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A Textbook of Clinical Pharmacology and Therapeutics

A Textbook of Clinical Pharmacology and Therapeutics

Drug interactions

Drug interactions Amiodarone potentiates warfarin by inhibiting its metabolism. It can precipitate digoxin toxicity (the digoxin dose should be reduced by 50% when amiodarone is added) and can cause severe bradycardia if used with β-adrenoceptor antagonists or verapamil. SOTALOL Use Sotalol has uses similar to amiodarone, but a different spectrum of adverse effects. The plasma K � concentration should be monitored during chronic use and corrected if it is low in order to reduce the risk of torsades de pointes (see below). Mechanism of action Sotalol is unique among β-adrenoceptor antagonists in possessing substantial class III activity. It is a racemate, the D-isomer possessing exclusively class III activity. A clinical trial of D-sotalol (the ‘SWORD’ study) indicated that it reduces survival in patients with ventricular ectopic activity. The racemate is preferred. Adverse effects and contraindications Since it prolongs the cardiac action potential (detected on the ECG as a prolonged QT interval) it can cause ventricular tachycardia of the torsades de pointes variety, like amiodarone. Hypokalaemia predisposes to this effect. The betablocking activity of sotalol contraindicates its use in patients with obstructive airways disease, unstable heart failure, peripheral vascular disease or heart block. Drug interactions Diuretics predispose to torsades de pointes by causing electrolyte disturbance (hypokalaemia/hypomagnesaemia). Similarly, other drugs that prolong the QT interval should be avoided. These include class Ia anti-dysrhythmic drugs (quinidine, disopyramide), which slow cardiac repolarization as well as depolarization, and several important psychotropic drugs, including tricyclic antidepressants and phenothiazines. Histamine H1-antagonists (terfenadine, astemizole) should be avoided for the same reason. VERAPAMIL Use Verapamil is used as an anti-dysrhythmic: • prophylactically to reduce the risk of recurrent SVT, by mouth; • to reduce the ventricular rate in patients with atrial fibrillation who are not adequately controlled by digoxin alone (but beware interaction causing digoxin toxicity, see below); • to terminate SVT in patients who are not haemodynamically compromised. In this setting it is given intravenously over five minutes. Adenosine is generally preferred, but verapamil may be useful in patients in whom adenosine is contraindicated (e.g. asthmatics). SELECTED ANTI-DYSRHYTHMIC DRUGS 225 Mechanism of action Verapamil blocks L-type voltage-dependent Ca2� channels. It is a class IV drug and has greater effects on cardiac conducting tissue than other Ca2� antagonists. In common with other calcium antagonists, it relaxes the smooth muscle of peripheral arterioles and veins, and of coronary arteries. It is a negative inotrope, as cytoplasmic Ca2� is crucial for cardiac contraction. As an anti-dysrhythmic drug, its major effect is to slow intracardiac conduction, particularly through the AV node. This reduces the ventricular response in atrial fibrillation and flutter, and abolishes most re-entry nodal tachycardias. Mild resting bradycardia is common, together with prolongation of the PR interval. Adverse effects and contraindications 1. Cardiovascular effects: Verapamil is contraindicated in cardiac failure because of the negative inotropic effect. It is also contraindicated in sick sinus syndrome or intracardiac conduction block. It can cause hypotension, AV block or other bradydysrhythmias. It is contraindicated in WPW syndrome complicated by supraventricular tachycardia, atrial flutter or atrial fibrillation, as it can increase the rate of conduction through the accessory pathway. Verapamil is ineffective in ventricular dysrhythmias and its negative inotropic effect makes its inadvertent use in such dysrhythmias extremely hazardous. 2. Gastrointestinal tract: About one-third of patients experience constipation, although this can usually be prevented or managed successfully with advice about increased dietary intake of fibre and use of laxatives, if necessary. 3. Other adverse effects: Headache, dizziness and facial flushing are related to vasodilatation (compare with similar or worse symptoms caused by other calciumchannel blockers). Drug rashes, pain in the gums and a metallic taste in the mouth are uncommon. Drug interactions The important pharmacodynamic interaction of verapamil with β-adrenoceptor antagonists, which occurs especially when one or other member of the pair is administered intravenously, contraindicates their combined use by this route. Verapamil reduces digoxin excretion and the dose of digoxin should therefore be halved when these drugs are combined. For the same reason, verapamil is contraindicated in patients with digoxin toxicity, especially as these drugs also have a potentially fatal additive effect on the AV node. ADENOSINE Use Adenosine is used to terminate SVT. In addition to its use in regular narrow complex tachycardia, it is useful diagnostically in patients with regular broad complex tachycardia which is suspected of being SVT with aberrant conduction. If adenosine terminates the tachycardia, this implies that the AV node is indeed involved. However, if this diagnosis is wrong

