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A Textbook of Clinical Pharmacology and Therapeutics

A Textbook of Clinical Pharmacology and Therapeutics

AT 1 receptor) produce

AT 1 receptor) produce good 24-hour control. Their beneficial effect in patients with heart failure (Chapter 31) or following myocardial infarction (Chapter 29) makes them or an ACEI (above) useful in hypertensive patients with these complications. Similarly, an ACEI or a sartan is preferred over other anti-hypertensive drugs in diabetic patients where they slow the progression of nephropathy. Head to head comparison of losartan versus atenolol in hypertension (the LIFE study) favoured the sartan. Their excellent tolerability makes them first choice ‘A’ drugs for many physicians, but they are more expensive than ACEI. First-dose hypotension can occur and it is sensible to apply similar precautions as when starting an ACEI (first dose at night, avoid starting if volume contracted). Mechanism of action Most of the effects of angiotensin II, including vasoconstriction and aldosterone release, are mediated by the angiotensin II subtype 1 (AT1) receptor. The pharmacology of sartans differs predictably from that of ACEI, since they do not inhibit the degradation of bradykinin (Figure 28.5). This difference probably explains the lack of cough with sartans. Adverse effects Adverse effects on renal function in patients with bilateral renal artery stenosis are similar to an ACEI, as is hyperkalaemia and fetal renal toxicity. Angio-oedema is much less common than with ACEI, but can occur. Pharmacokinetics Sartans are well absorbed after oral administration. Losartan has an active metabolite. Half-lives of most marketed ARB are long enough to permit once daily dosing. Drug interactions There is a rationale for combining a sartan with an ACEI (not all angiotensin II is ACE-derived, and some useful effects of ACEI could be kinin-mediated); clinical experience suggests that this has little additional effect in hypertensive patients, however. Clinical trial data on this combination in heart failure are discussed in Chapter 31. B DRUGS �-ADRENOCEPTOR ANTAGONISTS Use See Chapter 32 for use of β-adrenoceptor antagonists in cardiac dysrhythmias. Examples of β-adrenoceptor antagonists currently in clinical use are shown in Table 28.1. Beta-blockers lower blood pressure and reduce the risk of stroke in patients with mild essential hypertension, but in several randomized controlled Change in flow (%) (a) Change in flow (%) (b) 20 0 �20 �40 �60 �80 600 400 200 0 DRUGS USED TO TREAT HYPERTENSION 189 10 1 10 2 10 1 Placebo Enalapril Losartan Angiotensin II (pmol/min) Placebo Enalapril Losartan Bradykinin (pmol/min) trials (particularly of atenolol) have performed less well than comparator drugs. The explanation is uncertain, but one possibility is that they have less effect on central (i.e. aortic) blood pressure than on brachial artery pressure. ‘B’ drugs are no longer preferred over ‘A’ drugs as first line in situations where an A or B would previously have been selected, as explained above. They are, however, useful in hypertensive patients with an additional complication such as ischaemic heart disease (Chapter 29) or heart failure (Chapter 31). The negative inotropic effect of beta-blocking drugs is particularly useful for stabilizing patients with dissecting aneurysms of the thoracic aorta, in whom it is desirable not only to lower the 10 3 10 3 Figure 28.5: Differential effects of angiotensin converting enzyme inhibition (enalapril) and of angiotensin receptor blockade (losartan) on angiotensin II and bradykinin vasomotor actions in the human forearm vasculature. (Redrawn with permission from Cockcroft JR et al. Journal of Cardiovascular Pharmacology 1993; 22: 579–84.)

