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116 Cards in this Set
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Physostigmine |
Reversible anticholinesterase/indirect cholinomimetic Tertiary Amine Postganglionic parasympathetic synapse Half life: 30mins Treats: Glaucoma + Atropine poisoning Mechanism of action: donates carbamyl group to cholinesterase active site (hydrolysis of mins not msecs) |
Type of drug Chemical structure Location of action Half life Used to treat Mechanism of action |
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Neostigmine |
Reversible anticholinesterase/indirect cholinomimetic Has a quaternary nitrogen - more polar and therefore cannot enter CNS Greater effect than physostigmine on skeletal muscle Half life: 2-4 hours Treats: non-depolarizing neuromuscular block + myasthenia gravis Side effect: headache, brow pain, blurred vision Mechanism of action: donates carbamyl group to cholinesterase active site (hydrolysis of mins not msecs) |
Noteable chemical structure Noteable location of action Half life Treats Side effects Mechanism of action |
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Ecothiopate |
Irreversible anticholinesterase/indirect cholinomimetic Organophosphate New anticholinesterases must be made by the cell Treats: glaucoma Side effects: sweating, blurred vision, gi pain, bradycardia, hypotension, respiratory difficulty Mechanism of action: labile group used to phosphorylate cholinesterase active site leaving a blocking group that is resistant to hydrolysis |
Type of drug Chemical structure Effect Treats Sideffect Mechanism of action |
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Bethanecol |
Direct cholinomimetic Choline ester M3 AChR agonist More resistant to degradation Limited access to the brain Half life: 3-4 hours as opposed to ACh's 1-2msec Treats: assist bladder emptying + enhance gastric motility Side effects: sweating, impaired vision, nausea, bradychardia, hypotension, respiratory difficulty
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Type of drug Chemical structure Target Comparison to ACh Half life Use Side effect |
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Pilocarpine |
Direct cholinomimetic Alkaloid Non-selective muscarinic agonist Good lipid solubility Half life: 3-4 hours Use: local treatment for glaucoma Side effects: blurred vision, sweating, gastrointestinal disturbance and pain, hypotension, respiratory distress |
Type of drug Chemical structure Target Lipid solubility Use Side effects |
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Suxamethonium |
Depolarising NMJ blocking drug Use: Skeletal muscle relaxant MoA: Splits into two and acts as an agonist on both alpha subunits of AChr Duration: 5mins Degraded by butyrylcholinesterase + acetylcholinesterase |
ToD Use MoA Duration Degraded by |
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Donepezil + Tacrine |
Reversible anticholinesterase Use: relieve Alzheimer's symptoms Mechanism of action: potentiation of central cholinergic transmission relieves Alzheimer's symptoms |
Type of drug Use MoA |
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Hexamethonium |
First anti hypertensive No longer in use due to Side effects: lack of thermoregulation, sweating, constipation, paleness due to loss of vessel tone |
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Trimetaphan |
Use: anti hypertensive during surgery to reduce bleeding MoA: dominant autonomic tone for blood vessels and kidneys is sympathetic. Is a nicotinic receptor antagonist therefore blocks nAChR on ganglion - vasodilstion and reduced renin secretion |
Use MoA |
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Alpha-bungarotoxin |
Nicotinic receptor antagonist in snake venom Use: killin' a bitch via respiratory paralysis Skeletal muscle Is a complete block unlike other ganglion blocking drugs |
ToD Use Target Comparison to other ganglion blocking drugs |
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Atropine |
Muscarinic receptor antagonist Target: M1 + M5 Low dose effect: mild restlessness - agitation High dose effect: Same as Hyoscine - agitation MoA: M1 + M3 + M5 antagonism - increased phospholipase C - increased tissue response Administration: Oral Volume of distribution: 1-6 L/kg Distribution: ppb 50% Metabolism: partially liver and >30% in kidney Half life: 2-5 hours |
ToD Target Low dose effect High dose effect MoA Administration Volume of distribution Distribution Metabolism Half life |
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Hyoscine |
