Passing the FRACP Written Examination E-Book

Jonathan Gleadle

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 754

Veröffentlichungsjahr: 2013

Beschreibung

Passing the FRACP Written Examination is the ideal study aid for candidates of the Fellow of the Royal Australasian College of Physicians (FRACP) examination. Written by a team of physicians based at Flinders Medical Centre, and covering the key components of the FRACP basic training syllabus, this guide presents over 500 multiple-choice questions on all major topics covered in the examination. It provides coverage of rapidly evolving topics such as healthcare in an ageing population, disparity in indigenous health outcomes, advances in molecular science and genetics, and the complexity of care arising from multiple chronic illnesses. Questions echo the written examination, including those on both ‘Basic Sciences’ and ‘Clinical Practice’.

Many of the questions are similar to those in the actual examination; others are designed to ‘teach’ particularly important issues or to draw attention to contemporary topics. Each question has an answer that fully explains the correct and incorrect responses.

This study aid also includes:
• Questions and answers linked to a reference that is usually the best and most contemporary review for further reading and as additional guide to study
• QR code links to all the references
• Hints and tips from previous candidates on examination strategies
• A large number of the new style extended matching questions (EMQs).

This brand new study aid gives all FRACP candidates a unique opportunity to practise for the examination and improve their medical knowledge of the syllabus as a whole.

Leseprobe

Table of Contents

Title page

Copyright page

Introduction

Acknowledgements

Features contained in your study aid

1: Cardiology

Basic Science

Clinical

Basic Science

Clinical

2: Respiratory and sleep medicine

Basic Science

Clinical

Basic Science

Clinical

3: Gastroenterology

Basic Science

Clinical

Basic Science

Clinical

4: Nephrology

Basic Science

Clinical

Basic Science

Clinical

5: Endocrinology

Basic Science

Clinical

Basic Science

Clinical

6: Neurology

Basic Science

Clinical

Basic Science

Clinical

7: Rheumatology

Basic Science

Clinical

Basic Science

Clinical

8: Dermatology

Basic Science

Clinical

Basic Science

Clinical

9: Oncology

Basic Science

Clinical

Basic Science

Clinical

10: Infectious diseases

Basic Science

Clinical

Basic Science

Clinical

11: Haematology

Basic Science

Clinical

Basic Science

Clinical

12: Clinical immunology

Basic Science

Clinical

Basic Science

Clinical

13: Clinical pharmacology

Basic Science

Clinical

Basic Science

Clinical

14: Clinical genetics

Basic Science

Clinical

Basic Science

Clinical

15: General medicine, geriatric medicine and other topics

Basic Science

Clinical

Basic Science

Clinical

16: Psychiatry

Basic Science

Clinical

Basic Science

Clinical

17: Statistics, epidemiology and research

Basic Science

Clinical

Basic Science

Clinical

18: Intensive care medicine

Basic Science

Clinical

Basic Science

Clinical

Index

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Library of Congress Cataloging-in-Publication Data

Gleadle, Jonathan, author.

Passing the FRACP written examination : questions and answers / Jonathan Gleadle, Tuck Yong, Jordan Li, Surjit Tarafdar, Danielle Wu.

p. ; cm.

Passing the Fellow of the Royal Australasian College of Physicians written examination

Includes bibliographical references and index.

ISBN 978-1-118-45495-4 (pbk. : alk. paper) – ISBN 978-1-118-45502-9 (eMobi) – ISBN 978-1-118-45503-6 (ePdf) – ISBN 978-1-118-45504-3 (ePub)

I. Yong, Tuck, author. II. Li, Jordan, author. III. Tarafdar, Surjit, author. IV. Wu, Danielle, author. V. Title. VI. Title: Passing the Fellow of the Royal Australasian College of Physicians written examination.

[DNLM: 1. Medicine–Australia–Examination Questions. 2. Medicine–New Zealand–Examination Questions. WB 18.2]

R834.5

610.76–dc23

2013017941

A catalogue record for this book is available from the British Library.

Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.

Cover image: © iStockphoto.com/Kalawin

Cover design by Sarah Dickinson

Introduction

If you want to get out of medicine the fullest enjoyment, be students all your lives.

David Reisman (1867–1940)

Background to the examination

The Royal Australasian College of Physicians (RACP) examination consists of two parts – a written examination and a clinical examination. The written examination has two papers – Paper 1 (70 questions) and Paper 2 (100 questions), which focus on ‘Basic Sciences’ and ‘Clinical Practice’, respectively. The primary focus of this book is to help candidates prepare for the written component of the examination. The written examination is important because trainees are required to pass this before proceeding to the clinical examination and commencing advanced training in a subspecialty. Questions in the written examination are based on the curriculum and all candidates should familiarise themselves with the RACP curriculum for Basic Physician training, which is available electronically from the College website (http://www.racp.edu.au/page/curricula/adult-internal-medicine). It is vital to carefully read the most updated examination instructions (https://www.racp.edu.au/page/basic-training/written-exam), and any past questions provided by the RACP (https://www.racp.edu.au/share/page/site/pastexams/documentlibrary).

Although this book is written mainly for trainees in Australia and New Zealand, physician trainees in other programmes should still find these questions provide an opportunity for self-assessment and learning.

Questions are of two styles – multiple choice questions (MCQs) and extended matching questions (EMQs). In the MCQs, one correct answer must be selected from five possible responses to the stem. Commencing in 2013, EMQs will also be included. EMQs are organised into four parts:

1.Theme. There is a theme for each EMQ. This can include a symptom, investigation, diagnosis or treatment, e.g. back pain, dyspnoea, diabetes, corticosteroids.

2.A list of possible answers, also called an option list. This is a list of eight possible answers marked A–H.

3.The question, also called the lead in statement. This tells you what is being asked and clarifies the question being asked. It indicates the relationship between the clinical vignettes and the options.

4.Clinical problems or vignettes, also called the stems. This will usually consist of a clinical problem. There may be more than one clinical vignette for each theme.

This book has included a significant number of EMQs to help trainees familiarise themselves with this new and likely expanding format of assessment.

Question answering strategies

In Paper 1, the questions posed are commonly of the type, ‘What is the likely mechanism for this disease process or treatment modality?’, requiring the candidate to understand the underlying mechanism of disease pathophysiology and/or mechanism of actions for treatments that are used.

The knowledge and evidence gained from textbooks or journal articles and its application to clinical situations is one of the most challenging tasks in medicine. The retention of information, organisation of facts and recall of a myriad of data in relation to a patient is one of the crucial processes in clinical reasoning. One of the purposes of this book is to facilitate this process.

There are typically several steps in patient clinical management – making the diagnosis, assessing the severity of the disease, administering treatment according to the stage of disease and following the patient's response to treatment. Often in the MCQs or EMQs, more focused information is provided and candidates have to look for discriminating features to narrow the differential diagnosis. This is often a challenging but essential step to master as a physician. The question ‘What is the next step?’ is challenging because the next step may be more diagnostic evaluation, or staging, or therapy.

In general, the questions will assess knowledge of the following:

Aetiology, epidemiology and geneticsAnatomy, physiology, pathology and pathogenesisClinical manifestationsDiagnosis and investigationsTreatment and prevention of diseaseComplications and outcomesEthical, legal, social, economic, humanistic and historical aspects.

Candidates taking the written examination can sometimes be troubled by the wording of the questions, as when asked which features are classical, characteristic or typical of certain disorders, whether events are likely, frequent, common, unusual or rare and whether findings are expected in the majority or minority of cases or in few or many patients. For this reasons, we prefer, wherever possible, to minimise language problems with stems and responses. However it is not always possible to provide accurate numeric percentages (even approximate ones).

