Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Cardio Revision > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Atropine

A

Muscarinic antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Tubocurarine

A

Nicotinic antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Edrophonium

A

Anticholinesterase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Neostigmine/pyridostigmine

A

Anticholinesterase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Donepezil

A

Anticholinesterase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Clinical use of edrophonium

A

Diagnosis of myaesthenia gravis (short duration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Clinical uses of neostigmine

A

Reversal of non-depolarising neuromuscular blockers

Treatment of myaesthenia gravis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the Tensilon test?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Clinical use of donepezil

A

Treatment of AD (enters CNS well)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Varenicline

A

Partial agonist of nicotinic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Nm type nicotinic receptor

A

Somatic nicotinic receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Nn type nicotinic receptor

A

Ganglion nicotinic receptor (both branches of ANS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Clinical uses of tubocurarine/vecuronium

A

Pre-surgical skeletal muscle relaxant (non-depolarising)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Mechanism of action of non-depolarising block

A

Competitive antagonist at motor end plate nicotinic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Hexamethonium

A

Ganglion nicotinic receptor blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Side effects of muscarinic agonists

A 
Salivation
Lacrimation
Urination
Defecation
Sweating
Bradycardia
Bronchoconstriction
Vasodilation (non-neural)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Pilocarpine

A

Muscarinic agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Clinical use of pilocarpine

A

Glaucoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Clinical use of hyoscine

A

Motion sickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Clinical use of ipratropium

