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A Textbook of Clinical Pharmacology and Therapeutics

A Textbook of Clinical Pharmacology and Therapeutics

deficiency. Potassium

deficiency. Potassium iodide (3 mg daily p.o.) prevents further enlargement of the gland, but seldom actually shrinks it. Iodized salt is used to prevent this type of endemic goitre in areas where the diet is iodine deficient, according to a defined World Health Organization (WHO) policy. Preoperative treatment with Lugol’s iodine solution (an aqueous solution of iodine and potassium iodide) in combination with carbimazole or propylthiouracil (see below) is used to reduce the vascularity of the gland and inhibit thyroid hormone release. This action of iodine in inhibiting thyroid hormone release is only maintained for one to two weeks, after which thyroid hormone release is markedly increased if the cause of the hyperthyroidism has not been dealt with. THYROXINE AND TRI-IODOTHYRONINE Use L-Thyroxine is used in the treatment of uncomplicated hypothyroidism, the dose being individualized according to serum TSH. The dose is titrated every four weeks until the patient has responded clinically and the TSH level has fallen to within the normal range. Excessive dosage may precipitate cardiac complications, particularly in patients with ischaemic heart disease in whom the starting dose should be reduced. If angina pectoris limits the dose of thyroxine, the addition of a beta-blocker (e.g. atenolol) will allow further increments in thyroxine dosage. Long-term overdosage is undesirable and causes osteoporosis, as well as predisposing to cardiac dysrhythmias. Congenital hypothyroidism is treated similarly and thyroxine must be given as early as possible. In the UK, the adoption of the Guthrie test has greatly facilitated the early detection of neonatal hypothyroidism. The rapid action of T3 is useful in treating myxoedema coma. It is given intramuscularly while starting maintenance therapy with thyroxine. Hypothyroidism sometimes coexists with Addison’s disease (also autoimmune in aetiology) and hydrocortisone is given empirically to patients with myxoedema coma. Hypothyroidism may result from hypopituitarism. This is also treated with oral thyroxine in the usual doses. Glucocorticosteroid replacement must be started first, otherwise acute adrenal insufficiency will be precipitated. Mechanism of action Thyroxine is a prohormone. After entering cells it is converted to T3, which binds to the thyroid hormone nuclear receptor and the ligand–receptor complex increases transcription of genes involved in the following cellular functions: • stimulation of metabolism – raised basal metabolic rate; • promotion of normal growth and maturation, particularly of the central nervous system and skeleton; • sensitization to the effects of catecholamines. Adverse effects The adverse effects of the thyroid hormones relate to their physiological functions and include cardiac dysrhythmia, angina, myocardial infarction and congestive cardiac failure. ANTITHYROID DRUGS 293 Tremor, restlessness, heat intolerance, diarrhoea and other features of hyperthyroidism are dose-dependent toxic effects of these hormones. Chronic thyroxine excess is an insidious cause of osteoporosis. Pharmacokinetics Thyroid hormones are absorbed from the gut. The effects of T4 are not usually detectable before 24 hours and maximum activity is not attained for many days during regular daily dosing. T3 produces effects within six hours and peak activity is reached within 24 hours. The t1/2 of T4 is six to seven days in euthyroid individuals, but may be much longer than this in hypothyroidism, and that for T3 is two days or less. It is unnecessary to administer thyroid hormone more frequently than once a day. The liver conjugates thyroid hormones, which undergo enterohepatic recirculation. Key points Iodine and thyroid hormones • Iodized salt is used to prevent endemic goitre in regions where the diet is iodine-deficient. Lugol’s iodine (a solution of iodine in aqueous potassium iodide) is also used pre-operatively to reduce the vascularity of the thyroid. • Thyroxine (T 4) is used as a physiological replacement in patients who are hypothyroid. It is converted in the tissues to the more active tri-iodothyronine (T 3). • T 3 has a shorter elimination half-life than T 4 and is therefore used for emergency treatment of myxoedema coma (often with glucocorticoids because of the possibility of coexisting hypoadrenalism). ANTITHYROID DRUGS CARBIMAZOLE Use Carbimazole is used to treat hyperthyroidism. The patient is usually rendered euthyroid within four to six weeks, and the dose is then reduced. Treatment is maintained for one to two years and the drug is then gradually withdrawn. If relapse occurs, the dose is raised until clinical improvement is restored. If dosage adjustment proves difficult, smoother control may be obtained by giving a replacement dose of thyroxine together with a blocking dose of carbimazole. Mechanism of action The action of carbimazole is via its active metabolite methimazole, which is a substrate-inhibitor of peroxidase and is itself iodinated and degraded within the thyroid, diverting oxidized iodine away from thyroglobulin and decreasing thyroid hormone biosynthesis. Methimazole is concentrated by cells with a peroxidase system (salivary gland, neutrophils and macrophage/monocytes, in addition to thyroid follicular cells). It has an immunosuppressive action within the thyroid