226 CARDIAC DYSRHYTHMIAS (as is not infrequently the case) and the patient actually has VT, little or no harm results, in contrast to the use of verapamil in VT. Mechanism of action Adenosine acts on specific adenosine receptors. A1-receptors block AV nodal conduction. Adenosine also constricts bronchial smooth muscle by an A1 effect, especially in asthmatics. It relaxes vascular smooth muscle, stimulates nociceptive afferent neurones in the heart and inhibits platelet aggregation via A2-receptors. Adverse effects and contraindications Chest pain, flushing, shortness of breath, dizziness and nausea are common but short-lived. Chest pain can be alarming if the patient is not warned of its benign nature before the drug is administered. Adenosine is contraindicated in patients with asthma or heart block (unless already paced) and should be used with care in patients with WPW syndrome in whom the ventricular rate during atrial fibrillation may be accelerated as a result of blocking the normal AV nodal pathway and hence favouring conduction through the abnormal pathway. This theoretically increases the risk of ventricular fibrillation; however, this risk is probably small and should not discourage the use of adenosine in patients with broad complex tachycardias of uncertain origin. Pharmacokinetics Adenosine is rapidly cleared from the circulation by uptake into red blood cells and by enzymes on the luminal surface of endothelial cells. It is deaminated to inosine. The circulatory effects of a bolus therapeutic dose of adenosine last for 20–30 seconds, although effects on the airways in asthmatics persist for longer. Drug interactions Dipyridamole blocks cellular adenosine uptake and potentiates its action. Theophylline blocks adenosine receptors and inhibits its action. DIGOXIN For more information on digoxin, see also Chapter 31. Use The main use of digoxin is to control the ventricular rate (and hence improve cardiac output) in patients with atrial fibrillation. Digoxin is usually given orally, but if this is impossible, or if a rapid effect is needed, it can be given intravenously. Since the t1/2 is approximately one to two days in patients with normal renal function, repeated administration of a maintenance dose results in a plateau concentration within about three to six days. This is acceptable in many settings, but if clinical circumstances are more urgent, a therapeutic plasma concentration can be achieved more rapidly by administering a loading dose. The dose is adjusted according to the response, sometimes supplemented by plasma concentration measurement. Mechanism of action 1. Digoxin inhibits membrane Na � /K � adenosine triphosphatase (Na �� K � ATPase), which is responsible for the active extrusion of Na � from myocardial, as well as other cells. This results in accumulation of intracellular Na � , which indirectly increases the intracellular Ca 2� content via Na � /Ca 2� exchange and intracellular Ca 2� storage. The rise in availability of intracellular Ca 2� accounts for the positive inotropic effect of digoxin. 2. Slowing of the ventricular rate results from several mechanisms, particularly increased vagal activity: • delayed conduction through the atrioventricular node and bundle of His; • increased cardiac output due to the positive inotropic effect of digoxin reduces reflex sympathetic tone; • small doses of digitalis sensitize the sinoatrial node to vagal impulses. The cellular mechanism of this effect is not known. ATROPINE Use Atropine is administered intravenously to patients with haemodynamic compromise due to inappropriate sinus bradycardia. (It is also used for several other non-cardiological indications, including anaesthetic premedication, topical application to the eye to produce mydriasis and for patients who have been poisoned with organophosphorous anticholinesterase drugs; see Chapter 54). Mechanism of action Acetylcholine released by the vagus nerve acts on muscarinic receptors in atrial and cardiac conducting tissues. This increases K� permeability, thereby shortening the cardiac action potential and slowing the rate of increase of pacemaker potentials and cardiac rate. Atropine is a selective antagonist of acetylcholine at muscarinic receptors, and it thereby counters these actions of acetylcholine, accelerating the heart rate in patients with sinus bradycardia by inhibiting excessive vagal tone. Adverse effects and contraindications Parasympathetic blockade by atropine produces widespread effects, including reduced salivation, lachrymation and sweating, decreased secretions in the gut and respiratory tract, tachycardia, urinary retention in men, constipation, pupillary dilatation and ciliary paralysis. It is contraindicated in patients with narrow-angle glaucoma. Atropine can cause central nervous system effects, including hallucinations. Pharmacokinetics Although atropine is completely absorbed after oral administration, it is administered intravenously to obtain a rapid