190 HYPERTENSION Table 28.1: Examples of β-adrenoceptors in clinical use Drug Selectivity Pharmacokinetic features Comment Propranolol Non-selective Non-polar; substantial presystematic metabolism; variable dose requirements; multiple daily dosing First beta-blocker in clinical use Atenolol β1-selective Polar; renal elimination; once daily dosing Widely used; avoid in renal failure Metoprolol β1-selective Non-polar; cytochrome P450 (2D6 isoenzyme) Widely used Esmolol β1-selective Short acting given by i.v. infusion; Used in intensive care unit/theatre renal elimination of acid metabolite (e.g. dissecting aneurysm) Sotalol Non-selective Polar; renal elimination A racemate: the D-isomer has class (L-isomer) III anti-dysrhythmic actions (see Chapter 31) Labetolol Non-selective Hepatic glucuronidation Additional alpha-blocking and partial β2-agonist activity. Used in the latter part of pregnancy Oxprenolol Non-selective Hepatic hydroxylation/glucuronidation Partial agonist mean pressure, but also to reduce the rate of rise of the arterial pressure wave. Classification of β-adrenoceptor antagonists β-Adrenoceptors are subdivided into β1-receptors (heart), β2-receptors (blood vessels, bronchioles) and β3-receptors (some metabolic effects, e.g. in brown fat). Cardioselective drugs (e.g. atenolol, metoprolol, bisoprolol, nebivolol) inhibit β1-receptors with less effect on bronchial and vascular β2-receptors. However, even cardioselective drugs are hazardous for patients with asthma. Some beta-blockers (e.g. oxprenolol) are partial agonists and possess intrinsic sympathomimetic activity. There is little hard evidence supporting their superiority to antagonists for most indications although individual patients may find such a drug acceptable when they have failed to tolerate a pure antagonist (e.g. patients with angina and claudication). Beta-blockers with additional vasodilating properties are available. This is theoretically an advantage in treating patients with hypertension. Their mechanisms vary. Some (e.g. labetolol, carvedilol) have additional α-blocking activity. Nebivolol releases endothelium-derived nitric oxide. Mechanism of action β-Adrenoceptor antagonists reduce cardiac output (via negative chronotropic and negative inotropic effects on the heart), inhibit renin secretion and some have additional central actions reducing sympathetic outflow from the central nervous system (CNS). Adverse effects and contraindications • Intolerance – fatigue, cold extremities, erectile dysfunction; less commonly vivid dreams. • Airways obstruction – asthmatics sometimes tolerate a small dose of a selective drug when first prescribed, only to suffer an exceptionally severe attack subsequently, and β-adrenoceptor antagonists should ideally be avoided altogether in asthmatics and used only with caution in COPD patients, many of whom have a reversible component. • Decompensated heart failure – β-adrenoceptor antagonists are contraindicated (in contrast to stable heart failure, Chapter 31). • Peripheral vascular disease and vasospasm – β-adrenoceptor antagonists worsen claudication and Raynaud’s phenomenon. • Hypoglycaemia – β-adrenoceptor antagonists can mask symptoms of hypoglycaemia and the rate of recovery is slowed, because adrenaline stimulates gluconeogenesis. • Heart block – β-adrenoceptor antagonists can precipitate or worsen heart block. • Metabolic disturbance – β-adrenoreceptor antagonists worsen glycaemic control in type 2 diabetes mellitus. Pharmacokinetics β-Adrenoceptor antagonists are well absorbed and are only given intravenously in emergencies. Lipophilic drugs (e.g. propranolol) are subject to extensive presystemic metabolism in the gut wall and liver by CYP450. Lipophilic beta-blockers enter the brain more readily than do polar drugs and so

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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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  • Page 178 and 179: ● Introduction: inflammation 167
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  • Page 240 and 241: Case history A 24-year-old medical
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    Drug interactions Although synergis

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    use in asthma has declined consider

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    α 1-antitrypsin deficiency, neutro

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    PART VI THE ALIMENTARY SYSTEM

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    ● Peptic ulceration 247 ● Oesop

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    PEPTIC ULCERATION 249 • With rega

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    Ranitidine has a similar profile of

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    Vestibular stimulation ? via cerebe

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    cortical centres affecting vomiting

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    • in hepatocellular failure to re

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    Ciprofloxacin is occasionally used

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    withdrawal), small doses of benzodi

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    Table 34.7: Dose-independent hepato

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    ● Introduction 265 ● General ph

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    dinucleotide (NAD) and nicotinamide

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    Table 35.1: Common trace element de

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    PART VII FLUIDS AND ELECTROLYTES

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    ● Introduction 273 ● Volume ove

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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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