Muscarinic receptor antagonist Target: M1 + M5 Low dose effect: sedation High dose effect: Same as atropine - agitation MoA: M1 + M3 + M5 antagonism - increased phospholipase C - increased tissue response Administration: IV or IM Distribution: ppb 10% + reversible, can cross bbb and placenta Metabolism: hepatic + >2% in kidney Half life: 8 hours Excretion: Urine as metabolites |
ToD Target Low dose effect High dose effect MoA Administration Distribution Metabolism Half life Excretion |
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Tropicamide |
Muscarinic receptor antagonist Use: retinal examination upon pupil dilation via myrdriasis and cycloplegia |
ToD Use |
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Anaesthetic premedication |
Muscarinic receptor antagonist Use: bronchodilation for improved absorption of anaesthetics administered through airway, reduced salivary secretion for reduced risk of aspiration, slightly increase in heart rate to protect against anaesthetic induced bradychardia |
ToD Use |
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Digoxin |
Cardiac glycoside
Binds to an extracellular site on Na+/K+ ATPase pump in myocytes and decreases its function - Increase in Na+ in myocytes - Increase in intracellular Ca++ |
ToD MoA |
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Dimercarpol |
Chemical antagonist Chelating agent |
ToD Use |
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Hyoscine |
Muscarinic receptor antagonist Reduces flow of information from parasympathetic muscarinic receptors in vestibular apparatus to vomiting centres in brain |
ToD MoA |
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Muscarinic receptor antagonists in treatment of Parkinson's disease |
Loss of nigrostriatal dopaminergic neurones - reduced dopamine released into striatum M4 receptor antagonism reduces its inhibition of D1 receptors - Increases the sensitivity to dopamine - relieve symptoms of Parkinson's |
Define Parkinson's with regards to neurones and neurotransmitter MoA + Use |
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Ipratropium Bromide |
Muscarinic receptor antagonist Asthma/Obstructive airway disease Derivative of atropine with a large ammonium group (high positive charge) which prevents diffusion into bloodstream and crossing BBB- reducing side effects |
ToD Use MoA |
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Muscarinic receptor antagonists in treatment of irritable bowel syndrome |
High GI motility and tone - high intra-colonic pressure - pain Antagonists interfere with parasympathetic effect - decreased motility and tone - relieving intra-colonic pressure |
Define the cause of pain in IBS MoA |
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Side effects of muscarinic receptor antagonists |
Hot as hell - reduced sweating and loss of thermoregulation Dry as a bone - reduced secretions Blind as a bat - Cyclopegia (ciliary muscle paralysis) Mad as a hatter - CNS disturbance |
4 Hot as hell... etc. |
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Botulinum Toxin |
Protease enzyme Interferes with exocytosis of ACh Breaks down an important SNARE protein that allows for fusion of the vesicle with presynaptic membrane Remove wrinkles by paralysing skeletal muscle (NMJ) Treat excessive sweating (Muscarinic receptors in sweat glands (sympathetic nervous system))
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ToD Effect MoA Use (2) |
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Phenylephrine |
Chemically related to adrenaline More resistant to COMT but not MAO Selective for a1 at low doses Vasoconstrictor (IV + topically): local anaesthetics, anaphylactic shock, stop superficial bleeding from skin and mucous membranes Mydriatic (eye drops): constricts radial muscle - pupillary dilation - allows for inspection of fundus of eye Nasal decongestant (nose drops + orally): colds, flu, hayfever - vasoconstriction - less fluid released by transudation Unwanted effects: CVS hypertention |
ToD Resistance to degradation Selectivity Effect + administration + MoA+ Use (3): Vasoconstrictor: Mydriatic: Nasal deocongestant: Unwanted effects |
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Clonidine |
Sympathomimetic Selective for a2 Treats hypertension and migraine (orally + IV) Reduces sympathetic tone via a2 adrenoceptor mediated pre-synaptic inhibition of NA release Target: brainstem - baroreceptor pathway to reduce sympathetic outflow |
ToD Selectivity MoA Target |
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Isoprenaline |
Sympathomimetic Unselective beta agonist Less susceptible to Uptake 1 and MAO than adrenaline Plasma half life: 2 hours Treatment of heart block, cardioenic shock, acute heart failure + MI (IV): very potent B1 effect on heart - increased HR and contractility Discontinued use in asthma due to unwanted reflex tachycardia and dysrhythmias |