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    A Textbook of Clinical Pharmacology

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    A Textbook of Clinical Pharmacology

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    This fifth edition is dedicated to

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    FOREWORD viii PREFACE ix ACKNOWLEDG

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    PREFACE Clinical pharmacology is th

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    PART I GENERAL PRINCIPLES

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    ● Use of drugs 3 ● Adverse effe

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    and acquired factors, notably disea

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    100 Effect (%) 0 0 5 10 1 10 100 (a

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    Dose ratio -1 100 50 The relationsh

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    ● Introduction 11 ● Constant-ra

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    In reality, processes of eliminatio

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    lood (from which samples are taken

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    ● Introduction 17 ● Bioavailabi

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    ROUTES OF ADMINISTRATION ORAL ROUTE

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    Transdermal absorption is sufficien

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    FURTHER READING Fix JA. Strategies

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    and thromboxanes are CYP450 enzymes

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    and lorazepam. Some patients inheri

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    Orally administered drug Parenteral

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    ● Introduction 31 ● Glomerular

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    ACTIVE TUBULAR REABSORPTION This is

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    DISTRIBUTION Drug distribution is a

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    Detailed recommendations on dosage

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    DIGOXIN Myxoedematous patients are

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    ● Introduction 41 ● Role of dru

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    25 20 10 Life-threatening toxicity

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    ● Introduction 45 ● Harmful eff

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    vagina in girls in their late teens

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    an anti-analgesic effect when combi

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    Case history A 20-year-old female m

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    METABOLISM At birth, the hepatic mi

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    lifelong effects as a result of tox

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    DISTRIBUTION Ageing is associated w

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    DIGOXIN Digoxin toxicity is common

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    FURTHER READING Dhesi JK, Allain TJ

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    Factors involved in the aetiology o

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    analgesic. Following its release, t

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    antibiotics, such as penicillin or

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    predisposes to non-immune haemolysi

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    ● Introduction 71 ● Useful inte

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    Response Therapeutic range Toxic ra

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    Table 13.1: Interactions outside th

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    Table 13.5: Competitive interaction

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    ● Introduction: ‘personalized m

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    Table 14.2: Variations in drug resp

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    lipoprotein (LDL) is impaired. LDL

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    Key points • Genetic differences

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    • Discovery • • Screening Pre

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    Too many statistical comparisons pe

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    ETHICS COMMITTEES Protocols for all

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    Table 16.1: Recombinant proteins/en

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    duration and benefit. Adenoviral ve

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    ● Introduction 97 ● Garlic 97

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    A case report has suggested a possi

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    including hypericin and pseudohyper

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    PART II THE NERVOUS SYSTEM

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    ● Introduction 105 ● Sleep diff

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    and daytime sleeping should be disc

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    Key points • Insomnia and anxiety

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    Box 19.1: Dopamine theory of schizo

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    The Boston Collaborative Survey ind

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    Oral medication, especially in liqu

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    e.g. interpersonal difficulties or

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    Partial response to first-line trea

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    Key points Drug treatment of depres

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    Case history A 45-year-old man with

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    Levodopa PRINCIPLES OF TREATMENT IN

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    • pulmonary, retroperitoneal and

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    CHOREA The γ-aminobutyric acid con

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    Cholinergic crisis Treatment of mya

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    ● Introduction 133 ● Mechanisms

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    absolute arbiter. The availability

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    Table 22.2: Metabolic interactions

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    FURTHER ANTI-EPILEPTICS Other drugs

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    Case history A 24-year-old woman wh

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    Assessment of migraine severity and

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    ● General anaesthetics 145 ● In

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    is the theoretical concern of a ‘

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    • Respiratory system - apnoea fol

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    Competitive antagonists (vecuronium

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    have also proved useful in combinat

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    ● Introduction 155 ● Pathophysi

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    ASPIRIN (ACETYLSALICYLATE) Use Anti

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    Key points Drugs for mild pain •

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    increases, correlating with the hig

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    • If possible, use oral medicatio

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    PART III THE MUSCULOSKELETAL SYSTEM

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    ● Introduction: inflammation 167

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    Chapter 33). All NSAIDs cause wheez

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    • Stomatitis suggests the possibi

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    Pharmacokinetics Allopurinol is wel

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    Key points Diuretics Diuretics are

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    is sometimes caused by drugs, notab

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    or with potassium-sparing diuretics

