Pathology Interviews

THE SKILFUL PATHOLOGIST
Pathology Interviews
2017
Osama Sharaf Eldin, PhD, FRCPath
Copyright © 2017 by Osama Sharaf Eldin, MBBCh, MSc, PhD
All Rights Reserved. No part of this publication may be reproduced or

transmitted in any form or by any means without the permission of the
copyright owner
Library of Congress Control Number:
ISBN 978-0-244-92380-8
2
Table of Contents
PREFACE
ACKNOWLEDGEMENT
CHAPTER1: INTRODUCTION
Purposes of the Interviews
Conditional Questions
Staged Question
How to get prepared?
General rules during any interview
What will you do after the interview?
CHAPTER2: PATHOLOGY
General Pathology Overview
Pathology challenges
Management and pathology
Research in pathology
Clinical governance
Clinical Audit
Quality Control/ assurance
Errors in pathology
Clinicopathologic correlation/MDT
CHAPTER 3 : PATHOLOGIST
Pathologist-An overview
Pathologist as a leader
Pathologist as a team player
Portfolio-CV
Pathologist as a problem solver
CHAPTER4: PRACTICAL PATHOLOGY

Practical pathology skills
Histopathology
Frozen section
Autopsy
CHAPTER 5: OSPES EXAMPLES

Example number 1
Example number 2
CHAPTER 6: APPENDIX
Pathological staging and grading
Miscellaneous
3
Preface
This book is the second edition of the only published Pathology

interview book. This book points up how the Pathology interviews
differ from other medical and non-medical interviews.
Pathology interviews are one of the toughest interviews. The grounds
behind this are many. Firstly, the interviewer, who is a pathologist,
usually looking for certain details which should be precise and
concise at the same time. Secondly, the subject of the interview;
Pathology, is limitless and under continuous update with some
subjects like quality control, governance, audits.....etc, -which are new
to the interviewee- forms a significant part of the interview, either with
direct or indirect questions. Furthermore, some questions may require
certain practical experience level, which could be only acquired after
some training in histopathology.
Lastly, the interviewee knowledge about pathology who just finished
their internship or foundation year may be backdated to second or
third year of medical study.
In this book, I highlighted the hot topics in Pathology interviews in the

form of questions and simplified answers with many advices that will
help you to impress the interviewers.
Osama Sharaf Eldin, South Wales, 2017
4
Dedication
I dedicate this work to the soul of my father, to my mother, my wife

and my lovely kids.
Acknowledgments
I would like to thank the supervisors, colleagues and friends who

inspired me with ideas and knowledge and for their continuous
motivations in the following institutes:
 Mansoura Faculty of Medicine – Egypt

 Centre of Cancer Research, Belfast and Royal Victoria Hospital
 University College Dublin
 St. Vincent’s University Hospital, Dublin
 St. James's University Hospital, and Trinity College, Dublin
 The Whittington Hospital, North London
 Frimley Park Hospital, Surrey, UK
 Hartland Hospital, Birmingham, UK
 Arrowe Park Hospital, Wirral, UK
 Weston General Hospital: Dr Javed Wazir and Dr Wycliffe
Mbagaya.
 Royal Glamorgan Hospital, South Wales, UK
5
Disclaimer:
This is a study guidebook, designed in the Power Point (bullet) format,

employing the least possible number of words to convey the meaning.
It does not follow the classical complex textbook or the grammatical
English writing roles. As a self-published book, this book may contain
spelling or grammatical errors. In self-publishing, the author writes,
edits and designs his own book aiming to reduce the costs and to
provide a cheaper book for the buyers.
6
CHAPTER 1
INTRODUCTION
7
The interview is an essential tool for selecting the appropriate

candidate for the advertised job. Other tools including assessment of
the CV (curriculum vitae, resume), application form or presentation
The new trend of Pathology interviews is to be a panel interview in

which three or more consultants will be seating before the interviewee
accompanied by clerics and other non-medical staff. There could be
two or three slots in each interview.
These interviews usually are OBJECTIVE-STRUCTURED
INTERVIEWS, where the interviewers ask questions related to the job
description and person specifications (for example, a question
designed to test the leadership skill).
Currently a combination of panel interview and OSPE (Objective

Structured Pathology Exam) is employed. In OSPEs, you may be
given a written question, a photo or clinical scenario and then you are
asked to write the answer or to answer orally.
OSPE EXAM COMPONENTS
 The interview panel includes 5-7 interviewers.

 The exam comprises 6 stations of 3 to 4 OSPE –10 minutes each
+ a written exam, 20 min long
 You will be a paper including title of a presentation- 10 minutes
talk. The presentation usually would include a public topic (e.g.,
screening programs, breast cancer, autopsy, etc). You will be
allowed to prepare the topic in 20 minutes
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PURPOSES OF THE INTERVIEWS
The interviews test the following:

 Presentation skills
 Planning and organisation
 Problem solving / initiative kills
 How do you cope with stress
 Persuasiveness
 Teamwork / leadership
 Ability to learn
 Flexibility
CONDITIONAL QUESTIONS
Examples “What would you do if …….?” Such questions may be built

up to test a problem solving skill, audit, time management or team
work and you should come up with an example of each.
STAGED QUESTION
The interviewer will ask more questions based on the interviewee’s

answer. These questions are usually impulsive and either indicate a
curiosity of the interviewer to know more about the candidate level
(good indicator) or he wants to be sure that the interviewee deserves
a lower grade (bad indicator). This is why the interviewee should not
talk too much!
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HOW TO GET PREPARED?
 Read this book!

 Talk to others who are trained or working in histopathology and
ask questions such as:
o Why did you choose this specialty?
o What are the good and bad points of working in the
specialty?
o What is the lifestyle like here?
 Create a question bank

 Mock interview (rehearsal) - Practice Makes Perfect!
 Read the job description/person specification. You will be asked
questions related to core competencies in the field
 Re-read your application form
 Read your CV
 Why you have chosen Pathology as a life-long career?
 Know your weaknesses and your strengths
 Wear an appropriate suit /glasses and watch your body language
 Arrive early to review the exam paperwork.
GENERAL RULES DURING ANY INTERVIEW
 Be punctual and smart for the interview - first impressions are very
important. Speak calmly and clearly and make eye contact with
members of the panel.
 Try to come across as a confident, interesting person with a strong
personality and plenty of enthusiasm.
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 Keep time
 Well dressed up
 Body language: smile, keep eye contact, keep hands straight and
fest open, use your hands when required to illustrate, don't play with
your tie.....etc
 Listen carefully to the question
 DON’T give general examples
 DO give specific examples. The examples can be from your
personal experience or from your professional life.
 Do not answer a question that was not asked!
 Ask for re-phrasing if you do not understand the question
 Answer briefly and don’t talk too much
 Focus on your strengths
 If you are asked at the end of the interview if you have any
question, your reply should be “No, I would like just to thank you for
giving me this opportunity to meet you. Thank you very much". Or
similar! With a confident smile.
WHAT WILL YOU DO AFTER THE INTERVIEW?
 Write down all the questions and your answers

