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A Textbook of Clinical Pharmacology and Therapeutics

A Textbook of Clinical Pharmacology and Therapeutics

to cause pupillary

to cause pupillary dilatation, namely muscarinic antagonists (anticholinergics) and sympathomimetics. Short-acting relatively weak mydriatics, such as tropicamide, facilitate retinal examination. Cyclopentolate and atropine are preferred for producing cycloplegia (paralysis of the ciliary muscle) for refraction in young children. Atropine is also used for the treatment of iridocyclitis mainly to prevent posterior synechiae, when it is often combined with phenylephrine. Table 52.2 shows some commonly used agents, their receptor effects, dose schedule and toxicity. Agents that dilate the pupil may abruptly increase the intra-ocular pressure in closed-angle glaucoma by causing obstruction to the outflow tract, and are contraindicated in this condition. Patients should be asked whether they are driving before having their pupils dilated and should be warned not to drive afterwards until their vision has returned to normal. Cornea Aqueous humour Iris Tears Systemic circulation Conjunctiva Sclera Ciliary body Figure 52.2: Potential absorption pathways for drugs applied to the eye. Table 52.2: Drugs commonly used to dilate the pupil DRUGS USED TO CONSTRICT THE PUPIL AND TO TREAT GLAUCOMA 425 DRUGS USED TO CONSTRICT THE PUPIL AND TO TREAT GLAUCOMA PHYSIOLOGY OF AQUEOUS HUMOUR DYNAMICS AND REGULATION OF INTRA-OCULAR PRESSURE Aqueous humour is produced at a rate of 2–2.5 mL per minute and flows from the posterior chamber through the pupil into the anterior chamber. Around 80–95% of it exits via the trabecular meshwork and into the canal of Schlemm and subsequently into the episcleral venous plexus and eventually into the systemic circulation. Fluid can also flow via the ciliary muscles into the suprachoroidal space. The geometry of the anterior chamber differentiates the two forms of glaucoma, namely open-angle glaucoma (the more common form) and angle-closure glaucoma (closed-angle glaucoma). Open-angle glaucoma is usually treated medically in the first instance, by reducing aqueous humour flow and/or production. Closed-angle glaucoma is treated by iridectomy following urgent medical treatment to reduce the intra-ocular pressure in preparation for surgery. PRINCIPLES OF THERAPY FOR GLAUCOMA Acute glaucoma is a medical emergency. Mannitol can reduce the intra-ocular pressure acutely by its osmotic effect. In addition, therapy with a carbonic anhydrase inhibitor (intravenous acetazolamide or topical dorzolamide) may be required. This is then supplemented with either a topical β-adrenergic antagonist (e.g. timolol) or a cholinergic agonist (e.g. pilocarpine), or both. Drug Receptor Dose, onset of mydriasis Toxicity and other and schedule comments Anticholinergics Tropicamide Single drop of 0.5% solution, Photosensitivity, blurred vision and maximum onset of effect is in 20–40 min and lasts 3–6 h systemic absorption can occur Cyclopentolate All anticholinergics are Single drops of 0.5 or 1.0% As for tropicamide antagonists at the solution, maximum onset of M3 receptor on the effect is in 30–60 min and ciliary muscle lasts 24 h Atropine Sympathomimetics Single drop of 0.5 or 1.0% solution, maximum onset of effect is 30–40 min and lasts 7–10 days As for tropicamide Phenylephrine One of two drops of 10% Systemic absorption can occur (avoid in solution, lasts up to 12 h patients with coronary artery disease or hypertension)