A

Inhaled for COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Ipratropium

A

Anti-muscarinic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Hyoscine

A

Anti-muscarinic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Isoprenaline
B1 and B2 agonist
26
Propanolol
B1 and B2 antagonist
27
Dobutamine
B1 agonist
28
Atenolol
B2 antagonist
29
Clinical use of dobutamine
Short term support in acute HF (increased HR and contractility)
30
Clinical use of atenolol
Hypertension (reduced HR and contractility)
31
Salbutomol
B2 agonist
32
Clinical use of salbutomol
Asthma (bronchodilation)
33
Phentolamine
a1 and a2 antagonist
34
Phenylephrine
a1 agonist
35
Clinical use of phenylephrine
Nasal decongestant (vasoconstriction)
36
Prazosin
a1 antagonist
37
Clinical use of prazosin
Hypertension (vasodilation)
38
What is the "triple response" of histamine?
Reddening (vasodilation) Wheal (increased vascular permeability) Flare (spreading response through sensory fibres)
39
3 classes of H1 blockers and characteristics of each
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
40
Chlorpheniramine
Sedative H1 blocker
41
Promethazine
Sedative H1 blocker
42
Terfenadine
Non-sedative H1 blocker
43
Astemizole
Non-sedative H1 blocker
44
Cetirizine
Newer non-sedative H1 blocker
45
Loratidine
Newer non-sedative H1 blocker
46
Cimetidine
H2 blocker
47
Ranitidine
H2 blocker
48
Clinical use of H2 blockers
Peptic ulcer
49
Bradykinin
Local peptide mediator of pain and inflammation
50
Kininase II/ACE
Degrades bradykinin
51
Side effects of ACEI mediated by increased bradykinin
Cough (bronchoconstriction) Angioedema and/or rash Hypotension Inflammation-related pain
52
Actions of bradykinin
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
53
Icatibant
BK2 antagonist
54
Clinical use of icatibant
Limited (hereditary angioedema)
55
Cause of hereditary angioedema
C1esterase inhibitor deficiency
56
C1esterase inhibitor
Inhibits kallikrein to reduce bradykinin production
57
Effect of ACh on endothelium vs vascular smooth muscle
Endothelium: stimulates release of NO (EDRF) | Vascular smooth muscle: contracts at high enough concentration
58
L-NAME (N-nitro-L-arginine methyl ester)
NOS inhibitor (causes vasoconstriction, hypertension)
59
Physiological roles of NO
"Flow-dependent" vasodilation Inhibits platelet adhesion and aggregation Neurotransmitter
60
What stimulates NO release?
ACh or bradykinin acting on receptor of endothelial (or other) cell
61
Constitutive COX
COX-1
62
Inducible COX
COX-2 (inflammatory stimuli e.g. IL-1)
63
Effects of PGE2
``` Vasodilation Natriuretic Hyperalgesic Pyrogenic Angiogenic Stimulates mucus secretion Reduces gastric acid secretion ```
64
Effects of PGF2
Bronchoconstrictor
65
Effects of PGD2
Bronchoconstrictor
66
Mechanism of action of stable prostaglandins
``` Act locally (do not circulate) at site of production Degraded by endothelial cells of pulmonary capillaries ```
67
Mechanism of IL-1 induced hyperalgesia
Increases BK1 receptors | Increases COX-2 and PLA2
68
How do NSAIDs cause gastric ulcers?
Decreased mucosal blood flow and angiogenesis Decreased mucus secretion Increased gastric acid secretion
69
Which cells produce prostacyclin (PG12)?
Endothelial
70
Which cells produce thromboxane A2 (TXA2)?
Platelets
71
Actions of PGI2
Vasodilation | Reduces platelet activation
72
Actions of TXA2
Vasconstriction | Increases platelet activation
73
How does aspirin provide vascular protection?
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
Activation of 5-lipoxygenase
By increased IC Ca2+ caused by stimuli produced in inflammation (no known physiological role)
75
Effects of LTA4
Bronchoconstrictor Vasodilation Increased vascular permeability
76
Effects of LTB4
Promotes inflammation by attracting leucocytes
77
Action of class I antidysrhythmics
Na+ channel block
78
Action of class II antidysrhythmics
B-adrenoceptor antagonists
79
Action of class III antidysrhythmics
K+ channel block
80
Action of class IV antidysrhythmics
Ca2+ channel block
81
Characteristics and effects of class Ia Na+ channel blockers
Moderate Na+ block | Prolong repolarisation and increase ERP
82
Characteristics and effects of class IIa Na+ channel blockers
Mild Na+ block | Shorten repolarisation and decrease ERP
83
Characteristics and effects of class IIIa Na+ channel blockers
Marked Na+ block | Same repolarisation and ERP
84
Describe the concentration-dependent side effects seen in lignocaine
1st side effect noticed is lip and tongue numbness at 4ug/mL | Respiratory arrest and CV depression occurs at >20ug/mL
85
Which class of antidysrhythmics can be used to control aberrant pacemaker activity?
Class II
86
What is the effect of class II antidysrhythmics on the Purkinje fibres?
Membrane stabilising effects (similar to class I)
87
List 4 adverse effects of class II antidysrhythmics
Bradycardia Hypotension AV conduction block Bronchoconstriction
88
Mechanism of action of class III antidysrhythmics
Prolong cardiac (myocyte) AP by slowing phase 3 repolarisation
89
Uses of class III antidysrhythmics
Decrease incidence of re-entry arrhythmias (but increased risk of triggered events)
90
Amiodarone
Class III antidysrhythmic but also blocks Na+, Ca2+ and B adrenoceptors
91
Adverse effects of amiodarone
Reversible: photosensitisation, skin discolouration, hypothyroidism Long term: pulmonary fibrosis
92
Mechanism of action of class IV antidysrhythmics
Cardioselective Ca2+ channel blockers (acting preferentially on SA and AV nodal tissue) slow conduction velocity and increase ERP (phase 4)
93
What other drugs/approaches are used to manage dysrhythmias (besides class I, II, III, IV antidysrhythmics)?
``` Anti-muscarinics Adenosine Cardiac glycosides Electrolyte supplements DC shock, defibrillators, implantable pacemakers ```
94
What is the current definition of hypertension?
BP >140/90mmHg
95
4 classes of antihypertensives
``` Angiotensin system inhibitors B-adrenoceptor antagonists Ca2+ channel blockers Diuretics Others ```
96
Effects of angiotensin II
``` Cell growth (including cardiac remodelling) Vasoconstriction via AT 1 receptors Aldosterone secretion via AT 1 receptors ```
97
"Pril"s
ACEI (captropril, enalapril, perindopril, ramipril)
98
Effects of ACEIs
Blocks angiotensin II production: vasodilation, reduced aldosterone, reduced cardiac hypertrophy Prevents bradykinin degradation: vasodilation, cardioprotection
99
Adverse effects of ACEIs
``` First dose hypotension Dry cough Ageusia Itching, rash, angioedema Hyperkalaemia (use with thiazide diuretic) ARF Foetal malformations ```
100