ToD Selectivity Resistance to degradation Half-life MoA in CVS MoA in lungs |
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Dobutamine |
Sympathomimetic Selective B1 agonist Lacks isoprenaline's reflex tachycardia Half-life: 2 mins - rapid degradation by COMT Treats heart block, cardiogenic shock, acute heart failure + MI (IV) |
ToD Selectivity Comparison to isoprenaline Half-life and degradation Use |
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Salbutamol |
Sympathetic catecholamine derivative Selective for B2 Relative resistance to MAO + COMT Treats asthma (inhalation + oral): relaxes bronchial smooth muscle + inhibits release of bronchoconstrictor mediators from mast cells Treats threatened uncomplicated premature labour (IV) Unwanted effects: reflex tachycardia, tremor Caution: cardia patients, hyperthyroidism and diabetes |
ToD Selectivity Resistance to degradation Treatment and MoA in Lungs Treatment in child birth Unwanted effects Caution with use in |
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Cocaine |
Adrenergic neurons Inhibits Uptake 1 (MAO) Rare use as local anaesthetic in opthalmology Half-life: 30 mins Well absorbed at all sites and readily crosses BBB Degraded by plasma esterases and hepatic enzymes |
Target MoA Use Half-life Tissue perfusion Degradation |
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Unwanted effects of Cocaine |
CNS: euphoria, excitement, increased motor activity, activation of vomiting centres and maybe psychological dependence syndrome (no evidence for physical dependence) and depression of medullary respiratory centre CVS: tachycardia, vasoconstriction, raised BP Other: Tremors and convulsions |
CNS (6) CVS (3) Other (2) |
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Tyramine |
Indirectly acting sympathomimetic Weak adrenoceptor agonist Competes with catecholamines (A) for Uptake 1 (nerve terminal) Displaces NA from intracellular storage vesicles NA and tyramine compete for sites on MAO-A Cytoplasmic NA leaks through the neuronal membrane to act on postsynaptic adrenoceptors Not a problem when monoamine degradation is functional however when MAO-A is inhibited tyramine ingestion -> hypertensive crisis |
ToD Receptor activity Intracellular activity Complication with monoamine oxidase inhibitors |
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5 common examples of SNS antagonists |
Labetalol (a1 + b1) Phentolamine (a1 + a2) Propanolol (b1 + b2) Prazosin (a1) Atenolol (b1) |
L P P P A |
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Selective and non-selective cardioselective SNS antagonist |
Selective - Atenolol (B1) Non-selective - Propanolol (B1 + B2) |
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Beta-adrenoceptor antagonist effect in tissues |
Reduce TPR |
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Unwanted effect of beta-antagonists in the lungs |
Bronchoconstriction There is no direct sympathetic drive to the lungs - responds to circulating adrenaline Normally of no-importance however in the presence of airway disease e.g. asthma or bronchitis - can be life threatening |
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Unwanted effects of beta-antagonists in the heart |
Cardiac failure Patients with heart disease may rely on a degree of sympathetic drive to the heart to maintain adequate CO Beta-blockers remove the sympathetic drive - cardiac failure |
C
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Unwanted effects of beta-antagonists in hypoglycaemia |
Sympathetic response to hypoglycaemia produces symptoms (sweating, palpitations, tremor) which are useful in warning diabetics of urgent need for carbohydrates/glucose B-antagonists block B2 receptor driven glycogenolysis B1 selective agents would be preferable since glucose release from liver is only controlled by B2 receptors |
Problem for diabetics in controlling sugar levels Prevents what process that is essential for diabetics An alternative and why |
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Unwanted effects of beta-antagonists on fatigue |
Reduced CO Reduced muscle perfusion Increase fatigue |
Effect Effect Symptom |
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Unwanted effects of beta-antagonists in cold extremities |
Loss of B-receptor mediated vasodilation in cutaneous vessels Causes cold extremities |
Effect Symptom |
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Unwanted effects of beta-antagonists on dreams |
Bad dreams |
1 |
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Propanolol |