 Search for the ideal answers and optimise them
 Add the questions to your question bank
 Read the feedback if you were not successful and know your
weak points
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CHAPTER 2
PATHOLOGY
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GENERAL PATHOLOGY OVERVIEW
1. WHAT IS PATHOLOGY?
Answer:
Pathology = the study of disease. (Pathos; disease, ology; to study)
2. WHAT IS HISTOPATHOLOGY?
Answer:
Histopathology is the science that deals with microscopic examination
of lesion-diseased- tissue (surgical pathology) or cells (cytology) for
the purpose of diagnosis.
Histopathological diagnosis is the most accurate diagnostic tool in
Medicine.
3. WHAT ATTRACTS YOU TO THE HISTOPATHOLOGY

SPECIALTY?
Answer:
Histopathology related factors:
-Decision making specialty
-Has important implications in clinical management (diagnosis,
prognosis, assessment of post-treatment effect)
-Wide range of knowledge (all body systems are included)
-Continuously updated and linked to up to date research
-Different subspecialties
Personal factors:
-I always keep attention to details.
-I always curious about mechanism of disease
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-I am interested in histopathology since I was a medical student.

-I feel that this specialty acts as a bridge between clinical and
research (connects bed side -to- lab bench)
4. WHAT ARE THE MOST INTERESTING ADVANCES IN

HISTOPATHOLOGY AND HOW DO YOU SEE IT DEVELOPING IN
THE FUTURE?
Answer:
A- Advances in knowledge
Histopathology is continuously updated in the following areas:
 Pathological staging ( last staging is the TNM 7th edition, 2009 )
 New classifications, based on advances in clinical research, better
characterization of diseases following molecular and genetic
studies and consensus of expert pathologists.
 New entities. Examples include provisional lymphoma subtypes.
 Research related issues. Examples include the prognostic values
of Fuhrman's nuclear grading of renal cell carcinoma, Nottingham
grading of breast carcinoma, and Gleason's scoring for prostate
carcinoma.
B- Advances in regulations
- Royal College of pathologists, UK (RCPath) and College of
American Pathologists (CAP), continuously update their regulations,
recommendations and publications. These need to be followed up by
pathologists for consistency of reporting.
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C- Advances in Auxiliary techniques:

-Immunohistochemistry (IHC): There is prominent development of
the immunohistochemical automated staining to shorten the staining
time, promote the quality of staining and enhancement of
economically efficient methods. Double staining using two
complementary antibodies is one of sometimes with different colours
is an example. Examples. Racemase and 34BE12 to differentiate
between normal (racemase-and 34BE12+) and prostatic
adenocarcinoma (racemase+ and 34BE12-).
-Molecular techniques: These are useful adjuncts to

immunohistochemistry in the diagnosis of lymphoma, soft tissue
tumours and in detection of certain prognostic markers in some
tumours especially childhood tumours.
D-Clinical advances that are linked with Histopathology

-The advances in radiology added the following:
 Better targeting of the lesion with less false negative tissue
sampling
 Useful description of the targeted lesion : cystic/solid, necrosis,
haemorrhage, effect on surrounding tissue/organs
 Accurate measurements of the lesion
- Advances of other laboratory tests:

Helicobacter pylori detection (CLO test) replaced the histopathological
evaluation.
16
In the future, I expect that there will be more introduction of molecular

genetics in diagnosis and prognosis. There will be more use of digital
pathology in teaching undergraduate students and in training, with
more applications in the field of diagnosis and telepathology
consultation.
5. WHAT ELECTRONIC TOOLS ARE USED IN PATHOLOGY?

Answer:
-Computers are used for:
 Report typing,
 Searching for specimen and patient information
 Ordering extra work (levels, special stain or IHC..etc)
 Using laboratory information management system (LIMS). The
new LIMS which is widespread through the UK is WinPath
enterprise. The old system is TelePath.
-Digital pathology, where the glass slide is scanned by a high

resolution scanner into a digital image, which can be used for teaching
and diagnosis without any need for the microscope. The image can be
viewed using computers and shared by many users at different
locations.
-Telepathology, in which a pathologist in one location looks at

specimens under a microscope or as a digital image that is located
hundreds of miles away.
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6. WHAT IS THE VALUE OF PATHOLOGY REPORT?

Answer:
 Diagnosis (including initial diagnosis by biopsy and pathologic
staging after resection of the whole tumour)
 Prognosis (Oestrogen and Her2 status of breast cancer have
prognostic implications. The pathological staging also affects
prognosis)
 Efficacy of current treatment (Examples include excision in
resection specimen, the report will state if surgical margin are clear
enough so no re-excision required and examination of post-
chemo/radiotherapy specimens, e.g., breast tissue and rectal cancer
post treatment specimen. The response will be graded according to
the percentage of the necrotic/fibrotic tumour to the whole tumour
before treatment)
 Guide for further treatment (the pathological staging will
determine if a particular patient will require chemo/radio therapy, e.g.,
lymph node positive breast and colon cancer.
 Data for research and quality control
 Warning for the presence of an underlying lesion, e.g.,
precancerous lesion which means recurrence and multifocality are
expected. The presence of hereditary or familial aetiology which
requires genetic screening and/or examination of the rest of the family
for possible mutations. Examples, Familial Adenomatous polyposis
FAP), Hereditary non polyposis colorectal cancer (HNPCC), BRCA1
mutation in breast and ovarian cancer .
 Medico-legal importance
 Reference for probable progress in the lesion
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INPUT (Request +specimen)……….OUTPUT (Report + slides)
7. WHAT ARE THE COMPONENTS OF THE PATHOLOGY

REPORT?
Answer:
 Demographic data of the patient: name, age,…etc
 Clinical History: including investigations, previous treatments,
clinical differential diagnosis
 Gross (macroscopic) description, including cassettes numbers and
labelling
 Microscopic features: detailed description of the pathologic
process, pattern, cell characteristic and diagnostic clues
 Diagnosis statement: includes the category, subcategory and
subtyping, ancillary studies requested and their results, pathologic
staging and grading, recommendations to the clinician
8. WHAT IS IT (INFORMATION TECHNOLOGY)? HOW IT CAN

AFFECT PATHOLOGY PRACTICE AND SERVICE.
Answer:
Image analysis can improve practice while networking can improve
service. The introduction of digital pathology using high quality full
slide scan has an important contribution in teaching, e-learning, and
telepathology
9. WHAT IS PATHOLOGY MODERNISATION/REFORMING?