When answering questions and taking the examination we would emphasise the following:

Read the question carefully!Read the possible answers carefully!Answer all of the questions! (Make an informed guess if you are uncertain)If you are uncertain about the correct response, look at which options you think are definitely incorrect. Think about why the question is being asked; what it is ‘getting at?’; what are the important ‘teaching points’ that are being tested? If you still are uncertain, move to the other questions and then come back to those you are not certain of.

‘Hints and tips’ for preparing for the FRACP examination

The best way of preparing for the physician examination, both written and clinical, is to learn from every encounter with a patient and the rest of the treating team (consultant physicians, advanced physician trainees, nurses and other health team members). Then, trainees are encouraged to use information gained from medical books (and increasingly electronic books) and journal articles to complement their education through reflection on their patient encounter. All trainees are encouraged to make the most of their learning encounters with patients; question what a symptom or sign indicates, what the most specific or sensitive diagnostic test to undertake is, what the evidence for the treatment being recommended is, how a complication can be prevented or a patient outcome improved. Even a small amount of reading or thought around a specific patient can be a very powerful learning experience.

Study effectively, do not just randomly read an article from a journal or a few pages in a textbook. Link your study to a question you could not answer or to a patient you saw last night. Cover the RACP curriculum fully, including the less obviously mainstream topics, such as statistics and psychiatry. Make sure you are studying not just reading. Make your own study notes, write down important facts, and practise relevant examination questions. Be disciplined about your study, switch off your phone, disconnect the internet and reward yourself with well-defined and enjoyable breaks.

Many trainees have found getting together as a small group to discuss and learn from each other is a useful way of preparing for this examination. Such small group dynamics are also a helpful way of supporting one another through the intense preparation.

Ensure that you have undertaken practice examinations multiple times under examination conditions and timings. Make sure you have answered and understood all of the practice questions provided by the RACP.

Using this book as a learning tool

This book is intended as a tool to direct basic physician trainees in their learning of core knowledge and skills in internal medicine, as well as the development of sound clinical reasoning. The content of this book sets out factual information, but also translates knowledge to clinical practice. Preparing for the physician examination is part of a lifelong process of learning, which should expand the trainee's attitude, skills and knowledge. It is this process of learning that enables a physician to cope with the ever-changing context in the practice of internal medicine. The trainee or groups of trainees can use this book in their personal studies or as part of their study group discussion. This book is not intended to cover the entire internal medicine curriculum comprehensively, but we have attempted to cover in particular topics that are rapidly evolving. For example, we have given attention to issues related to healthcare in an ageing population, disparity in indigenous health outcomes, advances in molecular science and genetics, and the complexity of care arising from multiple chronic illnesses in individual patients.

Whist we hope that many of the questions are similar to those in the actual examination, some are designed to ‘teach’ particularly important issues or to draw attention to contemporary topics. The commentaries explain the correct and incorrect responses. These commentaries have been prepared by the authors with input from experienced specialist physicians. For many subjects we have provided a reference, usually the best and most contemporary review we could identify at the time of writing. Reference texts are listed for further reading and as additional guides to study.

Some of the electronic or written resources on general internal medicine we recommend for use in the examination preparation are:

Up-to-date (www.uptodate.com)

New England Journal of Medicine (www.nejm.org)

Lancet (www.thelancet.com)

British Medical Journal (www.bmj.com)

Internal Medicine Journal (www.racp.edu.au/page/publications/internal-medicine-journal)

Medical Journal of Australia (www.mja.com.au)

Preparation time

In the lead-up to the examinations, it is important to maintain a healthy life of adequate sleep, exercise, food intake and socialization. Trainees are encouraged to set aside time for their clinical work, studies, family, social and recreational activities in a manner that is appropriate to each of them. It is best to study when the trainee's mind is fresh and able to concentrate on learning. As already mentioned, trainees should also make the most of their time in clinical work where experience will enhance the learning process.

Preparing for this examination should not lead to ‘burn-out’ for trainee-physicians. During the preparation period, the trainee should value the support received from family, peers and friends.

Disclaimer

Clinical practice and basic biomedical sciences are constantly changing and today's incontrovertible facts can quickly become outdated. Therefore, trainees are strongly encouraged to keep up-to-date with their reading and learning, and to check appropriate drug selection, dosage and route of administration. If you have any questions or suggestions, please write to us care of the publisher.

We hope that our contribution will assist you in your preparation for the examination in internal medicine. For every trainee that uses this book for their preparation, we wish you success in the RACP written examination or equivalent.

To all students of medicine who listen, look, touch and reflect;

may they hear, see, feel and comprehend.

Professor John B. Barlow in Perspectives on the Mitral Valve

Jonathan Gleadle

Tuck Yong

Jordan Li

Surjit Tarafdar

Danielle Wu

Acknowledgements

We would like to thank the following for their expert reviews and suggestions: A/Professor Nicholas Antic FRACP, Consultant Respiratory and Sleep Physician

Paul Hakendorf MPH, Clinical Epidemiologist

Dr Matthew Doogue FRACP, Consultant Endocrinologist and Clinical Pharmacologist

Dr Ganessan Kichenadasse FRACP, Consultant Medical Oncologist

A/Professor Ann Kupa FRACP, Consultant Immunologist

Dr Stephen Lam FRACP, Intensive Care Consultant

Dr Timothy Lu FRACP, Consultant Rheumatologist

Dr Anand Rose FRACP, Consultant Respiratory and Sleep Physician

Dr Roshan Prakash, Advanced Trainee in Cardiology

Dr Su Yin Lau, Advanced Trainee in Gastroenterology and Hepatology

Basic physician trainees in the Southern Adelaide Local Health Network who have ‘tested’ these questions and provided valuable feedback.

Features contained in your study aid

Question and answer sections are clearly indicated for quick reference.Question sections:

Answer sections:

Answers are linked to an authoritative reference to supplement your study. Scan the QR code on your mobile device to be taken directly to the reference.

1

Cardiology

Questions

Basic Science

Answers can be found in the Cardiology Answers section at the end of this chapter.

1. Beta-blockers are recommended as first-line therapy for stable angina by both the American College of Cardiology/American Heart Association (ACC/AHA) and the European Society of Cardiology. Their mechanism of action in this condition is explained by:

A. Plaque stabilisation

B. Increased coronary blood flow

C. Reduction in blood pressure

D. Reduction in myocardial oxygen demand

E. Reduction in systemic vasodilatation

2. Which one of the following compensatory mechanisms occurs in heart failure?

A. Decreased ventricular preload

B. Peripheral vasodilatation

C. Increased renal sodium and water excretion

D. Activation of the adrenergic nervous system

E. Myocardial atrophy

3. Which is the most common origin of idiopathic ventricular tachycardia in the absence of structural heart disease?

A. Aortic annulus

B. Aortic sinuses

C. Great cardiac vein

D. Epicardium

E. Right ventricular outflow tract

4. Which one of the following viral infections is the commonest cause of myocarditis in developed countries?

A. Enterovirus

B. Cytomegalovirus

C. Hepatitis C virus

D. Human immunodeficiency virus (HIV)

E. Influenza virus

5. Which one of the following statements is correct regarding the electrical conduction and contraction of the heart?

A. Electrical conduction is transmitted from the sino-atrial node to the bundle of His to the atrioventricular node to the Purkinje fibres to the myocardium

B. Muscle contraction is associated with release of calcium by the sarcoplasmic reticulum

C. Repolarisation of cardiac muscle is due to flow of potassium into the myocytes

D. On an electrocardiogram the QRS complex corresponds to ventricular repolarisation

E. The perfusion of the coronary arteries increases during systole

6. Perhexiline has been used in patients with chronic heart failure and refractory angina. Which one of the following statements about perhexiline is correct?