426 DRUGS AND THE EYE Chronic simple glaucoma is due to a limitation of flow through the trabecular meshwork. Initial treatment is with a topical β-blocker. Other drugs (e.g. dipivefrine, a prodrug of adrenaline (epinephrine) designed to penetrate the cornea readily, or pilocarpine) are added as necessary. Disappointingly, visual impairment may progress despite adequate control of intra-ocular pressure and surgery has a place in this, as well as in the acute form of glaucoma. DRUGS USED TO TREAT GLAUCOMA MANNITOL Mannitol (Chapter 36) is an osmotic diuretic. It is used in an emergency or before surgery, and is given as an intravenous infusion (e.g. 100–200 mL of a 20% solution) over 30–60 minutes. It shifts water from intracellular and transcellular compartments (including the eye) into the plasma, and promotes loss of fluid by its diuretic action on the kidney. Its major adverse effect is dehydration. CARBONIC ANHYDRASE INHIBITORS Acetazolamide is used in acute and chronic glaucoma, and it also has highly specialized uses in certain seizure disorders in infants, and in adapting to altitude. It was previously used as a diuretic (see Chapter 36). It is a sulphonamide. It is a competitive inhibitor of carbonic anhydrase, the enzyme that converts CO2 and H2O into H2CO3. Inhibition of this enzyme in the eye reduces aqueous humour production by the ciliary body. Adverse effects Adverse effects include the following: • paraesthesiae and tingling; • nausea, vomiting and loss of taste; • metabolic acidosis; • polyuria due to its mild diuretic properties; • hypersensitivity reactions – particularly of the skin; • bone marrow suppression (rare). Acetazolamide is poorly tolerated orally, although a slowrelease preparation exists which can be given twice daily and has reduced incidence of side effects. Dorzolamide is a topically applied carbonic anhydrase inhibitor, whose use may reduce the need for systemic acetazolamide therapy (see below). Acetazolamide should not be used in patients with renal failure, renal stones or known hypersensitivity to sulphonamides, or in pregnant women. TOPICAL AGENTS FOR GLAUCOMA DORZOLAMIDE Dorzolamide is a topically applied carbonic anhydrase inhibitor, which may be used either alone or as an adjunct to a β-blocker. Systemic absorption does occur and systemic side effects (e.g. rashes, urolithiasis) may require drug withdrawal. Typical adverse effects include local irritation of the eye and eyelid with burning, stinging and visual blurring, and a bitter taste. PROSTAGLANDIN ANALOGUES Latanoprost is a prostaglandin F2α analogue. It can be used in patients who are intolerant of β-blockers or as add-on therapy when the response to the first drug has been inadequate. Latanoprost is an inactive prodrug which readily penetrates the cornea and is hydrolysed to the free acid. The free acid diffuses out of the cornea into the aqueous humour and lowers the intra-ocular pressure by increasing uveoscleral outflow. Systemic absorption does occur via conjunctival and mucous membranes. Latanoprost is cleared by hepatic metabolism. The main side effects are local irritation with stinging, burning and blurred vision. Punctate keratopathy has occurred, and it increases the amount of brown pigment in the iris in patients with mixed-coloured eyes, which may be a cosmetic problem, especially if treatment is only needed for one eye. Travoprost and bimatoprost are related prostaglandin analogues. α2-AGONISTS Brimonidine is a selective α2-agonist, used for chronic openangle glaucoma when other drugs are unsatisfactory. It is used alone or as an adjunct to β-blocker therapy in chronic glaucoma. It decreases aqueous humour production and increases uveoscleral flow. Trace amounts do get into the circulation and undergo hepatic metabolism. The major toxicities include local ocular irritation and occasional corneal staining, and systemic adverse effects include dry mouth (25% of cases), headache, fatigue, drowsiness and allergic reactions. It is contraindicated in patients taking monoamine oxidase inhibitors (MAOIs) and should be used with caution in those with severe coronary artery disease (CAD) or taking tricyclic antidepressants. Apraclonidine is another selective α2-agonist which is formulated for ophthalmic use. Key points Drugs and the pupil • Miosis (pupillary constriction) – Parasympathetic stimulation: muscarinic agonists (e.g. carbachol, pilocarpine); cholinesterase inhibitors (e.g. neostigmine, physostigmine). – Sympathetic blockade: α1-antagonists (e.g. phentolamine). • Mydriasis (pupillary dilatation) – Parasympathetic blockade: muscarinic antagonists (e.g. atropine, tropicamide). – Sympathetic stimulation: α1-agonists (e.g. phenylephrine).

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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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    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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  • Page 392 and 393: Plasma membrane Signal transduction
  • Page 394 and 395: Table 48.10: Monoclonal antibodies
  • Page 396 and 397: INTERFERON-ALFA 2B Interferon-alfa
  • Page 398 and 399: PART X HAEMATOLOGY
  • Page 400 and 401: ● Haematinics - iron, vitamin B 1
  • Page 402 and 403: one marrow to produce red cells. Th
  • Page 404 and 405: EPO Erythroid precursors Erythrocyt
  • Page 406 and 407: Therapeutic principles The extent o
  • Page 408 and 409: PART XI IMMUNOPHARMACOLOGY
  • Page 410 and 411: ● Introduction 399 ● Immunity a
  • Page 412 and 413: Key points Antigen recognition Expr
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  • Page 418 and 419: DRUGS THAT ENHANCE IMMUNE SYSTEM FU
  • Page 420 and 421: PART XII THE SKIN
  • Page 422 and 423: ● Introduction 411 ● Acne 411
  • Page 424 and 425: DERMATITIS (ECZEMA) PRINCIPLES OF T
  • Page 426 and 427: SPECIALISTS ONLY SPECIALISTS ONLY E
  • Page 428 and 429: TREATMENT OF OTHER SKIN INFECTIONS
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  • Page 432 and 433: PART XIII THE EYE
  • Page 434 and 435: ● Introduction: ocular anatomy, p
  • Page 438 and 439: Table 52.3: Antibacterial agents us
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  • Page 442 and 443: PART XIV CLINICAL TOXICOLOGY
  • Page 444 and 445: ● Introduction 433 ● Pathophysi
  • Page 446 and 447: Table 53.2: Central nervous system
  • Page 448 and 449: which provide anonymized data to th
  • Page 450 and 451: Peak plasma levels after smoking ci
  • Page 452 and 453: Key points Acute effects of alcohol
  • Page 454 and 455: FURTHER READING Goldman D, Oroszi G
  • Page 456 and 457: Table 54.2: Common indications for
  • Page 458 and 459: Table 54.5: Antidotes and other spe
  • Page 460 and 461: Commission on Human Medicines (CHM)
  • Page 462 and 463: Note: Page numbers in italics refer
  • Page 464 and 465: atrial fibrillation 217, 221 digoxi
  • Page 466 and 467: Cushing’s syndrome 302 cyclic ade
  • Page 468 and 469: 5-fluorouracil 375-6 fluoxetine, mo
  • Page 470 and 471: children 54 diazepam 108 iron prepa
  • Page 472 and 473: non-steroidal anti-inflammatory dru
  • Page 474 and 475: puberty (male), delay 314 puerperiu
  • Page 476: tolerance 9, 433 benzodiazepines 10
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