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Davidson’s
Self-assessment in
Medicine
This page intentionally left blank
Davidson’s
Self-assessment in
Edited by

Deborah Wake
MB ChB (Hons), BSc, PhD, Diploma Clin Ed, MRCPE
Clinical Reader, University of Edinburgh; Honorary Consultant
Physician, NHS Lothian, Edinburgh, UK

Patricia Cantley
MB ChB, FRCP, BSc Hons (Med Sci)
Medicine
Consultant Physician, Midlothian Enhanced Rapid Response and
Intervention Team, Midlothian Health and Social Care Partnership
and also Royal Infirmary of Edinburgh and Midlothian Community
Hospital, Edinburgh, UK

Edinburgh London New York Oxford Philadelphia

St Louis Sydney 2018
© 2018, Elsevier Limited All rights reserved.

No part of this publication may be reproduced or transmitted in any form or

by any means, electronic or mechanical, including photocopying, recording,
or any information storage and retrieval system, without permission in writing
from the publisher. Details on how to seek permission, further information
about the Publisher’s permissions policies and our arrangements with
organizations such as the Copyright Clearance Center and the Copyright
Licensing Agency, can be found at our website: www.elsevier.com/
permissions.
This book and the individual contributions contained in it are protected
under copyright by the Publisher (other than as may be noted herein).

Notices
Practitioners and researchers must always rely on their own experience and
knowledge in evaluating and using any information, methods, compounds or
experiments described herein. Because of rapid advances in the medical
sciences, in particular, independent verification of diagnoses and drug
dosages should be made. To the fullest extent of the law, no responsibility is
assumed by Elsevier, authors, editors or contributors for any injury and/or
damage to persons or property as a matter of products liability, negligence or
otherwise, or from any use or operation of any methods, products,
instructions, or ideas contained in the material herein.

ISBN: 978-0-7020-7151-5
International ISBN: 978-0-7020-7145-4

Printed in China
Last digit is the print number: 9 8 7 6 5 4 3 2 1

Executive Content Strategist: Laurence Hunter

Content Development Specialist: Carole McMurray
Project Manager: Louisa Talbott
Design: Miles Hitchen
Illustration Manager: Nichole Beard
Illustrator: MPS North America LLC
Marketing Manager: Deborah Watkins
 Contents
Preface vii
Introduction ix
Contributors xi
Abbreviations xv

1. Clinical decision-making 1
2. Clinical therapeutics and good prescribing 6
3. Clinical genetics 14
4. Clinical immunology 22
5. Population health and epidemiology 28
6. Principles of infectious disease 32
7. Poisoning 37
8. Envenomation 46
9. Environmental medicine 51
10. Acute medicine and critical illness 54
11. Infectious disease 73
12. HIV infection and AIDS 96
13. Sexually transmitted infections 103
14. Clinical biochemistry and metabolic medicine 107
15. Nephrology and urology 115
16. Cardiology 132
17. Respiratory medicine 154
18. Endocrinology 185
19. Nutritional factors in disease 203
20. Diabetes mellitus 212
21. Gastroenterology 225
vi • Contents

22. Hepatology 245

23. Haematology and transfusion medicine 261
24. Rheumatology and bone disease 278
25. Neurology 299
26. Stroke medicine 325
27. Medical ophthalmology 330
28. Medical psychiatry 336
29. Dermatology 345
30. Maternal medicine 366
31. Adolescent and transition medicine 370
32. Ageing and disease 377
33. Oncology 383
34. Pain and palliative care 393
35. Laboratory reference ranges 402

Colour illustrations 415

Index 423
 Preface
This is the first edition of Davidson’s Self-assessment in Medicine, designed as an accompanying
volume to the internationally renowned textbook Davidson’s Principles and Practice of Medicine.
Since the original Davidson’s was first published in 1952, it has acquired a large following of medical
students, doctors and health professionals. Alongside the success of the main textbook, a demand
has emerged for a complementary self-assessment book covering a broad range of general medicine
topics. Our new book uses typical clinical scenarios to test the reader. Each chapter is written by a
specialty expert and the contents follow the style and chapter layout of Davidson’s. This book can
be used either independently or in conjunction with the main book.
This book has been built around modern educational principles and utilises a contemporary assess-
ment style, in line with current undergraduate and postgraduate teaching. It is designed to help and
support students in their final undergraduate years and in the early years after qualification. The style
is compatible with that used in modern postgraduate examinations across the world.
The clinical scenarios have been chosen to be suitable for clinicians at any stage in their career,
supporting ongoing professional development. Clinical reasoning and judgement are encouraged,
with questions mirroring the situations and presentations that clinicians will meet in their everyday
practice. The content is applicable to a global audience and is based on current evidence-based best
practice.
The modern physician needs not only a sound knowledge base but also the ability to apply that
understanding appropriately to individual patients. The vision of the editors is to create a resource
that stimulates readers to build and apply their clinical knowledge to real-life scenarios, resulting in
excellent patient-centred care.
Deborah Wake and Patricia Cantley
Edinburgh, 2018
This page intentionally left blank
 Introduction
This book offers a broad education through formative self-assessment in general internal medicine.
The majority of the questions have been designed around clinical scenarios, with a number of optional
answers offered to the question posed. In general, the ‘best fit’ answer is sought unless otherwise
stated. Full explanations are given as appropriate to assist the reader in their learning.
The questions aim to cover a wide range of topics, divided into specialist chapters in line with
Davidson’s Principles and Practice of Medicine. The questions have in general been based on UK
clinical practice and pharmacology, but where appropriate generic drug names are used and the
underlying principles are applicable internationally. Whilst the answers given are in line with best evidence-
based clinical practice, patient choice and cultural factors should always be considered when applying
the learning in individual patients and situations.

How to use this book

This self-assessment book can be used either independently or in conjunction with Davidson’s.
Readers may find it useful to read the relevant section of the main textbook in advance of tackling
the self-assessment; or they can use it subsequently to explore the topic in greater detail.
The questions, followed by their corresponding answers, have been arranged in the same chapter
order as Davidson’s. The chapters are free-standing and can be read independently in any order.
Some of the questions are based on accompanying clinical images and radiology. Where it is
appropriate to see the image in colour, it has also been reproduced in a colour photographic section
at the back of the book.
Normal Reference Ranges for tests have not been used within the questions or explanations, but
can be found in the laboratory reference range chapter, at the end of the book.
Standard abbreviations are found within the text and are generally explained at first use. A full list
of abbreviations can be found at the front of the book.
This page intentionally left blank

Anna Anderson MBChB, MRCP, PhD
Specialist Registrar Diabetes and Endocrinology,
Western General Hospital, Edinburgh, UK
Brian J Angus BSc (Hons), DTM&H, FRCP,
MD, FFTM(Glas)
Associate Professor, Nuffield Department of
Medicine, University of Oxford, UK
Quentin M Anstee BSc (Hons), MBBS, PhD,
MRCP, FRCP
Professor of Experimental Hepatology, Institute
of Cellular Medicine, Newcastle University,
Newcastle upon Tyne, UK; Honorary Consultant
Hepatologist, Freeman Hospital, Newcastle upon
Tyne NHS Hospitals Foundation Trust, Newcastle
upon Tyne, UK
Jennifer Bain MBChB, MRCP, FRCA, FFICM
Fellow in Vascular Anaesthesia, Scottish
Thoraco-abdominal & Aortic Aneurysm Service,
Royal Infirmary of Edinburgh, Edinburgh, UK
Leslie Burnett MBBS, PhD, FRCPA
Chief Medical Officer, Genome.One,
Garvan Institute of Medical Research,
Darlinghurst, Sydney; Honorary Professor,
University of Sydney, Sydney Medical School,
Sydney; Conjoint Professor, UNSW, St
Vincent’s Medical School, Darlinghurst,
Sydney, Australia
Mark Byers OBE, FRCGP, FFSEM, FIMC,
MRCEM
Consultant in Pre-Hospital Emergency Medicine,
Institute of Pre-Hospital Care, London, UK
Contributors
Harry Campbell MD, FRCPE, FFPH, FRSE
Professor of Genetic Epidemiology and Public
Health, Centre for Global Health Research, Usher
Institute of Population Health Sciences
and Informatics, University of Edinburgh,
Edinburgh, UK
C Fiona Clegg BSc (MedSci), MBChB,
MRCP (UK)
Clinical Lecturer in Gastroenterology, School of
Medicine, Medical Sciences and Nutrition,
University of Aberdeen, Aberdeen, UK
Gavin Clunie BSc, MBBS, MD, FRCP
Consultant Rheumatologist and Metabolic Bone
Physician, Cambridge University Hospitals NHS
Foundation Trust, Addenbrooke’s Hospital,
Cambridge, UK
Lesley A Colvin MBChB, BSc, FRCA, PhD,
FRCP (Edin), FFPMRCA
Consultant/Honorary Professor in Anaesthesia
and Pain Medicine, Department of Anaesthesia,
Critical Care and Pain Medicine, University
of Edinburgh, Western General Hospital,
Edinburgh, UK
Bryan Conway MB, MRCP, PhD
Senior Lecturer, Centre for Cardiovascular
Science, University of Edinburgh; Honorary
Consultant Nephrologist, Royal Infirmary
Edinburgh, Edinburgh, UK
Nicola Cooper MBChB, FAcadMEd, FRCPE,
FRACP
Consultant Physician, Derby Teaching Hospitals
NHS Foundation Trust; Honorary Clinical
Associate Professor, Nottingham University,
Division of Medical Sciences and Graduate Entry
Medicine, Nottingham, UK
xii • Contributors
Dominic J Culligan BSc, MBBS, MD, FRCP,
FRCPath
Consultant Haematologist and Honorary
Senior Lecturer, Aberdeen Royal Infirmary,
Aberdeen, UK
Ruth Darbyshire MB BChir, MA(Cantab)
Specialty Trainee in Ophthalmology, Yorkshire
and Humber Deanery, Yorkshire, UK
Graham Dark MBBS, FRCP, FHEA
Senior Lecturer in Medical Oncology and Cancer
Education, Newcastle University, Newcastle upon
Tyne, UK
Richard J Davenport DM, FRCP (Edin),
BM BS, BMedSci
Consultant Neurologist and Honorary Senior
Lecturer, University of Edinburgh, Edinburgh, UK
David Dockrell MD, FRCPI, FRCP (Glas),
FACP
Professor of Infection Medicine, MRC/University of
Edinburgh Centre for Inflammation Research,
University of Edinburgh, Edinburgh, UK
Emad El-Omar BSc (Hons), MBChB,
MD (Hons), FRCP (Edin), FRSE
Professor of Medicine, St George and Sutherland
Clinical School, University of New South Wales,
Sydney, Australia
Sarah Fadden BA, MB BChir, FRCA
Senior Registrar in Anaesthesia, Royal Infirmary of
Edinburgh, Edinburgh, UK
Catriona M Farrell MBChB, MRCP (UK)
Specialist Registrar Endocrinology and Diabetes,
Ninewells Hospital, Dundee, UK
Amy Frost MA (Cantab), MBBS, MRCP
Clinical Genomics Educator, Affiliated to St
George’s University NHS Foundation Trust,
London, UK
Neil Grubb MD, FRCP
Cardiology Consultant, Royal Infirmary of
Edinburgh; Honorary Senior Lecturer,
Cardiovascular Sciences, University of Edinburgh,
Edinburgh, UK
Jyoti Hansi
Department of Gastroenterology, Royal Infirmary
of Edinburgh, Edinburgh, UK
Sally H Ibbotson BSc (Hons), MBChB (Hons),
MD, FRCP (Edin)
Professor of Photodermatology, Photobiology
Unit, Dermatology Department, University of
Dundee, Dundee, UK
Sara J Jenks Bsc (Hons), MRCP, FRCPath
Consultant in Metabolic Medicine, Department of
Clinical Biochemistry, Royal Infirmary of
Edinburgh, UK
Sarah Louise Johnston MB ChB, FCRP,
FRCPath
Consultant in Immunology & HIV Medicine,
Department of Immunology and Immunogenetics,
North Bristol NHS Trust, Bristol, UK
David E J Jones MA, BM BCh, PhD, FRCP
Professor of Liver Immunology, Institute of Cellular
Medicine, Newcastle University; Consultant
Hepatologist, Freeman Hospital, Newcastle upon
Tyne, UK
Peter Langhorne MBChB, PhD, FRCP (Glas),
Hon FRCPI
Professor of Stroke Care, Institute of
Cardiovascular and Medical Sciences, University
of Glasgow, Glasgow, UK
Stephen Lawrie MD (Hons), FRCPsych,
Hon FRCP (Edin)
Professor of Psychiatry, University of Edinburgh,
Edinburgh, UK
John Paul Leach MD, FRCP
Consultant Neurologist, Institute of Neurological
Sciences, Glasgow; Head of Undergraduate
Medicine, University of Glasgow, Glasgow, UK
Andrew Leitch MBChB, BSc (Hons), PhD,
MSc (Clin Ed), FRCPE (Respiratory)
Consultant Respiratory Physician, Western
General Hospital; Honorary Senior Lecturer,
University of Edinburgh, Edinburgh, UK
Gary Maartens MBChB, FCP(SA), MMed
Professor of Medicine, University of Cape Town,
Cape Town, South Africa
Lucy Mackillop BM BCh, MA (Oxon), FRCP
Consultant Obstetric Physician, Oxford University
Hospitals NHS Foundation Trust; Honorary Senior
Clinical Lecturer, Nuffield Department of
Obstetrics and Gynaecology, University of Oxford,
Oxford, UK