A. It is metabolised by cytochrome P450 3A4

B. About 7–10% of Caucasians are slow metabolisers

C. The recommended dose for slow metabolisers is 100 mg on alternate days

D. It can cause hyperglycaemia in diabetic patients

E. It improves 5-year survival

Theme: Beta-blockers (for Questions 7 and 8)

A. Propranolol

B. Metoprolol

C. Nebivolol

D. Atenolol

E. Pindolol

F. Sotalol

G. Bisoprolol

H. Carvedilol

Select the drug that best fits the description in each of the following statements.

7. A non-selective beta-blocker with α1-adrenoreceptor blocking activity.

8. A selective β1-adrenoreceptor blocker with nitric-oxide potentiating vasodilatory effect.

Clinical

9. A 47-year-old man presents with chest pain. He reports moderately severe central chest pain of 24 h duration. The pain is worse with inspiration and is alleviated by maintaining an upright position. He also reports having had a fever recently. His medical history and physical examination are unremarkable. His ECG is shown below. What is the most likely diagnosis and the most appropriate treatment approach for this patient?

A. Acute pericarditis; perform an echocardiogram in 1 week to confirm diagnosis

B. Acute pericarditis; start a non-steroidal anti-inflammatory drug (NSAID)

C. Acute pericarditis; start prednisolone

D. ST elevation myocardial infarction; start thrombolytics

E. Pericardial tamponade; requires pericardiocentesis

10. A 21-year-old Aboriginal woman presents with a sore throat for 2 days. She has fever (38° C) and coryza. On physical examination, the patient appears well but has a markedly infected posterior pharynx and exudates over her tonsils. Streptococcal pharyngitis is suspected. Which one of the following approaches to management is most appropriate?

A. A throat swab is adequate to establish diagnosis in Aboriginal patients

B. Intravenous benzylpenicillin 1.2 g four times a day for 10 days is the treatment of choice in eradicating Group A streptococci from the nasopharynx

C. Treatment should be started within 9 days of the onset of symptoms to prevent acute rheumatic fever

D. Aspirin can prevent rheumatic chorea

E. Asymptomatic family contacts of patients with streptococcal pharyngitis should have throat swabs for streptococcal infection

11. A 50-year-old man presents with a 2-h history of severe chest pain. The pain started suddenly while eating, was constant and radiated to the back and interscapular region. His past medical history includes hypertension and hyperlipidaemia. On examination, his heart rate is 120 beats/min and his blood pressure is 80/40 mmHg. Jugular venous pressure is not visualised. All peripheral pulses are present and equal. While stabilising the patient, which one of the following investigations should be undertaken?

A. Serum lipase

B. Computed tomography (CT) angiography of the chest

C. D-dimer

D. Lung ventilation–perfusion scan

E. Upper gastrointestinal endoscopy

12. Which one of the following best describes the use of plasma brain natriuretic peptide (BNP) in the assessment of congestive heart failure (CHF)?

A. BNP level is more useful in detecting diastolic heart failure than systolic heart failure

B. Measurement of BNP is recommended as routine in the diagnosis of CHF

C. BNP offers additional diagnostic information beyond that provided by echocardiogram

D. BNP levels have been shown to predict all-cause mortality, including sudden death

E. Plasma BNP or N-terminal pro-BNP measurement is not useful in patients presenting with new-onset breathlessness

13. A 46-year-old woman presents with a 2-week history of shortness of breath and ankle swelling. On examination her jugular venous pressure (JVP) is elevated and there are fine crackles at the bases of both lungs on auscultation. She was diagnosed with breast cancer a year ago and has been treated with surgery, doxorubicin, cyclophosphamide and radiotherapy. She has no cardiac risk factors or family history of cardiac disease. Computed tomography pulmonary angiography (CTPA) is normal and chest X-ray shows interstitial pulmonary oedema. What is the most likely cause for this presentation?

A. Anthracycline cardiotoxicity

B. Constrictive pericarditis

C. Pulmonary fibrosis

D. Radiation-induced cardiomyopathy

E. Pulmonary embolism

14. All of the following drugs can be utilised in patients with heart failure. Which one is the most effective in improving systolic function?

A. Spironolactone

B. Angiotensin converting enzyme (ACE) inhibitor

C. Digoxin

D. Frusemide

E. Hydralazine

15. A 72-year-old man describes substernal chest pressure while walking for more than 100 m and this is relieved by rest. His medical history is remarkable for hypertension and a myocardial infarction 3 years ago. His medications include aspirin 150 mg daily; metoprolol 50 mg twice daily; atorvastatin 40 mg daily; perindopril 5 mg daily; and isosorbide mononitrate 120 mg daily. He had a cardiac catheterisation 1 month ago that showed a left main coronary artery stenosis of 85%, a proximal left anterior descending artery stenosis of 70% and a 80% stenosis of the first obtuse marginal branch. His left ventricular ejection fraction (LVEF) was estimated at 45%. Which one of the following therapies would be most beneficial for this patient?

A. Addition of clopidogrel

B. Regular exercise programme

C. Percutaneous transluminal angioplasty (PCTA)

D. Coronary artery bypass grafting (CABG)

E. Transmyocardial revascularisation procedure (TMR)

16. The use of computed tomography coronary angiography (CTCA) is most appropriate in which one of the following patients?

A. An asymptomatic patient who has a strong family history of ischaemic heart disease

B. A patient with coronary stents presenting with chest pain in whom you suspect in-stent restenosis

C. A patient presenting with severe crushing chest pain and an ECG showing ST-elevation myocardial infarction (STEMI)

D. A patient presenting with chest pain and palpitations and an ECG showing rapid atrial fibrillation (heart rate: 125 beats/min)

E. A patient with chest pain with normal serial cardiac enzymes and ECGs who you think has a low-to-intermediate pre-test probability of coronary artery disease

17. An 86-year-old woman with a history of ischaemic heart disease, atrial fibrillation and type 2 diabetes presented to the emergency department with flank pain and symptomatic anaemia with haemoglobin of 69 g/L. After abdominal CT imaging, she was found to have a retroperitoneal haemorrhage. Three weeks prior to the presentation she had been changed from warfarin to dabigatran (taking a standard dose of 150 mg twice a day) for stroke prevention. Prior to this change, her INR has been within the target range for 6 years. What is the most likely explanation for the significant haemorrhagic complication in this patient after commencing dabigatran?

A. She is also taking phenytoin

B. She has impaired renal function

C. Her atrial fibrillation had reverted to sinus rhythm

D. Her INR has not been checked during the 3 weeks on the new medication

E. She is also taking digoxin

18. A 60-year-old man has had an inferior myocardial infarction 5 days ago. Today he is feeling lightheaded and his pulse rate is 40 beats/min. Blood pressure is 85/65 mmHg. An ECG is done immediately. Which one of the following findings is an indication for temporary pacing?

A. (ECG A)

B. (ECG B)

C. (ECG C)

D. (ECG D)

E. (ECG E)

19. During pregnancy, which one of the following heart diseases is associated with the highest maternal mortality?

A. Aortic stenosis

B. Atrial septal defect

C. Coarctation of aorta

D. Eisenmenger syndrome

E. Mitral stenosis

20. A 22-year-old man who is known to have hypertrophic cardiomyopathy undergoes physical and echocardiographic examination. Which one of the following findings is most predictive of this patient's risk of sudden cardiac death?

