Brown BSc MBBS MRCP(UK) FHEA / Brown / Loudon MBBS | Pass the PSA e-Book | E-Book | sack.de
E-Book

E-Book, Englisch, 310 Seiten

Brown BSc MBBS MRCP(UK) FHEA / Brown / Loudon MBBS Pass the PSA e-Book

Pass the PSA e-Book

E-Book, Englisch, 310 Seiten

ISBN: 978-0-7020-5517-1
Verlag: Elsevier HealthScience EN
Format: EPUB
Kopierschutz: 6 - ePub Watermark



Drug prescribing is one of the most important parts of clinical practice. Yet it remains one of the most commonly failed components of undergraduate assessments, and accounts for an uncomfortably high proportion of medical errors. To remedy this, the Prescribing Safety Assessment (PSA) exam has been introduced in the UK. It is compulsory and will set a minimum standard for safe prescribing. Failure will preclude GMC registration. Pass the PSA is written specifically for the exam, with one chapter dedicated to each PSA section. Each chapter includes: The marking scheme for the PSA exam section and how to approach it. All the theory condensed into a few pages of memorable, illustrated text. Multiple worked questions covering the most common exam scenarios. In addition:Introduces a simple, memorable and failsafe approach to prescribing (the 'PReSCRIBER' mnemonic). Specifies the universal basic principles of prescribing for all sections. Over 300 worked questions, structured identically to the exam. Data interpretation made memorable and simple including ECG, ABGs, chest X-rays and basic bloods. Common traps highlighted throughout.Two mock exams.
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1;Front Cover;1
2;Pass the PSA;4
3;Copyright Page;5
4;Contents;6
5;Foreword;8
6;Preface;10
7;List of abbreviations;12
8;1 Basic principles of prescribing;14
8.1;Introduction;14
8.2;How to Use this Book;14
8.3;Basic Principles for All Prescribing;14
8.4;Enzyme Inducers and Inhibitors (See Chapters 8 and 9);15
8.5;Prescribing for Surgery;15
8.5.1;Drugs to Increase During Surgery;15
9;2 Prescription review: a foolproof plan;16
9.1;Structure of this Section within the PSA;16
9.2;A Safe Routine for Prescribing;19
9.2.1;PReSCRIBER;19
9.2.1.1;PReSCRIBER explained;19
9.2.1.1.1;Patient details;19
9.2.1.1.2;Reactions;19
9.2.1.1.3;Sign chart;19
9.2.1.1.4;Contraindications;19
9.2.1.1.5;Route;19
9.2.1.1.6;Intravenous fluids;20
9.2.1.1.6.1;Replacement: which fluid? ;20
9.2.1.1.6.2;Replacement: how much fluid and how fast? ;20
9.2.1.1.6.3;Maintenance: which fluids and how much? ;20
9.2.1.1.6.4;Maintenance: how fast to give fluids ;20
9.2.1.1.7;Blood clot prophylaxis;20
9.2.1.1.8;Antiemetics (see Table 2.1);20
9.2.1.1.9;Pain relief (see Table 2.2);21
9.3;Questions;22
10;3 Data interpretation;40
10.1;Structure of this Section within the PSA;40
10.2;Introduction;43
10.3;General Data Interpretation;43
10.3.1;Blood Tests: Haematology;43
10.3.1.1;Low haemoglobin (anaemia);43
10.3.2;Blood Tests: Biochemistry;43
10.3.2.1;Urea and electrolytes (U&E);43
10.3.2.1.1;Sodium (normal range 135–145 mmol/L);43
10.3.2.1.2;Potassium (normal range 3.5–5.0 mmol/L);43
10.3.2.1.3;Acute kidney injury (AKI);44
10.3.3;Liver Function Tests (LFTs);44
10.3.4;Thyroid Function Tests (TFT);45
10.3.5;Chest X-Rays;46
10.3.5.1;Quality of film;46
10.3.5.2;Structures;46
10.3.5.3;Difficult areas;46
10.3.6;Arterial Blood Gases;46
10.3.7;ECG;47
10.4;Drug-Specific Data;47
10.4.1;An Introduction to Drug Monitoring;47
10.4.1.1;Gentamicin monitoring;48
10.4.1.2;Once-daily regimen monitoring;48
10.4.1.3;Divided daily dosing;48
