candesartan)

102
Q

Losartan

A

Short-acting competitive reversible AT receptor antagonist

103
Q

Candesartan

A

Long-acting competitive irreversible AT receptor antagonist

104
Q

Effects of AT receptor antagonists

A

Reduced vasoconstriction
Reduced aldosterone
Reduced cardiac hypertrophy
Reduced sympathetic activity

105
Q

Adverse effects of AT receptor antagonists

A

Hyperkalaemia (use with thiazide diuretic)

Headache, dizziness

106
Q

Contraindications for AT receptor antagonists

A

Pregnancy
Bilateral renal stenosis
Angioneurotic oedema

107
Q

“Olol”s

A

B-blockers (propanolol, atenolol, pindolol, timolol, metoprolol)

108
Q

Effects of B-blockers

A

Reduced CO (due to decreased HR and contractility)
Decreased HR also causes increased diastole, leading to increased coronary perfusion and therefore blood supply (use in angina)
Reduced renin release (effects on BV and TPR)

109
Q

Non-selective B-blockers

A

Propanolol

Timolol

110
Q

B1-selective B-blockers

A

Atenolol

Metoprolol

111
Q

Partial agonist B1 and B2 B-blocker

A

Pindolol

112
Q

Adverse effects of B-blockers and their mechanisms

A

Cold extremities: due to blockade of dilatory B2-adrenoceptors and reflex a1-adrenoceptor constriction
Fatigue: due to decreased CO (can cause hypoglycaemia) and B2-blockade constriction of skeletal muscle blood vessels
Dreams, insomnia: CNS effects related to lipid solubility
Bronchoconstriction: B2-blockade in airway smooth muscle

113
Q

Contraindications for B-blockers

A

Diabetes (and in PVD due to effects on circulation in extremities)
Asthma
AV block
(Care with HF and metabolic syndrome)

114
Q

Verapamil

A

Ca2+ channel blocker with effects on cardiac and vascular muscle

115
Q

Diltiazem

A

Ca2+ channel blocker with less pronounced effects on cardiac muscle

116
Q

Felodipine

A

Dihydropyridine: vascular-selective Ca2+ channel blocker

117
Q

Nifedipine

A

Dihydropyridine: vascular-selective Ca2+ channel blocker

118
Q

Mechanism of Ca2+ channel blockers

A

Inhibit voltage-gated L-type Ca2+ channels in vasculature and myocardium
Reduces Ca2+ entry and therefore contractility

119
Q

“Pine”s

A

Dihydropyridines: vascular-selective Ca2+ channel blocker

120
Q

Adverse effects of non-selective Ca2+ channel blockers

A

Oedema, flushing
Headache (increased cerebral perfusion)
Bradycardia (use with care in HF)

121
Q

Adverse effects of vascular-selective (dihydropyrimidine) Ca2+ channel blockers

A

Oedema, flushing
Headache (increased cerebral perfusion)
Reflex tachycardia (use with care in tachyarrhythmias)

122
Q

Hydrochlorothiazide

A

Thiazide diuretic

123
Q

Mechanism of thiazide diuretics

A

Inhibit Na+/Cl- cotransporter in DCT
Decrease Na+ and Cl- reabsorption
Increase Na+ and H20 excretion from kidney (causes K+ loss from collecting duct)
Lowers BV and therefore BP

124
Q

Adverse effects of thiazide diuretics

A

Hypokalaemia
Gout
Hyperglycaemia
Allergic reaction

125
Q

“Other” drugs used to treat hypertension

A

Older: a1 and a2 antagonists
Newer: renin inhibitors

126
Q

Digoxin

A

Cardiac glycoside

127
Q

Mechanism of cardiac glycosides

A

Inhibits Na+/K+-ATPase
Increased [Na+] IC causes decreased Ca2+ extrusion (due to a reduction in the concentration gradient of Na+, remembering that Ca2+ is exchanged for Na+)
Increased Ca2+ stored in SR
Increased Ca2+ release from SR with each AP

128
Q

Limitations of cardiac glycosides

A

Low therapeutic index (narrow margin of safety)

129
Q

Adverse effects of cardiac glycosides (due to effects on excitable tissues)

A

Gut: anorexia, nausea, diarrhoea
CNS: drowsiness, confusion, psychosis
Cardiac: ventricular dysrhythmias

130
Q

Factors increasing toxicity of cardiac glycosides and underlying mechanisms

A

Low K+: decreased competition for binding
High Ca2+: decreased gradient or Ca2+ efflux
Renal impairment: due to effects on Na+/K+ exchange in the kidney

131
Q

Short term support for acute heart failure and cardiogenic shock

A

B-adrenoceptor agonists

PDEI

132
Q

Adverse effects of B-adrenoceptor agonists and PDEI

A

Increase cardiac work and O2 demand (not good long term solution)
Risk of arrhythmias (effects on SA node)

133
Q

Amrinone

A

PDEI

134
Q

Milrinone

A

PDEI

135
Q

What changes lead to decompensation in CHF?