HOW IT IS DESIGNED AND WHAT ARE THE GOALS?
Answer:
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Pathology reforming is a part of the NHS modernisation. The NHS

modernisation has the following purposes:
 To improve service quality
 To improve the distribution of workload for the staff
 To expand the workforce
 To allow quicker access to the service that is patient-centred
 Integration into clinically-managed network, where patients,
clinicians and other healthcare workers can cooperate to improve the
service quality
The main aims of reforming Pathology service are to improve the
service excellence by producing high quality reports in the least
possible turnaround time and to minimize diagnostic errors. This could
be achieved when there are approved standards, clear guidelines for
processing and reporting, better supervision and training, quality
control, CPD, well-organised system, reasonable distribution of
workload and fair reward for pathologists. In order to integrate
Pathology in multidisciplinary healthcare network, there should be an
easy-to-use database and clinically managed networks.
Summary of goals of Pathology Modernisation

 Patient-centred service
 Faster access to results (shorter turnaround time)
 Better quality (use of best practice, lab accreditation, EQA/IQA,
perfection of the standard of Pathology staff)
 Error-free results
 Evidence-based diagnosis
 Increased cost-effectiveness
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10. WHAT ARE THE CURRENT PROBLEMS/CHALLENGES IN

PATHOLOGY?
Answer:
 Excess workloads: Pathology is undermanned due to decreased
number of training posts, increased rate of retirement or
emigration among consultants due to different reasons. In
addition, there is increased demand on pathology service by
different clinical specialties and the screening programs.
 Clinicopathologic discrepancy and misunderstanding which
requires MDT meetings and more communications between
pathologists and clinicians. It is found that 30% of pathology
reports are misunderstood by physicians and surgeons (Arch
Pathos Lab Med 2000)
 The HTA (human tissue authority) regulations limited the tissue
retention and the use of tissues in research and education.
 Changing perception of the public regarding autopsy and tissue
retention after a few scandals of unlawful tissue retention. This led
to decreased frequency of consented (hospital) autopsy.
 Increased complexity of classification and frequent updates in
classifications. e.g., lymphoma classification. This should be
resolved by Continuous Professional Development (CPD).
 Low inter-observer reproducibility in certain lesion subtyping e.g.,
in non-Hodgkin’s lymphoma. Further auxiliary studies including
immunohistochemistry or molecular techniques may be required.
 IT changes: the introduction of image analysis, virtual microscopy
and telepathology added challenges. These techniques are less
understandable by senior pathologists and require training.
21
 Changes in the accuracy of other diagnostic techniques including

radiology puts more pressure in order to correlate with the radiologic
findings. Example: slice X-ray for DCIS, requires more and accurate
sampling to match the X-ray films, sometimes by extensive sampling
or composite blocks.
11. IF YOU ARE ASKED TO ADVISE A FIRST YEAR MEDICAL

STUDENT ABOUT HISTOPATHOLOGY AS A LIFELONG CAREER,
HOW WOULD YOU DESCRIBE TO HIM THE ADVANTAGES AND
DISADVANTAGES OF HISTOPATHOLOGY?
Histopathology advantages over other clinical specialities: No
overnight shifts ( 9-5 work ), No direct patient contact, histopathology
is in demand as a job, you get knowledge of almost all Medical
specialties.
Histopathology disadvantages: Exposure to formalin, stressful as a
decision making career
PATHOLOGY CHALLENGES
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Pathology as a clinical practice faces many problems. Pathology is a

decision-making and demanding practice that requires full attention to
details. It is subjective and uses descriptive rather than quantitative
terms -in many instances-, which created poor reproducibility in
certain diagnostic entities. The subjectivity of Pathology created
problems with standardisation & clinical communication, in addition to,
the poor handling of uncertainty
Pathology as a clinical practice faces the following challenges:
 Workforce shortage
 Changed perception of people re: autopsy and tissue retention,
especially after certain scandals of unlawful tissue retention in UK
 Changes in the HTA (Human Tissue Act) regulations, added more
restrictions to the use of tissues in research and teaching
 Changes in other diagnostic methods, e.g., urease test for
Helicobacter Pylori replaced gastric biopsy as the gold standard for
diagnosis
 Changes in clinical practice and referral system resulted in
increased workload (e.g., cervical and breast screening programs)
 IT advancement (seldom used by senior pathologists) drawbacks
include technical complexity, cost and maintenance
 Continuous updates in pathology knowledge changed the old
concepts. This should be handled by CME
 Introduction of new techniques, like molecular diagnosis. Although
they are valuable, they are time consuming and expensive
 The use of sophisticated terms that have no clinical correlation,
resulted in poor communication. It is found that 30% of pathology
reports were not understandable by clinicians
 Poor reproducibility of subtyping, e.g., in lymphoma diagnosis
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12. WHAT ARE THE MOST IMPORTANT ISSUES IN PATHOLOGY

NOWADAYS?
Answer:
- Workload issues and short staffing
- Modernisation and integration of pathology service with other
clinical specialties
- Introduction of Digital pathology
- Decline in Autopsy
More details above!
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MANAGEMENT AND PATHOLOGY
13. WHAT IS CLINICAL MANAGEMENT?

Answer:
Management is the proper use of time, staff and resources. Within the
clinical practice, the fields of management includes patient diagnosis
(all diagnostic specialties, including histopathology, Laboratories,
Radiology...etc) and patient treatment (surgery, radiotherapy..etc)
Management means goal-oriented planning.

Management and administration are used alternatively to indicate
planning skills.
Types:
 Time management
 Clinical management
 Laboratory management
 Information Management
TIME MANAGEMENT
Time management means maximum use of time, aiming to increase
the efficiency of the service. This can be achieved by setting the work
prioritization and creation of “to-do-list”.
Pathology-related time management include:
 Routine time management: for routine daily activity
 Emergency time management: this is essential in urgent
situations where you do not have the full capacity to handle all duties.
Delegation is often essential.
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Steps of time management:

1. To do list : daily or weekly
2. Setting priorities
3. Do
4. Re-check
Questions:
14. GIVE AN EXAMPLE WHEN YOU HAD TO TAKE UP EXTRA
WORK AT SHORT NOTICE
15. HOW CAN YOU ORGANISE YOUR WORK TIME AND
OBJECTIVES?
16. HOW CAN YOU MANAGE TO MEET A TIGHT DEADLINE?
17. HOW CAN YOU SET PRIORITIES IN A BUSY LAB?
WORK PRIORITISATION
A- High priority work in Pathology
Generally
 Critically ill patient
 Patients who will benefit from early diagnosis
 Frozen sections
Special examples:
Histopathology:
 FNAB from clinically suspicious mass
 Biopsy from suspected metastasis
26
Cytology
 FNA from clinically suspicious mass
 FNA from clinically suspicious effusion
Autopsy
 Cases of high turnover of metabolic or enzymatic changes
 Infectious cases
B- Low priority work
Generally
 Screening tests
 Experimental tests
 Research
 Teaching
 Autopsies
 Cosmetic or plastic surgery biopsies
 Mild inflammatory or autoimmune conditions
Special examples:
Histopathology:
 Hysterectomy for uterine prolapse/ectropion
 Abortion
 Products of conception
 Ectopic pregnancy
 Congenital megacolon
 Skin lesions removed for cosmetic purposes
 Gall bladder removed for the presence of stone
 Appendicectomy from a child
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 Lipectomy
 Gangrene
Cytology
 Routine cervical screening
 Ascetic fluid from inflammatory conditions: e.g., hepatic fibrosis
Autopsy
 Most of cases are of low priority
18. EXAMPLE QUESTION OF WORK PRIORITIZATION:

