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A Textbook of Clinical Pharmacology and Therapeutics

A Textbook of Clinical Pharmacology and Therapeutics

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or with potassium-sparing diuretics (see above). Hyperkalaemia is particularly likely to occur in patients with impaired renal function, in the elderly (in whom renal impairment may be unrecognized because the plasma creatinine concentration is normal) and in patients receiving ACE inhibitors, K � supplements or NSAID. Treatment 1. Calcium gluconate is a potentially life-saving emergency treatment in patients with dysrhythmias caused by hyperkalaemia (Chapter 32). It is given intravenously with ECG monitoring. 2. Glucose and insulin shift extracellular K� into cells. 3. Sodium bicarbonate, given intravenously, also shifts K� into cells. 4. High-dose nebulized β2-agonists shift K� into cells. 5. Ion-exchange resin made of sodium or calcium polystyrene sulphonate removes potassium from the body in stool. The main adverse effect when resins are given chronically for patients with chronic renal failure is constipation, which can be avoided if the resins are suspended in a solution of sorbitol. 6. Emergency haemofiltration or dialysis. Key points Drugs and plasma potassium • Hypokalaemia (and hypomagnesaemia) predisposes to digoxin toxicity and to torsades de pointes caused by drugs that prolong the QT interval (e.g. amiodarone, sotalol). Mild hypokalaemia associated with thiazide or loop diuretics is common and seldom harmful per se. • Where hypokalaemia is clinically important it can be corrected and/or prevented with K � supplements or more conveniently with K � -retaining diuretics. However, these predispose to hyperkalaemia. • Hyperkalaemia can cause dysrhythmias that can be fatal. ACEI predispose to hyperkalaemia, especially when there is renal impairment. • Emergency treatment of broad complex tachycardia caused by hyperkalaemia includes i.v. calcium gluconate. • Glucose and insulin i.v. cause redistribution of potassium into cells. • Sodium bicarbonate i.v. can cause redistribution of potassium into cells in exchange for hydrogen ions. • β 2-Agonists i.v./high-dose nebulized cause intracellular shift of K � . • Haemodialysis or haemofiltration is frequently indicated in acute hyperkalaemic emergencies. • Ion-exchange resins administered by mouth are useful. DRUGS THAT ALTER URINE pH ACIDIFICATION Ammonium chloride given orally results in urinary acidification and is used in specialized diagnostic tests of renal tubular DRUGS THAT AFFECT THE BLADDER AND GENITO-URINARY SYSTEM 279 acidosis. It is a gastric irritant and is given as enteric-coated tablets. The elimination of some basic drugs (e.g. amfetamine) is enhanced by acidification of the urine, though this is rarely used in clinical practice. ALKALINIZATION Sodium bicarbonate causes urinary alkalinization; intravenously it is used to alkalinize the urine in salicylate overdose (see Chapter 54). However, if given by mouth it reacts with hydrochloric acid in the stomach to produce carbon dioxide, so it is poorly tolerated and not very effective. Instead, a citric acid/potassium citrate mixture can be used orally, as citrate is absorbed from the gut and metabolized via the tricarboxylic acid cycle with generation of bicarbonate. Potassium must be avoided in renal failure, as retention of potassium ions may cause hyperkalaemia. Use Alkalinization of the urine is used to give symptomatic relief for the dysuria of cystitis and to prevent the formation of uric acid stones, especially in patients who are about to undergo cancer chemotherapy. The use of alkaline diuresis to increase urinary excretion of salicylate following overdose is discussed in Chapter 54. DRUGS THAT AFFECT THE BLADDER AND GENITO-URINARY SYSTEM DRUGS TO INCREASE BLADDER ACTIVITY Drugs that increase bladder activity (e.g. muscarinic agonists, such as bethanechol, or anticholinesterases, such as distigmine) have been used to treat patients with chronic retention of urine, but catheterization is usually preferable. DRUGS FOR URINARY INCONTINENCE Stress incontinence is usually managed without drugs, often surgically, although duloxetine (an amine uptake inhibitor) is licensed for use in women with moderately severe stress incontinence in conjunction with pelvic floor exercises. Alpha blockers (e.g. doxazosin, see Chapter 28) can worsen incontinence in women with pelvic floor pathology and should be discontinued if possible. Urge incontinence is common. Infection should be excluded. When unstable detrusor contraction is responsible, drug treatment to reduce bladder activity is of limited use, combined with pelvic floor exercises and bladder training. Antimuscarinic drugs, such as oxybutynin, have a high incidence of antimuscarinic side effects (e.g. dry mouth, dry eyes, blurred vision, constipation, confusion). These may be minimized by starting with a low dose and by slow release formulation. Solifenacin is a newer and more expensive drug.