294 THYROID and interferes with the generation of oxygen radicals by macrophages, thereby interfering with the presentation of antigen to lymphocytes. Methimazole does not affect hormone secretion directly. Thus hormone release decreases after a latent period, during which time the thyroid becomes depleted of hormone. Adverse effects Carbimazole is usually well tolerated, although pruritus and rashes are fairly common. These usually respond to switching to propylthiouracil (see below). Neutropenia is a rare but potentially fatal adverse effect. Patients must be warned to report sore throat or other evidence of infection immediately, an urgent white cell count must be obtained and the drug should be stopped if there is neutropenia. Nausea, hair loss, drug fever, leukopenia and arthralgia are rare, but recognized adverse effects. Use of carbimazole during pregnancy has rarely been associated with aplasia cutis in the newborn. Pharmacokinetics Carbimazole is rapidly absorbed after oral administration and hydrolysed to methimazole, which is concentrated in the thyroid within minutes of administration. Methimazole has an apparent volume of distribution equivalent to body water and the t1/2 varies according to thyroid status, being approximately seven, nine and 14 hours in hyperthyroid, euthyroid and hypothyroid patients, respectively. It is metabolized in the liver and thyroid. PROPYLTHIOURACIL Use Propylthiouracil has similar actions, uses and toxic effects to carbimazole, but in addition inhibits the peripheral conversion of T4 to active T3. As with carbimazole, dangerous leukopenia may develop, but is very rare. The scheme of attaining a euthyroid state with a large initial dose which is then reduced is as for carbimazole. Propylthiouracil is rapidly absorbed from the intestine. The plasma t1/2 is short, but the duration of action within the thyroid is prolonged and, as with carbimazole, propylthiouracil can be given once daily. It is used (by specialists) in pregnancy (see below) and has some advantages over carbimazole in this setting. β-ADRENOCEPTOR ANTAGONISTS Beta-blockers improve symptoms of hyperthyroidism, including anxiety, tachycardia and tremor. They inhibit the conversion of T4 to T3 in the tissues. They are useful: • while awaiting laboratory confirmation, if the diagnosis is in doubt; • during initiation of therapy with antithyroid drugs; • before treatment with radio-iodine, because they do not interfere with the uptake of iodine by the gland; • in thyroid crisis; • with iodine, as a rapid preparation for surgery on a hyperactive thyroid goitre; • in neonatal hyperthyroidism due to thyroid-stimulating immunoglobulin from the mother – this remits within about six weeks as maternal-derived immunoglobulin is cleared by the infant. Hyperthyroid patients treated with beta-blockers are not biochemically euthyroid, even if they appear clinically euthyroid, and thyroid crisis (‘storm’) can supervene if treatment is discontinued. RADIOACTIVE IODINE Radioactive iodine is an effective oral treatment for thyrotoxicosis caused by Graves’ disease or by toxic nodular goitre. It is safe, causes no discomfort to the patient and has largely replaced surgery, except when there are local mechanical problems, such as tracheal compression. It is contraindicated in pregnancy. Dosing has been the subject of controversy. It is now standard practice in many units to give an ablative dose followed by replacement therapy with thyroxine, so late-onset undiagnosed hypothyroidism is avoided. The isotope usually employed is 131I with a t1/2 of eight days. Thyroxine replacement is started after four to six weeks and continued for life. There is no increased incidence of leukemia, thyroid or other malignancy after therapeutic use of 131I, but concern remains regarding its use in children or young women. However, the dose of radiation to the gonads is less than that in many radiological procedures and there is no evidence that therapeutic doses of radioactive iodine damage the germ cells or reduce Key points Antithyroid drugs • Carbimazole works via its active metabolite, methimazole. This is concentrated in cells that contain peroxidase, including neutrophils as well as thyroid epithelium. It is iodinated in the thyroid, diverting iodine from the synthesis of T 3 and T 4 and depleting the gland of hormone. It does not inhibit secretion of preformed thyroid hormones, so there is a latent period before its effect is evident after starting treatment. • Neutropenia is an uncommon but potentially fatal adverse effect. Patients who develop sore throat or other symptoms of infection need to report for an urgent white blood count. Pruritus and rash are more common but less severe. • Propylthiouracil is similar in its effects and adverse effects to carbimazole/methimazole, but in addition it inhibits peripheral conversion of T 4 to the more active T 3, and is therefore preferred in thyroid storm. • β-Adrenoceptor antagonists suppress manifestations of hyperthyroidism and are used when starting treatment with specific antithyroid drugs, and in treating thyroid storm (together with propylthiouracil and glucocorticoids, which also suppress the conversion of T 4 to T 3). • Radioactive iodine ( 131 I) is safe in non-pregnant adults and has largely replaced surgery in the treatment of hyperthyroidism, except when there are local mechanical complications, such as tracheal obstruction. Replacement therapy with T 4 is required after functional ablation.