THREE CONSULTANTS ARE AWAY FOR DIFFERENT REASONS
AND YOU ARE THE HEAD OF DEPARTMENT. HOW COULD YOU
COPE WITH SUCH SHORTAGE IN WORK FORCE AND HOW
WOULD YOU BE SURE THAT THE SERVICE IS NOT
COMPROMISED
Answer:
A. In-house
 Inform the clinicians that you will prioritise the work so that biopsies
come first and excisions at the end of the list
 Senior registrars can take some responsibilities.
 BMS (basic medical scientists) do part of cut up –keep eye on
them
 Reduce some activities. Example, decrease number of MDMs or
use video-conference or send a trainee.
 No autopsies
B. If the above did not work, ask for help from local network
(SLA- service level agreement network hospitals. You send some
cases to neighbouring hospitals.
C. If A&B did not work, hire a locum consultant histopathologist.
28
D. Send work away (specific companies who employ other

consultants in other parts of the country)
Disadvantages:
 Transport
 Chain of custody
 Need to keep patient data safe (anonymous)
 IT is important
 Calculation
 Reports need to be reviewed
E. After few months: Advertise for sustentative consultant the
job.
- Write job description approved by FRCPath (number of PAs
(program activities) and describe hospital facilities.
- Trust manager should agree
19. GIVE AN EXAMPLE WHEN BIOPSY FROM NON-NEOPLASTIC

LESION COULD BE OF HIGH PRIORITY.
Answer:
Any critically ill patient, e.g., in severe immunologic disease that could
be life threatening as in severe systemic lupus eryhtmatosus (SLE)
20. HOW CAN YOU DETERMINE THE SEVERITY OF SYSTEMIC

LUPUS ERYHTMATOSUS –SLE- BY BIOPSY?
Answer:
By renal biopsy. Lupus nephritis WHO classification can determine the
prognosis
WHO classification of lupus nephritis (Renal bx):
29
● WHO I: normal
● WHO II: pure mesangial lesions
● WHO III: focal proliferative glomerulonephritis
● WHO IV: diffuse proliferative glomerulonephritis
● WHO V: membranous glomerulonephritis
● WHO VI: advanced sclerosing glomerulonephritis;
chronic renal failure, unlikely to respond to therapy
RESEARCH IN PATHOLOGY
21. DEFINE RESEARCH. WHAT IS THE DIFFERENCE BETWEEN

BASIC AND CLINICAL RESEARCH.
Answer:
Definition: Research means to identify or to find out a new
knowledge. The pathologist should use his diagnostic eye and
academic background to prove/disprove proposals.
Types of research: Basic research is to detect a fact or to

bookmark an observation without any link to the clinical data, while
Medical (clinical) research is the use of scientific methods to
improve the patient’s health by increasing the precision of diagnosis
and management. For example, to find a link between a specific
morphologic observations or protein expression level and the
prognosis of a certain tumour
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22. GIVE AN EXAMPLE OF HOW RESEARCH CONTRIBUTED TO

PATIENT MANAGEMENT
Answer:
Two important examples of the retrospective study of the expression
of oestrogen receptors and Her-2 status in breast carcinoma and their
correlation with patient prognosis and subsequent effect on patients
survival after the use of antioestrogen and Herceptin treatment.
23. DO YOU THINK THAT MEDICS (DOCTORS) SHOULD

CONTRIBUTE TO RESEARCH?
Answer:
Yes. Research is part of clinical governance and part of evidence
based Medicine / evidence based Pathology
24. FROM SCRATCH DESCRIBE HOW YOU CAN START A

RESEARCH PROJECT (RESEARCH STEPS)
Answer:
Research steps
 Find a defect in the knowledge in a certain subject
 Search the database using MEDLINE, for example, to find out if it
is a novel project or has been done before
 Suggest a hypothesis (your expectations)
 Write down the objectives (divide the hypothesis into achievable
small goals)
 Look for funding resources (e.g., apply for a grant)
 Look for the contributors (other authors, technicians…etc)
 Find out the best materials and method (internet and papers)
 Organise a plan and deadlines for each stage (timetable)
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 Type an abstract
 Read key papers in the subject and type the introduction (Review)
 Look for citations and arrange references (e.g., Reference
manager, Endnote software)
 Start the practical work
 Collect all data (Results)
 Compile data
 Do statistical analysis (e.g., SPSS, PRISM, ORIGIN software)
 Interpretation of data
 Write the discussion: correlate the hypothesis and objectives with
the results
 Format your research into a thesis or a paper using the appropriate
cast
 Review the whole work with the aid of supervisors or principal
investigators (PI)
 Submit for publication in the appropriate journal
25. WHAT IS THE VALUE OF RESEARCH IN PATHOLOGY?

Answer:
 Evidence-based pathology (EBP), e.g., retrospective study of
breast tissues showed that ER/PR expressions are determinant
factors in the prognosis of breast cancer (this also show the value of
Pathology in patient management)
 Research is part of clinical governance
 Research is one of the pathologist’s professional performance
indicators (PPPI):
 To find out the origin and the mechanism of a disease
 To validate a classification
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 To relate the pathologic staging to prognosis

 To document the effect of a treatment morphologically
 Clinicopathologic correlation (e.g., to relate the pathological
grade to the clinical stage)
26. DESCRIBE EVIDENCE-BASED PATHOLOGY (EBP) AND GIVE

AN EXAMPLE?
Answer:
EBP ( Evidence Based Pathology) means the use of scientific
methods (e.g., Laboratory methods) to support and justify the
diagnosis (bench-bed correlation). By other means, it is the
application of scientific evidence ( including laboratory methods,
statistics, meta-analysis and clinical trials) or experience to Pathology
diagnosis, classification and prognosis. It aims to improve the
accuracy of diagnosis and to disseminate new knowledge. EBP is a
way to decrease the subjectivity of Pathology diagnosis.
27. WHAT ARE THE EVIDENCES USED TO SUPPORT EBP?

Scientific evidences include:
 Laboratory methods
 Statistical analysis
 Meta-analysis (retrospective study)
 RCT (randomised clinical trial)
 Expert opinion
EBP generally, integrates Pathology into clinical practice as well as
scientific research and makes Pathology a part of Evidence Based
Medicine (EBM).
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28. WHAT ARE THE VALUES OF EBP?