10.4.1.4;Paracetamol nomograms;49
10.4.1.5;Warfarin (excessive anticoagulation with warfarin);49
10.5;Questions;50
11;4 Planning management;62
11.1;Structure of the Section within the PSA;62
11.2;Introduction;64
11.3;Management of Acute Conditions;64
11.3.1;Cardiovascular (CV) Emergencies (Fig. 4.1);64
11.3.1.1;Tachycardia > 125 b.p.m.;64
11.3.2;Anaphylaxis (Fig. 4.3);66
11.3.3;Respiratory Emergencies;66
11.3.3.1;Acute exacerbation of asthma (Fig. 4.4);66
11.3.3.2;Acute exacerbation of chronic obstructive pulmonary disease (COPD);66
11.3.3.3;Pneumothorax;66
11.3.3.4;Pneumonia;66
11.3.3.5;Pulmonary embolism (PE, Fig. 4.6);66
11.3.4;Gastroenterology Emergencies;67
11.3.4.1;Gastrointestinal bleeding (Fig. 4.7);67
11.3.5;Neurological Emergencies;67
11.3.5.1;Bacterial Meningitis;67
11.3.5.2;Seizures and status epilepticus;67
11.3.5.3;Stroke (Fig. 4.10);67
11.3.6;Metabolic Emergencies;68
11.3.6.1;Hyperglycaemia (DKA and HONK, Fig. 4.11);68
11.3.6.1.1;Diabetic ketoacidosis;68
11.3.6.1.2;Hyperglycaemic HONK coma;68
11.3.6.2;Hypoglycaemia (BM blood glucose <3 mmol/L);68
11.3.6.3;Acute kidney injury (AKI, previously known as acute renal failure) (Fig. 4.12);68
11.3.6.4;Acute poisoning (Fig. 4.13);68
11.4;Management of Chronic Conditions;69
11.4.1;Cardiovascular Conditions;69
11.4.1.1;Hypertension;69
11.4.1.1.1;When to treat (see Fig. 4.14);69
11.4.1.1.2;Target blood pressures on treatment;69
11.4.1.2;Chronic heart failure (adapted from NICE guideline CG108, 2010);69
11.4.1.3;Atrial fibrillation (adapted from NICE guideline CG36, 2006);70
11.4.1.3.1;Stroke prevention;70
11.4.1.3.2;Determine the aim of the treatment according to the patient:;70
11.4.1.4;Stable angina (angina pectoris);70
11.4.1.4.1;Management of stable angina (adapted from NICE clinical guideline CG126, 2011);70
11.4.2;Respiratory Conditions;71
11.4.2.1;Chronic asthma (see Fig. 4.15);71
11.4.2.2;COPD;71
11.4.3;Diabetes;71
11.4.3.1;Management of both type 1 and 2 diabetes;71
11.4.3.1.1;Blood glucose lowering therapy in type 1 diabetes;71
11.4.3.1.2;Blood glucose lowering therapy in type 2 diabetes;71
11.4.4;Neurological Conditions;73
11.4.4.1;Parkinson’s disease;73
11.4.4.2;Epilepsy;73
11.4.4.3;Alzheimer’s disease;73
11.4.5;Crohn’s Disease (Adapted from NICE CG152, 2012);73
11.4.5.1;Inducing remission;73
11.4.5.2;Maintaining remission;73
11.4.5.2.1;Azathioprine or 6-mercaptopurine;73
11.4.6;Rheumatoid Arthritis;73
11.5;Symptoms;73
11.5.1;Fever;73
11.5.2;Constipation;73
11.5.3;Diarrhoea;73
11.5.4;Insomnia;73
11.6;Questions;74
12;5 Communicating information;84
12.1;Structure of the Section within the PSA;84
12.2;Introduction;84
12.3;Questions;84
13;6 Calculation skills;96
13.1;Structure of this Section within the PSA;96
13.2;Introduction;96
13.3;Questions;96
14;7 Prescribing: doing it yourself;108
14.1;Structure of this Section within the PSA;108
14.2;Prescribing Pitfalls;108
14.3;Remember PReSCRIBER;115
14.4;Remember the Basic Principles for all Prescribing;115
14.5;Questions;116
15;8 Drug monitoring;136
15.1;Structure of this Section within the PSA;136
15.2;Introduction;136
15.3;Questions;136
16;9 Adverse drug reactions;152
16.1;Structure of this Section within the PSA;152
16.2;Introduction;152
16.3;Type 1: Adverse Effects of Common Drugs;152
16.4;Type 2: Recognizing the Common Reactions;152
16.5;Type 3: Clinically Important Drug Interactions;154
16.6;Type 4: Recognizing and Managing an ADR;155
16.7;Questions;156
17;10 Mock examinations;166
17.1;Exam 1;166
17.2;Exam 2;235
18;Index;304