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    Greger R, Lang F, Sebekova, Heidlan

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    PART VIII THE ENDOCRINE SYSTEM

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    ● Introduction 285 ● Pathophysi

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    in prefilled injection devices (‘

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    Metformin should be withdrawn and i

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    FURTHER READING American Diabetes A

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    deficiency. Potassium iodide (3 mg

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    fertility. It is contraindicated du

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    ● Introduction 297 ● Vitamin D

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    effective in life-threatening hyper

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    Further reading Block GA, Martin KJ

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    Table 40.1: Actions of cortisol and

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    injection may be useful, but if don

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    CHAPTER 41 REPRODUCTIVE ENDOCRINOLO

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    elease by the pituitary via negativ

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    Treatment with depot progestogen in

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    infusion using an infusion pump to

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    significant proportion of men who r

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    with symptoms caused by the release

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    FURTHER READING Birnbaumer M. Vasop

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    PART IX SELECTIVE TOXICITY

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    ● Principles of antibacterial che

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    2. transfer of resistance between o

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    Pharmacokinetics Absorption of thes

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    Mechanism of action Macrolides bind

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    asic quinolone structure dramatical

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    Case history A 70-year-old man with

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    PRINCIPLES OF MANAGEMENT OF MYCOBAC

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    Pharmacokinetics Absorption from th

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    MYCOBACTERIUM LEPRAE INFECTION Lepr

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    POLYENES AMPHOTERICIN B Uses Amphot

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    therapy is adequate though more fre

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    NUCLEOSIDE ANALOGUES ACICLOVIR Uses

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    Table 45.3: Summary of available ac

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    Uses Interferon-α when combined wi

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    ● Introduction 351 ● Immunopath

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    Table 46.1: Examples of combination

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    NON-NUCLEOSIDE ANALOGUE REVERSE TRA

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    FUSION INHIBITORS Uses Currently, e

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    salvage therapy include azithromyci

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    ● Malaria 361 ● Trypanosomal in

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    Pharmacokinetics Chloroquine is rap

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    Table 47.2: Drug therapy of non-mal

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    ● Introduction 367 ● Pathophysi

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    Table 48.1: Classification of commo

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    Polymorph count/mm 3 (a) (b) 10 000

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    doses are used to prepare patients

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    Adverse effects Methotrexate Inhibi

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    Table 48.7: Summary of clinical pha

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    Table 48.9: Summary of the clinical

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    Plasma membrane Signal transduction

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    Table 48.10: Monoclonal antibodies

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    INTERFERON-ALFA 2B Interferon-alfa

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    PART X HAEMATOLOGY

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    ● Haematinics - iron, vitamin B 1

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    one marrow to produce red cells. Th

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    EPO Erythroid precursors Erythrocyt

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    Therapeutic principles The extent o

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    PART XI IMMUNOPHARMACOLOGY

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    ● Introduction 399 ● Immunity a

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    Key points Antigen recognition Expr

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    Table 50.1: Novel anti-proliferativ

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    Key points Treatment of anaphylacti

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    DRUGS THAT ENHANCE IMMUNE SYSTEM FU

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    PART XII THE SKIN

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    ● Introduction 411 ● Acne 411

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    DERMATITIS (ECZEMA) PRINCIPLES OF T

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    SPECIALISTS ONLY SPECIALISTS ONLY E

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    TREATMENT OF OTHER SKIN INFECTIONS

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    effect of too high a dose of UVB in

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    PART XIII THE EYE

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    ● Introduction: ocular anatomy, p

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    to cause pupillary dilatation, name

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    Table 52.3: Antibacterial agents us

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    Table 52.6: Common drug-induced pro

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    PART XIV CLINICAL TOXICOLOGY

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    ● Introduction 433 ● Pathophysi

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    Table 53.2: Central nervous system

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    which provide anonymized data to th

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    Peak plasma levels after smoking ci

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    Key points Acute effects of alcohol

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    FURTHER READING Goldman D, Oroszi G

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    Table 54.2: Common indications for

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    Table 54.5: Antidotes and other spe

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    Commission on Human Medicines (CHM)

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    Note: Page numbers in italics refer

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    atrial fibrillation 217, 221 digoxi

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    Cushing’s syndrome 302 cyclic ade

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    5-fluorouracil 375-6 fluoxetine, mo

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    children 54 diazepam 108 iron prepa

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    non-steroidal anti-inflammatory dru

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    puberty (male), delay 314 puerperiu

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    tolerance 9, 433 benzodiazepines 10

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