SNS antagonist Non selective beta-receptor antagonist B1+ B2 At rest: very little change in HR, CO and arterial pressure Reduces effect of exercise and stress on HR, CO and arterial pressure Produces all unwanted effects |
Selectivity Effect at rest Effect during exercise + stress Side effects |
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Atenolol |
SNS antagonist Selective B1 antagonist Mainly antagonises the effect of NA on the heart but also other tissue like kidney Less effect on airways due to selectivity but can still produce adverse effects at high concentrations (not safe for asthmatics) |
Selectivity Effect on heart Effect on airways |
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Lebatolol |
SNS antagonist Selective for B1 and a1 but higher ratio of B1:a1, 4:1 Lowers blood pressure via reduction in TPR No long term change in HR or CO |
Selectivity Effect Long term effects on HR and CO? |
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General effects of non-selective alpha adrenoceptor antagonists |
Fall in arterial pressure (main mediators of peripheral resistance) Postural hypotension Increased CO + HR (reflex) Increased blood flow to cutaneous and splanchnic beds (only slight increased to vascular SM) |
F P I I |
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Phentolamine |
SNS antagonists Non-selective alpha antagonist Vasodilation and fall in BP due to blockade of a-1 receptors Enhanced reflex tachycardia due blockade of a-2 receptors causing NA release Increased GIT motility - Diarrhoea |
Selectivity Effect 1 + cause Effect 2 + cause Effect 3 |
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Prazosin |
SNS antagonist Highly selective for a-1 Fall in BP via vasodilation (a1) Less reflex tachycardia than non-selective antagonists CO decrease due to fall in venous pressure as a result of capacitance vessel dilation Modest LDL decrease with increase HDL |
Tod Selectivity Comparison to non-selective SNS antagonists Effect on CO Effect on cholesterol |
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Other beneficial effects of prazosin that are making it increasingly popular |
Overall decrease in LDL, vLDL and total triglyceride levels
Increase in HDL - reduced risk of CAD |
Decreases what Increases what |
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Effects of Methyldopa |
False transmitter Antihypertensive agent Stimulates vasopressor centre of brain to inhibit sympathetic outflow Also maintains renal and CNS blood flow - can be used in hypertensives with renal insufficiency/cerebrovascular disease No adverse effects on foetuses despite crossing blood-plancenta barrier |
ToD Direct vascular effects CNS effects Renal + CNS benefit Pregnancy benefit |
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MoA of Methyldopa |
Taken up by noradrenergic neurons Decarboxylated and hydroxylated to form methyl-noradrenaline Not deaminated by MAO Accumulates and displaces NA from synaptic vesicles Less active than NA on a-1 receptors - less vasoconstriction More active on pre-synaptic a-2 - increases auto-inhibitory feedback mechanism - reduces transmitter release |
6 |
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Adverse effects of Methyldopa |
Dry mouth Sedation Orthostatic hypotension Male sexual dysfunction |
D S O M |
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Name a non-selective b-antagonist class II antiarrhythmic + list its effects |
Propanolol Effects mainly attributed to b1 antagonism B antagonism increases refractory period of AV node - interference of AV conduction in arterial tachycardia - reduced ventricular rate Reduces mortality in MI Particularly successful in arrhythmias that occur during exercise |
Drug Cause of antiarrhythmic effects MoA + effect Effect on mortality Particularly successful in what |
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Metoprolol |
SNS antagonist B-1 antagonist that loses selectivity at high doses (propanolol-like effects) Decreases HR, cardiac contractile activity and systolic BP Used to treat angina |
ToD Selectivity Effects Use |
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Adverse effects of metoprolol |
Fatigue Insomnia Dizziness Sexual Dysfunction Bronchospasm Bradycardia Heart block Hypotension Decreased myocardial contractility |
F I D S B B H H D |
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Which kinds of patients is metoprolol not used on |
Bradycardia (<55bpm) Bronchospasm Hypotension (systolic <90mmhg) AV block Severe congestive heart failure |
B B H A S |
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Effect of B-1 adrenoceptors in they eye |
Facilitate the action of cabronic anhydrase - increase production of aq humour Antagonism used to treat glaucoma |