1 Basic principles of prescribing
Chapter objectives . Understand the premise of this book and how it will help you to pass the Prescribing Safety Assessment (PSA). . Learn how best to work your way through this book and how to follow the basic principles of safe prescribing. Introduction
Drug prescribing is one of the most important parts of clinical practice. Yet it remains one of the most commonly failed components of undergraduate assessments and accounts for an uncomfortably high proportion of medical errors. To remedy this the PSA has been introduced. The General Medical Council expects that all UK undergraduates will pass this exam during their final year (though at the time of going to press, there is uncertainty over the date of such enforcement). The exam comprises eight ‘sections’ within which different facets of prescribing are assessed (see Fig. 1.1). Students must complete the assessment within 2 hours. There are 200 marks available; the Prescribing and Prescription Review sections are assessed extensively and carry the most marks (112/200 marks in total). Figure 1.1 The Prescribing Safety Assessment structure. How to use this Book
Pass the Prescribing Safety Assessment is written specifically for the exam, with one chapter dedicated to each PSA section. This chapter outlines the universal basic principles of prescribing for all sections and includes discussions of two common concepts applicable throughout. Chapter 2 introduces a simple, memorable and fail-safe approach to prescribing (the PReSCRIBER mnemonic) and each subsequent chapter builds on the previous, creating a robust prescribing method for both the PSA and foundation years. Each chapter also discusses the section’s question structure and how to approach it. Questions (structured identically to the exam) conclude each chapter and cover all scenarios suggested for questioning in the PSA blueprint (2012). Finally, two mock exams (which should be completed within 2 hours each) enable consolidation of previous learning. The chapter order imitates clinical practice and each chapter consolidates the work of previous ones. Knowing the correct diagnosis reflects accurate data interpretation (Chapter 3), which in turn enables the deduction of appropriate management strategies (Chapter 4). Some treatments require communication of specific information to patients (Chapter 5) and others require calculation skills (Chapter 6), before safely prescribing (Chapter 7). Finally, drug monitoring (Chapter 8) attempts to prevent some adverse drug reactions (Chapter 9). A secondary aim of the book is to summarize the clinical knowledge required to pass the PSA. There is little merit in limiting learning to drug-related data interpretation or management while ignoring the substantial non-pharmacological remainder: this arbitrary distinction does not avail itself in clinical practice, and the PSA will include scenarios where a drug is not to blame. Consequently, Chapters 3 and 4 include concise, yet comprehensive, summaries of data interpretation and management algorithms, with the most common causes emboldened, and drug-related causes (which will of course be over-represented in the exam) emboldened/italicized. In the exam you will have access to the British National Formulary (BNF) for every section. If in doubt, look it up! Many questions will require even the most capable candidate to look up an answer, so you should become familiar with it during your preparations. The BNF will even tell you what to prescribe in common clinical situations (just look up the symptom or diagnosis in the index), but you will not have time to do this for each question. It is therefore advisable to learn the theory in each chapter and use the BNF as a backup. The BNF includes sections on antibiotic choice for different infections; you can use this or your local antibiotic policy while preparing, but you should know the first line antibiotic choices for common infections. Drug charts have been provided where written prescriptions are required (Chapter 7), so no additional materials beyond a BNF are needed whilst using this book. Basic Principles for all Prescribing