Michael MacMahon MBChB, FRCA, FICM,
EDIC
Consultant in Anaesthesia and Intensive Care,
Victoria Hospital, Kirkcaldy, Fife, UK
Rebecca Mann BMedSci, BMBS, MRCP,
FRCPCh
Consultant Paediatrician, Taunton and Somerset
NHS Foundation Trust, Taunton, UK
Lynn Manson MBChB, MD, FRCP, FRCPath
Consultant Haematologist, Scottish National
Blood Transfusion Service, Department of
Transfusion Medicine, Royal Infirmary of
Edinburgh, Edinburgh, UK
Amanda Mather MBBS, FRACP, PhD
Consultant Nephrologist, Department of Renal
Medicine, Royal North Shore Hospital; Conjoint
Senior Lecturer, Faculty of Medicine, University of
Sydney, Sydney, Australia
Simon R Maxwell BSc, MBChB, MD, PhD,
FRCP, FRCPE, FHEA
Professor of Student Learning/Clinical
Pharmacology & Prescribing, Clinical
Pharmacology Unit, University of Edinburgh,
Edinburgh, UK
David McAllister MBChB, MD, MPH, MRCP,
MFPH
Wellcome Trust Intermediate Clinical Fellow
and Beit Fellow, Senior Clinical Lecturer in
Epidemiology and Honorary Consultant in
Public Health Medicine, University of Glasgow,
Glasgow, UK
Mairi H McLean BSc (Hons), MBChB (Hons),
PhD, MRCP
Senior Clinical Lecturer in Gastroenterology,
School of Medicine, Medical Sciences and
Nutrition, University of Aberdeen; Honorary
Consultant Gastroenterologist, Digestive Disorders
Department, Aberdeen Royal Infirmary, Aberdeen,
UK
Francesca E M Neuberger MBChB,
MRCP (UK)
Consultant Physician in Acute Medicine and
Obstetric Medicine, Southmead Hospital,
Bristol, UK
Contributors • xiii
David E Newby BA, BSc (Hons), PhD, BM,
DM, DSc, FMedSci, FRSE, FESC, FACC
British Heart Foundation John Wheatley Chair of
Cardiology, British Heart Foundation Centre for
Cardiovascular Science, University of Edinburgh,
Edinburgh, UK
John Olson MD, FRPCE, FRCOphth
Consultant Ophthalmic Physician, Aberdeen
Royal Infirmary; Honorary Reader, University of
Aberdeen, UK
Paul J Phelan MBBCh, MD,
FRCP (Edin)
Consultant Nephrologist and Renal Transplant
Physician, Honorary Senior Lecturer, University of
Edinburgh, Royal Infirmary of Edinburgh,
Edinburgh, UK
Eric M Przybyszewski BS, MD
Resident Physician, Department of Medicine,
Massachusetts General Hospital, Boston, USA
Stuart H Ralston MBChB, MRCP, FMedSci,
FRSE
Professor of Rheumatology, Rheumatic Diseases
Unit, University of Edinburgh, Edinburgh, UK
Jonathan Sandoe MBChB, PhD, FRCPath
Associate Clinical Professor, University of Leeds,
UK
Gordon Scott BSc, FRCP
Consultant in Genitourinary Medicine, Chalmers
Sexual Health Centre, Edinburgh, UK
Alan G Shand MD, FRCP (Ed)
Consultant Gastroenterologist, Gastrointestinal
Unit, Western General Hospital, Edinburgh, UK
Robby Steel MA, MD, FRCPsych
Department of Psychological Medicine, Royal
Infirmary of Edinburgh; Honorary (Clinical) Senior
Lecturer, Department of Psychiatry, University of
Edinburgh, Edinburgh, UK
Grant D Stewart BSc (Hons),
FRCSEd (Urol), MBChB, PhD
University Lecturer in Urological Surgery,
Department of Surgery, University of Cambridge;
Honorary Consultant Urological Surgeon,
Department of Urology, Addenbrooke’s Hospital,
Cambridge; Honorary Senior Clinical Lecturer,
University of Edinburgh, Edinburgh, UK
xiv • Contributors

David R. Sullivan MBBS, FRACP, FRCPA Henry Watson MBChB, MD

Clinical Associate Professor, Clinical Biochemistry,
Royal Prince Alfred Hospital, Camperdown, NSW,
Australia
Victoria Ruth Tallentire BSc (Hons), MD,
FRCP (Edin)
Consultant Physician, Western General Hospital;
Honorary Clinical Senior Lecturer, University of
Edinburgh, Edinburgh, UK
Simon H Thomas MD, FRCP
Professor of Clinical Pharmacoloy and
Therapeutics, Medical Toxicology Centre,
Newcastle University, Newcastle upon Tyne, UK
Consultant Haematologist, Aberdeen Royal
Infirmary, Aberdeen, UK
Julian White MBBS, MD
Professor and Department Head, Toxinology
Department, Women’s & Children’s Hospital,
North Adelaide, Australia
Miles D Witham BM BCh, PhD, FRCP (Ed)
Clinical Reader in Ageing and Health, Department
of Ageing and Health, University of Dundee,
Dundee, UK

Craig Thurtell BMedSci (Hons), MBChB

MRCP
Specialty Registrar, Department of Diabetes &
Endocrinology, Ninewells Hospital, Dundee, UK
 Abbreviations
11β-HSD 11β-Hydroxysteroid APL Acute promyelocytic leukaemia
dehydrogenase APS Antiphospholipid syndrome
131
I Radioisotope iodine-131 APTT Activated partial thromboplastin
2,3-DPG 2,3-Diphosphoglycerate time
20WBCT 20-Minute whole-blood clotting ARDS Acute respiratory distress
test syndrome
5-ASA 5-Aminosalicylic acid ART Antiretroviral therapy
5-HIAA 5-Hydroxyindoleacetic acid AS Ankylosing spondylitis
AAV ANCA-associated vasculitis AST Aspartate aminotransferase
ACE Angiotensin-converting enzyme ATCG Adenine, thymine, cytosine,
AChR Acetylcholine receptor guanine
ACPA Anti-citrullinated peptide antibody ATG Anti-thymocyte globulin
ACR Albumin : creatinine ratio ATN Acute tubular necrosis
ACTH Adrenocorticotrophic hormone AVNRT Atrioventricular nodal re-entrant
ADH Antidiuretic hormone, vasopressin tachycardia
ADP Adenosine diphosphate AVP Arginine vasopressin
ADR Adverse drug reaction AVRT Atrioventricular re-entrant
AED Antiepileptic drug tachycardia
AFLP Acute fatty liver of pregnancy axSpA Axial spondyloarthritis
AFP Alpha-fetoprotein BAL Bronchoalveolar lavage
AICTD Autoimmune connective tissue BCC Basal cell carcinoma
disease BCG Bacille Calmette–Guérin
AIDS Acquired immune deficiency BD Behçet’s disease
syndrome BiPAP Bi-level positive airway pressure
AIH Autoimmune hepatitis BMD Bone mineral density
AK Actinic keratosis BMI Body mass index
AKI Acute kidney injury BNP Brain natriuretic peptide
ALL Acute lymphoblastic leukaemia BP Blood pressure
ALP Alkaline phosphatase BPH Benign prostatic hypertrophy
ALT Alanine transaminase BPPV Benign paroxysmal positional
AMA Antimitochondrial antibody vertigo
AMD Age-related macular degeneration BRCA1 BReast CAncer genes 1
AML Acute myeloid leukaemia BRCA2 BReast CAncer genes 2
ANA Antinuclear antibody Ca2+ Calcium
ANCA Antineutrophil cytoplasmic CA-MRSA Community-acquired meticillin-
antibody resistant Staphylococcus aureus
anti-EMA Anti-endomysial antibody CAH Congenital adrenal hyperplasia
anti-tTG Anti-tissue transglutaminase cAMP Cyclic adenosine monophosphate
APC Argon plasma coagulation CAP Community-acquired pneumonia
APKD Autosomal dominant polycystic CBT Cognitive behavioural therapy
kidney disease CCF Congestive cardiac failure
xvi • ABBREVIATIONS

CD4 Cluster of differentiation 4 DIPJ Distal interphalangeal joints

CDC Centers for Disease Control and DIT Diiodotyrosine
Prevention DKA Diabetic ketoacidosis
CF Cystic fibrosis DLBL Diffuse large B-cell lymphoma
CFTR Cystic fibrosis transmembrane DLQI Dermatology Life Quality Index
conductance regulator DM1 Myotonic dystrophy type 1
CGA Comprehensive Geriatric DMARD Disease-modifying antirheumatic
Assessment drug
CGH Comparative genomic DMSA Dimercaptosuccinic acid
hybridisation DNA Deoxyribonucleic acid
CGRP Calcitonin gene-related peptide DOAC Direct oral anticoagulant
CIDP Chronic inflammatory DPP-4 Dipeptidyl peptidase 4
demyelinating polyneuropathy DRE Digital rectal examination
CIM Critical illness myopathy DRESS Drug reaction and eosinophilia
CJD Creutzfeldt–Jakob disease with systemic symptoms
CK Creatine kinase DVT Deep vein thrombosis
CKD Chronic kidney disease DXA Dual X-ray absorptiometry
CLL Chronic lymphocytic leukaemia E, V, M Eye, verbal, motor (in Glasgow
CML Chronic myeloid leukaemia Coma Scale)
CMV Cytomegalovirus EBUS-FNA Endobronchial ultrasound-guided
CN Cranial nerve fine needle aspiration
CNS Central nervous system EBV Epstein–Barr virus
CNV Copy number variant ECF Extracellular fluid
CO2 Carbon dioxide ECF Epirubicin, cisplatin and
COL4A5 Collagen type IV alpha 5 chain fluorouracil (cancer chemotherapy
COPD Chronic obstructive pulmonary combination)
disease ECG Electrocardiography
COX Cyclo-oxygenase ECMO Extracorporeal membrane
CPAP Continuous positive airway pressure oxygenation
CPE Carbapenemase-producing ECT Electroconvulsive therapy
Enterobacteriaceae ED Erectile dysfunction
CPPD Calcium pyrophosphate disease ED50 Median effective dose: the dose
CPR Cardiopulmonary resuscitation that produces a quantal effect (all
CRP C-reactive protein or nothing) in 50% of the
CRPS Complex regional pain syndrome population that takes it
CSF Cerebrospinal fluid EEG Electroencephalography
CT Computed tomography eGFR Estimated glomerular filtration rate
CT-PET CT positron emission tomography EGFR Epidermal growth factor receptor
CTKUB CT scan of kidneys, ureters and EIA Enzyme immunoassay
bladder ELISA Enzyme-linked immunosorbent
CTPA CT pulmonary angiogram assay
CTS Carpal tunnel syndrome EMG Electromyography
CVC Central venous catheter ENA Extractable nuclear antigens
CVD Cardiovascular disease ENT Ear, nose and throat
CVP Central venous pressure EPO Erythropoietin
CXR Chest X-ray ERCP Endoscopic retrograde
CYP Cytochrome P cholangiopancreatography
DBS Deep brain stimulation ESR Erythrocyte sedimentation rate
DDAVP Desmopressin ESRD End-stage renal disease
DGI Disseminated gonococcal ESWL Extracorporeal shockwave
infection lithotripsy
DILI Drug-induced liver injury ET Essential tremor
DILS Diffuse inflammatory EUS Endoscopic ultrasound
lymphocytosis syndrome FAP Familial adenomatous polyposis
 ABBREVIATIONS • xvii