Answer:
 Reduces the uncertainty in Pathology diagnosis
 Provides solutions for problematic cases
 Increases the patients’ satisfaction of the health service
 Provides ways of better communication between the pathologist
and clinicians in relation to patient management
 A way of disseminating the best practice
 Encourages methodical re-evaluation of diagnostic criteria and
tumour classifications
29. ENUMERATE DIFFERENT RESEARCH METHODS

Answer:
 Audit
 Clinical trial
 Content analysis
 Correlation (negative or positive)
 Experimental studies
 Frequency distribution
 Inter-observer reliability
 Meta-analysis
 Response rate
 Statistical analysis
 Statistical significance
 Survey
34
30. GIVE EXAMPLES WHERE PATHOLOGY RESEARCH

AFFECTED THE CLINICAL MANAGEMENT.
Answer:
HER-2: Her2+ breast tumours: can be treated with herceptin (anti
Her2), poor prognosis. Her2+ gastric carcinoma: can be treated with
hereceptin, good prognosis
ER (oestrogen receptor): In breast cancer, predicts response to

tamoxifen (anti-estrogen). ER+ tumours have good prognosis
p53 a cell cycle regulator. Its mutation is found to be associated with

cancer progression. Therefore, it is used in combination with
proliferation marker Ki67 to detect dysplasia and carcinoma in situ
(cancer signature)
Ras (KRAS and NRAS) mutations are linked with poor response to
anti epidermal growth factor receptor (EGFR) drugs in Colorectal
cancer
31. WHAT IS HER2 AND WHAT IS HERCEPTIN?

Answer:
Her2/neu is the decapitated receptor of epidermal growth factor
receptor (EGFR). The decapitated receptor discharges growth signals
autonomously to stimulate the proliferation of tumour cells without a
need to bind to the growth factor.
35
Herceptin (Trastuzumab) is used as treatment for HER2 positive

breast and stomach cancer (one in five tumours are HER2+) . It is a
monoclonal antibody that interfers with HER2/neu receptor.
32. WHAT IS A "GENE EXPRESSION SIGNATURE" FOR A

TUMOUR?
Answer:
These are group of genes that are expressed constantly higher or
lower in the tumour > the population standard for same type of non-
neoplastic tissue.
Example in breast cancer, there are ER-positive and ER-negative
phenotypes. ER-positive group is also separated into three distinct
subgroups; luminal A, B, and, C based on gene expression pattern.
Survival and treatment outcome/prognosis are different in these
groups.
33. WHAT IS RESEARCH GOVERNANCE (RG) ? WHO DOES IT

APPLY TO? AND WHY IT IS ESSENTIAL?
Answer:
Definition: Regulations and standards of good practice that
continuously improve research quality nationally and internationally
RG applies to everyone connected to healthcare research (any

research that involves humans). Examples include surveys, imaging,
use of tissue or blood samples, drug trials or any use of patients data.
RG is essential to ensure the following

 Protect researchers
36
 Protect patients
 Ensure the ethical role in research
 Observe the performance of participants
34. WHAT IS THE DIFFERENCE BETWEEN SENSITIVITY AND

SPECIFICITY?
Answer:
Specificity = true negative rate = % of negatives that are properly
identified as being negative. Example; % of normal females who are
properly identified as being breast cancer free after breast core biopsy
Sensitivity = true positive rate = % of positives that are properly

identified as being positive. Example; % of cancer breast patients
who are correctly identified to have breast cancer after a breast core
biopsy.
37
CLINCAL GOVERNANCE
35. WHAT IS CLINICAL GOVERNANCE?

Answer:
CG defined by Scally and Donaldson as “A framework through which
NHS organisations are accountable for continually improving the
quality of their services and safeguarding high standards of care by
creating an environment in which excellence in clinical care will
flourish”
36. WHAT ARE THE COMPONENTS OF CLINICAL

GOVERNANCE/ WHAT CONTRIBUTIONS CAN A PATHOLOGIST
MALE TO CLINICAL GOVERNANCE IN THEIR TRUST?
Answer:
Components of clinical governance: 6 components: C2OR2E
 Clinical audit: Clinical audit is the measurement of performance

against agreed standards - a cyclical process of improving the quality
of clinical care.
 Clinical effectiveness: the extent to which a particular
intervention works. In pathology, high quality reports in short turn
round time
 Openness: Pathology service should be open to quality
assurance, so that poor performance can be managed.
 Risk management: Minimising risk to patients by audit and
learning from complaints. Poor quality of service is another risk to the
service.
38
 Research and development: Research includes review of the

literature & project management, in addition to, development of
guidelines & protocols.
 Education and Training: CME, the pathologist should be up-to-
date.
37. WHAT IS THE FRAMEWORK (CONNECTIONS) OF CLINICAL

GOVERNANCE:
Answer: These include:
 NICE (National Institute for Health and Clinical Excellence)
 CHI (Commission for Health Improvement)
 CPD (Continuous Professional Development)
 National audits
 Lab accreditation
38. WHAT CONTRIBUTIONS CAN A PATHOLOGIST MAKE TO
CLINICAL GOVERNANCE?
Answer: The pathologist contributes to all parts of clinical governance
(C2OR2E) the pathologist should share in clinical audit annually and
clinical research. Quality improvement is part of daily practice of the
pathologist to assure clinical effectiveness. Risk management is
employed by audit and learning from complaint to minimise the risk to
the patient. Continuous medical education is and attending the
training sessions/conferences are an important part of any pathologist
appraisal and revalidation by GMC.
39
39. WHAT THE CLINICAL GOVERNANCE DATA ARE REQUIRED

FOR?
Answer:
 Risk assessment
 Research
 Clinical audit
 Information management
 Education for patients and public
 Education and training for doctors
 Staffing and workload
AUDIT IN PATHOLOGY
40. WHAT IS AN AUDIT?

Answer:
CA defined by NHS as “a quality improvement process that seeks to
improve patient care and outcomes through systematic review of care
against explicit criteria and the implementation of change”.
This is to ensure that what should be done is being done. Clinical
audit is an essential and integral part of clinical governance.
41. WHAT ARE THE TYPES OF AUDIT?

Answer:
 Standard audit :assessing the practice against the standards
 Problem audit: problematic MDT meeting cases.
 Peer review: unusual cases reviewed by colleagues.
40
42. WHERE THE AUDIT REPORT SHOULD GO TO ON THE

NATIONAL LEVEL?
Answer:
The National Institute for Health and Clinical Excellence (NICE)
43. WHAT IS NICE?

Answer:
The National Institute for Health and Clinical Excellence (NICE)
supports the application of guidance/recommendation by clinical audit
to improve the quality of patient care (Audit implementation)
`
44. WHAT ARE PHASES/STEPS OF AUDIT?
Answer:
1. Find the problem (audit topic): the topic could be recommended
by NICE or a problem was found.
2. Define criteria & standards
 A criterion is a quantifiable outcome of care
 A standard is the threshold of the likely compliance for each
criterion (measured in a percentage).
3. Data collection
Data include sample size, duration, clinicians involved…etc
4. Compare performance with criteria and standards
After comparison, a conclusion is issued. The conclusion states if
standards were met or not. If not, the causes should be defined.
5. Implementing change
Recommendations for change should be notified to who shared in the
audit and nationally to plan for re-audit or best practice
41
th
Closing the loop is the ultimate goal for an audit (i.e., to reach the 5
step of change implementation)
6. Re-audit = to ensure sustained Improvements, the audit should
be repeated. This is essential for successful audit.
7. Dissemination: Results of good audit should be distributed locally
and nationally as a part of best practice.
45. WHAT ARE THE COMPONENTS OF AN AUDIT REPORT?