2 |
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Non-selective B-antagonists used to treat glaucoma and mechanism of action |
Carteolol hydrochloride Levobunolol hydrochloride Timolol maleate Block receptors on ciliary body Possible by blocking effect of circulating adrenaline |
3 drugs 2 MoA |
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Selective B-antagonists used to treat glaucoma |
Betaxolol hydrochloride |
1 |
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Non B-antagonist drugs used to treat glaucoma |
Pilocarpine Adrenaline Physostigmine Ecothiopate |
P A P E |
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Other uses of B-antagonists |
Anxiety states - control somatic symptoms associated with sympathetic over reactivity Migraine prophylaxis Benign essential tremor |
A M B |
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Drugs which affect central processes |
Spasmolytics Diazepam Baclofen |
D B |
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Drugs which affect the conduction of nerve AP in motor neurones |
Local anaesthetics (not their primary use) |
L |
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Drugs which affect ACh release |
Hemicholinum (Indirect acetylcholine antagonist) Blockers Neurotoxins (botulinum toxin) |
H B N |
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Drugs which affect depolarisation of motor end-plate |
Tubocurarine Suxamethonium |
T S |
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Drugs which affect propagation of AP along muscle fibre
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Spasmolytics (Dantrolene - reduces intracellular Ca2+ - reduced force of contraction) |
S (D) |
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Non-depolarising NMJ blocking drugs |
Competitive antagonists Tubocurarine Atracurium |
T A |
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Depolarising NMJ blocking drugs |
Agonists Suxamethonium |
S |
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Tubocurarine |
ToD: Non-depolarising NMJ blocking alkaloid MoA: Competitive nAChr antagonist 70-80% block required for desired effects (Graded block - different proportions of fibres blocked) Effects: Flaccid paralysis in the following order: extrinsic eye muscles (double vision), small muscles of face, limbs and pharynx, respiratory muscles Administration: IV (since it is highly charged (cant oral)) Onset of action: 2-3 mins Duration of action: 40-60mins Excretion: 70% urine, 30% bile (careful in hepatic/renal failure) |
ToD MoA Effects Administration Onset of action Duration of action Excretion |
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Why is tubocurarine used in surgery and how can its actions be reverse |
Relaxation of skeletal muscle means less anaesthetic is required Permits artificial ventilation Reversed by anticholinesterases e.g neostigmine - Increases ACh concentration at all NMJ and in PNS Co-administered with atropine to prevent unwanted overstimulation of PNS |
Why (2) Reverse (4) |
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Unwanted effects of tubocurarine |
Hypotension - Ganglion block (low TPR) + Histamine release from mast cells Reflex tachycardia - blockade of vagal ganglia (decreases HR) Bronchospasm + excess bronchial and salivary secretions - histamine release Apnoea |
H R B A |
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Drug similar to tubocurarine |
Atracurium Same effect but shorter duration |
A |
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Use of atropine in MI |
mAChr antagonist After MI there is normally increased vagal (PNS) activity - bradycardia - reduced BP + CO - reduced cardiac perfusion - worsen damage of MI IV atropine given short term post-MI to increase HR |
ToD Problem associated with MI and how atropine is used to treat it |
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Muscarinic antagonists used to modify bronchial smooth muscle tone |
Ipratropium (1x daily) + tiotropium (4x daily) Administered through inhaler/nebulizer Administered to target organ - avoids hepatic metabolism - lower dose required Used for COPD and acute treatment of asthma (B-agonist preferred) |
I T Administration Use |
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Muscarinic antagonists used to modify bladder function |
Oxybutynin, Tolterodine, Solfenacin For overactive bladder, incontinence and enuresis May result from MS or spinal injury Decrease bladder activity - decreased detrussor activity and increased activity of internal sphincter |
O T S Use Effect |
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Use of tropicamide in the eye |