FAST HUG Feeding, analgesia, sedation, HBeAg Hepatitis B e antigen

thromboprophylaxis, head of bed HBsAg Hepatitis B surface antigen
elevation, ulcer prophylaxis, glucose HBV Hepatitis B virus
control (mnemonic to help prevent HCC Hepatocellular carcinoma
intensive care complications) hCG Human chorionic gonadotrophin
FDG Fludeoxyglucose HCO3− Bicarbonate
FEV1 Forced expiratory volume in 1 HCV Hepatitis C virus
second HDL High-density lipoprotein
FFP Fresh frozen plasma HDV Hepatitis D virus
FHH Familial hypocalciuric HELLP Haemolysis, elevated liver
hypercalcaemia enzymes, low platelet count
FiO2 Fraction of inspired oxygen HER Human epidermal growth factor
FODMAP Fermentable oligosaccharides, receptor
disaccharides, monosaccharides HEV Hepatitis E virus
and polyols HG Hyperemesis gravidarum
FSGS Focal segmental HHS Hyperosmolar hyperglycaemic
glomerulosclerosis state
FSH Follicle-stimulating hormone HIT Heparin-induced
FVC Forced vital capacity thrombocytopenia
FXR Farnesoid X receptor HIV Human immunodeficiency virus
G-CSF Granulocyte colony-stimulating HIVAN HIV-associated nephropathy
factor HL Hodgkin lymphoma
G6PD Glucose-6-phosphate HLA Human leucocyte antigen
dehydrogenase HLH Haemophagocytic
GABA γ-Aminobutyric acid lymphohistiocytosis
GAD Glutamic acid decarboxylase HMS Hypermobility syndrome
GBD Global Burden of Disease HNF Hepatocyte nuclear factor
GBL Gamma butyrolactone HPOA Hypertrophic pulmonary
GBM Glomerular basement membrane osteoarthropathy
GBS Guillain–Barré syndrome HPV Human papilloma virus
GCA Giant cell arteritis HRCT High-resolution CT
GCS Glasgow Coma Scale HSV Herpes simplex virus
GFR Glomerular filtration rate HTLV Human T-cell lymphotropic virus
GGE Genetic generalised epilepsies HUS Haemolytic uraemic syndrome
GGT γ-Glutamyl transferase IA-2 Islet antigen 2
GH Growth hormone IABP Intra-aortic balloon pump
GHB Gamma hydroxybutyrate IARC International Agency for Research
GI Gastrointestinal on Cancer
GIP Gastric inhibitory polypeptide IBD Inflammatory bowel disease
GIST Gastrointestinal stromal cell IBS Irritable bowel syndrome
tumour ICD Implantable cardiac defibrillator
GLP-1 Glucagon-like peptide-1 ICD International Classification of
GLUTs Glucose transporters Diseases
GnRH Gonadotrophin-releasing hormone ICF Intracellular fluid
GORD Gastro-oesophageal reflux disease ICP Intracranial pressure
GPA Granulomatosis with polyangiitis ICS Inhaled corticosteroid
GVHD Graft-versus-host disease ICU Intensive care unit
H+ Hydrogen ion IDU Intravenous drug user
HACE High-altitude cerebral oedema Ig Immunoglobulin
HAP Hospital-acquired pneumonia IgA Immunoglobulin A
HAPE High-altitude pulmonary oedema IgE Immunoglobulin E
HAV Hepatitis A virus IGF Insulin-like growth factor
HbA1c Glycated haemoglobin IgG Immunoglobulin G
HBc Hepatitis B core antigen IgM Immunoglobulin M
xviii • ABBREVIATIONS

IGRA Interferon-gamma release assay MERS-CoV Middle East respiratory syndrome

IIH Idiopathic intracranial hypertension coronavirus
ILD Interstitial lung disease Mg2+ Magnesium
IM Intramuscular MGUS Monoclonal gammopathy of
INN International non-proprietary name uncertain significance
INR International normalised ratio MHC Major histocompatibility complex
IPF Idiopathic pulmonary fibrosis MI Myocardial infarction
IPSS International Prostate Symptom MIT Monoiodotyrosine
Score MM Multiple myeloma
IRIS Immune reconstitution MMF Mycophenolate mofetil
inflammatory syndrome MODY Maturity-onset diabetes of the
ITP Immune thrombocytopenia young
IV Intravenous MPA Microscopic polyangiitis
IVIg Intravenous immunoglobulins MRCP Magnetic resonance
JC virus John Cunningham virus cholangiopancreatography
JIA Juvenile idiopathic arthritis MRD Minimal residual disease
JVP Jugular venous pressure MRI Magnetic resonance imaging
K+ Potassium mRNA Messenger ribonucleic acid
KCO Carbon monoxide transfer MRSA Meticillin-resistant Staphylococcus
coefficient aureus
LABA Long-acting β2-agonist MS Multiple sclerosis
LADA Latent autoimmune diabetes of MSE Mental state examination
adulthood MSM Man who has sex with men
LAMA Long-acting muscarinic antagonist MSU Mid-stream urine
LDH Lactate dehydrogenase MTP Metatarsophalangeal
LDL Low-density lipoprotein MuSK Muscle-specific kinase
LEMS Lambert–Eaton myasthenic MVA Mosaic variegated aneuploidy
syndrome Na+ Sodium
LFTs Liver function tests NAD Nicotinamide adenine dinucleotide
LH Luteinising hormone NAFLD Non-alcoholic fatty liver disease
LMWH Low-molecular-weight heparin NASH Non-alcoholic steatohepatitis
LR Likelihood ratio NFFC Non-front-fanged colubrid (snake)
LSD Lysosomal storage disease NGS Next-generation sequencing
LUL Left upper lobe NHL Non-Hodgkin lymphoma
LUTS Lower urinary tract symptoms NICE National Institute for Health and
MALT Mucosa-associated lymphoid Care Excellence
tissue NIV Non-invasive ventilation
MAP Mean arterial pressure NMDA N-methyl-D-aspartate
MCI Minimal cognitive impairment NMO Neuromyelitis optica
MCP Metacarpophalangeal NNRTI Non-nucleoside reverse
MCPJ Metacarpophalangeal joint transcriptase inhibitor
MCTD Mixed connective tissue disease NNT Number needed to treat
MCV Mean corpuscular volume NR Normalised ratio
MDP Methylene diphosphonate NRTI Nucleoside reverse transcriptase
MDRD Modification of Diet in Renal inhibitor
Disease NSAID Non-steroidal anti-inflammatory
MDS Myelodysplastic syndromes drug
MEGX Monoethylglycinexylidide NSIP Non-specific interstitial pneumonia
MELAS Mitochondrial encephalopathy, O2 Oxygen
lactic acidosis and stroke-like OA Osteoarthritis
episodes OBMT Omeprazole, bismuth subcitrate,
MELD Model for End-Stage Liver metronidazole and tetracycline
Disease OCD Obsessive–compulsive disorder
MEN Multiple endocrine neoplasia OCP Oral contraceptive pill
MERS Middle East respiratory syndrome OGD Oesophago-gastroduodenoscopy
 ABBREVIATIONS • xix

OGTT Oral glucose tolerance test PTE Pulmonary thromboembolism

OPIDN Organophosphate-induced PTH Parathyroid hormone
delayed polyneuropathy PTLD Post-transplant lymphoproliferative
OSA Obstructive sleep apnoea disorder
PaCO2 Partial pressure of carbon dioxide PTSD Post-traumatic stress disorder
in arterial blood PUO Pyrexia of unknown origin
pANCA Perinuclear antineutrophil PVD Posterior vitreous detachment
cytoplasmic antibody RA Rheumatoid arthritis
PaO2 Partial pressure of oxygen in RAAS Renin–angiotensin–aldosterone
arterial blood system
PARP Poly-ADP ribose polymerase RAPD Relative afferent pupillary defect
PASI Psoriasis Area and Severity RBILD Respiratory bronchiolitis–interstitial
Index lung disease
PBC Primary biliary cirrhosis RFA Radiofrequency ablation
PBI Pressure bandage and RIC Reduced-intensity conditioning
immobilisation RNA Ribonucleic acid
PCI Percutaneous coronary ROSC Return of spontaneous
intervention circulation
PCNL Percutaneous nephrolithotomy ROSIER Rule Out Stroke In the Emergency
PCOS Polycystic ovary syndrome Room (clinical stroke tool)
PCP Pneumocystis pneumonia RPR Rapid plasma reagin
PCR Polymerase chain reaction rt-PA Recombinant tissue plasminogen
PD Parkinson’s disease activator
PDB Paget’s disease of bone RTA Renal tubular acidosis
PDT Photodynamic therapy RV Residual volume
PEA Pulseless electrical activity SAAG Serum–ascites albumin gradient
PEEP Positive end-expiratory pressure SABA Short-acting β2-agonist
PEFR Peak expiratory flow rate SaO2 Arterial oxygen saturation
PEP Post-exposure prophylaxis SARS Severe acute respiratory
PET Positron emission tomography syndrome
PHT Pulmonary hypertension SBP Spontaneous bacterial peritonitis
PIP Proximal interphalangeal SCC Squamous cell carcinoma
PIPJ Proximal interphalangeal joints SCLC Small cell lung cancer
PI Protease inhibitor SCRA Synthetic cannabinoid receptor
PKD Polycystic kidney disease agonist
75
PLE Polymorphic light eruption SeHCAT Se-homocholic acid taurine
PMF Progressive massive fibrosis SGLT2 Sodium and glucose
PMR Polymyalgia rheumatica co-transporter 2
PO2 Partial pressure of oxygen SHBG Sex hormone-binding globulin
POCT Point-of-care test SIADH Syndrome of inappropriate
POEM Peroral endoscopic myotomy antidiuretic hormone (vasopressin)
POMC Pro-opiomelanocortin secretion
PPARγ Peroxisome proliferator-activated SIJ Sacroiliac joint
receptor gamma SLE Systemic lupus erythematosus
PPCI Primary percutaneous coronary SO2 Saturation of haemoglobin with
intervention oxygen
PPI Proton pump inhibitor SOFA Sequential Organ Failure
PRV Polycythaemia rubra vera Assessment
PSA Prostate-specific antigen SpA Spondyloarthritis
PsA Psoriatic arthritis SPC Summary of product
PSC Primary sclerosing cholangitis characteristics
PSP Primary spontaneous SPECT Single-photon emission computed
pneumothorax tomography
PSS Primary Sjögren’s syndrome SpO2 Peripheral capillary oxygen
PT Prothrombin time saturation
xx • ABBREVIATIONS