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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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    PART IV THE CARDIOVASCULAR SYSTEM

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    ● Introduction 177 ● Pathophysi

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    esponsible for the strong predilect

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    Ezetimibe Fat Muscle Dietary fat In

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    educed). The risk of muscle damage

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    ● Introduction 185 ● Pathophysi

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    Each of these classes of drug reduc

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    AT 1 receptor) produce good 24-hour

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    Table 28.2: Examples of calcium-cha

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    Key points Drugs used in essential

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    Case history A 72-year-old woman se

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    Assess risk factors Investigations:

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    Persistent ST segment elevation Thr

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    Mechanism of action GTN works by re

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    Because of the risks of haemorrhage

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    Intrinsic pathway XIIa XIa the acti

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    that the pharmacodynamic response i

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    used with apparent benefit in acute

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    ● Introduction 211 ● Pathophysi

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    The drugs that are most effective i

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    therapeutic plasma concentration ca

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    ● Common dysrhythmias 217 ● Gen

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    BASIC LIFE SUPPORT CARDIOPULMONARY

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    arrest. The electrocardiogram is li

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    should be given to insertion of an

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    Drug interactions Amiodarone potent

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    effect when treating sinus bradycar

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    Case history A 24-year-old medical

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    PART V THE RESPIRATORY SYSTEM

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    CHAPTER 33 THERAPY OF ASTHMA, CHRON

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    STEP 5: CONTINUOUS OR FREQUENT USE

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    Adenylyl cyclase Table 33.1: Compar

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    Drug interactions Although synergis

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    use in asthma has declined consider

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  • Page 256 and 257: PART VI THE ALIMENTARY SYSTEM
  • Page 258 and 259: ● Peptic ulceration 247 ● Oesop
  • Page 260 and 261: PEPTIC ULCERATION 249 • With rega
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  • Page 282 and 283: PART VII FLUIDS AND ELECTROLYTES
  • Page 284 and 285: ● Introduction 273 ● Volume ove
  • Page 286 and 287: Key points Diuretics Diuretics are
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  • Page 294 and 295: PART VIII THE ENDOCRINE SYSTEM
  • Page 296 and 297: ● Introduction 285 ● Pathophysi
  • Page 298 and 299: in prefilled injection devices (‘
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  • Page 306 and 307: fertility. It is contraindicated du
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  • Page 310 and 311: effective in life-threatening hyper
  • Page 312 and 313: Further reading Block GA, Martin KJ
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  • Page 322 and 323: Treatment with depot progestogen in
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  • Page 328 and 329: with symptoms caused by the release
  • Page 330 and 331: FURTHER READING Birnbaumer M. Vasop
  • Page 332 and 333: PART IX SELECTIVE TOXICITY
  • Page 334 and 335: ● Principles of antibacterial che
  • Page 336 and 337: 2. transfer of resistance between o
  • Page 338 and 339: Pharmacokinetics Absorption of thes
  • Page 340 and 341: Mechanism of action Macrolides bind
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  • Page 344 and 345: Case history A 70-year-old man with
  • Page 346 and 347: PRINCIPLES OF MANAGEMENT OF MYCOBAC
  • Page 348 and 349: Pharmacokinetics Absorption from th
  • Page 350 and 351: MYCOBACTERIUM LEPRAE INFECTION Lepr
  • Page 352 and 353: 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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