Contraindications for ACEIs
Pregnancy Bilateral renal stenosis Angioneurotic oedema
101
"Sartan"s
AT receptor antagonists (losartan, candesartan)
102
Losartan
Short-acting competitive reversible AT receptor antagonist
103
Candesartan
Long-acting competitive irreversible AT receptor antagonist
104
Effects of AT receptor antagonists
Reduced vasoconstriction Reduced aldosterone Reduced cardiac hypertrophy Reduced sympathetic activity
105
Adverse effects of AT receptor antagonists
Hyperkalaemia (use with thiazide diuretic) | Headache, dizziness
106
Contraindications for AT receptor antagonists
Pregnancy Bilateral renal stenosis Angioneurotic oedema
107
"Olol"s
B-blockers (propanolol, atenolol, pindolol, timolol, metoprolol)
108
Effects of B-blockers
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
Non-selective B-blockers
Propanolol | Timolol
110
B1-selective B-blockers
Atenolol | Metoprolol
111
Partial agonist B1 and B2 B-blocker
Pindolol
112
Adverse effects of B-blockers and their mechanisms
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
Contraindications for B-blockers
Diabetes (and in PVD due to effects on circulation in extremities) Asthma AV block (Care with HF and metabolic syndrome)
114
Verapamil
Ca2+ channel blocker with effects on cardiac and vascular muscle
115
Diltiazem
Ca2+ channel blocker with less pronounced effects on cardiac muscle
116
Felodipine
Dihydropyridine: vascular-selective Ca2+ channel blocker
117
Nifedipine
Dihydropyridine: vascular-selective Ca2+ channel blocker
118
Mechanism of Ca2+ channel blockers
Inhibit voltage-gated L-type Ca2+ channels in vasculature and myocardium Reduces Ca2+ entry and therefore contractility
119
"Pine"s
Dihydropyridines: vascular-selective Ca2+ channel blocker
120
Adverse effects of non-selective Ca2+ channel blockers
Oedema, flushing Headache (increased cerebral perfusion) Bradycardia (use with care in HF)
121
Adverse effects of vascular-selective (dihydropyrimidine) Ca2+ channel blockers
Oedema, flushing Headache (increased cerebral perfusion) Reflex tachycardia (use with care in tachyarrhythmias)
122
Hydrochlorothiazide
Thiazide diuretic
123
Mechanism of thiazide diuretics
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
Adverse effects of thiazide diuretics
Hypokalaemia Gout Hyperglycaemia Allergic reaction
125
"Other" drugs used to treat hypertension
Older: a1 and a2 antagonists Newer: renin inhibitors
126
Digoxin
Cardiac glycoside
127
Mechanism of cardiac glycosides
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
Limitations of cardiac glycosides
Low therapeutic index (narrow margin of safety)
129
Adverse effects of cardiac glycosides (due to effects on excitable tissues)
Gut: anorexia, nausea, diarrhoea CNS: drowsiness, confusion, psychosis Cardiac: ventricular dysrhythmias
130
Factors increasing toxicity of cardiac glycosides and underlying mechanisms
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
Short term support for acute heart failure and cardiogenic shock
B-adrenoceptor agonists | PDEI
132
Adverse effects of B-adrenoceptor agonists and PDEI
Increase cardiac work and O2 demand (not good long term solution) Risk of arrhythmias (effects on SA node)
133
Amrinone
PDEI
134
Milrinone
PDEI
135
What changes lead to decompensation in CHF?
Reduced B1-adrenoceptor expression and impaired coupling, causing reduced sensitivity to sympathetic drive
136
How is pressure overload as a cause of HF treated?
By reducing afterload
137
How is volume overload as a cause of HF treated?
By reducing preload
138
How is loss of myocardial muscle (e.g. in IHD or cardiomyopathy) as a cause of HF treated?
By reducing contractility
139
List 4 classes of drugs used to reduce preload in the treatment of HF
Venodilators (nitrates) Diuretics Aldosterone receptor antagonists Aquaretics
140
Limitations of nitrates
1st pass metabolism (can be administered sublingually) | Tolerance
141
Frusemide
Loop diuretic
142
Aquaretics
Vasopressin (ADH) receptor antagonists
143
Spironolactone
Aldosterone receptor antagonist
144
Mechanism of aldosterone receptor antagonists
Inhibits aldosterone action on cortical and distal tubules
145
Benefit of aldosterone receptor antagonists over other HF treatments
Improves survival with combination therapy in severe HF
146
Adverse effects of aldosterone receptor antagonists
Hyperkalaemia (K+ sparing) | May impact renal functioning
147
List 4 classes of drugs used to reduce afterload in the treatment of HF
Arterial vasodilators ACEI AT1 receptor antagonists B-adrenoceptor antagonists
148
Adverse effects of arterial vasodilators
Reflex tachycardia
149
What is the effect of ACEI on prognosis in HF?
``` Improves symptoms Delays progression May improve survival in combination Effective at all grades of HF Used as 1st line treatment ```
150
Effect of B1-blockers in HF
SV increases (due to restoration of pump efficiency) Reduces tachycardia Inhibits renin release (and therefore fluid retention/preload)
151
Carvedilol
B1 and a1 blocker
152
Effects of carvedilol
Cardiac effects (reduced HR and contractility) Vasodilation also reduces afterload Increases EF and reduces mortality
153
Clinical uses of cardilol
Early and mild to moderate CHF
154
Drugs for HF which reduce mortality
AT1 receptor antagonists B-blockers Aldosterone antagonists (e.g. spironolactone)
155
Surgical interventions for HF
Pacemaker, defibrillator, valve replacement | Heart transplant
156
Clinical use of sodium bicarbonate
Aspirin overdose
157
Use of probenecid
Inhibits secretion of banned substances in sport
158
4 classes of diuretics
Loop Thiazide K+ sparing Osmotic
159
Mechanism of loop diuretics
Inhibit Na+/K+/2Cl- carrier into cells of ascending LOH
160
Classes of drugs used to treat angina
Nitrates Ca2+ channel blockers B-blockers Ivabradine
161
Mechanism of action of nitrates
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
GTN
Glyceryl trinitrate | Administered sublingually for acute attack or before exercise, transdermally for prophylaxis, or IV for emergency
163
Isosorbide dinitrate
Longer acting nitrate for angina | Undergoes 1st pass metabolism to produce the active metabolite
164
Drug interaction between nitrate and sildenafil
Sildenafil prevents breakdown of cGMP by inhibiting PDE, can lead to massive hypotension when used with nitrate
165
Limitation of nitrates
Tolerance
166
Mechanism of action of ivabradine
Specific and selective inhibition of inward Na+-K+ funny current in SA node to reduce slope of phase 4 (reduces HR)
167
How is variant angina treated?
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions