Clinical Phase 3 Cls Handbook 2011 12

School of Molecular Medical Sciences

A104 Medicine – BM BS – Year 5

2011 – 2012

A14ACE

Clinical Practice 3

Handbook

Specialty Contacts: Clinical Chemistry: [email protected] Haematology: [email protected] Immunology: [email protected] Microbiology: [email protected] Pathology: [email protected]

This guide is available on the NLE in the following areas:

Clinical Phase 3 A14ACE/log books and guides

Clinical Phase 3 A14ACE/learning materials

INTRODUCTION

Clinical Laboratory Sciences incorporates the Divisions of Clinical Chemistry,

Haematology, Immunology, Microbiology and Pathology. This document is a Study Guide

for teaching in Clinical Laboratory Sciences for Clinical Phase 3 in Year 5.

OBJECTIVES

The objectives for this part of the course are incorporated into the learning objectives for

Medicine and Surgery. Please note that these should not be regarded as a finite

description of the work to be undertaken for examinations but as a general description of

the areas to be covered for this purpose. Students are expected to develop skills in self-

learning which will make them aware of important advances in the clinical and laboratory

aspects of medicine. The reading lists are regarded as very important parts of your

studies in Clinical Laboratory Sciences.

SMALL GROUP TEACHING

Small group teaching is provided at each Trust during the attachment indicated below:

Specialty Small group teaching Attachment

Clinical chemistry Seminars Medicine

Haematology Seminars Medicine

Microbiology Cases of infection Medicine

Pathology Tutorials Medicine & Surgery

TIMETABLES

Teaching is arranged locally and will be timetabled differently at each hospital site so you

will need to look at local noticeboards in each hospital to find out the place and time

teaching will occur.

For local timetable enquiries please see the Clinical teaching coordinator at your hospital

site. In case of specific difficulty with aspects of teaching you can contact teaching co-

ordinators for each Division.

Clinical Chemistry Professor Noor Kalsheker (QMC) [email protected] Haematology Dr Andrew Haynes (NCH) [email protected] Immunology Dr Ian Todd (QMC) [email protected] Microbiology Dr David Turner (QMC) [email protected] Pathology Professor Ian Ellis (NCH) [email protected]

CENTRAL TEACHING

Two interactive Friday afternoon central teaching sessions cover the Interpretation of

Laboratory Tests in Common Clinical Scenarios. A third central teaching session focuses

on haematological malignancies and haemoglobinopathies. Further details are available

on the Central Teaching timetable.

WORKBOOKS

Workbooks are included at the end of this handbook providing a set of clinical and

laboratory data for students to use for self-directed learning

ASSESSMENTS

Formative assessments in CLS will be incorporated into the Progress Tests at the end of

each attachment, and into the final MCQ assessment at the end of Clinical Phase 3.

Although there is no specific CLS examination, students should be aware that the

material covered in the Clinical Phase 3 course will be assessed.

CLINICAL CHEMISTRY

OUTLINE OF TEACHING

Students are constantly exposed to clinical chemistry results where they relate to patient

management. They are encouraged to become familiar with normal and abnormal result

profiles in this context and to seek guidance from clinical teachers on appropriate

requesting and interpretation of biochemical investigations for individual patients under

their care. This teaching is underpinned by seminars in clinical chemistry held during

year 5. Wherever possible the teaching is illustrated by patients‘ results.

TEACHING:

Seminars. A series of three seminars covering routine clinical chemistry tests will

take place during your attachment in medicine. Titles of sessions and times will be

arranged individually at each hospital site by your clinical teaching coordinator.

Timetables should be on noticeboards at each hospital site.

Central Teaching. Clinical chemistry tuition on relevant topics will be incorporated

into Friday afternoon central teaching

Workbook. A workbook of clinical chemistry data interpretation exercises for self-

assessment. [See Workbook sections at the end of this Study Guide.]

CLINICAL CHEMISTRY GENERAL OBJECTIVES

To understand the biochemical and pathophysiological processes underlying clinical

chemistry.

To recognise which tests are useful in common clinical situations; to develop

interpretive skills in clinical chemistry.

CLINICAL CHEMISTRY SESSION OBJECTIVES

The topics covered in the seminars and central teaching are listed below. The objectives

for each session are as listed in the Clinical Phase 3 guide.

Electrolyte and water homeostasis

Acid-base balance

Markers of myocardial damage

Hypo- and hyper-calcaemia

Diabetes and hypoglycaemia

Thyroid function

Adrenal function

Liver function

RECOMMENDED READING

The recommended textbook is W.J.Marshall‘s Illustrated Textbook of Clinical

Chemistry.

Many students find the biochemistry section in the Oxford Handbook of Clinical

Medicine useful for revision purposes.

HAEMATOLOGY

OUTLINE OF TEACHING

Haematology teaching in the clinical part of the course builds upon work done in the

Preclinical course related to structure and function of blood cells and blood clotting.

During the Clinical part of the course, students are constantly exposed to haematology

results where they relate to patient management. They are encouraged to become

familiar with normal and abnormal results profiles in this context and to seek guidance

from clinical teachers on appropriate requesting and interpretation of haematology

investigations for individual patients under their care. This clinical teaching is

underpinned by seminars in Haematology

TEACHING IN YEAR 5 Details of the teaching arrangements will be distributed separately. A series of seminars covering red cell disorders, white cell disorders, coagulation problems and transfusion medicine will take place during your attachment. Times and exact details of the sessions will be arranged individually at each hospital

Workbook

A workbook of haematology data interpretation exercises for self-assessment. [See

Workbook sections at the end of this Study Guide.]

RECOMMENDED SUPPORT READING

Essential Haematology: Hoffbrand and Pettit. Blackwell Scientific Publications. Third

Edition 1993: Chapters 5, 6, 7, 11, 12, 14, 15,18, 19 ,21

Clincal Medicine:Kumar and Clarke. Bailliere Tindall: Chapter Six.

IMMUNOLOGY

OUTLINE OF TEACHING

Immunology teaching in the clinical part of the course builds upon (and assumes

knowledge of) work done earlier in the medical course and aims to provide the necessary

expertise and experience required to practice as a foundation level doctor and to provide

a foundation for postgraduate continuing professional development.

During their clinical attachments students will be frequently exposed to test results

undertaken by clinical immunology related to patient management. They are encouraged

to become familiar with normal and abnormal result profiles and to seek guidance from

clinical teachers on appropriate requesting and interpretation of immunological

investigations for individual patients under their care. This clinical teaching is

underpinned by a session on ‗Interpretation of Common Laboratory Tests‘ within the

Friday afternoon central topic teaching, a workbook (this document) and recommended

reading.

TEACHING IN YEAR 5 Workbook

A workbook containing datasets, questions and answers for self-assessment. [See

Workbook sections at the end of this Study Guide.]

IMMUNOLOGY GENERAL OBJECTIVES Aim To introduce students to the direct application of immunology to investigation,

diagnosis and management of patients

Objectives Describe the underlying pathophysiology of the important immunological disorders

Describe how immunological principles may be applied directly to the diagnosis, assessment of prognosis, follow up and management of patients with immunological disorders.

Describe the indications for and the interpretation of the commonly requested immunology tests

Review of defence mechanisms Describe the variety of innate and adaptive immunological defence mechanisms.

Describe the normal immune response to bacterial and viral infection, relating this to

patients‘ symptoms, signs and laboratory results. Immunodeficiency Describe the clinical features that should alert clinicians to the possibility of an

underlying immunodeficiency. Describe the principles of investigation and management of immunodeficiency.

Describe the clinical features and immunopathology of HIV infection.