A. Hypertension

B. Double apex beat

C. Atrial dilatation

D. Intensity of systolic murmur

E. Septal wall thickness of 3 cm or greater

21. Which is the commonest organism causing prosthetic valve infective endocarditis?

A.Staphylococcus aureus

B. Coagulase-negative staphylococcus

C.Streptococcus bovis

D. Candida

E.Streptococcus viridans

22. A 16-year-old girl has a cardiac arrest while visiting her grandmother in hospital and has the ECG shown below. She revives after DC shock and all the subsequent ECGs show a prolonged QT interval. Blood tests rule out any metabolic derangement. Two of her first-degree relatives died suddenly at a young age. She should be treated with:

A. An implantable cardioverter–defibrillator

B. Beta-blocker

C. Quinidine

D. Sotalol

E. Verapamil

23. A 35-year-old man who is from an indigenous community in New Zealand has had mitral stenosis due to rheumatic heart disease. He has experienced some exertional dyspnoea recently. He attends a cardiology clinic with his most recent echocardiography results. Which one of the following features should prompt a referral for him to have a percutaneous balloon mitral valvuloplasty (PBMV)?

A. Mitral orifice area of 1.2 cm2 with minimal calcification

B. The presence of severe mitral regurgitation

C. Dyspnoea classified as New York Heart Association functional class I

D. Mitral orifice area of 3 cm2 with fusion of the subvalvular apparatus

E. Large left atrial thrombus

24. A 68-year-old male farmer is transferred from a country hospital following a late presentation with acute myocardial infarction. He suffered severe chest pain 2 days ago but did not seek medical treatment. While you are examining the patient you hear a pericardial rub and make a diagnosis of peri-infarction pericarditis. Which one of the following statements is correct?

A. Aspirin and heparin infusion should be stopped immediately

B. The patient should be commenced on ibuprofen

C. Reperfusion therapies are associated with a reduced incidence of peri-infarction pericarditis

D. The patient should be commenced on high-dose prednisolone

E. The echocardiogram is likely to show preserved ejection fraction

25. A 35-year-old man presents to the emergency department with a 1-h history of feeling his heart racing and slight chest discomfort. He has had two similar episodes previously following alcohol binges. An electrocardiography shows a regular narrow complex tachycardia with a rate of 180 beats/min. He otherwise feels well, his blood pressure is 98/68 mmHg and pulse oximetry on air shows oxygen saturation of 97%. What treatment should be administered?

A. Electrical cardioversion

B. Intravenous lignocaine

C. Intravenous adenosine

D. Intravenous digoxin

E. Intravenous verapamil

26. A 45-year-man presents with a 24-h history of palpitations and chest discomfort. He had one similar episode 5 years ago. He is known to have asthma since childhood and uses a salbutamol inhaler two to three times a week. His initial examination reveals blood pressure of 110/60 mmHg, pulse rate 152 beats/min and oxygen saturation on room air of 95%. There is a scattered expiratory wheeze but no cardiac murmur. His ECG taken 5 years ago when he was admitted with an acute asthma attack is shown below (A) and his current ECG (B). His biochemistry results are unremarkable and the troponin T level is normal. Which one of the following medications should be administered to achieve rate control?

A. Intravenous adenosine

B. Intravenous atenolol

C. Intravenous loading dose of digoxin

D. Intravenous flecainide

E. Intravenous verapamil

27. A 75-year old man presents to hospital with a 2-week history of malaise and low-grade fever. He also has had chronic diarrhoea for the past 3 months and a 5-kg weight loss. On examination, his blood pressure is 100/70 mmHg, heart rate 110 beats/min and temperature of 38.4° C. A diastolic murmur (3/6) is heard at the left sternal edge. He is mildly anaemic with mean cell volume (MCV) of 76 fL (normal reference range 80–100 fL). Blood cultures grow Streptococcus bovis and transoesophageal echocardiography reveals vegetations on the aortic valve. What additional investigations should be undertaken?

A. Cardiac magnetic resonance imaging

B. Computed tomography of the abdomen

C. Orthopantomogram (OPG)

D. Colonoscopy

E. White cell scan

28. Which one of the following disorders does NOT cause high-output heart failure?

A. Hyperthyroidism

B. Paget disease

C. Brachio-cephalic arteriovenous fistula

D. Cirrhosis

E. Amyloidosis

29. A 60-year-old woman is diagnosed with Streptococcus viridians endocarditis involving the mitral valve. Which one of the following is a poor prognostic factor?

A. Left ventricular ejection fraction of 50%

B. Perivalvular extension of infection

C. Recent dental extraction

D. Previous adverse drug reaction to penicillin

E. Previous abdominal aortic aneurysm repair

30. A 72-year-old man presents with a 2-day history of pain in his toes. He presented to another hospital with chest pain and received a coronary angiography 7 days ago. His other medical problems include hypertension, type 2 diabetes, chronic kidney disease with a serum creatinine of 156 μmol/L and osteoarthritis. He is taking aspirin, clopidogrel, metformin, atorvastatin and perindopril. On examination, he is afebrile, peripheral pulses are difficult to palpate and toes are painful to touch. His initial blood test results are shown below. Which one of the following diagnoses is most likely?

ValueReference rangeHaemoglobin82 g/L115–155 g/LWhite blood cells13.0 × 109 cells/L4.0–11.0 × 109 cells/LPlatelet count593 × 109 cells/L150–400 × 109 cells/LLactate dehydrogenase344 U/L110–230 U/LCreatinine287 μmol/L80–120 μmol/LUrate0.69 μmol/L0.21–0.48 μmol/L

A. Contrast nephropathy

B. Renal embolus

C. Cholesterol emboli

D. Cryoglobulinaemia

E. Metformin-induced renal failure

31. A 72-year-old man who was admitted with an inferior myocardial infarction has a cardiac arrest on the way to the angiogram suite. After three cycles of cardiopulmonary resuscitation (CPR), two boluses of 1 mg epinephrine (adrenaline) and two defibrillator shocks, his electrocardiography remains unchanged and is shown below. What is the next most appropriate step?

A. 3 mg of epinephrine (adrenaline)

B. 40 units of vasopressin

C. 10 ml of 10% calcium chloride

D. 10 ml of magnesium sulphate

E. 300 mg of amiodarone

32. A 66-year-old woman is admitted for fixation of a left hip fracture. She has a history of osteoporosis and hypertension, but is otherwise in good health. She has no history of chest pain, but she says she experiences dyspnoea after walking about 400 m. She has a 30 pack-year smoking history but stopped 5 years ago. She is currently taking an angiotensin converting-enzyme inhibitor for her hypertension. What is the next most appropriate step in her assessment?

A. Transthoracic echocardiography

B. Dobutamine stress echocardiography

C. Coronary angiography

D. No further cardiac investigation

E. Cardiac magnetic resonance imaging

33. Which one of the following is the modality of choice for diagnosing and monitoring transplant coronary artery disease after orthotopic heart transplantation?

A. Clinical history

B. Coronary angiography

C. Exercise electrocardiography (ECG)

D. Myocardial contrast echocardiography

E. Intravascular ultrasound

34. A 53-year-old woman presents with dyspnoea and ankle oedema for 1 month. Her blood pressure is 110/80 mmHg. On examination, her jugular venous pressure rises with inspiration. She has a soft systolic murmur and a third heart sound. Electrocardiography (ECG) shows poor R-wave progression. An echocardiogram shows no pericardial effusion, increased ratio of early diastolic filling-to-atrial filling and systolic function is mildly impaired. Which one of the following is the most likely diagnosis?