SScl Systemic sclerosis TPPA Treponema pallidum particle

SSRI Selective serotonin re-uptake agglutination assay
inhibitor TRAbs TSH receptor antibodies
STI Sexually transmitted infection TRM Treatment-related mortality
SVR Sustained viral response tRNA Transfer ribonucleic acid
T3 Triiodothyronine TSH Thyroid-stimulating hormone
T4 Thyroxine TTP Thrombotic thrombocytopenic
TAC Trigeminal autonomic purpura
cephalalgia UDCA Ursodeoxycholic acid
TACE Transarterial chemoembolisation UFH Unfractionated heparin
TB Tuberculosis UMOD Uromodulin
TBG Thyroxine-binding globulin USS Ultrasound scan
TCO Transfer factor for carbon UVB Ultraviolet B
monoxide V̇ /Q̇ Ventilation–perfusion
TEN Toxic epidermal necrolysis V2 Vasopressin 2
TFTs Thyroid function tests VAP Ventilator-associated pneumonia
TGA Transient global amnesia Vd Volume of distribution
TGF Transforming growth factor VEGF Vascular endothelial growth factor
TIA Transient ischaemic attack VGCC Voltage-gated calcium channel
TIPSS Transjugular intrahepatic VIP Vasoactive intestinal peptide
portosystemic stent shunt VLDL Very low-density lipoprotein
TKI Tyrosine kinase inhibitor VSD Ventricular septal defect
TKR Total knee replacement VTE Venous thromboembolism
TNF Tumour necrosis factor vWD von Willebrand disease
TNM System used in cancer staging: vWF von Willebrand factor
T = size and extent of the main/ vWF:Ag von Willebrand factor antigen
primary tumour; N = number VZV Varicella zoster virus
of nearby lymph nodes involved; WCC White cell count
M = metastasis WHO World Health Organization
TPOs Thyroid peroxidise antibodies ZnT8 Zinc transporter 8
 N Cooper
1
Clinical decision-making
Multiple Choice Questions
1.1. In the specialty of internal medicine, 1.4. A test is performed to detect the presence
diagnostic error occurs in approximately what of a disease in a specific population. The
percentage of cases? results of the test can be summarised in the
A. 0–5% table below.
B. 6–10%
C. 11–15% Disease No disease
D. 16–20% Positive test A B
E. 21–25% Negative test C D

1.2. A doctor is considering whether a patient Which of the following describes the positive
presenting with headache, fever and nuchal predictive value of the test?
rigidity may have meningitis. Regarding A. A/(A + B) × 100
likelihood ratios (LRs) for each clinical finding, B. A/(A + C) × 100
which of the following statements is true? C. A/(A + D) × 100
A. An LR greater than 1 decreases the D. D/(D + B) × 100
probability of disease E. D/(D + C) × 100
B. An LR greater than 1 increases the
probability of disease 1.5. An elderly woman fell and hurt her left hip.
C. An LR is the probability of the finding in On examination the left hip was extremely
patients with the disease painful to move and she was unable to stand.
D. An LR of 0 means the diagnosis is unlikely The pre-test probability of a hip fracture was
E. An LR of 1 means the diagnosis is certain deemed to be high. Plain X-rays of the pelvis
and left hip were requested.
1.3. A test is performed to detect the presence Which of the following statements best
of a disease. The results of the test can be describes ‘post-test probability’?
summarised in the table below. A. The adjustment of probability after
Disease No disease taking individual patient factors in
Positive test A B to account
Negative test C D B. The chance that a test will detect true
positives
Which of the following describes the C. The prevalence of disease in the population
sensitivity of the test? to which the patient belongs
A. A/(A + B) × 100 D. The probability of a disease after taking
B. A/(A + C) × 100 new information from a test result into
C. A/(A + D) × 100 account
D. D/(D + B) × 100 E. The proportion of patients with a test result
E. D/(D + C) × 100 who have the disease
2 • Clinical decision-making
1.6. A doctor is considering whether to treat a
patient with antibiotics for a urinary tract
infection. The term ‘treatment threshold’
describes a situation in which various factors
are evenly weighted. What is the best
description of the factors involved?
A. The cost of the treatment, and whether the
treatment is likely to succeed
B. The quality of life of the patient, and risks
and benefits of treatment
C. The risk and benefits of treatment
D. The risks of the test, and risk and benefits of
treatment
E. The wishes of the patient, and whether the
treatment is likely to succeed
1.7. Dual process theory describes two distinct
processes of human decision-making. What is
the accepted estimate of the proportion of time
we spend engaged in type 2 (analytical)
thinking?
A. 5%
B. 25%
C. 50%
D. 75%
E. 95%
1.8. In terms of human thinking and
decision-making, what tendency does
confirmation bias describe?
A. To look for supporting evidence to confirm
a theory and ignore evidence that
contradicts it
B. To rely too much on the first piece of
information offered
C. To stop searching because we have found
something that fits
D. To subconsciously see what we expect to
see
E. To want to confirm our diagnoses with
others before making a decision
1.9. Which of these factors is most likely to lead
to an increased incidence of errors in clinical
decision-making?
A. Age
B. Fatigue
C. Gender
D. Use of checklists
E. Working alone
1.10. In a case of suspected pulmonary
embolism in an ambulatory care setting, which
of the following individual signs on physical
examination carries the most diagnostic weight
in either a positive or negative direction?
A. Blood pressure greater than 120/80 mmHg
B. Heart rate less than 90 beats/min
C. Oxygen saturations greater than 94% on air
D. Respiratory rate less than 20 breaths/min
E. Temperature less than 37.5°C
1.11. Which of the following statements best
describes ‘patient-centred evidence-based
medicine’?
A. The application of best available evidence
taking individual patient factors into account
B. The application of best available evidence to
patient care
C. The application of clinical decision aids in
decision-making
D. The implementation of a management plan
based on patient wishes
E. The use of evidence-based care bundles
1.12. According to research, under what
circumstances are patients more likely to
comply with recommended treatment and less
likely to re-attend?
A. If relative risk instead of absolute risk is used
in explanations
B. If the consultation is longer
C. If the patient is male
D. If they feel that they have been listened to
and understand the treatment plan
E. If visual aids have been used instead of text
to explain the treatment plan
1.13. Which of the following statements best
describes what is meant by the term ‘human
factors’?
A. An understanding of diagnostic error
B. How equipment is designed to take human
behaviour into account
C. How fatigue affects human thinking and
decision-making
D. How healthcare professionals communicate
in a team
E. The science of the limitations of human
performance
1.14. In terms of human thinking and
decision-making, anchoring describes what
tendency?
A. To look for supporting evidence to confirm
a theory and ignore evidence that
contradicts it

B. To rely too much on the first piece of
information offered
C. To stop searching because we have found
something that fits
D. To subconsciously see what we expect to
see
E. To want to confirm our diagnoses with
others before making a decision
1.15. The D-dimer test has a sensitivity of at
least 95% in detecting acute venous
thromboembolism (VTE). However, it has a low
specificity of around 40%. Which of the
Answers
1.1. Answer: C.
It is estimated that diagnosis is wrong 11–15%
of the time in the undifferentiated specialties
of internal medicine, emergency medicine
and general practice. Diagnostic error is
associated with greater morbidity than other
types of medical error, and the majority of
diagnostic errors are considered to be
preventable.
1.2. Answer: B.
Likelihood ratios (LRs) are clinical diagnostic
weights.
probability of finding in patients
with disease
LR =
probability of finding in patients
without disease
An LR greater than 1 increases the
probability of disease (the greater the value, the
greater the probability). An LR less than 1
decreases the probability of disease. LRs are
developed against a diagnostic standard (in the
case of meningitis, lumbar puncture results) so
do not exist for all clinical findings. LRs illustrate
how a probability changes – but do not
determine the prior probability of disease. If the
starting probability is high to begin with, an LR
of around 1 does not affect this.
1.3. Answer: B.
Sensitivity = A ( A + C ) × 100
Sensitivity is the ability to detect true
positives; specificity is the ability to detect true
negatives. There is no test that can 100% of
the time detect people with a disease and
Clinical decision-making • 3
following statements is true regarding the
interpretation of a D-dimer result?
1
A. A negative D-dimer result in a high clinical
probability patient excludes acute VTE
B. A positive D-dimer result means that acute
VTE is present
C. D-dimer is a useful screening test in patients
presenting with breathlessness
D. D-dimer testing in suspected acute VTE
results in lots of false negatives
E. D-dimer testing in suspected acute VTE
results in lots of false positives
exclude those without it. Even a very good test,
with 95% sensitivity, will miss 1 in 20 people
with the disease. Every test therefore has ‘false
positives’ and ‘false negatives’.
A very sensitive test will detect most
disease but may generate abnormal findings in
healthy people. A negative result will therefore
reliably exclude the disease, but a positive test
is likely to require further evaluation. On the
other hand, a very specific test may miss
significant pathology but is likely to establish
the diagnosis beyond doubt when the result is
positive.
1.4. Answer: A.
Positive predictive value = A (A + B) × 100
Predictive values combine sensitivity,
specificity and prevalence. Sensitivity and
specificity are characteristics of the test; the
population does not change this. However, as
doctors, we are interested in the question,
‘What is the probability that a person with a
positive test actually has the disease?’ The
positive predictive value is the proportion of
patients with a test result who have the disease
and is calculated from a table of results in a
specific population. It is not possible to transfer
this value to a different population.
1.5. Answer: D.
Post-test probability is the probability of a
disease after taking new information from a test
result into account. The pre-test probability of
disease is decided by the doctor – it is an
opinion based on gathered evidence prior to
ordering the test. Bayes’ Theorem can be used
4 • Clinical decision-making
to calculate post-test probability for a patient in
any population. It is a mathematical way to
describe the post-test probability of a disease
by incorporating pre-test probability, sensitivity
and specificity.
1.6. Answer: D.
The treatment threshold combines factors such
as the risks of the test, and the risks versus
benefits of treatment. The point at which the
factors are all evenly weighted is the threshold.
If a test or treatment for a disease is effective
and low risk, then one would have a lower
threshold for going ahead. On the other hand,
if a test or treatment is less effective or high
risk, one requires greater confidence in the
clinical diagnosis and potential benefits of
treatment first. In principle, if a diagnostic test
will not change the management of the patient,
then it should not be requested, unless there
are other compelling reasons to do so.
1.7. Answer: A.
Psychologists believe we spend 95% of our
daily lives engaged in type 1 thinking – the
intuitive, fast, subconscious mode of
decision-making. In everyday life we spend little
time (5%) engaged in type 2 thinking. Imagine
driving a car; it would be impossible to function
efficiently if every decision and movement was
as deliberate, conscious, slow and effortful as
in our first driving lesson. With experience,
complex procedures become automatic, fast
and effortless. The same applies to medical
practice.
1.8. Answer: A.
Cognitive biases are subconscious errors that
lead to inaccurate judgement and illogical
interpretation of information. In evolutionary
terms, it is thought that cognitive biases
developed because speed was often more
important than accuracy. This property of
human thinking is highly relevant to clinical
decision-making. Confirmation bias is the
tendency to look for confirming evidence to
support a theory rather than looking for
contradictory evidence to refute it, even if the
latter is clearly present. Confirmation bias is
common when a patient has been seen first by
another doctor.
1.9. Answer: B.
Cognition is affected by things like fatigue,
illness, emotions, interruptions, cognitive
overload and time pressure. Poor team
communication and poorly designed equipment
or clinical processes also increase the likelihood
of error. Age, gender and working alone are not
factors that affect cognition. Use of checklists
has been shown to improve decision-making in
clinical settings.
1.10. Answer: B.
Suspected pulmonary embolism is a
common problem referred to UK ambulatory
emergency care centres. Unexplained pleuritic
chest pain and/or a history of breathlessness
are the most common symptoms. Vital signs at
rest and the physical examination may be
normal. The only feature presented with a
negative likelihood ratio in the diagnosis of
pulmonary embolism is a heart rate of less than
90 beats/min. In other words, the other normal
physical examination findings (including normal
oxygen saturations) carry little diagnostic
weight.
1.11. Answer: A.
‘Patient-centred evidence-based medicine’
refers to the application of best available
research evidence while taking individual patient
factors into account – these include clinical
factors (e.g. bleeding risk when considering
anticoagulation) and non-clinical factors (e.g.
the patient’s inability to attend for regular blood
tests if started on warfarin).
1.12. Answer: D.
Many studies demonstrate a correlation
between effective clinician–patient
communication and improved health outcomes.
If patients feel they have been listened to and
understand the problem and proposed
treatment plan, they are more likely to adhere
to their medication and less likely to re-attend.
Whenever possible, doctors should quote
numerical information using consistent
denominators (e.g. ‘90 out of 100 patients who
have this operation feel much better, 1 will die
during the operation and 2 will suffer a stroke’).
Visual aids can be used to present complex
statistical information.
Relative risk exaggerates small effects that
distort people’s understanding of true
probability. Longer consultations and the use
of visual aids are tools to facilitate good
communication but in themselves do not
guarantee this is the case. Gender by itself is
not a factor.