Allergy Describe the clinical features of type 1 hypersensitivity; outline the investigation and

management of a patient with suspected type 1 hypersensitivity. Describe the immunopathology and investigation of common allergic diseases

including food allergy and anaphylaxis, urticaria, rhinitis.

Autoimmune diseases Describe the immunopathology and investigation of common autoimmune diseases,

including vasculitis. Describe the indications for, and interpretation of, the autoimmune screen and other

autoantibodies.

Outline the main features of myeloma and Interpret paraprotein reports. Connective tissue disease (during the Rheumatology attachment) Describe the clinical features of connective tissue disease (in particular Systemic

Lupus Erythematosus and Scleroderma) and indicate those features which may suggest that the patient may require urgent treatment.

Outline the differences between Raynaud‘s Disease (primary) and Raynaud‘s phenomenon secondary to connective tissue or other disease

Outline the immunopathology and management of connective tissue diseases.

Outline the investigation of a patient with suspected connective tissue disease.

Describe the indications for and the interpretation of anti-nuclear antibodies.

RECOMMENDED READING Rather than suggest a separate immunology text book we have compiled a reading list based upon the most popular general medical text. Similar chapters/sections may be found in the other general medical texts. The pages listed will therefore contain general as well as immunological information. We suggest you concentrate on immunological aspects and laboratory investigation. Further information can be obtained in ―Essentials of Clinical Immunology‖ by Chapel, Haeney, Misbah & Snowden (5th edition) and ‗Pathology‘ by Stevens & Lowe Clinical Medicine, Kumar & Clark, Page numbers for the 6th Edition Basic components 197-213 Immunodeficiency 213-220 C reactive protein / ESR/ white cell count 421 HIV 129-152 Myeloma 516-518 Asthma and Allergy Mechanisms of damage 220-226 Asthma 912-922 Rhinitis / Hay fever 895-898 Atopic eczema 1327-1329 Food allergy and intolerance 261-262, 1283-1284 Urticaria 1334-1335 Drug allergy 1358-1359, 1365 Skin-prick test 262, 893, 897, 918 Autoimmunity Mechanisms of damage 220-226 Rheumatoid arthritis 555-564 SLE 574-577, 1344 Thyroid disease 1071-1079 Type 1 diabetes mellitus 1103-1106 Pernicious anaemia 432-433 Autoimmune liver disease 373-374 Coeliac disease (and DH) 301-303 Systemic vasculitis 633-636 Goodpasture‘s syndrome 226, 582, 633-634, 940 Cryoglobulins 628-629, 582-584 Raynaud‘s phenomenon 869

MICROBIOLOGY & INFECTIOUS DISEASES

OUTLINE OF TEACHING

By the beginning of the fifth year, you will have had exposure to Microbiology and

Infectious Diseases through:

Lectures in microbiology and infectious diseases during A11CLS and A12CLS modules

Microbiology Optional module A13MMB in Semester 4

Treatment and Prevention of Infection (A13AMC)

Teaching in Clinical Phase 1

The clinical course in Microbiology and Infectious Diseases will build on this previous

teaching. Clinical Phase 3 is intended to consolidate and extend your knowledge of

common and important infections and, in particular, to provide the expertise necessary to

recognize and manage such infections in your role as a pre-registration house officer. The

sessions will be delivered as part of Central Teaching, but will also be taught locally in

each of the five centres (QMC, CHN, Derby, Lincoln and Kings Mill Hospital).

TEACHING IN YEAR 5

SESSIONS:

Central Teaching. Central teaching in Microbiology and Infectious Disease will be

lecture based and is intended to have a strong practical application. Sessions may either

focus on selected infections or form part of a multidisciplinary approach to important

clinical syndromes. Topics which will be covered during Clinical Phase 3 will be Infectious

Emergencies and Hospital Acquired Infection.

Local Teaching. The remaining objectives specified in the integrated guide for Medicine

and Surgery will be met by a combination of self-directed learning and a continuation of

the previous ‗Case of Infection‘. Three Cases will be delivered to students in each of the

four teaching centres during your attachment in Medicine. These sessions will be

problem-orientated and relatively informal in style. The content of the ‗Case of Infection‘

sessions may vary in different Trusts, and you will receive a timetable at the beginning of

each attachment. Please note that the limited time available for formal teaching does not

permit delivery of the entire curriculum and self-directed learning is essential. Workbook. Please note that this workbook is to be used both as self assessment and as a guide to self directed learning. The questions and answers highlight key subjects for further reading.

MICROBIOLOGY GENERAL OBJECTIVES

To identify and develop clinical skills necessary for the recognition and further

assessment of patients with important infectious diseases

To become familiar with the indications for common microbiological/ serological

investigations and their interpretation

To acquire a rationale for the use of antimicrobial therapy in clinical practice RECOMMENDED RESOURCES: Problem-orientated Clinical Microbiology and Infection 2nd Ed 2004 (Humphreys and

Irving) Medical Microbiology 16th Ed 2002 (Greenwood, Slack and Peutherer) Infection (Finch and Ball) Instant notes in Medical Microbiology 2005 (Irving, Ala‘Aldeen, Boswell) Antimicrobial Chemotherapy 2007 (Greenwood, Finch, Davey, Wilcox) 2007

www.survivingsepsis.org

http://www.survivingsepsis.org/

PATHOLOGY

OUTLINE OF TEACHING

Students entering the clinical part of the course have had a strong grounding in general

pathology, provided by teaching in years 1 and 2 as well as tutorial teaching and directed

reading from Clinical Phase 1.

The teaching programme aims to provide the necessary expertise and experience

required to practice as a pre-registration house officer. However, it should be seen as

part of the overall training required to become a post-registration medical practitioner

and as the start of continuing medical education which will be required to maintain high

standards during the whole of a professional career.

Teaching in pathology involves the gradual acquisition of factual information, practical

skills and attitudes such that the student will become familiar with the aetiology,

pathobiology and clinical course of diseases. In addition, the student has to be familiar

with the very wide range of clinical diseases in which Histopathology is used to establish

a diagnosis and determine clinical management. In Clinical Phase 1 the pathology of

common diseases was covered. In Clinical Phase 2 Histopathology learning was related

as part of clinical experience special subjects of child health, obstetrics & gynecology,

health care of the elderly, psychiatry, dermatology, and otorhinolaryngology. In Clinical

Phase 3 the emphasis will be to increasing the breadth of your knowledge of the

pathology of organ systems and apply this to differential diagnosis.

Clinicopathological co-operation in patient management is very important and the

student should participate in clinicopathological meetings and multidisciplinary team

meetings (MDTs) which are held as part of their firm-based activities. Such experience is

vital in developing communication skills.

Students have to gain experience in medico-legal aspects of medicine. Towards the end

of Clinical Phase 3, in the preparation for Foundation Course, students will become

conversant with the medico-legal aspects of death certification and the histopathologist‘s

and Coroner‘s role in the investigation of sudden and unnatural death, exclusive of

criminal cases.

TEACHING IN CLINICAL PHASE 3

Tutorials. Tutorials based on directed reading.

Post Mortem/Autopsy. All students should make efforts to attend autopsy

examinations on patients who have died if they have been in their care on admission

to hospital. Any medical student is welcome to attend autopsy sessions at any time

providing this is arranged with mortuary staff and the attending pathologist.

Normally this can be done at short notice by a telephone call to the mortuary office.

Post mortems generally take place between 9.00am and 1.30pm each day.

Firm-based clinico-pathological meetings and MDTs. These sessions should be

attended in the context of the working schedules which exist on different ward

attachments. Not all clinical attachments will feature such an activity.

PATHOLOGY GENERAL OBJECTIVES

To become familiar with natural history, macroscopic and histological features of

common medical and surgical conditions.

To become broadly familiar with the techniques involved in carrying out a full autopsy

and arriving at a clinico-pathological correlation

RECOMMENDED READING The recommended course textbooks are Pathology (Stevens & Lowe), 2nd Edition published in 2000 by Mosby and the new edition Core Pathology, A Stevens, J Lowe, I Scott 978-0723434443 (2009) with student consult online access. Please note, we recognise students will have purchased Pathology (Stevens & Lowe), 2nd Edition, the pages listed in the reading list below are taken from the 2000 publication. Students who have purchased Core Pathology (2009) with online access are reassured should refer to the relevant pages within this publication. We reassure students both publication have appropriate text for their BMedSci and BMBS studies. Copies of both publications are available in the library. TUTORIAL SESSION DETAILS

Directed reading and small group tutorials Each student will be allocated to a

pathology tutor (a list is provided by the teaching coordinator at each site). The time

of teaching sessions is planned in the context of the working schedules which exist on

different ward attachments and will be scheduled by the Teaching Coordinators in

each Trust. The main method of learning is directed reading which is supported by

tutorial-style teaching sessions. In preparation for each teaching session students

must undertake directed reading (see schedule of topics later). Tutorials are not

meant to be didactic teaching sessions but are meant to address problems which have

been encountered in the course of directed reading. The recommended course

textbook is Pathology (Stevens & Lowe), 2006 Edition, Mosby.

SESSION OBJECTIVES

IT IS IMPORTANT THAT YOU READ THE CHAPTERS LISTED AS PART OF YOUR

DIRECTED STUDY as some topics may initially seem large, but in reality the objectives

you need to meet are quite limited. The pathology-specific objectives have been

abstracted from the guide for use in the tutorials. Please note that several sessions

include an OBJECTIVES CHECK — this is all work you have covered before and is

designed for you to identify any small gaps in your knowledge so they can be discussed

and clarified in a tutorial, hence the large number of objectives to check. We have listed

7 recommended areas of reading for each Medicine/Surgery attachment. We appreciate

it may not be possible to deliver all as tutorial sessions so students are encouraged to be

proactive in their learning needs and to discuss the direction of tutorial content in

advance with their tutors to capture areas of concern.. Students should NOT need to be

doing all this work from scratch.

Tutorial topics and directed reading

Pathology Stevens &

Lowe, 2006 Edn.

Medical Tutorials

Session 1

OBJECTIVES CHECK: Revision. This session is designed for you

to check for gaps in your attainment of the following objectives —

there are a lot because this is all work you have covered in detail

in the past related to Atherosclerotic vascular disease,

Aneurysms, Ischaemic heart disease, and heart failure

Define atherosclerosis and list the risk factors for its

development.

Distinguish between macrovascular disease and microvascular

disease

List the specific sites where there is a predilection to develop

atheroma and explain why such predilections exist.

List the clinical sequelae of atheroma.

Describe the common sites and relative incidence of

atherosclerotic arterial aneurysms.

Define a mycotic aneurysm.

161-166,175-

180, 173-175

Describe the pathophysiology of a dissecting aneurysm,

complications and causes of death.

Describe the anatomy of the cardiac chambers, valves,

coronary arteries, the great arteries and the cardiac

conduction system.

Discuss the possible underlying causes of angina including

coronary artery disease, valvular heart disease,

cardiomyopathy and anaemia.

List recognised risk factors for coronary artery disease and

describe the pathology of the coronary arteries in patients

presenting with angina.

Describe the morphology and pathological consequences of

AMI.

Discuss the differential diagnosis of AMI.

Describe the complications and describe their presentation:

o immediate: arrhythmias particularly ventricular

tachycardia and fibrillation

o short term: pulmonary oedema, cardiogenic shock,

thromboembolism, VSD, ruptured chordae tendineae

o long term: heart failure, Dressler‘s syndrome

Understand the spectrum between stable angina, unstable

angina, non-Q wave infarction and Q-wave infarction.

Understand the difference in prognosis between AMI (high

early death rate, relatively good prognosis) and unstable

angina/acute coronary syndromes (patients with elevated CK

or troponin have a low early death rate but a high risk of

death or AMI in the next three months).

List the common causes of pulmonary oedema.

Describe the morphology and histological changes of the lungs

in pulmonary oedema.

Discuss the differential diagnosis of pulmonary oedema

including chest infection, pulmonary embolism and adult

respiratory distress syndrome.

Define heart failure and classify common causes.

List the common causes of CCF.

Describe the morphology and histological changes of the lungs

and liver in heart failure

Session 2

OBJECTIVES CHECK: This majority of this session is designed

for you to check for gaps in your attainment of the following

objectives — there are a lot because this is all work you have

covered in detail in the past related to Hypertension, Venous

thrombosis and pulmonary thromboembolism. New work is on

Vasculitis

Describe the clinical and pathological features of ‗accelerated

phase‘ or ‗malignant‘ hypertension.

Discuss the differential diagnosis of hypertension and the

causes of secondary hypertension including renal disease,

endocrine disease and coarctation of the aorta.

Describe the pathological consequences of hypertension as

they affect the cardiovascular, cerebrovascular and renal

152-159, 166-

169, 169-171

systems.

Identify the usual initial anatomic location of deep venous

thrombosis.

Describe the risk factors for venous thrombosis.

Describe the range of clinical presentation and associated

pathology of pulmonary embolic disease depending on clot

size and cardiopulmonary haemodynamics.

Outline the pathophysiology of vasculitis and discuss the

conditions associated with vasculitis including autoimmune

disease (SLE, polyarteritis, temporal arteritis), infection,

malignancy and haematological disease.

Session 3 Disease of heart valves

Classify the causes of valvular heart disease into congenital

(bicuspid aortic valve), rheumatic, ischaemic (mitral

regurgitation), and infective (endocarditis).

Define what bacterial endocarditis is

Describe the morphology and histological changes seen on an

affected heart valve in endocarditis.

Describe the pathological complications of infective

endocarditis including valve destruction with heart failure,

embolic disease and glomerulonephritis.

183-186

Session 4

OBJECTIVES CHECK: This session is designed for you to check

for gaps in your attainment of the following objectives — there

are a lot because this is all work you have covered in detail in the

past related to Infection, Bronchiectasis, Asthma, Chronic

obstructive airways disease. Carcinoma of the lung

Describe the pathology of acute lobar pneumonia and

bronchopneumonia.

Describe the complications of pneumonia including

septicaemia, lung abscess and empyema.


asthma.

Define the term chronic obstructive pulmonary disease

(COPD).

Describe the pathology underlying COPD and emphysema.

List recognised risk factors for the condition including

smoking, pollution and alpha-1 anti-trypsin deficiency.

Outline the morphology and pathological consequences of

bronchiectasis

List recognised risk factors for bronchiectasis including

inherited causes (Kartagener‘s syndrome, cystic fibrosis-see

separate section), post-infectious, and immunocompromised

patients.

Outline the major pathological classification of lung cancers

and their prognosis.

194-200, 200-

205, 212-217

+220

Session 5

Fibrosing alveolitis, allergic alveolitis, occupational lung disease

Describe the pathological features of fibrosing alveolitis

List common causes of allergic alveolitis such as Farmer‘ lung,

bird fancier‘s lung etc.

Outline the pathological consequences of repeated allergen

exposure in allergic alveolitis

Describe the main conditions associated with asbestos

inhalation (pleural plaques, mesothelioma, asbestosis and

lung cancer).