A. Restrictive cardiomyopathy

B. Dilated cardiomyopathy

C. Constrictive pericarditis

D. Ischaemic cardiomyopathy

E. Pulmonary embolus

35. A patient with acute fulminant myocarditis is most likely to present with:

A. Dyspnoea

B. Palpitations

C. Hypotension

D. Fever

E. Chest pain

36. A 63-year-old woman is worried because her elder sister has just had a disabling stroke. Her blood pressure is 148/94 mmHg and her BMI is 30 kg/m2. She wishes to reduce her blood pressure by non-pharmacological means. You should recommend which one of the following evidence-based measures?

A. Weight reduction and a sodium intake of 5 g/day

B. A diet reduced in sodium intake to less than 1 g/day

C. Insist on starting an antihypertensive medication

D. A diet reduced in potassium and sodium intake

E. Weight reduction and the Dietary Approaches to Stop Hypertension (DASH) diet

Theme: Congenital heart disease (for Questions 37–40)

A. Ostium secundum atrial septal defect

B. Ventricular septal defect

C. Patent ductus arteriosus

D. Eisenmenger syndrome

E. Tetralogy of Fallot

F. Pulmonary stenosis

G. Bicuspid aortic valve

H. Coarctation of the aorta

For each of the following patients, select the most likely diagnosis.

37. A 32-year-old man presents to a hospital with fatigue and fever of 2 weeks' duration. He has no chest pain, dyspnoea or orthopnoea. He is known to have a ‘heart murmur’ since birth. On physical examination the only abnormal findings are a temperature of 38.3° C; a harsh systolic murmur is heard in the left lower sternal border; and the presence of small tender nodules are noted on two fingers. Which cardiac anomaly is most consistent with this patient's clinical presentation?

38. A 21-year-old woman is being evaluated for exertional dyspnoea. She has been having these symptoms for the past 4 months. Her medical history includes one episode of atrial fibrillation 1 month ago. Her physical examination shows fixed splitting of the second heart sound and a systolic murmur in the pulmonic area. An electrocardiogram shows slight right axis deviation and incomplete right bundle-branch block. A chest X-ray reveals an enlarged right atrium and main pulmonary artery. Which cardiac anomaly is the most likely diagnosis for this patient?

39. An 18-year-old man is being evaluated for a murmur and hypertension. He is asymptomatic. On physical examination his blood pressure is 170/100 mmHg in the right arm. The femoral pulses are diminished in amplitude compared to the radial pulses. His cardiac examination reveals a short mid-systolic murmur in the left infrascapular area. Which cardiac anomaly is the most likely diagnosis for this patient?

40. A 19-year-old woman presents with breathlessness on exertion and mild fatigue. She has no significant medical history. She does not smoke and is not on regular medication. Her cardiac examination reveals a systolic murmur at the second left intercostal space, which increases with inspiration. What is the most likely diagnosis for this patient?

Answers

Basic Science

1. Answer DThe beneficial effects of beta-blockers in stable angina are secondary to reduction in myocardial oxygen demand. Myocardial oxygen demand varies directly according to the heart rate, contractility and left ventricular wall stress, each of which is decreased by beta-blockers.Catecholamine activation of the beta-1 receptors, which are primarily found in the heart muscle, leads to increased heart rate, contractility and atrioventricular (AV) conduction, with a decrease in AV node refractoriness. Beta-blockers act by competitively inhibiting catecholamines from binding to these receptors.No randomised trials have studied the effect of beta-blockers on survival in patients with angina, but survival benefits have been seen in patients with systolic heart failure and following myocardial infarction.In the treatment of patients with angina, titrating the dose of beta-blocker to achieve a target resting heart rate of 55–60 beats/min is recommended. Adverse side effects can include bradycardia, AV node conduction problems, reduced contractility, bronchoconstriction (notably in patients who are taking a beta-2 adrenergic agonist), worsening of peripheral vascular disease, Raynaud phenomenon, fatigue, nightmares and erectile dysfunction.

2. Answer DCompensatory mechanisms that are activated in heart failure include: Increased ventricular preload with ventricular dilatation and volume expansionPeripheral vasoconstriction, which initially maintains perfusion to vital organsMyocardial hypertrophy to preserve wall stress as the heart dilatesRenal sodium and water retention to enhance ventricular preloadActivation of the adrenergic nervous system, which increases heart rate and contractile function.These processes are controlled mainly by activation of neurohormonal vasoconstrictor systems, including the renin–angiotensin–aldosterone system, the adrenergic nervous system, and non-osmotic release of arginine–vasopressin. These and other mechanisms contribute to the symptoms, signs and poor natural history of heart failure. In particular, an increase in wall stress along with neurohormonal activation facilitates pathological ventricular remodelling; this process has been closely linked to heart failure disease progression. Management of chronic heart failure targets these mechanisms and, in some instances, results in reverse remodelling of the failing heart (Krum and Abraham, 2009).

Krum, H. and Abraham, W.T. (2009). Heart failure. Lancet 373, 941–955.

http://www.ncbi.nlm.nih.gov/pubmed/19286093

3. Answer EVentricular tachycardia without structural heart disease is often referred to as idiopathic ventricular tachycardia (John et al., 2012). Idiopathic ventricular tachycardia in the absence of structural heart disease most often originates from the right ventricular outflow tract. Diseases such as arrhythmogenic right ventricular cardiomyopathy and sarcoidosis often need to be excluded before a diagnosis is made. Idiopathic ventricular tachycardia must be distinguished from ventricular tachycardia with structural heart disease, because the latter often warrants an implantable cardioverter defibrillator (ICD). Detection of ventricular scar on cardiac imaging can be helpful. Although idiopathic monomorphic ventricular tachycardia can cause syncope, sudden death is rare. Beta-blockers, calcium-channel blockers or catheter ablation are often effective.Catheter ablation is a reasonable first-line therapy for many patients with symptomatic idiopathic ventricular tachycardias. Success rates approach 80–90% in experienced centres. Success rates are lower for those tachycardias arising in less common locations, such as along the aortic annulus, within the aortic sinuses, within the great cardiac vein or from the epicardium. Failure of ablation is usually due to the inability to induce the arrhythmia for precise localisation, or ventricular tachycardia origin in a location that is inaccessible or in close proximity to a coronary artery, which precludes safe ablation.

John, R.M., Tedrow, U.B., Koplan, B.A., et al. (2012). Ventricular arrhythmias and sudden cardiac death. Lancet 380, 1520–1529.

http://www.ncbi.nlm.nih.gov/pubmed/23101719

4. Answer AMyocarditis is most commonly caused by a viral infection in developed countries (Magnani and Dec, 2006). Enteroviruses, including the Coxsackie virus, are the most commonly associated viral species. The Coxsackie virus has a myocardial affinity because of its easy entrance into the myocardial cell through the Coxsackie–adenoviral receptor, which triggers the host immune response.Cytomegalovirus is commonly associated with post-transplantation myocarditis. Influenza myocarditis is often associated with haemorrhagic pulmonary oedema. HIV has been reported to cause myocarditis. However, it may be difficult to determine the exact cause of cardiac dysfunction because symptoms may be due to the inflammatory response to HIV; the HIV infection itself; or coexisting opportunistic infections, side effects of anti-retroviral treatment, or a combination of these causes.Hepatitis C, adenovirus, parvovirus B19 and Epstein–Barr virus (EBV) have been reported to cause myocarditis.