A

Reduced B1-adrenoceptor expression and impaired coupling, causing reduced sensitivity to sympathetic drive

136
Q

How is pressure overload as a cause of HF treated?

A

By reducing afterload

137
Q

How is volume overload as a cause of HF treated?

A

By reducing preload

138
Q

How is loss of myocardial muscle (e.g. in IHD or cardiomyopathy) as a cause of HF treated?

A

By reducing contractility

139
Q

List 4 classes of drugs used to reduce preload in the treatment of HF

A

Venodilators (nitrates)
Diuretics
Aldosterone receptor antagonists
Aquaretics

140
Q

Limitations of nitrates

A

1st pass metabolism (can be administered sublingually)

Tolerance

141
Q

Frusemide

A

Loop diuretic

142
Q

Aquaretics

A

Vasopressin (ADH) receptor antagonists

143
Q

Spironolactone

A

Aldosterone receptor antagonist

144
Q

Mechanism of aldosterone receptor antagonists

A

Inhibits aldosterone action on cortical and distal tubules

145
Q

Benefit of aldosterone receptor antagonists over other HF treatments

A

Improves survival with combination therapy in severe HF

146
Q

Adverse effects of aldosterone receptor antagonists

A

Hyperkalaemia (K+ sparing)

May impact renal functioning

147
Q

List 4 classes of drugs used to reduce afterload in the treatment of HF

A

Arterial vasodilators
ACEI
AT1 receptor antagonists
B-adrenoceptor antagonists

148
Q

Adverse effects of arterial vasodilators

A

Reflex tachycardia

149
Q

What is the effect of ACEI on prognosis in HF?

A 
Improves symptoms
Delays progression
May improve survival in combination
Effective at all grades of HF
Used as 1st line treatment
150
Q

Effect of B1-blockers in HF

A

SV increases (due to restoration of pump efficiency)
Reduces tachycardia
Inhibits renin release (and therefore fluid retention/preload)

151
Q

Carvedilol

A

B1 and a1 blocker

152
Q

Effects of carvedilol

A

Cardiac effects (reduced HR and contractility)
Vasodilation also reduces afterload
Increases EF and reduces mortality

153
Q

Clinical uses of cardilol

A

Early and mild to moderate CHF

154
Q

Drugs for HF which reduce mortality

A

AT1 receptor antagonists
B-blockers
Aldosterone antagonists (e.g. spironolactone)

155
Q

Surgical interventions for HF

A

Pacemaker, defibrillator, valve replacement

Heart transplant

156
Q

Clinical use of sodium bicarbonate

A

Aspirin overdose

157
Q

Use of probenecid

A

Inhibits secretion of banned substances in sport

158
Q

4 classes of diuretics

A

Loop
Thiazide
K+ sparing
Osmotic

159
Q

Mechanism of loop diuretics

A

Inhibit Na+/K+/2Cl- carrier into cells of ascending LOH

160
Q

Classes of drugs used to treat angina

A

Nitrates
Ca2+ channel blockers
B-blockers
Ivabradine

161
Q

Mechanism of action of nitrates

A

Drug undergoes biotransformation, releases NO
NO stimulates guanylate cyclase in vascular smooth muscle
Guanylate cyclase converts GTP to cGMP
cGMP causes dephosphorylation of myosin light-chain to induce vascular relaxation
Effect most important in VEINS to REDUCE PRELOAD
Usually used in combination with B-blocker or Ca2+ channel blocker to prevent reflex tachycardia

162
Q

GTN

A

Glyceryl trinitrate

Administered sublingually for acute attack or before exercise, transdermally for prophylaxis, or IV for emergency

163
Q

Isosorbide dinitrate

A

Longer acting nitrate for angina

Undergoes 1st pass metabolism to produce the active metabolite

164
Q

Drug interaction between nitrate and sildenafil

A

Sildenafil prevents breakdown of cGMP by inhibiting PDE, can lead to massive hypotension when used with nitrate

165
Q

Limitation of nitrates

A

Tolerance

166
Q

Mechanism of action of ivabradine

A

Specific and selective inhibition of inward Na+-K+ funny current in SA node to reduce slope of phase 4 (reduces HR)

167
Q

How is variant angina treated?

A

Relieve coronary spasm with short acting nitrate
Prophylaxis with Ca2+ channel blocker
DON’T USE B-BLOCKERS (may cause vasopasm via a-adrenoceptor if vasodilatory action of B2-adrenoceptor on coronary arteries blocked)

Cardio Revision (6 decks)

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