Describe the natural history of pleural plaques, mesothelioma

and asbestosis and outline the relation between these

conditions and the duration of exposure to asbestos.

Describe the pathology of simple and complicated coalworkers

pneumoconiosis.

208-210

Session 6

OBJECTIVES CHECK: This majority of this session is designed

for you to check for gaps in your attainment of the following

objectives - there are a lot because this is all work you have

covered in detail in the past related to Cerebrovascular disease

Define what a stroke is and outline the three major causes:

thrombotic, embolic and haemorrhagic.

Outline the major factors that predispose to stroke disease

including age, hypertension, cardiac disease and diabetes.


haemorrhagic and ischaemic stroke.

Describe the pathology of subarachnoid haemorrhage and the

predisposing factors including congenital berry aneurysms

(80%), A-V malformations and other non-aneurysmal causes.

436-441

Session 7

Nervous system: multiple sclerosis, peripheral nerve disease.

Tumours of peripheral nerves. Meningitis/ Encephalitis. Dementia

List the common sites of CNS involvement in multiple sclerosis

Describe the nature of demyelination and axonal loss in the

lesions of multiple sclerosis.

Outline the causes of neuropathy such as diabetes, post-

infectious demyelinating, vasculitis, drugs etc.

Describe common tumours of peripheral nerve


leptomeningitis

Discuss the aetiology of common types of viral encephalitis

Classify causes of dementia into pre-senile and senile causes

450-451, 464-

467, 446-450,

451-455

Surgical Tutorials

Session 1

OBJECTIVES CHECK: This session is designed for you to check

for gaps in your attainment of the following objectives — there

are a lot because this is mostly work you have covered in detail in

the past on Oesophagitis, Peptic ulceration, Inflammatory bowel

disease, Carcinoma of stomach, oesophagus, small bowel, colon

and rectum.


oesophagitis

List the two main causes of peptic ulcer disease.

List three rarer causes of peptic ulcer disease.

List the complications of peptic ulcer disease


Crohn‘s disease and ulcerative colitis.

Describe the pathology and natural history of a malignant

lesion of the oesophagus

Describe the classification of gastric neoplasms and discuss

their morphology and natural history.

Discuss the relative frequency of the most common small

bowel neoplasms and compare these frequencies with those of

large bowel neoplasms

Describe the aetiology, morphology, staging and pathological

consequences of carcinoma of the colon. Using Dukes

classification discuss the staging and five year survival of

carcinoma of the colon and rectum. Be able to discuss the

TNM system of staging cancer in respect of cancer of the

colon.

250-252, 257-

259, 252-254,

248-250, 259-

264

Session 2

This session is designed for you to check for gaps in your

attainment of the following objectives - there are a lot because

this is mostly work you have covered in detail in the past on

Pathology of hepatitis and cirrhosis. Complications of cirrhosis.

Portal hypertension. Tumours of the liver


acute and chronic hepatitis

Define cirrhosis in pathological terms.


cirrhosis.

List the causes of cirrhosis including alcohol, post-hepatitis

B/C infection, immunological, drugs and metabolic diseases

(Wilson‘s disease and haemochromatosis).

Outline the pathophysiology underlying the clinical features of

cirrhosis including hypoproteinaemia, abnormal clotting,

secondary hyperaldosteronism and portal hypertension.

Discuss the complications of cirrhosis and portal hypertension

including oesophageal varices, ascites and encephalopathy

and outline their management.

Define portal hypertension and classify its aetiology.

281-290, 293-

295, 295-296,

280-181

List the complications of portal hypertension.

Describe the aetiology and pathology of primary and

secondary liver neoplasms.

Session 3

Diverticular disease. Diseases associated with malabsorption,

Pancreatitis and carcinoma of pancreas

Outline the common causes of malabsorption in the UK

including coeliac disease, stagnant loops, pancreatic disease

and terminal ileal disease


coeliac disease

Classify pancreatitis on the basis of the severity of injury to

the organ.

Describe the aetiology and pathology of pancreatitis.

Discuss the potential early complications of acute pancreatitis.

List the pancreatic neoplasms; describe the pathology of each

with reference to cell type and function.

On the basis of pathology and cell type discuss the long-term

prognosis of pancreatic cancers.

265-266, 264-

265, 255-256,

300-303

Session 4

Lymphomas. Carcinoma of the breast.

Classify lymphomas into Hodgkin‘s disease and Non-Hodgkin‘s

type and to high and low grade

Outline the natural history of benign and malignant breast

neoplasms.

Describe the aetiology, morphology and pathological

consequences of carcinoma of the breast.

List the risk factors for carcinoma of the breast.

Describe the diagnosis of a breast lump, including cytology,

mammography and biopsy (trucut and open).

307-316 (NOTE

limited lymphoma

objectives despite

depth of reading)

424-430

Session 5

Carcinoma of the bladder. Carcinoma of the kidney, Obstruction

of urinary tract. Hydronephrosis. Testicular tumours, prostatic

carcinoma

Describe the causes of hydronephrosis and obstruction to the

pelviureteric junction.

Describe the natural history of renal cell carcinoma, Wilm‘s

tumour and transitional cell carcinoma.

Discuss the pathology of carcinoma of the prostate

Discuss the natural history of malignant tumours of seminoma

and teratoma of the testis.

374-376, 378-

380, 377-378,

386-390, 392

Session 6

This session is designed for you to check for gaps in your

attainment of the following objectives - there are a lot because

this is all work you have covered in detail in the past related to

Acute renal failure. Chronic renal failure. Nephrotic syndrome,

acute tubular necrosis. Hypertension and the kidney. Diabetes

and the kidney. Pyelonephritis.

Classify renal failure into pre-renal, renal and post-renal

causes and discuss common diseases that may cause each

type.

Pre-renal Hypovolaemic, cardiogenic and septicaemic shock;

renal artery stenosis

Renal Glomerulonephritis, chronic pyelonephritis, interstitial

nephritis, diabetic nephropathy, hypertension, vasculitis.

Post-renal Benign prostatic hyperplasia, prostate carcinoma,

renal stone disease, retroperitoneal fibrosis

List the common causes of chronic renal failure including

diabetes, glomerulonephritis, hypertension, chronic interstitial

nephritis, macrovascular disease, polycystic kidney disease,

and obstructive uropathy.


pyelonephritis, interstitial nephritis, polycystic kidney disease,

hypertensive renal damage to the kidney and obstructive

uropathy.

Discuss the effect of chronic renal failure on blood (anaemia of

chronic disease) and bone (renal bone disease)

Define the nephrotic syndrome. List the three main primary

renal causes; minimal change nephropathy, membranous

glomerulonephritis and proliferative glomerulonephritis and

outline briefly the key pathological features. List secondary

causes such as diabetes, amyloid disease etc.

Describe the pathological features and complications of acute

and chronic pyelonephritis.

350-353, 353-

356, 371-373,

368-371

Session 7

Glomerular diseases

Outline the main pathological processes affecting the

glomerulus including primary disease and those relating to

systemic disease particularly the vasculitic illnesses.

356-359 (Note

limited objectives -

you do not need to

know the details

about glomerulo-

nephritis - just

broad concepts)

WORKBOOK QUESTIONS

Clinical Chemistry ………………………………………………….. Page 15

Haematology ………………………………………………….. Page 19

Immunology ………………………………………………….. Page 21

Microbiology ………………………………………………….. Page 23

Answers can be found on the NLE:

Clinical Phase 3 (A14ACE)/learning materials

CLINICAL CHEMISTRY

1. An unconscious 45 year old man with a two day history of a febrile illness.

Temperature 39˚.