Every drug prescription must be:  Legible  Unambiguous (e.g. not a range of doses, such as 30–60 mg codeine which is a common error and entirely your fault if a patient is overdosed within your prescribed dosage range)  An approved (generic) name, e.g. salbutamol not Ventolin®. See Box 1.1. Box 1.1   Generic versus trade drug names There are a small number of exceptions when trade names should be used; one of the most important reflects the various preparations of tacrolimus (used for preventing the rejection of transplanted organs). The BNF states that trade names should be used for prescribing because switching between brands can result in toxicity (if relative levels increase) or rejection (if relative levels decrease). You will often see the brand name Tazocin® written instead of piperacillin with tazobactam – this is done for simplicity but is not acceptable, particularly because it masks the fact that the drug contains penicillin that is made obvious by the ‘cillin’ in piperacillin.  IN CAPITALS  Without abbreviations  Signed (even when practising or in an exam, sign and make up a bleep number in order to get into this habit)  If a drug is to be used ‘as required’ provide two instructions: (1) indication and (2) a maximum frequency (e.g. twice daily) or total dose in 24 hours (e.g. 1g)  If an antibiotic is being prescribed include the indication and stop/review date  Include of duration if the treatment is not long term (e.g. antibiotics) or if it is in a GP setting (e.g. 7 or 28 days). Marks are awarded for each of these points. Enzyme Inducers and Inhibitors (See Chapters 8 and 9)
Most of this book concerns the effects of drugs on the body (pharmacodynamics). Conversely, what the body does to the drug (known as pharmacokinetics, including absorption, metabolism and excretion) is slightly less relevant in a practical guide to prescribing, as these processes are reasonably stable and thus a drug’s effect is usually predictable. Problems arise, however, when other substances (in this case concomitantly administered drugs) unintentionally alter these complex systems resulting in increased or decreased drug levels and hence altered effects. Thus, from an early stage it is important to recognize that when you prescribe particular drugs (which are also enzyme inhibitors or enzyme inducers) they may affect seemingly unrelated drugs (Table 1.1). Table 1.1 Most common enzyme inhibitors and inducers Inducers Inhibitors ? Enzyme Activity? ? Drug Concentration ? Enzyme Activity? ? Drug Concentration PC BRAS: Phenytoin, Carbamazepine, Barbiturates, Rifampicin, Alcohol (chronic excess), Sulphonylureas AODEVICES: Allopurinol, Omeprazole, Disulfiram, Erythromycin, Valproate, Isoniazid, Ciprofloxacin, Ethanol (acute intoxication), Sulphonamides Most drugs are metabolized to inactive metabolites by the cytochrome P450 enzyme system in the liver, preventing them exerting infinite effects. The activity of these enzymes, however, may in turn be altered by the presence of other particular drugs, known as enzyme inducers and inhibitors. An enzyme inducer will increase P450 enzyme activity, hastening metabolism of other drugs with the result that they exert a reduced effect (and thus a patient will require more of some other drugs in the presence of an enzyme inducer). Conversely, an enzyme inhibitor will decrease P450 enzyme activity and, subsequently, there will be increased levels of other drugs (which in the hands of a diligent physician require a reduced drug dose). The classic example of this is the effect of newly introduced enzyme inhibitors on patients taking warfarin. In particular, the addition of erythromycin (an enzyme inhibitor) can sometimes and unpredictably cause a dangerous rise in international normalized ratio (INR) if the warfarin dose is not decreased; you should be aware of this in patients presenting with excessive anticoagulation (see Chapter...


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