1.13. Answer: E.
Human factors is the science of the limitations
of human performance and how technology,
our work environment and team communication
can adapt for this to reduce diagnostic and
other types of error. Analysis of serious adverse
events in health care show that human factors
and poor team communication play a
significant role when things go wrong. Human
factors training is being introduced into
undergraduate and postgraduate medical
curricula and multi-professional team training in
many countries.
1.14. Answer: B.
Cognitive biases are subconscious errors that
lead to inaccurate judgement and illogical
interpretation of information. In evolutionary
terms, it is thought that cognitive biases
developed because speed was often more
important than accuracy. This property of
human thinking is highly relevant to clinical
decision-making. Anchoring describes the
Clinical decision-making • 5
common human tendency to rely too heavily
on the first piece of information offered (the
1
‘anchor’) when making decisions.
1.15. Answer: E.
A very sensitive test will detect most disease
but generate abnormal findings in healthy
people. A negative result therefore means the
disease is unlikely, but a positive result is likely
to require further evaluation. As with all
diagnostic tests, a low pre-test probability plus
a negative D-dimer virtually excludes acute
VTE. However, if the pre-test probability is
very high, a negative D-dimer still leaves a small
but significant chance that acute VTE is
present.
D-dimer is commonly raised in conditions
that have nothing to do with acute VTE: for
example, old age, pregnancy, heart failure,
sepsis and cancer. This is the reason for its low
specificity. It should be used only when the
history and physical examination are consistent
with acute VTE.
 S Maxwell
2
Clinical therapeutics and
good prescribing
Multiple Choice Questions
2.1. Which of the following drugs exerts its E. Reacting chemically with the agonist to
action directly at an enzyme target? reduce the agonist concentration available to
A. Aspirin bind to receptors
B. Hydrocortisone
C. Insulin 2.4. Which of the following drugs induce the
D. Lidocaine hepatic cytochrome P450 enzymes that are
E. Morphine responsible for drug metabolism?
A. Cimetidine
2.2. Which of the following statements best B. Ciprofloxacin
describes the term ‘potency’? C. Erythromycin
A. A less potent drug will always have a lower D. Rifampicin
efficacy than a more potent drug E. Valproate
B. More potent drugs have a lower ED50
C. The potency of a drug has no bearing on 2.5. Which of the following drugs may exhibit
recommended dose ranges zero-order drug kinetics at therapeutic drug
D. The potency of a drug is the extent to which concentrations?
the drug can produce a response when all A. Carbamazepine
of the available receptors are occupied B. Ciprofloxacin
E. The potency of a drug is unrelated to its C. Lamotrigine
affinity for a receptor D. Phenytoin
E. Vancomycin
2.3. Which of the following statements best
describes how a non-competitive antagonist 2.6. Which of the following statements about
drug affects the pharmacodynamic actions of the estimated volume of distribution (Vd) of a
an agonist? drug is true?
A. Binding irreversibly with the receptor to A. Drugs that are highly bound to albumin have
remove receptors as potential binding sites a lower Vd
for the agonist B. Drugs with a large Vd are eliminated more
B. Binding to a different population of receptors rapidly after discontinuation
that produce a response antagonistic to that C. Larger Vd is associated with a shorter
of the agonist half-life
C. Causing cell death so that it cannot function D. Vd cannot be greater than the volume of the
D. Increasing the total number of receptors for body
the agonist, thereby reducing the proportion E. Vd of lipid-soluble drugs is larger in males
that it can occupy than females (of equivalent mass)
 Clinical therapeutics and good prescribing • 7
2.7. Which of the following factors might be
expected to favour increased bioavailability of a
drug that is given by mouth?
A. Enterohepatic circulation of the active drug
B. Gastroenteritis
C. Hypoalbuminaemia
D. Impaired renal function
E. Solid rather than liquid formulations
2.8. For which of the following drugs do
pharmacogenetic differences commonly
influence the clinical effect in Western
populations?
A. Amlodipine
B. Codeine
C. Gliclazide
D. Omeprazole
E. Simvastatin
2.9. Which of the following features is most
characteristic of hypersensitivity adverse drug
reactions?
A. They are associated with human leucocyte
antigen (HLA) class haplotypes
B. They are discovered early in the drug
development process
C. They are dose related
D. They manifest several months after initial
exposure
E. They occur at the higher part of the
therapeutic dose range
2.10. Which of the following is an advantage of
the spontaneous voluntary reporting methods
of pharmacovigilance?
A. It captures the majority of adverse drug
reactions
B. It is able to quantify the risk of an adverse
drug reaction (ADR) after exposure to a drug
C. It is specific for events that really are caused
by the drug
D. It provides early signal generation after
marketing of a new drug
E. Its information is generated by highly
qualified professionals
2.11. A 23 year old woman is taking a
combined oral contraceptive preparation. She
has developed an infection sensitive to a
number of common antibiotics. Which of the
following antibiotic choices is most likely to
interact with the contraceptive preparation to
cause contraceptive failure?
A. Amoxicillin
B. Ciprofloxacin
C. Doxycycline 2
D. Erythromycin
E. Rifampicin
2.12. A 71 year old woman with ischaemic
heart disease recently started taking
amiodarone 200 mg orally daily for control of
her atrial fibrillation. She has now been
admitted to hospital 3 months later with
episodes of dizziness and bradycardia (heart
rate 48 beats/min). The electrocardiogram
shows a prolonged QT interval (530 ms).
Which of her current regular medicines below
is most likely to interact with amiodarone to
cause the QT prolongation?
A. Clopidogrel
B. Moxifloxacin
C. Nicorandil
D. Simvastatin
E. Thyroxine
2.13. Which of the following is the commonest
cause of prescribing errors in hospital
practice?
A. Calculation errors
B. Duplicated prescribing
C. Failed medicines reconciliation
D. Prescribing without indication
E. Unintentional prescribing
2.14. Which of the following is NOT information
required as part of the regulatory process
leading to the granting of a marketing
authorisation (‘license’)?
A. Cost-effectiveness compared to standard
treatment
B. Efficacy in the licensed indication
C. Product information literature
D. Quality of the manufacturing process
E. Toxicology studies
2.15. A trial of 5000 hypertensive patients
randomised them to treatment with a new oral
anticoagulant or a matched placebo. After a
follow-up period of 5 years, 150 patients in the
active treatment arm and 250 patients in the
placebo arm had suffered a stroke.
What is the number of patients that need to
be treated (NNT) with the new treatment over 5
years to prevent one stroke?
A. 10
B. 15
8 • Clinical therapeutics and good prescribing
C. 20
D. 25
E. 30
2.16. An 82 year old man has a routine
medication review with his family physician.
He has a history of a transient ischaemic
attack, hypertension and attacks of gout.
Which of the following prescriptions should
probably be discontinued?
A. Allopurinol 100 mg orally daily
B. Amlodipine 5 mg orally daily
C. Aspirin 75 mg orally daily
D. Diclofenac 25 mg orally 3 times daily
E. Ramipril 5 mg orally daily
2.17. Which of the following drugs would pose
the greatest risk of teratogenic effects if
prescribed during the first trimester of
pregnancy?
A. Amoxicillin
B. Mebeverine hydrochloride
C. Rifampicin
D. Sodium valproate
E. Sulfasalazine
2.18. A 63 year old woman has progressively
deteriorating renal function presumed to be due
to the effects of renal scarring secondary to
chronic reflux nephropathy in childhood. Her
most recent estimated glomerular filtration rate
(eGFR) is 26 mL/min/1.73 m2.
Which of the patient’s prescriptions below
would need to be amended?
A. Clopidogrel 75 mg orally daily
B. Doxazosin 8 mg orally daily
C. Metformin hydrochloride 1 g orally
twice daily
D. Pregabalin 50 mg orally twice daily
E. Tamoxifen 20 mg orally daily
2.19. A 44 year old man with alcoholic cirrhosis
of the liver is admitted to hospital with delirium,
irritability and painful distension of the abdomen
as a result of ascites. His investigations show
that he is anaemic (haemoglobin 82 g/L),
jaundiced (bilirubin 65 µmol/L (3.8 mg/dL)),
hypoalbuminaemic (albumin 20 g/L) and has a
mild coagulopathy (international normalised
ratio (INR) 1.6).
His initial prescription chart contains the five
prescriptions below. Which of the prescriptions
should be discontinued?
A. Codeine phosphate 60 mg orally 4 times
daily
B. Lactulose 20 g 3 times daily
C. Pabrinex (vitamins B and C) intravenous
high-potency solution for injection 2 pairs of
5 mL ampoules 3 times daily
D. Spironolactone 100 mg orally daily
E. Terlipressin acetate 1.5 mg intravenously
4 times daily
2.20. The following dose expressions have been
found on a hospital inpatient chart.
Which dose expression violates acceptable
prescribing practice?
A. 1 sachet
B. 1.4 g
C. 20 mL
D. 26 units
E. 100 µg
2.21. Which of the following drugs should be
prescribed by its proprietary (brand) name in
preference to the generic international
non-proprietary name (INN)?
A. Atorvastatin
B. Ciclosporin
C. Ciprofloxacin
D. Irbesartan
E. Methyldopa
2.22. A 76 year old woman has been treated
successfully with digoxin 187.5 µg orally daily
over a number of months to control the
ventricular response rate to her atrial fibrillation.
She has recently complained of some nausea
and so the plasma digoxin concentration has
been measured to investigate the possibility
of digoxin toxicity as an explanation. On
examination, the radial pulse rate is irregularly
irregular and 64 beats/min. The plasma
digoxin concentration is 1.8 µg/L (target
0.8–2.0 µg/L).
What is the most appropriate course of
action with regard to her digoxin prescription?
A. Change digoxin dosage to 187.5 µg orally
on alternate days
B. Maintain the digoxin dosage at 187.5 µg
orally daily
C. Reduce the digoxin dosage to 62.5 µg orally
daily
D. Reduce the digoxin dosage to 125 µg orally
daily
E. Stop digoxin and start bisoprolol 2.5 mg
orally daily
 Clinical therapeutics and good prescribing • 9
2.23. A 56 year old man is being treated with
intravenous gentamicin for Gram-negative
septicaemia that is presumed to be of urinary
tract origin. He is well hydrated and his renal
function is normal. He has had two previous
doses of gentamicin 360 mg as a 30-minute
intravenous infusion at 1000 hrs on Wednesday
and Thursday. Both previous plasma
gentamicin concentrations have been checked
by the senior doctor in charge of the ward and
the third dose of gentamicin has been
prescribed and is now due (Friday morning at
1000 hrs).
When should the next plasma gentamicin
concentration be taken?
A. 0400 hrs (Saturday)
B. 1400 hrs (Friday)
C. 1800 hrs (Friday)
D. Immediately after the infusion is completed
E. Immediately before the third dose
Answers
2.1. Answer: A.
Aspirin acts on the enzyme cyclo-oxygenase
and is a non-selective and irreversible inhibitor.
Hydrocortisone is a corticosteroid and acts on
a DNA-linked receptor. Insulin acts on a
kinase-linked receptor. Lidocaine blocks a
voltage-sensitive Na+ channel. Morphine acts
on a G-protein-coupled receptor.
2.2. Answer: B.
The potency of a drug is related to its affinity
for a receptor. Less potent drugs are given in
higher doses. The lower potency of a drug can
be overcome by increasing the dose. Option D
refers to the ‘efficacy’ of a drug.
2.3. Answer: A.
The term ‘non-competitive antagonist’ is used
to describe two distinct situations where an
antagonist binds to a receptor, or its associated
signal transduction mechanism, to prevent the
agonist activating the receptor. The common
feature is that increasing the concentration of
agonist cannot outcompete the antagonist.
The receptor is rendered inactive and so the
maximal response of which the cell or tissue is
capable is reduced. This can occur in three
ways: (i) the antagonist binds to an allosteric
site of the receptor, (ii) the antagonist binds to
2.24. A 78 year old woman is reviewed in the
emergency department of a hospital with
bruising. She is taking warfarin 3 mg and 4 mg 2
orally on alternate days as prophylaxis against
recurrent pulmonary emboli. Her last 3-monthly
INR measurement was 2.7. She has been
otherwise well with no other new symptoms
and she has not been put on any new
medicines. Her investigations reveal a normal
full blood count but an INR of 6.7.
What is the appropriate course of action?
A. Stop warfarin and give phytomenadione
(vitamin K1) 1–3 mg by slow intravenous
injection
B. Stop warfarin and give phytomenadione
(vitamin K1) 1–5 mg by mouth
C. Stop warfarin and start apixaban
D. Stop warfarin and start low-molecular-weight
heparin injections
E. Stop warfarin for 2 days only
the same active site as the agonist but does so
irreversibly, or (iii) the antagonist interferes with
the signal transduction mechanism preventing
receptor–agonist binding resulting in a
pharmacological effect.
2.4. Answer: D.
Rifampicin is a very potent enzyme inducer.
All of the other options are well recognised as
enzyme inhibitors.
2.5. Answer: D.
The clearance rate of most drugs increases
progressively as their plasma concentration
increases (‘first-order metabolism’). For a
small number of common medicines, their
metabolism is ‘saturable’, meaning that the
rate of clearance cannot increase further
(‘zero-order kinetics’). For those drugs, further
dose increases can cause disproportionate
increases in exposure and the likelihood of
toxicity.
2.6. Answer: A.
The apparent volume of distribution (Vd) is the
volume into which a drug appears to have
distributed following intravenous injection. It is
calculated from the equation Vd = D/C0, where
D is the amount of drug given and C0 is the
Another random document with
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mentioned the “Lord Chancellor,” used by Maudslay before 1830. R.
Hoe & Company, of New York, in 1858, had a bench micrometer
reading up to 9 inches. But none of these could ever have influenced
mechanical standards generally as did the strong, compact little
instrument developed by Brown & Sharpe.
The circumstances surrounding its introduction are as follows: In
1867 the Bridgeport Brass Company had a lot of sheet brass
returned to them from the Union Metallic Cartridge Company as “out
of gauge.” Investigation showed that the sheets were to the gauge of
the manufacturer, but that the gauge used by the customer did not
agree, and, further, when both gauges were tested by a third, no two
of them agreed. All three gauges were supposed to be the regular U.
S. Standard, adopted by the wire manufacturers in 1857, of the well-
known round, flat form, with slits for the various sizes cut in the
circumference. Gauges of this form were the best and most accurate
method then known for measuring sheet metal.
S. R. Wilmot, then superintendent of the Bridgeport Brass
Company, seeing that the difficulty was likely to occur again, devised
the micrometer shown at A in Fig. 44, and had six of them made by a
skilled machinist named Hiram Driggs, under the direction of A. D.
Laws, who was then in charge of the mechanical department of the
Brass Company. The reading of the thousandths of an inch was
given by a pointer and a spiral line of the same pitch as the screw,
40 to the inch, running around the cylinder and crossed by a set of
25 lateral, parallel lines. In the early part of 1867, the matter was
taken up with J. R. Brown & Sharpe with a view to having them
manufacture the gauges, and the one shown, A, Fig. 44, with Mr.
Laws’ name stamped on it, is still in their possession. As submitted,
the tool was not considered to be of commercial value, for the
cylinder was completely covered with spiral and straight lines
intersecting each other so closely that it was impossible to put any
figures upon it, thus making it very difficult to read.
In 1848 Jean Laurent Palmer, a skilled mechanic in Paris,
patented a “screw caliper,” shown at B, Fig. 44, and began
manufacturing it under the name of “Systeme Palmer.” In this
micrometer the graduations were divided, one set being on the
cylinder of the frame and the other on the revolving barrel, an
arrangement which permitted all the markings necessary for
clearness. The importance of this tool does not seem to have been
appreciated until August, 1867, when J. R. Brown and Lucian
Sharpe saw one at the Paris Exposition. They at once recognized its
possibilities and brought one home with them. To use Mr. Sharpe’s
own words: “As a gauge was wanted for measuring sheet metal, we
adopted Palmer’s plan of division, and the Bridgeport man’s size of
gauge, adding the clamp for tightening the screw and the adjusting
screw for compensating the wear of end of points where the metal is
measured, and produced our ‘Pocket Sheet Metal Gauge.’... We
should never have made such a gauge as was shown us by the
Bridgeport man in 1867, to sell on our own account, as it would be
too troublesome to read to be salable. If we had not happened to find
the Palmer gauge, and thereby found a practical way to read
thousandths of an inch, no gauges would have been made. If we had
never seen the Bridgeport device we should have found the Palmer
at Paris, and without doubt have made such gauges, but possibly
would have made a larger one first. The immediate reason of making
the ‘Pocket Sheet Metal Gauge’ was the suggestion coming from the
Bridgeport Brass Company of the want of a gauge of the size of the
sample shown us for the use of the brass trade.”[194]
[194] From a letter of Lucian Sharpe, quoted in the American Machinist of
December 15, 1892, p. 10.
 A B