Plasma Sodium 165 mmol/L (135 to 145) Potassium 3.5 mmol/L (3.5 to 5.3) Urea 18.4 mmol/L (2.0 to 6.5) Creatinine 134 umol/L (60 to 120)

Why are the plasma sodium and urea high?

2. A 54 year old man with bronchial carcinoma

Plasma Sodium 125 mmol/L (135 to 145) Potassium 3.5 mmol/L (3.5 to 5.3) Urea 2.4 mmol/L (2.0 to 6.5) Creatinine 104 umol/L (60 to 120)

(a) What is the likely cause of hyponatraemia in this patient?

(b) Will the plasma osmolality be high, normal or low?

(c) Will the urinary osmolality be high or low relative to the plasma osmolality?

3. A 67 year old woman with congestive cardiac failure treated with frusemide.

Plasma Sodium 135 mmol/L (135 to 145) Potassium 2.6 mmol/L (3.5 to 5.3) Urea 13 mmol/L (2.0 to 6.5) Creatinine 110 umol/L (50 to 110)

(a) Why is the patient hypokalaemic?

(b) Why is the plasma urea high?

(c) Will the answer to part (b) affect renal potassium handling? 4. A 20 year old woman with psychogenic vomiting. Clinically dehydrated.


(a) What acid-base derangement is likely to be present?

(b) Why is the patient hypokalaemic? 5. A 16 year old boy with a two month history of weight loss. Impaired consciousness

on admission; respiratory rate 40 per minute.

Plasma Sodium 137 mmol/L (135 to 145) Potassium 6.2 mmol/L (3.5 to 5.3) Glucose 37 mmol/L Ketones Positive

Arterial pH 7.09 (7.35 to 7.45) Blood PC02 2.7 kPa (4.7 to 6.5) PO2 15kPa (10.6to 13.3) HC03 6 mmol/L (19 to 24)

(a) What type of acid-base disturbance is this?

(b) What is the cause?

(c) Why is the plasma potassium high?

(d) Is the total body potassium likely to be high, normal or low? 6. A 58 year old ex-miner with chronic obstructive airways disease.

Arterial pH 7.36 (7.35 to 7.45) Blood PC02 8.4 kPa (4.7 to 6.5) PO2 8.0kPa (10.6to 13.3) HC03 35 mmol/L (19 to 24)

What type of acid-base disturbance is this?

7. A 55 year old woman with a two week history of progressive jaundice.

Plasma GGT 269 U/L (up to 70) ALP 1079 U/L (40 to 120) ALT 63 U/L (up to 50) Bilirubin 310 umol/L (up to 17)

(a) Do these results suggest predominantly haemolytic, hepatocellular or

cholestatic jaundice?

(b) Will Bilirubin be detectable in the urine? 8. A 12 year old boy with a two day history of nausea, anorexia and vomiting


(a) Do these results suggest predominantly haemolytic, hepatocellular or

cholestatic jaundice?

(b) What is the likely diagnosis?

(c) Will Bilirubin be detectable in the urine? 9. A fit 29 year old man attending a medical examination for life insurance purposes.


(a) What is the most likely cause of the hyperbilirubinaemia?

(b) Is Bilirubin detectable in the urine in this condition?

10. A 61 year old woman presented with a three month history of increasing weakness

and weight loss over the last three weeks. On examination she was wasted, deeply pigmented, and had a blood pressure of 80/40 when lying down.


(a) What diagnosis do these results suggest?

(b) What further test would you perform to support this diagnosis? 11. A 52 year old woman complaining of tiredness.

Plasma Free thyroxine 8 pmol/L (12 to 24) TSH 45 mU/L (0.1 to 4.5)

What is the diagnosis?

12. A 65 year old woman with atrial fibrillation.

Plasma Free thyroxine 38 pmol/L (12 to 24) TSH < 0.1 mU/L (0.1 to 4.5)

What is the diagnosis?

13. A 49 year old woman with recurrent renal calculi over the last 5 years.

Plasma Calcium 2.92 mmol/L (2.2 to 2.6) Phosphate 0.5 mmol/L (0.7 to 1.4) Albumin 40 g/L (30 to 52) ALP 100 U/L (40 to 120)

(a) What are the two commonest causes of hypercalcaemia?

(b) Which is more likely in this case?

(c) What further chemistry test would you request to confirm the diagnosis? 14. A 53 year old man on AICU following abdominal surgery

Plasma Calcium 2.04 mmol/L (2.2 to 2.6) Phosphate 0.7 mmol/L (0.7 to 1.4) Albumin 25 g/L (30 to 52) ALP 116 U/L (40 to 120)

Why is the plasma calcium concentration low?

15. A 41 year old man brought to A&E with sudden onset of chest pain.

On admission After 24 hours CK 172 U/L 863 U/L (up to 200) Troponin I <0.1 ug/L 17 mg/L (up to 0.1)

What is the most likely diagnosis?

HAEMATOLOGY

1. A 23yr old Asian woman presents with a history of menorrhagia and the

following results:

Hb 7.2g/dL MCV66fL WBC 6 x 109/L Platelets 570 x 109/L Ferritin 3mcg/L Haemoglobin electrophoresis normal HbA2 <1%

(a) What is the likely diagnosis ?

(b) What is the significance of the normal HbA2 ?

2. A 65yr old alcoholic presents with the following results:

Hb 8.9g/dL MCV110fL WBC 2.6 x 109/L Platelets 46 x 109/L Serum B12 1000ng/ml (NR 200-800) Red Cell Folate 60 mcg/L (NR 130-400)

(a) What is the likely cause of the anaemia ?

(b) What are the possible explanations for the whole blood picture ?

3. A 60yr old woman presents with a 1 week history of worsening angina and at

admission had the following results recorded:

Hb 5.1g/dL MCV113fL WBC 8 x 109/L Platelets 260 x 109/L Reticulocytes 12% (NR < 2%) Blood film Spherocytes, Polychromasia and leucoerythoblastic changes Bilirubin 90uM/L Other LFT‘s Normal LDH 1200iu/L (NR <450) Direct Coomb‘s Test Positive at 37oC

(a) What is the diagnosis ?

(b) Which other investigations would you perform ?

(c) What aspect of the history is important ?

4. A 72yr old man warfarinised with a histrory of atrial fibrillation and previous

CVA presents to A+E unconscious with a history of haematuria. Initial

investigations show:

Hb 17 g/dL WBC 12 x 109/L Platelets 340 x 109/L INR 12 APTT 45/31 sec Alkaline Phosphatase 1200iu/L (NR up to 200) Gamma GT 264iu/L (NR up to 50)


(b) How would you manage this ?

5. A 82yr old woman presents with confusion and a mass in the left breast. Her

results are as follows:

Hb 9.0g/dL MCV87fL WBC12 x 109/L Platelets 62 x 109/L Blood film Leucoerythroblastic features Corrected calcium 3.1mM Alkaline Phosphatase 900 iu/L (NR up to 200)

(a) What are the causes of a leucoerythroblastic blood film ?

(b) What is the most likely diagnosis in her and how would you confirm it?

6. A 65yr old man presents with a Streptococcal pneumoniae lobar pneumonia

and associated shingles. His admission bloods show:

Hb 9.7g/dL WBC 36 x 109/L (Neutrophils 2 x 109 Lymphocytes 31 x 109) Blood film Smear cells present


(b) What might you expect to find on examination ?

(c) How would you confirm the diagnosis ?

(d) Why do these patients experience excess infection ?