Muscarinic antagonist Pupil dilation for eye examination |
2 |
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Use of mebeverine in the gut
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Used for IBS to reduce intra-colonic pressure by reducing gastric motility |
Use (1) Effect (2) |
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Unwanted effects of antimuscarinic drugs |
Dry eyes/blurred vision/increased intra-ocular pressure Dry mouth Tachycardia Constipation Urinary retention Erectile dysfunction |
Eyes Mouth Heart Gut Bladder Genitalia |
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Use of muscarinic receptor antagonists in CNS |
Benzhexol + Procyclidine Parkinson's disease Drug-induced Parkinsonism - parkinson symptoms induced by ACh-dopamine imbalance caused by drugs (TCA, antemetics, lithium, pheonothiazines) Acute dystonic reactions - sudden outburst of involuntary, jerky movements mainly involving the head and neck |
B P Uses (3) |
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Summarise the mechanism of action of B-1 receptor on the heart |
Activation of B-1 adrenoceptor Stimulaties adenylate cyclase to produce Cyclic AMP Acts as messenger to increase intracellular Ca2+ and stimulate Na/K ATPase in myocytes |
4 |
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Drugs used to treat supraventricular arrhythmias (improper electrical activity of the heart originating from or above AV node) |
Amidoarone Verapamil |
A V |
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Drugs used to treat ventricular arrhythmias |
Flecainide Lidocaine |
F L |
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Drugs used to treat complex arrhythmias (Supraventricular + Ventricular) |
Disopyramide |
D |
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Define the Vaughan-Williams classification |
Classification of anti-arrhythmic drugs (limited clinical significance) |
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Classes of Vaughan-Williams classification |
Class 1: Sodium channel blockade Class 2: Beta adrenergic blockade Class 3: Prolongation of repolarisation Class 4: Calcium channel blockade |
4 S B P C |
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Adenosine |
Supraventricular tachyarrythmias (SVT) DoA: 20-30secs MoA: endogenous mediator produced from ATP Acts on adenosine (A1) receptors to hyperpolarize cardiac tissue and slow conduction through AV node |
Use DoA MoA |
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Adverse effects of adenosine |
Chest pain Shortness of breath Dizziness Nausea (safer than verapamil) |
4 |
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Verapamil |
Prevents recurrence of paroxysmal SVT Reduces ventricular rate in px with atrial fibrilation (provided no wolff-parkinson-white or other abnormal conduction pathways) MoA: Is a phenylalkylamine class drug which acts on cardiac and smooth muscle. Act on intracellular portion of L-type Ca channels to reduce/slow entry |
Use (2) MoA |
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Amiodarone & Dronedarone |
Supraventricular & Ventricular tachyarrythmias MoA: Complex (probs ion channel block) |
Use MoA |
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Adverse effects of amiodarone & dronedarone (non-iodinated/less toxic) |
Amiodarone accumulates in the body (half life: 10-100 days) Photosensitive skin rashes Hypo/hyper-thyroidism Pulmonary fibrosis Corneal deposits Neurological and GI disturbances |
A P H P C N |
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MoA, Effects and Use of Digoxin and Cardiac glycosides |
MoA: Inhibition of Na+/K+ ATPase - increased accumulation og intracellular Na+ - increased intracellular Ca2+via increased Na+/Ca2+ exchange - Positive ionotropic effect. Central vagal stimulation - increased refractory period and reduced rate of conduction through AV node - slows ventricular rate Use: atrial fibrillation and relief of symptoms of chronic hearth failure |
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Adverse effects of Digoxin and Cardiac glycosides |
Dysrhythmias (AV conduction block and increased ectopic pacemaker activity) Hypokalaemia + hypomagnesaemia lower the threshold of digoxin toxicity (with use of diuretics) Amiodarone and Verapamil affect digoxin excretion and plasma binding (Fab ligand (Digibind) used for digoxin toxicity) |
D Toxicity Excretion and plasma binding |
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Ivabradine |
MoA: Blocks If (funny) channel (Na/K channel in SAN) Use: Angina in patients with normal sinus rhythm |
MoA Use |
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Contraindications of using Ivabradine |
