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A Textbook of Clinical Pharmacology and Therapeutics

A Textbook of Clinical Pharmacology and Therapeutics

Assess risk factors

Assess risk factors Investigations: full blood count (exclude polycythaemia, either primary or secondary to smoking, thrombocythaemia), plasma glucose and lipid profile No significant improvement in symptoms REFER TO CARDIOLOGIST OR CHEST PAIN CLINIC order to prevent pain. Alternatively, long-acting nitrates (e.g. isosorbide mononitrate) may be taken regularly to reduce the frequency of attacks. Beta-blockers (usually of the ‘cardioselective’ type, e.g. atenolol, metoprolol or bisoprolol) or calcium-channel blockers (most commonly diltiazem, less commonly verapamil or one of the dihydropyridine drugs, such as nifedipine or amlodipine) are also useful for chronic prophylaxis (see below). Nicorandil combines nitrate-like with K � -channel-activating properties and relaxes veins and arteries. It is used in acute and long-term prophylaxis of angina, usually as an add-on to nitrates, beta-blockers and/or calcium-channel blockers where these have been incompletely effective, poorly tolerated or contraindicated. Statins (e.g. simvastatin or atorvastatin) should be prescribed routinely for cholesterol lowering unless there is a contraindication, regardless of serum cholesterol (unless it is already very low: total cholesterol �4 mmol/L and/or LDL cholesterol �2 mmol/L), as numerous large studies have shown prognostic benefit in terms of prevention of cardiac events and reduction in mortality. CONSIDERATION OF SURGERY/ANGIOPLASTY Cardiac catheterization identifies patients who would benefit from coronary artery bypass graft (CABG) surgery or percutaneous coronary intervention (PCI, which most commonly involves balloon angioplasty of the affected coronary arteries with concomitant stent insertion). Coronary artery disease is progressive and there are two roles for such interventions: 1. symptom relief; 2. to improve outcome. Aspirin 75 mg daily Statin therapy Modification of risk factors Trial of anti-anginal medication Adequate control of symptoms Adequate control of risk factors ANNUAL REVIEW (Assessment of pain, risk factors) Worsening of symptoms or risk factors MANAGEMENT OF STABLE ANGINA 197 Figure 29.1: General management of stable angina. CABG and PCI are both excellent treatments for relieving the symptoms of angina, although they are not a permanent cure and symptoms may recur if there is restenosis, if the graft becomes occluded, or if the underlying atheromatous disease progresses. Restenosis following PCI is relatively common, occurring in 20–30% of patients in the first four to six months following the procedure, and various strategies are currently under investigation for reducing the occurrence of restenosis; one very promising strategy involves the use of ‘drug-eluting’ stents (stents which are coated with a thin polymer containing a cytotoxic drug, usually sirolimus or paclitaxel, which suppresses the hypertrophic vascular response to injury). PCI as currently performed does not improve the final outcome in terms of survival or myocardial infarction, whereas CABG can benefit some patients. Those with significant disease in the left main coronary artery survive longer if they are operated on and so do patients with severe triple-vessel disease. Patients with strongly positive stress cardiograms have a relatively high incidence of such lesions, but unfortunately there is no foolproof method of making such anatomical diagnoses non-invasively, so the issue of which patients to subject to the low risks of invasive study remains one of clinical judgement and of cost. Surgical treatment consists of coronary artery grafting with saphenous vein or, preferably, internal mammary artery (and sometimes other artery segments, e.g. radial artery) to bypass diseased segment(s) of coronary artery. Arterial bypass grafts have a much longer patency life than vein grafts, the latter usually becoming occluded after 10–15 years (and often after much shorter periods). PCI has yet to be shown to prolong life in the setting of stable angina, but can be valuable as a less demanding alternative to surgery in patients with accessible