7. A 28yr old presents with severe abdominal and left shoulder tip pain. The

admission bloods show:

Hb 10.7g/dL WBC 97 x 109/L Platelets 1200 x 109/L Blood film Neutrophilia, Myelocytes, Metamyelocytes

and Myeloblasts present. Basophilia Giant platelets Uric acid Very raised

Examination reveals massive splenomegaly.


(b) How would you confirm this ?

(c) What is the prognosis for this patient ?

8. A 32yr old Sculptor presents with a history of gum bleeding and bruising. His

results show:

Hb 7.2g/dL WBC 1.2 x 109/L (Neutrophils 0.2 Lymphocytes 0.9) Platelets 20 x 109/L Reticulocytes <0.1% (NR <1%)

(a) What are the possible diagnoses ?

(b) How would you prove the diagnosis in this case ?

(c) Which aetiological factors are relevant ?

IMMUNOLOGY

Case histories with immunological data are given, covering topics of the core curriculum. Students are advised to read the relevant topics as detailed in the recommended reading list before attempting the data interpretation exercises. Answers are provided.

1. A 23yr old Asian woman presents with a history of menorrhagia and the following

results:

C reactive protein 167 mg/l (normal range <10mg/l)

(a) Give three possible causes of this high CRP

2. A 19 year old student collapses while eating a picnic in the park. She is wheezing,

hypotensive and is covered in an erythematous itchy rash.

(a) What is the diagnosis? (b) What is the immediate management? (c) How could you identify the cause of this attack?

3. A 33 year old woman complains of feeling tired all the time. For each of the

results given below, suggest the most likely diagnosis and the tests you would

request to confirm this.

(a) Thyroid microsomal antibodies positive (b) IgA endomysial antibodies positive (c) Gastric parietal cell antibodies positive

4. A 24 year old woman complains of a facial rash, raynaud‘s, joint pains and feeling

unwell for the past 3 months. Urinalysis reveals blood and protein.

Anti-nuclear antibody strongly positive Rheumatoid factor weakly positive Mid Stream Urine no growth Urea & creatinine normal

(a) What is the most likely diagnosis? (b) List another cause of a positive ANA and another cause of a positive

rheumatoid factor. (c) Is this patient likely to require urgent treatment?

5. A 75 year old man complains of back pain. What tests would you request to

exclude myeloma?

6. A 75 year old man complains of back pain.

(normal range) Serum: IgG paraprotein (6.0 - 15.0 g/l) IgA 0.1 g/l (0.7 - 3.9 g/l) IgM 0.1 g/l (0.4 - 2.7 g/l) Serum IgG kappa paraprotein detected (47g/l) Urine:Free monoclonal kappa light chains detected

(a) What is the most likely cause of his paraprotein? (b) Why? (c) How could you confirm this?

7. A 75 year old man complains of back pain.

(normal range) Serum: IgG paraprotein (6.0 - 15.0 g/l) IgA 2.9 g/l (0.7 - 3.9 g/l) IgM 1.8 g/l (0.4 - 2.7 g/l) Serum IgG kappa paraprotein detected (1.7g/l) Urine: No monoclonal light chains detected

(a) What is the most likely cause of his paraprotein? (b) Why? (c) How would you follow up this result?

8. A child presents with recurrent infections and failure to thrive. A sweat test was

normal. He is scheduled to have some routine immunisations today.

(a) What diagnosis should be considered? (b) How could you confirm / exclude this? (c) Should the child be immunised?

MICROBIOLOGY

1. An 82 year old man is admitted to hospital following an acute stroke. He develops

urinary retention and a urinary catheter is inserted. Five days later he develops

rigors and is found to have a fever of 380C and an elevated white cell count.

a) what is the likely diagnosis

b) what microbiology investigations would you perform

c) what treatment would you give

2. A 30 year old solicitor is sent to Hong Kong for a six month period. Two weeks

after his return he develops anorexia, malaise and nausea and his friends tell him

that he has become yellow. He himself has noted that his urine has been very

dark for a few days. He has never injected drugs and has no past medical history

of note.

a) what is your differential diagnosis

b) what microbiology tests could you do to confirm the diagnosis

c) what further action should be taken

3. A 52 year old nurse performs venepuncture on a known intravenous drug user. On

attempting to resheath the needle, she sustains a needlestick injury to her finger.

She has been vaccinated against HBV.

a) what actions should be taken

4. A 36 year old poultry farmer‘s wife presents to her general practitioner with a 4

day history of fever, headache and shivering. The day before admission she

developed severe muscle aches, a non-productive cough, and became short of

breath. There is no past medical history of note.

a) what is the probable diagnosis

b) how would you confirm this diagnosis

c) are there any features of possible concern in this case

5. A 52 year old hospital administrator is admitted to hospital with a 2 day history of

high fever and confusion. He has recently returned from a trip to South Africa, and

had been advised that no anti-malarial prophylaxis was necessary. During his

vacation, he made a day trip to the Victoria Falls in Zimbabwe.

a) what diagnosis should you consider

b) what tests would confirm this diagnosis

c) what treatment would you give

d) was he given the correct advice on malarial prophylaxis

6. A 55 year old man is admitted to hospital with increasing breathlessness and

confusion. His respiratory rate is 35/min. Five days prior to admission he

developed a severe but nonproductive cough. CXR shows multi-lobe disease.

a) what microbiology tests must be performed

b) what treatment should be given

c) are there any other factors to consider in this case

7. An 18 year old medical student is admitted to hospital with a short history of

fever, neck stiffness and photophobia. On examination she is found to have a

widespread purpuric rash.

a) What treatment should immediately be given to the patient

b) What other essential steps must you take

8. A 15 year old boy falls when mountain biking and grazes his knees. 4 days later

the graze on the left knee has become erythematous and tender. There is a full

range of movement at the knee joint.

a) what is the diagnosis

b) what is the likely pathogen

c) what complications may follow this infection

9. A 27 year old woman is admitted to hospital with a short history of confusion.

Blood pressure found to be 68/40 with a heart rate of 120. Temperature is

elevated at 39.50C and WBC decreased at 1.5 x 109/l.


b) how would you manage this condition

c) are there any particular causes of this condition you would

consider in a young woman

10. A 21 year old Pakistani taxi driver is admitted to hospital with a 4 week history of

night sweats, fever and weight loss. He visited relatives in Pakistan 6 months

before becoming unwell. Temperature is 400C but blood pressure and respiratory

rate are normal and physical examination reveals no abnormality.

what features of the presenting history are important in

assessing the probable diagnosis

a) what microbiology investigations are likely to be helpful

b) what treatment would you give

11. A 72 year old woman develops watery diarrhea and vomiting 5 days after

admission to a general medical ward.

a) what infection control measures should be put in place

b) what would you do if 3 more patients developed the same symptoms

12. A 62 year old man is admitted with history of chest pain and a diagnosis of

unstable angina is made. A venflon is inserted in the right antecubital fossa.

Shortly before discharge the patient develops a fever. The venflon has not been

removed and the site is now erythematous with evidence of lymphangitis.


b) what organisms may cause this infection

c) how would you manage this case

CLINICAL CHEMISTRY WORKBOOK ANSWERS

1 Dehydration, causing haemoconcentration and impaired renal blood flow (pre-renal uraemia).

2 (a) Syndrome of inappropriate antidiuresis (SIADH)

(b) The plasma osmolality will be low

(c) The urine osmolality is inappropriately high in SIADH - although not always higher than the plasma osmolality.