Answer:
Clinical audit report
FRONT PAGE:
 Project title
 Name of Hospital
 Specialty
 Disciplines involved
 Project lead and staff members
BACKGROUND/RATIONALE
AIM, OBJECTIVES, STANDARDS
 Aim: overall purpose of the project.
 Objectives: individual steps to achieve the aim.
 Standards: The quantifiable criteria of care.
MATERIAL AND METHOD
RESULTS
CONCLUSION/ LEARNING POINTS
RECOMMENDATIONS/ ACTION PLAN
REFERENCES
42
46. GIVE AN EXAMPLE OF AN AUDIT THAT YOU CONTRIBUTED

IN AND DESCRIBE THE OUTCOME.
Answer:
Example audits and proposed outcome:
Example audits
 Audit of number of retrieved lymph nodes in colorectal
specimens:
 Audit of the proper use of RCPath minimum dataset in reporting
squamous cell carcinoma of the skin…. Or any other tumours…
 Audit of use of B codes in reporting breast biopsies
 Audit of C codes in reporting breast cytologic material
 Audit of the use of P codes in reporting
 Audit of the proper use of Q codes in reporting
 Audit of proper use of immunohistochemical stains in reporting
non small cell carcinoma of the lung
Outcome:
In any of the above audits, the standard will be compared with the
practice. For example in A, the standard number of lymph nodes in
colorectal cancer is 12 lymph nodes. If practically, there were less
lymph nodes retrieved, hence the methods that could be used to
maximize the number of lymph nodes ( longer fixation, xyline
clearance, slicing the fat for better fixation and embedding fat for
microscopical pick up of lymph nodes) should be introduced and re-
assessment should be done.
43
47. WHAT IS MEANT BY CLOSING THE LOOP IN A CLINICAL

AUDIT?
Answer:
Recommendations for change should be notified to who shared in the
audit and nationally to plan for re-audit or best practice . This is
called Closing the loop which is is the ultimate goal for an audit
th
(i.e., to reach the 5 step of change implementation)
QUALITY CONTROL /ASSURANCE IN

PATHOLOGY
QC controls the method that leads to a reliable service (prospective).

QA measures the standard (reliability) of the service (retrospective).
EXAMPLE: Setting Quality Standards for a cervical cytology lab
A. METHOD
B. SERVICE (OUTCOME)
A. Method
Includes:
 Staff: Experience, qualifications, time required to examine the
slides, no. of reports they can produce daily, sharing in CPD
 Report: standard format, scientific content, time round (time
needed to finalise it)
44
 Lab protocol: staining method, adequacy of the slides, technique,

IQA & EQA
External quality assurance (EQA)
UK National External Quality Assessment Service (UK NEQAS)

consortium is the main contributor of EQA system in UK
EQA involves:
 Annual slide circulation
 Recognition of poor performance
 Comparison of the rate of poor performance to that of colleagues
 Comparison of slide staining and quality
Internal quality assurance (IQA)
 Quick review of 100% slides (all the slides)

 Monitoring the differences between primary screening diagnosis
and final recorded diagnosis
 Screeners must attain 90% sensitivity overall and 95% sensitivity
for high grade lesions
 There should be a plan to avoid poor performance, if found
IQA (rapid review 100%) is the most precise test of QA in

Pathology
45
B. Service
 Rate of abnormal and inadequate smears should be recorded

 High quality reports produced
 Positive Predictive value (specificity) should be recognized
48. WHAT IS UKAS?

Answer: UK Accreditation Service (UKAS) is the main national
accreditation body responsible for providing certification (based on
international standards) to organisations/laboratories of their
competencies and performance.
49. WHAT IS UK NEQAS?

Answer:
UK NEQAS is UK National External Quality Assessment service
Its goal is to facilitate optimal patient care by providing a
comprehensive external quality assessment service in laboratory
medicine. It helps ensure that the results of investigations are reliable
and comparable wherever they are produced.
46
ERRORS IN PATHOLOGY DIAGNOSIS
50. HOW ERRORS MAY OCCUR IN PATHOLOGY DIAGNOSIS,

WHAT ARE THE SOURCES, TYPES OF ERRORS, HOW TO
MINIMISE THE ERRORS AND WHAT TO DO WHEN YOU FIND
THEM?
Answer:
INPUT (Request + specimen)……….OUTPUT (Report + slides)
CAUSES OF ERRORS
Clinician’s errors:
1. Poor sampling
2. Misidentification of the sample
3. Poorly fixed (this is also the technician’s responsibility)
samples
4. Incomplete or hidden clinical information (often intended by
the clinician)
5. Poor request; requesting inappropriate test or providing
incorrect differential diagnosis (e.g., in skin lesions)
Technician’s errors:
1- The use of inappropriate fixative (alcohol in glycogen storage
disease or formalin in bone marrow, lymph node, or testicular biopsy)
2- Irregular trimming by the microtome (leads to artefacts). This
is common in frozen section (varied tissue consistencies)
3- Poor staining quality; the presence of stains inclusions (e.g.,
formalin stains) or inaccurate titration of the pH (e.g., Ulcian /PAS)
47
4- Poor orientation of the tissue fragments in the cassettes

5- The presence of floaters (tissue fragments from other
specimens during tissue processing)
6- Coagulated or clogged cytology
Pathologist’s errors:
1. Poor performance (Most Dangerous) could be due to
improper training or inadequate exposure to diverse pathological
lesions
2. Rushing in diagnosis
3. The use of No-history slide technique (where the
pathologist diagnoses a case regardless of the clinical data). The
opposite is equally dangerous; when the pathologist diagnoses a case
based on clinician’s interest and ignores the pathological data
4. Misuse of auxiliary techniques (e.g., IHC)
5. Poor dealing with uncertainty, e.g., reluctant to refer a case for
a second opinion or subspecialist when indicated
6. Poor communication with clinicians
Typist’s errors:
1. Typos (typographic) or data errors
2. Misidentification (Dangerous!) of the specimen/slide
48
CLASSIFICATION OF ERRORS
1. Diagnosis Error
 Another Category error: benign instead of malignant (False
negative) or malignant instead of benign (False positive)
 Another Subcategory error: wrong subtype of a malignant
lesion
2. Report errors
1. Patient misidentification
 Report content (data) error, e.g., right instead of left arm
 Report layout and typos
Another classification of errors

 According to the patient risk: high or low
 According to the frequency: recurrent or sporadic
 According to the correctability: correctable or non
WHAT SHOULD YOU DO IF YOU DISCOVER AN ERROR?
1. Check the identification of the slide & report and contact the
clinician to confirm the clinical data
2. Immediate contact with the clinician or GP to describe the condition
and to allow him to take the appropriate action (e.g., remove the
patient from the operative list, stop therapy..etc)
3. Send the NEW report which could be named:
Amended (Revised) report: when there is an error in diagnosis
Corrected report: for report text errors
49
Addendum: for missed information or additional explanation
MEASURES TO MINIMIZE ERRORS
1- Problem-based audit and action learning

2- Better communication with the clinicians
3- Laboratory accreditation
4- Dissemination of Best Practice methods among technicians and
trainees
5- Continuous professional development (CPD) for pathologists
through:
 Continuous medical education (CME)
 Participation in audit, MDT meetings, EQA
 Research
False negative errors are the WORST and they were the sources
of some scandals in Pathology, lastly
51. ERROR SCENARIO QUESTION?