C D

Figure 44. Early Micrometer Calipers

A—Wilmot’s Micrometer, 1867

B—Palmer Micrometer, brought from Paris by J. R. Brown and Lucian Sharpe,
1867
C—“Pocket Sheet Metal Gauge,” Brown & Sharpe, 1868
D—One-inch Micrometer, Brown & Sharpe, 1877

This gauge, shown at C, in Fig. 44, was put on the market in 1868,
and appeared in the catalog of 1869. Comparison of A, B, and C in
Fig. 44 shows clearly their close relationship. The term “micrometer”
caliper was first applied to the one-inch caliper (D, Fig. 44) which
was brought out and illustrated in the catalog of 1877. In Machinery
of June, 1915, Mr. L. D. Burlingame has given an admirable and very
complete account of the various improvements which have been
brought out since that time. In connection with the article, a modern
micrometer is shown and its various features, with the inventors of
each, are clearly indicated.[195]
[195] The origin and development of the present form of micrometer is
further discussed in Machinery, August, 1915, p. 999, and September,
1915, pp. 11, 58.

The cylindrical grinder was first made as a crude grinding lathe in

the early sixties, and used for grinding the needle and foot bars of
the Wilcox & Gibbs sewing machines. In 1864 and 1865 the regular
manufacture of grinding lathes was begun by using parts of 14-inch
Putnam lathes modified to produce the automatic grinding lathes.
These modifications consisted in mounting a grinding wheel on the
carriage, providing an automatic feeding and reversing attachment,
and included the use of a dead center pulley. From 1868 until 1876
various plans were worked out for a complete universal grinder, and
by 1876 one had been built and was exhibited at the Centennial
Exposition. The first one used at the factory was put into service a
few days after Mr. Brown’s death, which occurred July 23, 1876. The
patent granted to Mr. Brown’s heirs for this machine included not
only the ordinary devices of the universal grinder so well known
today, but also provision for form grinding. The designing of surface
machines as well as many other varieties followed, the work being
done under the direction of Charles H. Norton, who later had charge
of the design of their grinding machinery.
The manufacture of automatic gear cutters was commenced by
the Brown & Sharpe Manufacturing Company in 1877, two designs
by Edward H. Parks, a small manufacturing machine for bevel and
spur gears and the larger machine for general use, being brought out
in that year.
In sixty years the Brown & Sharpe Company has grown from an
obscure local shop into a great plant employing thousands, but its
influence and its product represent a greater achievement. Many
mechanics of high ability have gone to other shops, among whom
are Henry M. Leland, president of the Cadillac Motor Car Company;
J. T. Slocomb, Horace Thurston, Elmer A. Beaman and George
Smith, of Providence; Charles H. Norton, of Worcester; John J.
Grant, of Boston; William S. Davenport, of New Bedford; A. J. Shaw,
of the Shaw Electric Crane Company, and H. K. LeBlond, of
Cincinnati. Hundreds of others, however, as managers,
superintendents, chief draftsmen and tool makers, have perhaps
done more to spread throughout the country the methods and
standards of accuracy which have made American machine tools
what they are.
Mr. Henry M. Leland, who was trained in the Providence shop,
says:
The man who is responsible for this and who thoroughly demonstrated his rare
ability and wonderful persistency in bringing out the accurate measuring tools and
instruments, and the advanced types of more efficient and unique machinery, was
the founder, Joseph R. Brown. I have often said that in my judgment Mr. Brown
deserved greater credit than any other man for developing and making possible
the great accuracy and the high efficiency of modern machine practice and in
making it possible to manufacture interchangeable parts, because the Brown &
Sharpe Company were the first people to place on the market and to educate the
mechanics of the country in the use of the vernier caliper. They were also the first
to make the micrometer caliper.
I remember that in those early days people came to Brown & Sharpe from all
over the world to consult with Mr. Brown in reference to obtaining great accuracy
and securing difficult results which had been deemed insurmountable by other
high-grade mechanics. The mechanical engineers are now searching the records
for men who have made themselves eminent in the industrial world as inventors
and manufacturers; for a list of men to have honorable mention and to have their
achievements and ability so recorded that the modern world may bestow upon
them the credit and gratitude which they so richly deserve. Among these names I
know of none who deserves a higher place than, or who has done so much for the
modern high standards of American manufacturers of interchangeable parts as
Joseph R. Brown.
 CHAPTER XVII
CENTRAL NEW ENGLAND
At the close of the chapter on “Early American Mechanics” we referred to
the spread of machinery building northward from Rhode Island to the
Merrimac Valley and central Massachusetts. This by no means implies that
all the northern shops were started by Rhode Island mechanics, but their
influence is so strong as to be clearly seen; and here, as in Rhode Island, the
early shops were closely identified with the textile industry.
One of the first and most influential of these was the Amoskeag
Manufacturing Company. The beginnings of the Amoskeag Company were
made by a Benjamin Pritchard, of New Ipswich, N. H., who built a small
textile mill at Amoskeag Village, then Goffstown, in 1809. In 1822 it was
bought by Olney Robinson, from whom, that same year, Samuel Slater
received a letter asking for a loan of $3000. This was accompanied by a
magnificent salmon as a sample of the products of Amoskeag. Slater, with
the instincts of a good sportsman and a careful business man, went there to
investigate, with the result that he bought the property, which then consisted
of a water power, a two-story wooden mill and two or three small tenements.
Larned Pitcher soon joined him, and in 1825 four other partners were taken
in, Willard Sayles, Lyman Tiffany, Oliver Dean and Ira Gay. Three of the
partners were Pawtucket men—Slater, Pitcher and Gay. Slater and Gay were
very influential in the early history of the company. The business grew rapidly
and in 1841 they formed the Amoskeag Manufacturing Company, which has
had a long and successful career. Their charter was broad, and they
extended their operations until they included textile mills, extensive
improvements of the water powers on the Merrimac, the founding of the city
of Manchester, and the operation of a large machine shop.
The last, which interests us most, was started about 1840. At first it was
used only for building and repairing textile machinery, but before very long it
was actively engaged in the manufacture of steam boilers, locomotives,
steam fire engines, turbine wheels and machine tools. It comprised two
three-story shops, each nearly 400 feet long, with foundries and forge shops,
and employed in all 700 men—a large plant for seventy-five years ago.
William A. Burke, its first head, left in 1845 to organize the Lowell Machine
Shop, which built textile and paper machinery and locomotives, and did
general millwright work. One of the workmen who helped install the
machinery in the Amoskeag shop was William B. Bement. He remained there
for two years as foreman and contractor, and in 1845 joined Burke at Lowell.
O. W. Bayley, who succeeded Burke as head of the Amoskeag shop, left in
1855 and founded the Manchester Locomotive Works.
Ira Gay came to New Hampshire from Pawtucket in 1824. Besides the
Nashua Manufacturing Company and the Nashua Iron & Steel Works, he and
his brother, Ziba Gay, founded (about 1830) the Gay & Silver Company, later
the North Chelmsford Machine & Supply Company referred to in a previous
chapter. Frederick W. Howe, who did such important work with Robbins &
Lawrence, the Providence Tool Company, and Brown & Sharpe, learned his
trade in the Gay & Silver shop.
It has been claimed that the shop of Gage, Warner & Whitney, established
by John H. Gage at Nashua in 1837, was the first one devoted exclusively to
the manufacture of machine tools. If this is true, it does not involve as high a
degree of specialization as would seem, for Bishop in 1860 says: “Their
manufactures include iron planers of all sizes, engine lathes, from the
smallest watch maker’s up to a size suitable for turning locomotive driving
wheels six or eight feet in diameter, hand lathes of all sizes, chucking lathes
of all dimensions, with sliding bed, bolt cutting machines for rapidly
transforming any part of a plain bolt into a nice, evenly threaded screw,
upright and swing drills, boring machines for shaping the interior of steam
cylinders, or other bores of large diameter, slabbers of all kinds, gear-cutting
engines of all sizes for shaping and smoothing the teeth of gear wheels with
perfect accuracy, power punching machines of various sizes, etc.”[196] In
1852 they began building steam engines. With all this formidable list, it
seems never to have been a very large shop.
[196] “History of American Manufactures,” Vol. III, p. 451.