198 ISCHAEMIC HEART DISEASE MINIMAL/INFREQUENT SYMPTOMS Sublingual GTN as required (tablets or preferably spray Aspirin 75 mg once daily Statin therapy Figure 29.2: Drug therapy of stable angina. lesions whose symptoms are not adequately controlled by medical therapy alone. Several antiplatelet drugs are given at the time of PCI, including oral aspirin and clopidogrel, and a glycoprotein IIb/IIIa inhibitor given intravenously such as abciximab, eptifibatide or tirofiban (Chapter 30). Aspirin is usually continued indefinitely and clopidogrel is usually continued for at least one month following the procedure. MANAGEMENT OF UNSTABLE CORONARY DISEASE ACUTE CORONARY SYNDROME SIGNIFICANT/REGULAR SYMPTOMS Beta blocker (e.g. atenolol) Diltiazem or verapamil if intolerant to beta blocker Dihydropyridine calcium antagonist (e.g. amlodipine or nifedipine) or long acting nitrate (e.g. isosorbide mononitrate) if intolerant of above Consider nicorandil if above incompletely effective, poorly tolerated or contraindicated Acute coronary syndrome (ACS) is a blanket term used to describe the consequences of coronary artery occlusion, whether transient or permanent, partial or complete. These different patterns of coronary occlusion give rise to the different types of ACS, namely unstable angina (where no detectable myocardial necrosis is present), non-ST-segmentelevation myocardial infarction (NSTEMI) and ST-segmentelevation myocardial infarction (STEMI, usually larger in extent and fuller in thickness of myocardial wall affected than NSTEMI). A flow chart for management of ACS is given in Figure 29.3. Unstable angina and NSTEMI are a continuum of disease, and usually only distinguishable by the presence of a positive serum troponin test in NSTEMI (troponin now being the gold standard serum marker of myocardial damage); their management is similar and discussed further here. Management of STEMI is discussed separately below. All patients with ACS must stop smoking. This is more urgent than in other patients with coronary artery disease, because of the acute pro-thrombotic effect of smoking. Patients with ACS require urgent antiplatelet therapy, in the form of aspirin and clopidogrel (Chapter 30), plus antithrombotic therapy with heparin (nowadays most often lowmolecular-weight heparin administered subcutaneously; see Chapter 30). Data from the CURE trial suggest that combined aspirin and clopidogrel treatment is better than aspirin alone, and that this combination should be continued for several months, and preferably for up to a year, following which aspirin alone should be continued. This antiplatelet/antithrombotic regime approximately halves the likelihood of myocardial infarction, and is the most effective known treatment for improving outcome in pre-infarction syndromes. By contrast, GTN, while very effective in relieving pain associated with unstable angina, does not improve outcome. It is usually given as a constant-rate intravenous infusion for this indication. A β-blocker is prescribed if not contraindicated. If β-blockers are contraindicated, a long-acting Ca 2� -antagonist is a useful alternative. Diltiazem is often used as it does not cause reflex tachycardia and is less negatively inotropic than verapamil. β-Blockers and Ca 2� -antagonists are often prescribed together, but there is disappointingly little evidence that their effects are synergistic or even additive. Moreover, there is a theoretical risk of severe bradycardia or of precipitation of heart failure if β-blockers are co-administered with these negatively chronotropic and inotropic drugs, especially so for verapamil; where concomitant β-blockade and calcium-channel blockade is desired, it is probably safest to use a dihydropyridine calcium-channel blocker (e.g. nifedipine or amlodipine) rather than verapamil or diltiazem. Nicorandil is now often added as well, but again there is not much evidence of added benefit. Coronary angiography is indicated in patients who are potentially suitable for PCI or CABG, and should be considered as an emergency in patients who fail to settle on medical therapy. ST-ELEVATION-MYOCARDIAL INFARCTION (STEMI) ACUTE MANAGEMENT Oxygen This is given in the highest concentration available (unless there is coincident pulmonary disease with carbon dioxide retention) delivered by face mask (FiO2 approximately 60%) or by nasal prongs if a face mask is not tolerated. Pain relief This usually requires an intravenous opiate (morphine or diamorphine; see Chapter 25) and concurrent treatment with an anti-emetic (e.g. promethazine or metoclopramide; see Chapter 34).

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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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    ● 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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