3 (a) Frusemide causes distal renal tubular potassium loss

(b) Poor renal perfusion due to diminished plasma volume and cardiac failure (pre-renal uraemia)

(c) Poor renal perfusion stimulates the rennin-angiotensin-aldosterone system, increasing sodium reabsorption and potassium excretion by the distal tubules

4 (a) Metabolic alkalosis due to loss of gastric acid

(b) Loss of potassium in vomitus; cellular uptake of potassium due to metabolic alkalosis; renal loss of potassium due to hyperaldosteronism secondary to dehydration.

5 (a) Metabolic acidosis

(b) Diabetic ketoacidosis

(c) Intracellular potassium is redistributed into the extracellular compartment in metabolic acidosis.

(d) The patient is likely to be potassium depleted, in spite of the hyperkalaemia.

6 A well compensated chronic respiratory acidosis.

7 (a) Cholestatic jaundice

(b) Yes; bilirubin is in the conjugated, water soluble form in simple cholestatic jaundice

8 (a) Hepatocellular jaundice.

(b) Infectious hepatitis

(c) Yes; there is nearly always an element of impaired bilirubin excretion in hepatitis.

9 (a) Gilbert's syndrome

(b) No; Gilbert's syndrome is associated with unconjugated hyperbilirubinaemia

10 (a) Adrenal insufficiency, most likely to be due to Addison's disease.

(b) A Synacthen test.

11 Hypothyroidism

12 Thyrotoxicosis

13 (a) Hyperparathyroidism; hypercalcaemia of malignancy.

(b) Hyperparathyroidism (long time course of symptoms makes malignancy unlikely)

(c) Serum parathyroid hormone concentration (high in hyperparathyroidism; suppressed in hypercalcaemia of malignancy).

14 Hypoalbuminaemia causes a low total plasma calcium concentration, but does not affect the concentration of the biologically active ionised calcium. Many laboratories now report a ―corrected calcium‖ result, which adjusts for albumin concentration.

15 Myocardial infarction. Note that cardiac enzyme levels may be within reference limits for several hours post-infarct.

HAEMATOLOGY WORKBOOK ANSWERS

1 (a) Iron deficiency

(b) It excludes a diagnosis of beta thalassemia trait in which this would be raised

2 (a) Folate deficiency

(b) Pancytopenia due to – folate deficiency, ethanol or hypersplenism with portal hypertension

3 (a) Haemolytic anaemia

(b) Haptoglobins, Urinary haemosiderin and Autoantibody Screen

(c) Excluding an underlying cause: drugs, malignancy, connective tissue disease

4 (a) Cerebral haemorrhage due to overanticoagulation

(b) Immediate injection of 5mg vitamin K IV and prothrombin complex concentrate (25-50 ml/kg depending on INR). Infusion of fresh frozen plasma 15 ml/kg if no prothrombin complex concentrate available.

5 (a) Myelofibiosis disease, marrow infiltration

(b) Metastatic breast cancer; bone marrow biopsy

6 (a) Chronic lymphatic leukaemia

(b) Lymphadenopathy and hepatosplenomegaly

(c) Immunophenotyping of peripheral blood lymphocytes

(d) 60% have low immunoglobulin levels

7 (a) Chronic myeloid leukaemia

(b) Bone marrow examination and cytogenetics to show the Philadelphia chromosome. Molecular studies (RT PCR) show the presence of the bcr-abl fusion gene.

(c) A median survival of 4yrs but a >70% chance of cure by allogeneic Bone marrow transplantation. Give (imatinib) therapy for patients without a donor

8 (a) Aplastic anaemia, acute leukaemia or myelodysplasia

(b) Bone marrow examination to include a trephine biopsy

(c) As a sculptor he may have been exposed to chemicals

IMMUNOLOGY WORKBOOK ANSWERS

1 (a) Bacterial chest infection, pulmonary embolism, myocardial infarction (other possible but less likely causes include bronchial carcinoma, systemic vasculitis) CRP is an acute phase protein - it rises in response to tissue damage or inflammation.

2 (a) Anaphylaxis

(b) Drugs - intramuscular adrenaline is the most important; also anti-histamines and steroids. Supportive measures — oxygen and other measures such as intravenous fluids if necessary.

(c) The history is the most important - look for a precipitant eg ingestion of nuts, drugs, bee or wasp sting in the hour prior to the onset of symptoms. Testing serum for specific IgE to named allergens or skin testing (in a controlled setting) can help confirm your clinical suspicions.

3 (a) Autoimmune thyroid disease. Request thyroid function tests.

(b) Coeliac disease. Request tests to look for other evidence of malabsorption. Refer for small bowel biopsy (the definitive test)

(c) Pernicious anaemia. Full blood count, B12 levels, intrinsic factor antibody

4 (a) Systemic lupus erythematosus is most likely (however other diagnoses eg infection, other connective tissue diseases would have to be considered.)

(b) ANAs are found in other connective tissue diseases, autoimmune disease (eg autoimmune hepatitis, thyroid disease) and may also be found in some normal individuals (usually low titre), sometimes following infection. Positive rheumatoid factors are found in a proportion of patients with rheumatoid arthritis but are also found in other connective tissue disease and in some normal individuals (usually low titre), sometimes following infection.

(c) The presence of blood and protein in urine suggests renal involvement - this is an indication for early referral for treatment.

5 Serum and urine electrophoresis to look for a paraprotein. It is necessary to send urine as well as serum since 15-20% of myelomas secrete light chains only, and these may be detectable in urine but not serum.

6 (a) Multiple myeloma

(b) The paraprotein is present in high concentration, there is background immunoparesis ( ie the non-paraprotein immunoglobulins are suppressed) and there are free monoclonal light chains in the urine - these features all suggest that the paraprotein is associated with a malignant lymphoproliferative disease.

(c) A skeletal survey and/or bone marrow examination

7 (a) Monoclonal Gammopathy of Uncertain Significance (MGUS)

(b) The paraprotein is present in low concentration, there is no background immunoparesis and there are no free monoclonal light chains in the urine.

(c) Review the patient for symptoms / signs of myeloma or other lymphoproliferative disease. If there are none, arrange follow up monitoring of the paraprotein as a proportion of patients will develop myeloma in the future.

8 (a) Immune deficiency is suggested by the recurrent infections and failure to thrive

(b) Investigation of possible immune deficiency is a specialist area - discuss with a senior colleague / immunologist.

(c) Do not give any live vaccines (eg oral polio, BCG, MMR) until immune deficiency is excluded. As a general rule live vaccines should not be given to any patient who is immunocompromised in any way eg by high dose steroids etc. Helpful advice may be found in the British National Formulary or the HMSO book ―Immunisation against Infectious Disease‖.

MICROBIOLOGY WORKBOOK ANSWERS

1 a) The patient is catheterized and the likely diagnosis is infection arising from the urinary tract. Other common sources of sepsis in hospital such as lower respiratory tract infection and infection of intravenous line sites should also be considered.

b) The patient should have urine cultures and two sets of blood cultures performed before giving empirical antibiotic therapy.

c) Urosepsis is usually caused by Gram negative bacilli and recommended therapy is iv cefuroxime or oral ciprofloxacin. An additional single dose of gentamicin should be given if the patient is in septic shock. Note that multi-resistant Gram negative bacilli are increasing in frequency.

2 a) The combination of a short, non-specific prodromal illness, jaundice and

recent foreign travel suggest acute infectious hepatitis. b) The most important causes of infectious hepatitis acquired in the UK are

hepatitis viruses A–C. Other candidate agents include Epstein-Barr virus, cytomegalovirus, the ‗atypical‘ respiratory pathogens and leptospira. Hepatitis acquired abroad can be caused by a wide range of additional pathogens and cases should be discussed with Microbiology or Infectious Diseases. The microbiology request form must contain brief but clear details of the clinical presentation and travel history. Routine tests for acute hepatitis A-C are based on the detection of :

IgM antibody to hepatitis A virus (IgM antibody distinguishes acute infection from previous disease or response to vaccination).