A female patient had an ovarian mass. The ovarian biopsy showed
metastatic signet ring cell carcinoma (usually metastasis from
stomach. Such metastasis to the ovary is called Krukenberg tumour).
Previous gastric biopsy was reported negative. However, you pulled
the previous slide and ordered levels, which showed a signet ring
carcinoma. How will you manage at the MDT meeting?
Answer:
 See both reports and all the slides
 Error logging
50
 Talk to the patient or someone else will do (e.g., clinical

colleague)
 Talk to the head of department
 Write a clinical incident report as part of risk management
 Talk to risk management board (part of clinical governance). They
will ask you to do risk assessment if this happens again.
 Risk assessment board will see if this happened before by some
or other pathologists due to lab problem or pathologist problem
 Amended report
Pathology Reviews
Aims: to improve patient safety

Types:
A. Internal review
 Within the department
 Randomly selected cases or three months or 200 cases
around this case
B. External review:
 From outside the department
 Combination of RCPath and GMC review to improve patient
safety.
Buzz words: GMC safety procedures, Error logging, Risk

assessments, Clinical governance, Legal, Patient should be informed
51
MDM/MDT (CLINICOPATHOLOGIC
CORRELATION)
MDT: Multidisciplinary team

MDM: Multidisciplinary team meeting
52. WHAT IS THE MULTIDISCIPLINARY TEAM (MDT)?

Answer:
Multidisciplinary team (MDT) is a group of professionals from different
health care specialities, who share in diagnosis and treatment.
They meet up at a specific time to discuss a patient’s case.
The MDT report should be sent to the patient’s GP
53. WHAT ARE THE ROLES OF A PATHOLOGIST IN MDT?

Answer:
 Confirmation of the diagnosis and answering queries related to the
diagnosis
 Better communication with clinicians
 The diagnosis may change after better communication with the
clinicians. For example, a case that was diagnosed as carcinoma
in situ (CIS) by cytology while a mass was discovered
radiologically would alter the diagnosis into transitional cell
carcinoma (TCC)
 Explanation of pathology diagnosis. It is found that 30% of
pathology reports are misunderstood by physicians and surgeons
(Arch Pathos Lab Med 2000)
52
54. DESCRIBE THE WEAKNESSES (CONS) OF MDT MEETING?

Answer:
 Time consuming
 Requires extensive administrative work
 May interfere with other duties
55. WHAT ARE THE PRE-REQUISITES FOR EFFECTIVE MDT?

Answer:
 Administrative support
 Flexibility of the participants’ attitude
 The pathologist should understand the clinical management
56. WHAT WILL YOU SAY IN A MDT MEETING TO SURGEONS

WHO SENT YOU A COLON CANCER CASE THINKING THAT IT IS
LYMPH NODE METASTASIS FREE WHILE YOU FOUND A SMALL
LN THAT CONTAINS MICROMETASTASIS? (SENTINEL LN)?
Answer:
This is a case of clinicopathologic miscorrelation. Remember to
mention value of LN dissection, the technique of excision and the
value of sending the related part of the mesentery
53
54
CHAPTER 3
PATHOLOGIST
55
PATHOLOGIST- AN OVERVIEW
57. WHAT IS THE ROLE OF THE HISTOPATHOLOGIST IN

PATIENT MANAGEMENT/HEALTHCARE?
Answer:
 Clinical diagnosis: pathological diagnosis is the surest in clinical
practice. Based on pathological diagnosis, the surgeon can decide
serious operations like radical surgery or amputations. Detection of
the origin of metastasis is another example.
 Clinical management: pathologists provide evidence of efficacy
of clinical management, e.g., tumour cell ablation after radiotherapy
 Cancer prevention and early diagnosis: e.g., breast and
cervical screening reduced the incidence of corresponding cancers
 Infection control: e.g., through detection of new cases of TB
 Clinical audit of other clinicians’ work: e.g., the effect of
specific clinical intervention
 Autopsy and cause of death: Autopsy can detect a cause of
death that is different from the pre-mortem diagnosis. In 10% of cases
the cause of death could only known by autopsy
 Research: including clinical trials, often require pathologist’s
opinion
 Teaching: pathologist’s are involved in teaching of undergraduate
and postgraduate healthcare students
 Community awareness: pathologists have roles in increasing the
public awareness towards diseases prevalence and prevention
56
 Experimental Pathology: preclinical research is essential pre-

requisite for clinical/therapeutic trials. Basic research is fundamental
for clinical studies.
 The role of the pathologist in disasters: including epidemics,
atomic accidents or other catastrophes; the pathologist can assist in
identification of bodies, define the cause of death, collect pathologic
materials for investigations including microbiologic and DNA studies,
in addition to, histopathological reporting.
58. DO YOU THINK THAT PATHOLOGISTS SHOULD BE MEDICS

(MEDICALLY QUALIFIED)?
Answer:
Yes. A pathologist should have clinical background for proper clinico-
pathologic correlation.
59. DO YOU AGREE THAT BMS (BASIC MEDICAL SCIENTISTS)

COULD BE PATHOLOGISTS?
Answer:
Yes. Currently an FRCPath can be awarded to BMS after fulfilling
certain conditions (Please refer to RCPath guidelines). BMS can share
in surgical specimen cut up, quality control and with training they can
help in workload management. However, clinicopathologic correlation
requires good knowledge of clinical practice, which is an advantage of
medics.
57
60. WHAT ARE THE ITEMS DESCRIBING GOOD MEDICAL

PRACTICE IN PATHOLOGY?
Answer:
GOOD MEDICAL PRACTICE (GMP)
Def: Professional behaviour towards self and others (patient,

colleagues, supervisors, authority & community)
I. GENERAL GOOD MEDICAL PRACTICE: (for anyone wearing a

white coat including pathologists):
A-Towards yourself
 Improve your proficiency and skills by CPD, audit, EQA and
sharing in teaching, training and appraisal
 Protect your health by following the lab health & safety
 Ask for a second opinion when indicated
B-Towards the patients

 Probity: be honest and trustworthy
 Ask for consent when indicated
 Keep confidentiality of information
 Minimise patient’s risk
 Have a good communication with patients and their relatives,
carers and partners
C-Towards colleagues
 Work in a team: see team player
 Know the duties of a good leader: see leader
58
 Do not be confrontational
 Avoid racism
 Respect your colleagues
 Arrange cover, delegate or refer when indicated
 Share information with colleagues
D-Towards higher authority and government