Severe bradycardia Sick sinus syndrome 2nd-3rd degree heart block Cardiogenic shock Recent MI |
S S 2 C M |
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Adverse effects of Ivabradine |
Bradychardia First degree heart block Ventricular and supraventricular arrhythmias |
B F V |
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Cardiac inotropes |
Agents that increase force of contraction Treat acute heart failure Dobutamine - B1 adrenoceptor agonist stimulates contraction with little effect on HR Milrinon inhibits phophodiesterase - inhibit breakdown of cAMP in cardiac myocytes - Positive inotropic effect All reduce survival in CHF |
Definition Use Example 1 + MoA Example 2 + MoA |
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Effects of the renin-angiotensin-aldosterone system (RAAS) |
Angiotensin II Increased insulin resistance Activation of cellular immunity Pro-fibrotic Increased BP Increased NA+/fluid retention Cardiovascular remodelling Prothrombotic |
7 |
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List two ACE inhibitors |
Enalapril Captopril |
E C |
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Besides preventing the conversion of angiotensin I to angiotensin II, what else do ACE inhibitors do? |
Prevent breakdown of bradykinin into active metabolites (resulting in a cough being a side effect) |
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What are ACE inhibitors (ACEI) used for? |
Hypertension Heart failure Post MI Diabetic nephropathy Progressive renal insufficiency Patients at high risk of CVD |
H H P D P P |
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Adverse effects of ACEI |
Hypotension Dry cough Angioedema |
H D A |
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Angiotensin receptor blockers (ARB) |
Losartan |
L |
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Direct renin antagonists |
Aliskiren |
A |
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Losartan |
Insurmountable antagonists of type 1 (AT1) receptors for Ang II -prevents renal and vascular actions of Ang II Used in hypertension as an alternative to ACEI with fewer side effectsUsed in CHF in patients who can't tolerate ACEI |
ToD + MoA Use and side effects (2) |
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Aliskiren |
Inhibit enzyme activity of renin - prevent production of Ang I |
MoA |
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Unwanted effects of ACEI and ARB |
Generally well tolerated esp ARB Cough (ACEI) Hypotension (ACEI + ARB) Urticaria (hives)/Angiodema (rarely ACEI) Hyperkalaemia (care with K supplements/K sparing diuretics) Fetal injury (both) Renal failure in patients with renal artery stenosis (ACEI + ARB) |
C H U/A H F R |
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Aldosterone antagonist |
Spirinolcatone |
S |
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Spirinolactone |
Inhibits Na retaining effects of aldosterone Limited diuretic effect Useful in heart failure and resistant hypertension |
MoA (1) Effect (1) Use (2) |
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Adverse effects of spirinolactone |
Can cause hyperkalaemia Unwanted steroid-like effects e.g. gynaecomastia, menstural disorders and testicular atrophy |
H G M T |
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List three calcium antagonist drugs |
Dihydropyridine Diltiazem Verapamil |
D D V |
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Uses of dihydropyridine |
Hypertension Angina |
H A |
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2 things calcium antagonists can act on |
Afterload Cardiac muscle |
A C |
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Effect of dihydropyridine |
Reduced smooth muscle contraction |
1 |
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MoA of dihydropyridine |
Act on the extracellular portion of L-type Ca channels to inhibit calcium entry in vascular smooth muscle |
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Use of verapamil |
Angina Proxysmal SVT Atrial fibrillation |
A P A |
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Effect of verapamil and diltiazem |
Negative inotropic effect (verapamil > diltiazem) Smooth muscle action |
2 |
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MoA of verapamil and diltiazem |
Act on intracellular portion of L-type Ca channels to inhibit Ca entry in cardiac and smooth muscle |
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Unwanted effects of verapamil |
Bradycardia AV block Worsening of heart failure Constipation |
B A H C |
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Unwanted effects of dihydropyridine |
Ankle oedema Headache/flushing Palpitations |
A H P |