Hepatitis B virus surface antigen (HBsAg) and HBV DNA levels. RT-PCR for the detection of the hepatitis C virus RNA genome

c) The patient was HBsAg positive with high levels of circulating HBV DNA (2x109 virions per ml). These findings are consistent with acute HBV infection. The patient admitted to multiple (female) sexual partners in Hong Kong, which has a high prevalence of chronic HBV infection. He has had a number of sexual partners since his return. It is therefore imperative to trace those partners and consider both active and passive immunization for HBV.

3 a) The nurse is at risk of blood borne virus infection, including HIV. She should

wash the wound copiously with fresh water and thereafter follow Trust procedures for Post Exposure Prophylaxis (PEP) for HIV. These differ in detail at different sites but have in common: immediate assessment of the event by a responsible consultant with a decision on whether or not to offer PEP; counseling of the staff member and taking base line bloods for HIV and HCV; initiation of PEP if appropriate, ideally within one hour of the incident; follow up with Infectious Disease or Genitourinary Medicine. The donor patient should be tested for BBV infection if possible and the results used to inform further management.

4 a) This presentation is typical of influenza. Severe non-productive cough and

breathlessness may suggest the onset of viral pneumonia. b) Confirmatory tests are not performed for uncomplicated influenza in a

previously healthy adult. In more severe cases or in high risk patients, a nasopharyngeal aspirate and throat swab should be sent to the laboratory (in viral transport media) together with an acute serum sample. Viral pneumonia is a severe disease and is often complicated by bacterial super-infection. Current NICE guidelines focus on the use of neuraminidase (NA) inhibitors, zanamivir and oseltamivir, in high-risk patients within 48 hours of the onset of symptoms (NICE Technology Appraisal no 58). It would, however, be appropriate to treat this patient with a NA inhibitor and broad spectrum antibiotic.

c) This patient lives on a poultry farm and may therefore have come into contact with avian flu. Should there be any reports of avian flu in the locality, the case should be immediately discussed with the on-call

Infectious Disease or Microbiology service, who will advise on infection control procedures.

5 a) Malaria is the most important cause of fever in a returning traveler from a

malaria endemic region. b) The diagnosis is confirmed by examination of three thick and thin blood

films. Thick films increase the volume of blood screened and examination of thin films permits identification of the organism. An ELISA-based serological test for plasmodium antigens is also available.

c) Patients with suspected malaria should be initially treated for chloroquine resistant falciparum malaria (caused by Plasmodium falciparum) unless they have returned from a region known to be free of this pathogen. Treatment for falciparum malaria is with oral or intravenous quinine sulphate followed by either oral doxycycline or clindamycin. Other effective treatments for acute malaria are also available.

d) No. Much of South Africa is malaria free. The patient, however, planned a short visit to a location where P. falciparum is endemic and should have been advised against doing so without taking anti-malarial prophylaxis. Up to date information can be found in the British National Formulary or at www.who.int/ith

6 a) In any case of severe community acquired pneumonia two sets of blood

cultures should be taken prior to treatment and a urinary antigen test for Legionella should be requested.

b) This patient meets the CURB 65 criteria for severe community acquired pneumonia and should treated with iv cefuroxime and clarythromycin or iv benzyl penicillin and oral levofloxacin. The long prodrome and the presence of multi-lobe involvement on CXR are consistent with Legionnaire‘s Disease. In these circumstances, rifampicin should be added to empirical antibiotic regimens. Treatment of proven infection with Legionella pneumophila should be discussed with Microbiology.

c) Legionella spp. can cause sporadic and outbreak patterns of infection. Although not a notifiable disease, it is important to inform Public Health of a suspected case.

7 a) The diagnosis is meningococcal meningitis. Two sets of blood cultures and a

sample for meningococcal PCR should be taken and iv ceftriaxone started without delay at a dose of 2g bd. The patient should be considered for adjunctive therapy with dexamethasone (although the benefits in meningococcal disease are unproven).

b) All cases of meningococcal disease must be notified to Public Health. Close contacts must be given chemoprophylaxis with either rifampicin or ciprofloxacin (adults only). Public Health will consider the indications for a vaccination programme.

8 a) The diagnosis is soft tissue infection, or cellulites

b) The likely infecting organisms are Streptococcus pyogenes (Lancefield Group A β-haemolytic streptococcus) or Staphylococcus aureus. Oral flucloxacillin is used to treat mild disease and high dose iv flucloxacillin to treat severe infection.

c) Group A streptococcus infection can be complicated by either rheumatic fever or post-streptococcal glomerulonephritis

9 a) This patient has septic shock. Septic shock is defined as severe sepsis with

refractory hypotension and organ failure. b) This patient requires antibiotic therapy to cover likely organisms, together

with circulatory support and ventilatory support if necessary. Careful clinical exam and imaging to identify possible sources of sepsis are essential and blood, urine and other relevant biological samples must be sent for culture. If MRSA infection is unlikely but the site of infection remains unclear, broad spectrum therapy such as iv cefuroxime and gentamicin should be given.

http://www.who.int/ith

The patient should be considered for adjuvant therapy with activated protein C.

c) Severe sepsis in a previously well young woman is rare. This patient had toxic shock syndrome. Mortality for septic shock remains almost 50%. This patient died.

10 a) The patient has a long and non-specific prodromal illness. He is of Pakistani

origin and has recently visited Pakistan. These features strongly suggest a diagnosis of tuberculosis.

b) It is important to obtain a tissue confirmation of the diagnosis of tuberculosis and to determine the sensitivity of the organism. Sputum is the most easily accessible material. In patients who have a pulmonary syndrome but do not produce sputum, further investigation using bronchial lavage and trans-bronchial biopsy should be considered. In patients who present with an extra-pulmonary syndrome, such as TB meningitis, investigation is directed at the site most likely to be informative.

c) There are no features in this case to suggest drug resistance and treatment should be commenced according to British Thoracic Society guidelines with four drugs for the two month initial phase (rifampicin, isoniazid, pyrazinamide and ethambutol) followed by two drugs (rifampicin and isoniazid) for the four months continuation phase.

11 a) The patient should immediately be given their own toilet and nursed with

full enteric precautions, ideally in a side room. Infection Control should be contacted. The patient should be assessed for risk factors for the development of diarrhea, including a recent antibiotic history, and stool samples (x 3) should be sent for MC&S and testing for C. difficile toxin.

b) Three further cases suggest a highly infectious cause of the diarrhea and vomiting. All cases should be nursed as a cohort in one bay. Stool samples should be examined by ELISA for the presence of enteric viruses. If more patients, or members of staff, develop symptoms the ward should be considered for closure.

12 a) The diagnosis is cellulitis arising from an infected venflon site

b) Staphylococcus aureus is the likely pathogen and more than 40% of S. Aureus acquired in hospital are methicillin resistant (MRSA).

c) It is wise to treat this patient as if infected with MRSA until investigations prove otherwise. He should ideally be nursed in a side room. The venflon should be removed and the line site cultured. Blood cultures and swabs of the anterior nares and perineum should be performed. Cellulitis should be treated following discussion with Microbiology (MRSA currently circulating in Nottingham are sensitive to vancomycin and gentamicin). The patient should be considered for a 5 day course of Aquasept body wash and mupirocin nasal cream if swabs for MRSA are positive.

Clinical Phase 3 Cls Handbook 2011 12

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