280 NEPHROLOGICAL AND RELATED ASPECTS DRUGS FOR PROSTATIC OBSTRUCTION Prostatic obstruction is often managed surgically. Symptoms of benign prostatic hypertrophy may be improved by a 5αreductase inhibitor (e.g. finasteride, Chapters 41 and 48) or by an α 1-adrenoceptor antagonist (e.g. doxazosin, Chapter 28). Tamsulosin, an α 1-adrenoceptor antagonist selective for the α 1A-adrenoceptor subtype, produces less postural hypotension than non-selective α 1-adrenoceptor antagonists. Hormonal manipulation with anti-androgens and analogues of luteinizing hormone-releasing hormone (LHRH) is valuable in patients with prostatic cancer (Chapter 48). ERECTILE DYSFUNCTION Erectile failure has several organic, as well as numerous psychological, causes. Replacement therapy with testosterone, given by skin patch, is effective in cases caused by proven androgen deficiency. Nitric oxide is involved in erectile function both as a vascular endothelium-derived mediator and as a non-adrenergic non-cholinergic neurotransmitter. This has led to the development of type V phosphodiesterase inhibitors as oral agents to treat erectile dysfunction. Sildenafil (Viagra) was the first of these to be introduced, there are several other longer-acting agents in this class currently. These drugs are discussed in Chapter 41. Case history A 35-year-old woman has proteinuria (3 g/24 hours) and progressive renal impairment (current serum creatinine 220 μmol/L) in the setting of insulin-dependent diabetes mellitus. In addition to insulin, she takes captopril regularly and buys ibuprofen over the counter to take as needed for migraine. She develops progressive oedema which does not respond to oral furosemide in increasing doses of up to 250 mg/day. Amiloride (10 mg daily) is added without benefit and metolazone (5 mg daily) is started. She loses 3 kg over the next three days. One week later, she is admitted to hospital having collapsed at home. She is conscious but severely ill. Her blood pressure is 90/60 mmHg, heart rate is 86 beats/minute and regular, and she has residual peripheral oedema, but the jugular venous pressure is not raised. Serum urea is 55 mmol/L, creatinine is 350 μmol/L, K � is 6.8 mmol/L, glucose is 5.6 mmol/L and albumin is 3.0 g/dL. Urinalysis shows 4� protein. An ECG shows tall peaked Twaves and broad QRS complexes. Question Decide whether each of the following statements is true or false. (a) Insulin should be withheld until the patient’s metabolic state has improved. (b) Metolazone should be stopped. (c) The furosemide dose should be increased in view of the persistent oedema. (d) Ibuprofen could have contributed to the hyperkalaemia. (e) Captopril should be withheld. Answer (a) False (b) True (c) False (d) True (e) True Comment Although highly effective in causing diuresis in patients with resistant oedema, combination diuretic treatment with loop, K � -sparing and thiazide diuretics can cause acute prerenal renal failure with a disproportionate increase in serum urea compared to creatinine. Resistance to furosemide may be related to the combination of reduced GFR plus albuminuria. The combination of an NSAID, captopril and amiloride is extremely dangerous, especially in diabetics, and will have contributed to the severe hyperkalaemia. The NSAID may also have led to reduced glomerular filtration. Glucose with insulin would be appropriate to lower the plasma K � . Case history A 73-year-old man has a long history of hypertension and of osteoarthritis. Three months ago he had a myocardial infarction, since when he has been progressively oedematous and dyspnoeic, initially only on exertion but more recently also on lying flat. He continues to take co-amilozide for his hypertension and naproxen for his osteoarthritis. The blood pressure is 164/94 mmHg and there are signs of fluid overload with generalized oedema and markedly elevated jugular venous pressure. Serum creatinine is 138 μmol/L and K � is 5.0 mmol/L. Why would it be hazardous to commence furosemide in addition to his present treatment? What alternative strategy could be considered? Comment The patient may go into prerenal renal failure with the addition of the loop diuretic to the two more distal diuretics he is already taking in the co-amilozide combination. The NSAID he is taking makes this more likely, and also makes it more probable that his serum potassium level (which is already high) will become dangerously elevated. It would be appropriate to consider hospital admission, stopping naproxen (perhaps substituting paracetamol for pain if necessary), stopping the co-amilozide and cautiously instituting an ACE inhibitor (which could improve his prognosis from his heart failure as described in Chapter 31) followed by introduction of furosemide with close monitoring of blood pressure, signs of fluid overload and serum creatinine and potassium levels over the next few days. FURTHER READING Brater DC. Pharmacology of diuretics. American Journal of Medical Science 2000; 319: 38–50. Clark BA, Brown RS. Potassium homeostasis and hyperkalemic syndromes. Endocrinology and Metabolism Clinics of North America 1995; 24: 573–91.

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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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    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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