Magnani, J.W., and Dec, G.W. (2006). Myocarditis: current trends in diagnosis and treatment. Circulation 113, 876–890.

http://circ.ahajournals.org/content/113/6/876.long

5. Answer BElectrical propagation of the cardiac impulse is transmitted from the sino-atrial node to the anterior, middle, and posterior internodal tracts, to the AV node and to the bundle of His (AV bundle), and then via the right and left bundle branches to the Purkinje fibres and thence to the myocardium.Myocytes have a negative membrane potential when at rest. Stimulation induces the opening of voltage-gated ion channels, leading to flow of cations into the cell. The positively charged ions enter the cell, causing the depolarisation characteristic of an action potential. The action potential spreads through the muscle network of T-tubules, depolarising the inner portion of the muscle fibre. The depolarisation activates L-type voltage-dependent calcium channels (dihydropyridine receptors) in the T-tubule membrane, which are in close proximity to calcium-release channels (ryanodine receptors) in the adjacent sarcoplasmic reticulum. Activated voltage-gated calcium channels physically interact with calcium-release channels to activate them, causing the sarcoplasmic reticulum to release calcium. Calcium release is the main trigger of muscle contraction by causing alterations in the binding of troponin and tropomyosin to actin and leading to the ATP-driven myosin–actin bonding, sliding and releasing interactions that generates contraction. Repolarisation occurs due to a flow of potassium out of the cardiac cells.In an electrocardiogram the P wave corresponds to the depolarisation of the atria; the QRS complex to right and left ventricular depolarisation; the ST-T wave to ventricular repolarisation; the PR interval is the time from onset of atrial depolarisation (P wave) to onset of ventricular depolarisation (QRS complex); the QRS duration is duration of ventricular muscle depolarisation; and the QT interval is the duration of ventricular depolarisation and repolarisation.During diastole the pressure within the left ventricle is lower than that in aorta, allowing blood to circulate into the heart itself through the epicardial coronary arteries.

6. Answer BPerhexiline has been used in the treatment of congestive heart failure and refractory angina. It relieves symptoms of angina, improves exercise tolerance and increases workload needed to induce ischemia. The drug works in part by modifying myocardial substrate utilisation from fatty acids to carbohydrates, which is energetically more efficient for the heart to metabolise, thus reducing myocardial oxygen consumption. Study has demonstrated the effectiveness of perhexiline in relieving symptoms, but there is no evidence that it provides mortality benefit (Phan et al., 2009).Its major side effects include hepatotoxicity, peripheral neuropathy and hypoglycaemia. To prevent these toxicities, perhexiline plasma levels should be closely monitored and maintained between 0.15 and 0.60 mg/L. Perhexiline is metabolised by cytochrome P450 2D6. Drug level monitoring is essential to identify patients who are slow metabolisers, which occurs in about 7–10% of Caucasians who harbour mutations in CYP2D6. In normal metabolisers, perhexiline's half-life is between 3 and 12 days. In slow metabolisers this half-life can be as long as 30 days. The usual loading dose is 200 mg twice a day for 3 days, then 100 mg/day. Blood is taken 3 days after commencing the drug to determine metaboliser status. If there is no metabolite peak, then the patient is a slow metaboliser, and the dose should be reduced to 100 mg weekly. If the metabolite is present, dose is continued at 100 mg daily. Plasma perhexiline trough concentrations should be monitored monthly until stable, then 3–6 monthly.

Phan, T.T., Shivu, G.N., Choudhury, A., et al. (2009). Multi-centre experience on the use of perhexiline in chronic heart failure and refractory angina: old drug, new hope. Eur J Heart Failure 11, 881–886.

http://eurjhf.oxfordjournals.org/content/11/9/881.long

7. Answer H

8. Answer CCommentary for Questions 7 and 8:Beta-adrenoreceptor blocking agents, commonly known as beta-blockers, are useful in the treatment of angina, myocardial infarction, cardiac failure, hypertension and cardiac arrhythmias. Beta-blockers given long-term have been shown to diminish mortality following acute myocardial infarction.Some beta-blockers possess beta-agonist activity. Agents with partial agonist activity include pindolol, which causes little or no depression of resting heart rate (partial agonist effect) while blocking the increase in heart rate that occurs in response to exercise or the administration of a beta-agonist such as isoproterenol. The presence of partial agonist activity may be useful when bradycardia limits treatment in patients with slow resting heart rates. Pindolol also produces mild vasodilation. Agents with partial agonist activity cause less change in blood lipid levels than agents without agonist properties.Non-selective beta-blockers, such as propranolol, sotalol, timolol and carvedilol, induce competitive blockade of both β1 and β2 receptors. Metoprolol and atenolol possess relative selectivity for the β1 receptor. Although β1(cardiac)-selective agents have the theoretical advantage of producing less bronchoconstriction and less peripheral vasoconstriction, a clear clinical advantage of cardioselective agents is unestablished. Bronchoconstriction may occur when β1-selective agents are administered in therapeutic doses.Various beta-blockers differ in their water and lipid solubility. The lipophilic agents (e.g. propranolol, metoprolol, bisoprolol and carvedilol) are readily absorbed from the gastrointestinal tract, metabolised by the liver, have large volumes of distribution and penetrate the central nervous system well. The hydrophilic agents (e.g. atenolol) are less readily absorbed, not extensively metabolised and have relatively longer plasma half-lives, resulting in their ability to be administered once per day. Hepatic impairment may prolong the plasma half-life of lipophilic agents whereas renal impairment may prolong the action of hydrophilic agents. Nebivolol is a β1-receptor blocker with a nitric-oxide potentiating vasodilatory effect.Carvedilol has both α1-adrenoreceptor blockade and non-selective beta-blockade actions and is devoid of intrinsic sympathomimetic activity (Frishman, 1998). Carvedilol is indicated to slow the clinical progression of heart failure, as evidenced by reductions in hospitalisation rates and mortality. Contraindications to carvedilol therapy in patients with heart failure include severe decompensation requiring inotropic therapy, marked bradycardia, the sick sinus syndrome, and partial or complete atrioventricular block, unless a permanent pacemaker is in place.

Frishman, W.H. (1998). Carvedilol. N Engl J Med 339, 1759–1765.

http://www.ncbi.nlm.nih.gov/pubmed/10328713

Clinical

9. Answer BThe clinical diagnosis of acute pericarditis rests primarily on the findings of chest pain, pericardial friction rub and ECG changes (Imazio et al., 2010). The chest pain of acute pericarditis typically develops suddenly and is severe and constant over the anterior chest. In acute pericarditis, the pain worsens with inspiration – a response that helps to distinguish acute pericarditis from myocardial infarction. Low-grade fever and sinus tachycardia are often present. A pericardial friction rub can be detected in most patients when symptoms are acute. ECG changes are common in most patients with acute pericarditis, particularly in those with an infectious aetiology in which the associated inflammation in the superficial layer of myocardium is prominent. The characteristic change is an elevation in the ST segment in multiple leads. The diffuse distribution and the absence of reciprocal ST segment depression distinguish the characteristic pattern of acute pericarditis from acute myocardial infarction. Depression of the PR segment, which reflects superficial injury of the atrial myocardium, is as frequent and specific as ST segment elevation and is often the earliest ECG manifestation. Analgesic agents or non-steroidal anti-inflammatory drugs (NSAIDs) are often effective in reducing pericardial inflammation. Corticosteroids should be reserved for severe cases that are unresponsive to other therapy, because symptoms may recur after steroid withdrawal.