In 1825 the improvement of the water power at what is now Lowell was
begun. Almost at the very beginning of this development work, a large
machine shop was built and placed under the charge of Paul Moody, who
was regarded as one of the foremost mechanics of his day and was an
expert in cotton machinery. This shop was retained by the Water Power
Company for nearly twenty years, when it was sold (1845) and reorganized
as the Lowell Machine Shop under Burke’s leadership. It employed at times
one thousand men, and became one of the most important shops in the
whole Merrimac Valley. James B. Francis, the great hydraulic engineer,
began his life work as a draftsman here in 1833; and later Bement became
its chief draftsman, leaving it to go to Philadelphia.
From 1820 to 1840, other shops sprang up in the Merrimac Valley, such as
C. M. Marvel & Company, of Lowell, the Lawrence Machine Shop, and the
Essex Machine Shop, where Amos Whitney, of Pratt & Whitney, learned his
trade, almost all of them building textile machinery, as well as machine tools.
The output of these shops showed little specialization. They built almost
anything which they could sell.
Of the Massachusetts towns, Worcester and Fitchburg seem to have been
the first to develop successful shops producing machine tools only. In
Worcester also the machinery trade had its beginning in the manufacture of
textile machinery; in fact, Worcester antedates even Pawtucket in its attempts
at cotton spinning, but these at first were unsuccessful. Practically all the
early water privileges in and about the town, not used for sawmills, were
used for textile mills. Prior to 1810 there was a small clock shop, some paper
mills, and a few other enterprises, but they could hardly be dignified as
factories. One of these was the old shop where Thomas Blanchard invented
his copying lathe for turning irregular forms.
An Abraham Lincoln operated a mill and a forge with a trip hammer as
early as 1795. Here, in quarters rented from Lincoln, Earle & Williams
started, about 1810, the first machine shop in the city. The town grew slowly
and its interests were largely local. It was not until 1820 that Worcester took
first rank even among the towns in the county. There was quite an excitement
over the discovery of coal in 1823. It was found, however, to be so poor, that,
as someone put it at the time, “there was a —— sight more coal after burning
it than there was before.” The Providence & Worcester canal was opened in
1828, but its usefulness for navigation was greatly limited by the many power
privileges along its route. Its traffic was never large and it went out of
business in 1848. It served, however, to hasten the building of the Boston &
Worcester Railroad, which was built by Boston capital to deflect the trade of
the central Massachusetts towns from Providence to that city. It opened in
1835; and in 1836 there were listed in Worcester “seven machinery works,”
one wire mill and one iron foundry. Most of the earlier tool builders were
trained in the small textile-machinery shops which had sprung up after 1810,
such as Washburn & Goddard’s, Goulding’s, Phelps & Bickford’s, White &
Boyden’s. The rapid development of railroads created a demand for machine
tools which the Worcester mechanics were quick to recognize, as had
Nasmyth and Roberts in England.
Thomas Blanchard, who was born near Worcester, is one of the
picturesque and attractive figures in our mechanical history. He was a shy,
timid boy, who stammered badly, and was considered “backward.” The
ingenious tinkerer, laughed at by all, first secured his standing by devising an
apple-parer which made a hit, social and mechanical. At eighteen he began
building a tack machine and worked six years on it before he considered it
finished. The essentials of its design have been little changed since. It made
over two hundred tacks a minute and its product was more uniform and
better than the hand-made tacks. Blanchard sold the patent for it for $5000, a
large price for those days, but only a fraction of its real value.
A few years later, about 1818, he invented the lathe for turning irregular
forms which is associated with his name. It was first built for turning gun-
stocks at the Springfield Armory, and the original machine (Fig. 29) is still
preserved there in the museum. Blanchard worked at the Armory for several
years as an expert designer and invented or improved about a dozen
machines for the manufacture of firearms, chiefly mortising and turning
machines.
He was a fertile inventor and worked in many lines besides tool building.
His principal income came from royalties on his “copying” lathe. Many stories
are told of his ingenuity and homely wit. In his later life he was a patent
expert. His keen mechanical intuitions, his wide and varied experience and
unswerving honesty, gave weight to his opinions, and his old age was spent
in comfortable circumstances. He died in 1864.
In 1823 William A. Wheeler came to Worcester, and two years later he was
operating a foundry. He did some machine work, and had the first steam
engine and the first boring machine in Worcester, and also an iron planer
“weighing 150 lb., 4 ft. long and 20 in. wide,” the first one, it is said, in the
state. Beginning with three or four hands, this foundry employed at times two
hundred men. Its long career closed in the summer of 1914.
Samuel Flagg moved to Worcester from West Boylston in 1839, to be near
the Wheeler foundry from which he got his castings. “Uncle Sammy Flagg”
was the first man in Worcester to devote himself entirely to tool building, and
is considered the father of the industry there. He made hand and engine
lathes in rented quarters in the old Court Mills, which has been called the
cradle of the Worcester tool building industry. His first lathes were light and
crude, with a wooden bed, wrought-iron strips for ways, chain-operated
carriage, and cast gears, as cut gears were unheard of in the city at that time.
His first competitor, Pierson Cowie, began making chain planers about
1845. After a few years he sold his business to Woodburn, Light & Company,
which in a few years became Wood, Light & Company, one of the best known
of the older firms. About the same time S. C. Coombs began making lathes
and planers. Flagg meantime had organized the firm of Samuel Flagg &
Company, which included two of his former apprentices, L. W. Pond (whose
portrait appears in Fig. 46) and E. H. Bellows. Pond later bought out Flagg
and Bellows and developed the business greatly. It was incorporated as the
Pond Machine Tool Company, in 1875, specialized in heavy engine lathes,
and is now part of the Niles-Bement-Pond Company. Bellows went into the
engine business, and Flagg started another enterprise, the Machinist Tool
Company, which did not last long. It lasted long enough, however, to build
one of the largest lathes made up to that time, 35 feet long with ways 8 feet
wide.
From the old Phelps & Bickford and S. C. Coombs shops came the two
Whitcomb brothers, Carter and Alonzo, who formed the Carter Whitcomb
Company in 1849, which became the Whitcomb Manufacturing Company in
1872. From the Coombs company also came successively Shepard, Lathe &
Company; Lathe, Morse & Company, and the Draper Machine Tool Company.
P. Blaisdell & Company was founded in 1865 by Parritt Blaisdell, who had
been fifteen years with Wood, Light & Company; and S. E. Hildreth, who had
worked for more than twenty years with Flagg and Pond, became a partner in
this firm eight years later. The Whitcomb, Draper and Blaisdell companies
were united in 1905 into the present Whitcomb-Blaisdell Machine Tool
Company. From the old Blaisdell shop came also J. E. Snyder & Son through
Currier & Snyder, who began building drills in 1833 and were both old
workmen at Blaisdell’s. The original Reed & Prentice Company was started
by A. F. Prentice, who sold a half interest to F. E. Reed in 1875. The
Woodward & Powell Planer Company comes from the Powell Planer
Company, incorporated in 1876. This maze of relationships is made clear by
reference to the table given in Fig. 45. The Norton Company comes from F.
B. Norton, who began experimenting on vitrified emery wheels about 1873
and put them on the market in 1879. At his death the business was
incorporated as the Norton Emery Wheel Company, now the Norton
Company. Charles H. Norton’s work in developing precision grinding has
been perhaps the most distinguished contribution to the later generation of
Worcester mechanics. He began work in the shops of the Seth Thomas
Clock Company at Thomaston, Conn., under his uncle, N. A. Norton, who
was master mechanic there for about forty years. At his uncle’s death, Norton
became master mechanic. He was with the Clock Company about twenty
years in all, most of the time in charge of the design and building of all their
tools, machinery and large tower clocks.
 WILLIAM A. WHEELER, ICHABOD WASHBURN
1823 Cards and Textile Machry.
PHELPS &
Foundry—Came from
BICKFORD
Brookfield,
Textile Machinery
Plant closed in 1914
S. C. Coombs
WASHBURN & HOWARD
Cards, Textile Machry. and
J. A. FAY & CO. SAMUEL Wire
Woodworking FLAGG, 1839 1820
Machry First tool-builder
Keene, N. H. in city—came S. C. COOMBS & CO.
J. A. Fay and from West 1845
Edw. Josslyn. Boylston to be R. R. Shepard and Martin WASHBURN & GODDARD
1836 near Wheeler Lathe Textile, Machry. and Wire
foundry A. A. Whitcomb 1822
PIERSON
C. READ &
COWIE
CO.
THOS. E. About 1845—
Worcester
DANIELS Made chain
—Screws
Woodworking planers SHEPARD, LATHE & CO.
Machry. SAMUEL FLAGG & C. WHITCOMB & AMERICAN SCREW
Worcester CO. CO. CO.
L. W Pond, E. H. 1849—Carter and Providence, R. I.
Bellows, S. E. Hildreth Alonzo Whitcomb
E. C. Pond bought out other LATHE, MORSE & CO. LORING & A.
 TAINTER partners. G. COES
GARDNER 1847 1836
CHILDS
Daniels WOODBURN Began making
Planer, etc. , screw
Worcester LIGHT & CO. DRAPER MACH. TOOL wrenches
1846 CO. 1841
RICHARDSON, MERRIAM
& CO. F. B. NORTON
Worcester. Richardson was Began
Josslyn’s experiments
nephew. Name of J. A. Fay on wheels
was sold in 1873.
to Western agents, about WHITCOMB MFG. CO. Began sale in
1862 1872 1879.
Thomson, WOOD, Died 1885 and
Skinner of LIGHT & CO. business
Co. of Parritt incorporated
Chicopee Blaisdell 1886
WASHBURN
Falls,
& MOEN
bought
Wire 1850
out
Flagg’s
original NORTON
business EMERY
P. WHEEL CO.
NEW BLAISDELL & 1886
HAVEN CO.
MFG. 1865 A. F. PRENTICE
CO. P. Blaisdell, Sold half interest to F. E.
New S. E. Hildreth, Reed, 1875
Haven, Enoch
Conn. Earle, Currier,
Snyder
POND CHAS. H.
MACH. NORTON
TOOL CO. CURRIER & Invented
1875 SNYDER REED & PRENTICE Grinding
Both worked Reed bought whole Machines,
for Blaisdell. business in 1877 Came from
1883 Brown &
Sharpe
J. A. FAY & CO. NORTON
Cincinnati, Ohio, Moved to POWELL PLANER CO. Incorporated GRINDING
1862 Plainfield, 1887 later as CO.
N. J., Washburn & Grinding
1888
EGAN CO NILES-
 EGAN CO. NILES
Moen Machines
Cincinnati, BEMENT-POND Mfg. Co. 1900
Ohio, CO.
1873 Hamilton, O.—
Philadelphia—
Plainfield REED-PRENTICE CO. COES
J. E. SNYDER WRENCH CO.
WOODWARD & POWELL PLANER CO.
& SON 1888
J. A. FAY & NORTON
EGAN CO. CO.
WHITCOMB-BLASIDELL MACH.
Cincinnati, Ohio. AM. STEEL & WIRE CO. Emery
TOOL CO.
1893 Worcester Plant—1899 Wheels,
Worcester—1905
etc.
1906