Imazio, M., Spodick, D.H., Brucato, A., Trinchero, R., and Adler, Y. (2010). Controversial issues in the management of pericardial diseases. Circulation 121, 916–928.

http://circ.ahajournals.org/content/121/7/916.long

10. Answer CAcute rheumatic fever (ARF) remains common in the developing world. Indigenous populations in northern Australia have among the highest burden of ARF and rheumatic heart disease in the world, with one in 300 children developing ARF each year and up to 2% of people of all ages having rheumatic heart disease. Similar rates are seen throughout the Western Pacific region, including in Maori and Pacific Islander populations in New Zealand, where some of the most reliable data are available.Oral penicillin V is the drug of choice in treating streptococcal pharyngitis; twice-daily dosing is as effective as four times a day dosing and may improve compliance. Group A streptococci (GAS) are isolated from throat swabs in less than 10% of ARF cases in New Zealand, and less than 5% of cases in Australian Aboriginal people. Streptococcal antibody titres are therefore crucial in confirming the diagnosis. The most commonly-used tests are the plasma anti-streptolysin O (ASO) and the anti-DNase B titres. Previous data suggest that a rise in the ASO titre occurs in 75–80% of untreated Group A streptococci pharyngeal infections, and that the addition of anti-DNase B titre increases the sensitivity of testing.Treatment should be started within 9 days of the onset of symptoms to prevent rheumatic fever. Aspirin is recommended as the first-line treatment for arthritis or arthralgia in ARF. Sydenham chorea is self-limiting. Most cases will resolve within weeks and almost all cases within 6 months, although rare cases may last as long as 2–3 years. Because chorea is benign and self-limiting, and anti-chorea medications are potentially toxic, treatment should only be considered if the movements interfere substantially with normal activities. Aspirin does not have a significant effect on rheumatic chorea. Group A streptococci are responsible for only 5% of cases of pharyngitis in adults. Screening asymptomatic family contacts is controversial and probably unnecessary.

RHDAustralia (ARF/RHD writing group), National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand (2012). Australian Guideline for Prevention, Diagnosis and Management of Acute Rheumatic Fever and Rheumatic Heart Disease, 2nd edn. National Heart Foundation of Australia.

http://www.rhdaustralia.org.au/sites/default/files/guideline_0.pdf

11. Answer BThe sudden onset of chest pain radiating to the interscapular area and signs of shock suggest a diagnosis of acute aortic dissection, especially in those with risk factors such as hypertension, dyslipidaemia and peripheral vascular disease (Golledge and Eagle, 2008). Computed tomography (CT) angiography or echocardiography is usually needed in patients in whom acute aortic dissection is clinically suspected on the basis of presentation and initial investigations. A systematic review of the diagnostic accuracy of transoesophageal echocardiography, CT angiography and MRI reported a mean sensitivity and specificity of more than 95% for all three investigations. In addition to assisting in the diagnosis of aortic dissection, the results of imaging can help to plan management. Important findings include the extent of the dissection, the size of the true and false lumen, localisation of the intimal tear, the involvement of aortic branches, the presence and extent of aortic regurgitation, and the presence of periaortic haematoma, mediastinal haematoma, or effusion. Guidelines recommend the use of echocardiography or CT angiography, or both, in the initial imaging of patients suspected to have acute aortic dissection, whereas MRI is favoured for the assessment of chronic dissection. Contrast angiography is recommended in patients in whom visceral hypoperfusion is suspected or percutaneous interventions are being considered.Patients can present with aortic dissection either in the ascending aorta (type A) or in the more distal aorta (type B). The risk factors most probably relate to a combination of inherited and acquired weakening of the aortic media and intimal disease. Marfan syndrome is an important risk factor for aortic dissection, especially in young patients. Other inherited disorders, including Ehlers–Danlos syndrome type IV and Turner syndrome, have been associated with aortic dissection.

Golledge, J. and Eagle, K.A. (2008). Acute aortic dissection. Lancet 372, 55–66.

http://www.ncbi.nlm.nih.gov/pubmed/18603160

12. Answer DBrain natriuretic peptide (BNP) levels reflect the severity of congestive heart failure (CHF), the risk of hospitalisation and survival. Changes in BNP level in response to medical therapy also predict survival.Plasma BNP or N-terminal pro-BNP measurement may be helpful in patients presenting with recent-onset dyspnoea; it has been shown to improve diagnostic accuracy with a high negative predictive value. BNP measurement has been demonstrated to be useful for differentiating dyspnoea caused by CHF from dyspnoea due to other causes, especially in the Emergency Department. A cut-off value of 100 pg/mL has a sensitivity of 90% and a specificity of 76%. However, routine use of BNP in the diagnosis of CHF is not recommended. There is no evidence that BNP provides additional diagnostic information to that provided by echocardiogram.BNP levels appear more useful in detecting systolic heart failure than diastolic heart failure. BNP levels do not discriminate well between elderly female patients with diastolic heart failure (the most common patient group with this condition) and healthy age-matched controls.

National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand (Chronic Heart Failure Guidelines Expert Writing Panel) (2011). Guidelines for the Prevention, Detection and Management of Chronic Heart Failure in Australia Update 2011.

National Heart Foundation of Australia.

http://www.heartfoundation.org.au/sitecollectiondocuments/chronic_heart_failure_guidelines_2011.pdf

13. Answer ACardiomyopathy and heart failure are well recognised complications of prolonged anthracycline treatment (Yeh and Bickford, 2009). Anthracycline cardiotoxicity can be divided into acute/sub-acute or late/chronic, with the latter being more common. In adults, chronic anthracycline-related cardiotoxicity typically presents within 1 year after finishing chemotherapy, with the peak time for the appearance of symptoms being about 3 months after the last dose. Late cardiotoxicity is characteristically seen in survivors of childhood malignancy treated with an anthracycline.A number of risk factors for the development of chronic anthracycline cardiotoxicity have been identified. The strongest predictor is cumulative dose. Studies that have looked at the cumulative probability of doxorubicin-induced heart failure have found that it occurs in 3–5% at 400 mg/m2, 7–26% at 550 mg/m2 and 18–48% at 700 mg/m2. However, intravenous administration, concomitant administration of other cardiotoxic chemotherapeutic agents (particularly paclitaxel, cyclophosphamide and trastuzumab), concurrent or prior chest irradiation, pre-existing cardiovascular disease or risk (including coronary artery disease, hypertension and diabetes mellitus) are also major risk factors.Dexrazoxane is an EDTA-like chelator that significantly reduces the risk of chronic cardiotoxicity when used with anthracyclines. Dexrazoxane given with either doxorubicin or epirubicin significantly reduced the incidence of clinical and subclinical cardiotoxicity. It is recommended in patients who are being treated for metastatic disease and are receiving high cumulative doses of anthracyclines.All patients should have a baseline echocardiogram and serial monitoring of myocardial function during therapy with anthracyclines. Although chest radiotherapy in the past was associated with significant cardiotoxicity, con­temporary techniques with minimal exposure to the heart has lessened this complication.

Yeh, E.T. and Bickford, C.L. (2009). Cardiovascular complications of cancer therapy: incidence, pathogenesis, diagnosis, and management. J Am Coll Cardiol 53, 2231–2247.

http://www.ncbi.nlm.nih.gov/pubmed/19520246

14. Answer BPharmacological treatment of systolic heart failure consists of symptom relief with diuretics and disease modification is achieved with ACE inhibitors or angiotensin receptor blockers (ARBs), beta-blockers, spironolactone or a combination of hydralazine and isosorbide dinitrate (McMurray, 2010).ACE inhibitors are the first-line therapy for patients with systolic heart failure; therapy should be initiated promptly and continued indefinitely. ACE inhibitors reduce ventricular size, increase the ejection fraction modestly and reduce symptoms.The efficacy of ARBs is similar to ACE inhibitors but they are usually reserved for those who develop cough or other adverse effects with ACE inhibitors (on account of their higher cost). ARBs are sometimes prescribed for those who are symptomatic despite treatment with optimal doses of ACE inhibitors and beta-blockers.Beta-blockers are essential first-line therapy in patients with heart failure and left ventricular systolic dysfunction. Treatment with beta-blockers improves systolic function, resulting in an increase in ejection fraction of 5–10%, and reduces symptoms. Bisoprolol, carvedilol or metoprolol CR/XL (metoprolol succinate, controlled release or extended release) can reduce the rate of hospital admissions and mortality by up to 34%.Spironolactone is indicated in severe heart failure, that is NYHA class III or IV despite treatment with a diuretic, an ACE inhibitor (or ARB) and a beta-blocker. Digoxin when added to a diuretic and ACE inhibitor has no effect on mortality but may reduce risk of hospitalisation for heart failure.Diuretic treatments with loop diuretics should be prescribed to minimise fluid retention and pulmonary oedema.It is always important to also consider the underlying aetiology of the heart failure, correct this accordingly and address the possible need for anti-platelet agents, rhythm correction, implantable defibrillators, cardiac resynchronisation, coronary bypass surgery and lipid treatment. The presence of other problems such as renal insufficiency, thyroid disease and anaemia should be considered.

McMurray, J.J. (2010). Clinical practice. Systolic heart failure. N Engl J Med 362, 228–238.

http://www.ncbi.nlm.nih.gov/pubmed/20089973

15. Answer DCoronary artery bypass graft (CABG) is recommended in patients with any of the following criteria: significant left main coronary artery disease, three-vessel disease [in patients with three-vessel disease, those with left ventricular ejection fraction (LVEF) <50% have the greatest survival benefit] and two-vessel disease with significant left anterior descending coronary artery involvement or abnormal LV function (i.e. LVEF <50%) (Pfisterer et al., 2010). In patients with three-vessel disease and abnormal LVEF, the survival benefit and symptom relief of CABG are superior to those of percutaneous transluminal angioplasty (PCTA) or medical therapy. In transmyocardial revascularisation procedure (TMR), a laser is used to create channels in the myocardium to relieve angina. This procedure has been shown to improve severe refractory angina in patients who could not be treated with conventional revascularisation techniques (PCTA or CABG). For the patient described here, CABG is the preferred procedure.

Pfisterer, M.E., Zellweger, M.J., and Gersh, B.J. (2010). Management of stable coronary artery disease. Lancet 375, 763–772.

http://www.ncbi.nlm.nih.gov/pubmed/20189028

16. Answer EComputed tomography coronary angiography (CTCA) is a new imaging test that has been shown in meta-analyses to have excellent sensitivity (98%) and good specificity (88%) for significant coronary artery disease (stenosis >50%). Its high negative predictive value (96–100%) indicates that CTCA is an excellent test for ruling out significant disease in patients with low-to-intermediate pretest probability of coronary artery disease. Current data do not support the use of CTCA in asymptomatic patients. CTCA is not routinely recommended in patients with previous coronary stents since stents are likely to cause artefacts and make the results difficult to interpret. In patients who are likely to require invasive coronary angiograms, such as a patient with ST-elevation myocardial infarction, it is more appropriate to proceed with percutaneous coronary intervention without delay.To avoid artefacts that may hamper interpretation of the results, the patient should be in sinus rhythm with a heart rate of less than 65 beats/min, able to hold his/her breath for 10 s, able to tolerate beta-blockers and nitrates (nitrates are given to dilate the coronary arteries by most centres) and able to hold his/her arms above the head during the scan. Previous contrast allergy and renal impairment should be ruled out prior to CTCA.

Liew, G., Feneley, M., and Worthley, S. (2012). Appropriate indications for computed tomography coronary angiography. Med J Aust 196, 246–249.

https://www.mja.com.au/journal/2012/196/4/appropriate-indications-computed-tomography-coronary-angiography

17. Answer BDabigatran is 80% renally cleared (Hankey and Eikelboom, 2011). Therefore, care must be taken when used in patients with impaired renal function. Reduced kidney function in an elderly patient with diabetes is the most likely explanation for the bleeding complication in the patient described. In addition, bleeding rates with dabigatran increase with advanced age. The combination of aspirin and dabigatran is associated with higher bleeding rates.At present there are no available laboratory tests that have been validated for monitoring of dabigatran. The thrombin clotting time can be used to inform if dabigatran activity is present, but it does not reveal the extent of anti-coagulation. Unlike warfarin, one of the major drawbacks of dabigatran is the lack of an effective antidote for use in the event of a severe bleeding event.Dabigatran is given as the prodrug dabigatran etexilate, and this prodrug is a substrate for efflux by the p-glycoprotein transporter. Inhibitors of p-glycoprotein, such as ketoconazole (most azoles), protease inhibitors, macrolides, calcineurin inhibitors, amiodarone and verapamil, can increase dabigatran plasma concentrations by decreasing the efflux of the drug into the gastrointestinal lumen. Strong inducers of p-glycoprotein, such as rifampicin, carbamazepine and phenytoin, can reduce plasma concentrations and co-administration should be avoided. No significant interaction was seen with digoxin, also a p-glycoprotein substrate.

Hankey, G.J. and Eikelboom, J.W. (2011). Dabigatran etexilate: a new oral thrombin inhibitor. Circulation 123, 1436–1450.

http://circ.ahajournals.org/content/123/13/1436.long

18. Answer EThe ECGs show:

A. Bifascicular block

B. First-degree heart block

C. Left bundle branch block

D. Mobitz type I (Wenkebach) heart block

E. Mobitz type II 2:1 heart block

Temporary transvenous pacing is necessary for patients with severe and symptomatic bradyarrhythmias, but should also be considered for those at high risk of developing complete heart block as a consequence of acute myocardial infarction (AMI). High (second or third)-degree AV block is associated with an increase in mortality in patients with an inferior or anterior AMI (Vardas et al., 2007).Following an AMI, temporary transvenous pacing should be considered if there is: Complete (third-degree) heart blockNew or age-indeterminate bifascicular block (RBBB with LAFB or LPFB or LBBB) with PR prolongationSymptomatic bradycardia of any aetiology if hypotension is present and the bradyarrhythmia is not responsive to atropineMobitz type II second-degree AV blockBradycardia-induced tachyarrhythmias.Despite reperfusion treatment, the incidence of intraventricular conduction disturbances post acute myocardial infarction (AMI) has not changed, whereas the incidence of AV block post AMI has decreased but still remains high. AV block occurs in almost 7% of cases of AMI.

Vardas, P.E., Auricchio, A., Blanc, J.J., et al. (2007). Guidelines for cardiac pacing and cardiac resynchronization therapy: The Task Force for Cardiac Pacing and Cardiac Resynchronization Therapy of the European Society of Cardiology. Developed in collaboration with the European Heart Rhythm Association. Eur Heart J 28, 2256–2295.

http://eurheartj.oxfordjournals.org/content/28/18/2256.long

19. Answer D