Figure 45. Genealogy of the Worcester Tool Builders

In 1886 Mr. Norton went to the Brown & Sharpe Manufacturing Company
of Providence as assistant to Mr. Parks, their chief engineer. Soon afterward
he became designer and engineer for their work in cylindrical grinding
machinery, remaining in that capacity for four years. In 1890 he went to
Detroit with Henry M. Leland and formed a corporation called the Leland-
Falkner-Norton Company, Falkner being a Michigan lumber man. Associated
with them was Charles H. Strellinger, a well-known dealer in tools and
machinery. Six years later Mr. Norton returned to Brown & Sharpe and was
again their engineer of grinding machinery until he went to Worcester in
1900. The Norton Grinding Company, organized that year and financed by
men connected with the Norton Emery Wheel Company, have built cylindrical
and plain surface grinding machinery designed by Charles H. Norton, and
under his direction have been leaders in refining and extending the process
of precision grinding.
The Norton Company and the Norton Grinding Company should not be
confused. The former make grinding wheels; the latter build grinding
machines. Neither should F. B. Norton, who founded the grinding wheel
industry and who died in 1885, be confused with Charles H. Norton, who did
not come to Worcester until fifteen years later. There is no connection in their
work, and despite the similarity of name, they were in no way related.
The greatest industry in Worcester is the American Steel and Wire
Company, formerly the Washburn & Moen Company. While it is no longer
associated with tool building, it passed through that phase and traces back to
the textile industry as well. It was founded by Ichabod Washburn, who started
in as a boy in a cotton factory in Kingston, R. I., during the War of 1812.
Making up his mind to become a machinist, he served an apprenticeship and
then worked in Asa Waters’ armory and with William Hovey, one of the early
mechanics in Worcester. About 1820 he began the manufacture of woolen
machinery and lead pipe in partnership first with William Howard and later
with Benjamin Goddard. The enterprise prospered. As he was making cards
for cotton and woolen machinery, he determined to manufacture the
necessary wire himself by a new drawing process. His first experiments were
a failure, but by 1830 they were successful enough to justify his undertaking
regular manufacture. He superseded the old methods entirely and built up
the present great business. Goddard retired, and, after various changes in
partnership, Washburn took in his son-in-law, Philip L. Moen, in 1850. By
1868 the firm employed more than nine hundred men, and wire drawing,
which began as an incident in the manufacture of textile machinery, had
become their sole activity. Today the works employ eight thousand men. In
1833 Washburn, in order to make an outlet for his wire products, induced the
Read brothers to move to Worcester from Providence and begin the
manufacture of screws. This business was operated separately under the
name of C. Read & Company. Later it was moved back to Providence, where
it developed into the American Screw Company.
Worcester mechanics have made many things besides machine tools; in
small tools and in gun work they have long been successful. The Coes
Wrench Company was started in 1836 by Loring and A. G. Coes, and began
to make the present form of screw wrench in 1841. Asa Waters, in Millbury
near by, was one of the early American gun makers. After Waters came other
gun makers, Ethan Allen, Forehand & Wadsworth, Harrington & Richardson,
and Iver Johnson, who later moved to Fitchburg.
Much of Worcester’s prominence as a manufacturing center is due to the
unusual facilities it offered to mechanics to begin business in a small way.
Nearly every manufacturing enterprise in the city began in small, rented
quarters. There were a number of large buildings which rented space with
power to these small enterprises; one of them, Merrifield’s, was three stories
high, 1100 feet long, and had fifty tenants, employing two to eight hundred
men. Coes, Flagg, Daniels, Wood, Light & Company, Coombs, Lathe &
Morse, Whitcomb, Pond and J. A. Fay, all began, or at some time operated,
in this way. One is struck, in looking over the old records, with the constant
recurrence of certain names, as the Earles, Goddards, Washburns, and
realizes that he is among a race of mechanics which was certain sooner or
later to build up a successful manufacturing community.
Fitchburg, while not so large or so influential, is almost as old a tool
building community as Worcester. Its history centers about the Putnam
Machine Company which was started by John and Salmon W. Putnam, who
came from a family of mechanics. The latter’s portrait appears in Fig. 47.
They, too, began in cotton manufacturing, John as a contractor making cotton
machine parts, and Salmon as a bobbin boy and later as an overseer at New
Ipswich and Lowell. In 1836 they went to Trenton, N. J., intending to start a
machine shop there, but the panic of 1837 intervened and made it
impossible. They had themselves built most of the machines required; they
stored these and found employment until business conditions improved.
Finally, they started in a hired basement in Ashburnham, Mass., under the
name of J. & S. W. Putnam.
A year later they moved to Fitchburg and began repairing cotton
machinery. At first they did their work entirely themselves, but their business
increased rapidly and they soon hired an apprentice. Their first manufactured
product was a gear cutter. This gave them a start and they soon developed a
full line of standard tools. Though he was the younger brother, S. W. Putnam
was the leading spirit. He first built upright drills with a swinging table so that
the work could be moved about under the drill without unclamping. He
designed the present form of back rest for lathes, and is said to have
invented the universal hanger. The latter invention, however, has been
claimed for several other mechanics in both England and America. In 1849
the brothers were burned out, without insurance. They repaired their
machinery, built a temporary shed over it, and were at work again in two
weeks. The present company was formed in 1858.
The Putnam company has been influential in other lines than machine
tools. Putnam engines were for many years among the best known in the
country, and the company was also intimately concerned with the early
development of the rock drill, through Charles Burleigh, the head of their
planer department and the inventor of the Burleigh drill. In fact, the first
successful drills, those for the Hoosac tunnel, together with the compressors,
were designed and built in the Putnam shops. Sylvester Wright, who founded
the Fitchburg Machine Works, was for ten years foreman of their lathe
department, and most of the old mechanics in and about Fitchburg were
Putnam men.
Scattered here and there are other companies. At Nashua were Gage,
Warner & Whitney, to which we have referred, and the Flather Manufacturing
Company which was founded by Joseph Flather, an Englishman, in 1867.
The Ames Manufacturing Company of Chicopee Falls came from the old
Ames & Fisher shop at North Chelmsford. This was started by Nathan P.
Ames, Senior, in 1791, who operated a trip hammer and other machinery,
making edged tools and millwork. The shop was burned in 1810, and he
moved to Dedham, Mass., for a year or so, but returned and resumed his
former business on the old site. His sons, Nathan P., Jr., and James T.,
learned their trade with their father. The older brother, Nathan, moved to
Chicopee Falls in 1829. James joined him in 1834. The Ames Manufacturing
Company, formed the same year, lived for sixty years and employed at one
time over a thousand men. From the start they had close relations with the
Government and did an extensive business in all kinds of military supplies,
swords, bayonets, guns, cannon, cavalry goods, etc. They cast bronze
statuary, and the famous doors of the Capitol at Washington were made by
them. They rivaled Robbins & Lawrence in gun machinery and shared with
them the order for the Enfield Armory. This contract alone took three years to
complete. Their gun-stock machinery went to nearly every government in
Europe.
Figure 46. Lucius W. Pond
 Figure 47. Salmon W. Putnam

In addition to all this they built the famous Boydon waterwheel, mill
machinery, and a list of standard machine tools quite as catholic as that of
Gage, Warner & Whitney. They did their work well, contributed material
improvements to manufacturing methods and had one of the most influential
shops of their day.
Most of the plants for manufacturing woodworking machinery can be
traced back to a comparatively small area limited approximately by Fitchburg,
Gardner, Keene and Nashua. This section was poor farming land, rough and
heavily wooded, and the ingenuity of its inhabitants was early directed toward
utilizing the timber. Mr. Smith, of the H. B. Smith Company of Smithville, N.
J., came originally from Woodstock, Vt., and Walter Haywood started at
Gardner. J. A. Fay and Edward Josslyn began manufacturing woodworking
machinery as J. A. Fay & Company at Keene, in 1836. In 1853 they felt the
need of better facilities and purchased Tainter & Childs’ shop at Worcester,
which was manufacturing the Daniels wood planer. Mr. Fay died soon after,
and the business passed through the hands of H. A. Richardson, Josslyn’s
nephew, to Richardson, Merriam & Company. They built up a good business
before the Civil War, and had branch offices in New York, Chicago, and
Cincinnati.
In the early sixties the western agents bought the name of J. A. Fay &
Company and started manufacturing at Cincinnati. Later this was united with
the Egan Company, and the present J. A. Fay & Egan Company formed.
When J. A. Fay & Company was started at Cincinnati, machinery,
superintendent and mechanics were brought from Worcester, and, as the
name implies, the present company was a direct descendant from the old
Worcester and Keene enterprise.
Winchendon, in the center of the district referred to, has long been known
for its woodworking machinery. Baxter D. Whitney began there before 1840.
He died in 1915, aged ninety-eight years, the last of the early generation of
mechanics. For many years he was a leader in the development of
woodworking tools, and the business which he founded is still in successful
operation under the management of his son, William M. Whitney.
Springfield, although an important manufacturing city, has had few
prominent tool builders. One company, however, the Baush Machine Tool
Company, has built up a wide reputation for drilling machines, especially
large multiple spindle machines.
 CHAPTER XVIII
THE NAUGATUCK VALLEY
The most casual consideration of New England’s mechanical
development brings one squarely against a most interesting and baffling
phase of American industrial life, the brass industry of the Naugatuck
Valley. Here, in a narrow district scarcely thirty miles long, centering
about Waterbury, is produced approximately 80 per cent of the rolled
brass and copper and finished brass wares used in the United States, an
output amounting to upward of $80,000,000 a year. No concentration on
so large a scale exists elsewhere in the country. For example, in 1900,
Pennsylvania produced but 54 per cent of the iron and steel, and
Massachusetts but 45 per cent of the boots and shoes. Furthermore,
there seems to be no serious tendency to dislodge it. While there is more
competition from outside, its ascendency is nearly as marked today as it
was a generation ago. Why should this small district, a thousand miles or
more from its sources of raw material, far from its market, and without
cheap coal or adequate water power, gain and hold this leadership?[197]
[197] The best study of the brass industry of the Naugatuck Valley has been
made by William G. Lathrop, and has been published by him at Shelton, Conn.,
1909, under the name of “The Brass Industry.” Mr. Lathrop had intimate
knowledge of the subject and, in addition, unusual facilities for investigation. The
personal history of many of the men who have figured in its growth will be found
in Anderson’s “History of the Town and City of Waterbury,” 3 vols. 1895.

It was not the first in the field. The Revere Copper Company, in
Massachusetts, founded by Paul Revere, began rolling copper in 1801,
and the Soho Copper Company, at Belleville, N. J., in 1813. The brass
business in Connecticut had its origin with Henry Grilley, of Waterbury,
who began making pewter buttons there in 1790. In 1802 Abel and Levi
Porter joined him, and they started making brass buttons under the
name of Abel Porter & Company. In 1811 all the original partners retired
and a new firm was formed, Leavenworth, Hayden & Scovill. In 1827
Leavenworth and Hayden sold out to William H. Scovill, and the firm