 Follow the regulations
 Know the role of each organisation: UKNEQAS, NICE, CHI
II. SPECIFIC GOOD MEDICAL PRACTICE FOR PATHOLOGISTS:
A-Good microscopic skills

You should be able to interpret the relationship between cells and
tissues, to recognise growth patterns and to know the lesional from
normal tissue.
B-Manual skills
You should be able to dissect and select representative blocks for
processing.
C-Writing/dictation skill
You should be able to dictate/write clearly to produce a quality report.
D-Organisational skills
You should be able to memorise, to interconnect data and to know the
headings and subheadings of common subjects.
E-Strong clinical background
You should be aware of disease mechanisms, the different clinical
presentations and the clinicopathologic correlation. You should know
that certain diseases are commoner in certain age, sex, anatomic site
and you should anticipate the patient’s clinical picture from the slide.
59
F-Decision maker
You should be able to interpret and analyse data, suggest a logical
differential diagnosis and formulate a final diagnosis.
G-Approachable
You must be open to clinical colleagues when they enquire about
specific information.
H- Others
Sharing in EQA and appraisal, proper time management, being up-to-
date are essential. You should be able to work under stress, do not
take the risk, know your limitations, consult others when required and
know the importance of governance, audit, quality control and
research in Pathology .
61. WHAT MAKES A GOOD (QUALITY) PATHOLOGIST? OR HOW

CAN YOU BE SURE THAT YOUR (OR ANOTHER
PATHOLOGIST’S) PERFORMANCE MEETS THE STANDARD?
Answer:
The qualified pathologist should:
 Has a high professional performance (professional
performance indicators , PPPI)
 Follow good medical practice
A. Professional performance (professional performance

indicators
Sharing in: CARE
 CPD (continuous professional development) contribution

 Involvement in Audits
 Involvement in Research/teaching
60
 Involvement in EQA
 Practical level:
o The ability to produce high quality reports in a short time
round
o Pattern recognition & clinical correlations
o Prompt differential diagnosis based on clinicopathologic
data
o Attention to minor details
 Others: management/ leadership skills.
62. WHAT IS CPD? CME?

Answer:
Continuous Professional Development/Continuous Medical Education.
This is an important indicator of pathologist performance.
They can be achieved by continuous working in histopathology,
attending conferences and workshops, reading the new articles that
are related to new classification, new histological entities, new
immunohistochemical staining or molecular technique that aid in
diagnosis, and sharing in EQA.
Certain CPD/CME points are essentially required by the GMC
(General Medical Council, UK) for yearly appraisal (50 points/year)
and revalidation (250 points for the 5 years of appraisal). An example
is passing breast national EQA = 3 CME/CPD points.
61
PATHOLOGIST AS A LEADER
Leader is a guide who works with and through people. He should be a

role model for all other members of the team.
Good leader
 Goal-oriented
 Team player
 Follows delegates
 Uses the strengths of others
 Decisive
 No discrimination
 Does not blame other
 Takes responsibilities
PATHOLOGIST AS A TEAM PLAYER
Working as a team  more achievements, but it requires a high

degree of harmony between the team members, understanding the
personalities and motivations as well as needs for all members within
the team. A common goal for all is crucial.
Example questions
 Tell me about the last time that you had to work as part of a team
to achieve a specific outcome.
 Whilst part of team has there ever been a time where you
witnessed conflict?
 Describe a time when a colleague or friend has annoyed you.
62
 Have you ever had to modify your approach to take account of

someone else’s views?
 Can you recall a time where you have needed to offer constructive
feedback to a friend or colleague?
How to be an effective team player?
Effective team player is able to motivate the team to reach success.

He should have the following social skills:
 Responsibility
 Respect
 Teach other colleagues
 Be generous
 Set an example
 Never be confrontational
 Motivate other colleagues
 Do not be selfish
PORTFOLIO/CURRICULUM VITAE
Your curriculum vitae (Resume/Portfolio) could be part of the interview

questions and here are examples of the traditional questions:
63. WHY SHOULD WE CONSIDER YOU FOR THIS POST?
64. WHAT ARE YOU GOOD AT, OUTSIDE WORK?
65. WHAT ARE YOUR PARTICULAR STRENGTHS AND
WEAKNESSES?
66. HOW DO YOU MANAGE STRESS?
63
67. HOW DO YOU SEE YOUR CAREER DEVELOPING IN THE

NEXT FIVE YEARS?
68. WHAT DO YOU THINK ABOUT THE LATEST HEALTH-
RELATED NEWS IN THE PRESS?
69. WHAT ARE THE KEY ATTRIBUTES OF AN EFFECTIVE
TEAM?
70. HOW YOU WOULD MANAGE IF YOU FOUND YOURSELF IN
CONFLICT WITH ANOTHER MEMBER OF YOUR TEAM?
71. DO YOU THINK YOU A GOOD DOCTOR? WHAT SHOWS THIS
IN YOUR PORTFOLIO
72. GIVE AN EXAMPLE THAT BEST ILLUSTRATES YOUR DRIVE
AND INITIATIVE.
73. GIVE EXAMPLES OF WHAT YOU HAVE LEARNED FROM
WORKING IN THE MEDICAL FIELD.
74. WHAT IS YOUR GREATEST ACHIEVEMENT?
64
PATHOLOGIST AS A PROBLEM
SOLVER
75. IF YOU DID A BAD DISSECTION OF A RECTAL SPECIMEN,

WHAT ARE THE LIKELY MISTAKES THAT YOU HAVE DONE?
(WHAT ARE THE MOST LIKELY TO BE DONE BADLY IN
DISSECTION OF THE RECTUM?).
Answer:
 Circumferential margin. Sometimes this margin either forgotten or
poorly sampled.
 Lymph node dissection: This is specially a challenge in post
neoadjuvant specimen where the lymph nodes are too tiny (dwarf
lymph nodes). You can increase the yield of lymph nodes by the
following methods:
- Leave the specimen to fix for longer period. This will make the
lymph node firmer and easy to feel.
- Clearing method by leaving the pericolic fat in Xylene, which will
dissolve the fat and makes the lymph nodes more visible.
- Meticulous slicing of the fat at short to find the small lymph
nodes
- Leave the fat in a mixture of glacial acetic acid, alcohol and
buffered formalin. The lymph nodes will be easier to find.
- Put extra fat in the cassettes specially the fat around blood
vessels.
65
 Finding the tumour in post neoadjuvnat specimens, where the

tumour bed is hard to identify without a tattoo mark and may be
represented by just a dimple, a scar or a shallow ulcer. Hence,
slicing the rectal wall with a 5mm interval and choosing sequential
blocks will aid in finding the tumour bed (Quirke Method)
 A synchronous tumour may be overlooked especially if this tumour
arises in a polyp.
 Sampling of all polyps.
76. GIVE AN EXAMPLE WHEN YOU DISAGREED WITH THE

TEAM LEADER YOU WERE WORKING WITH AND HOW YOU
MANAGED TO SOLVE THE PROBLEM.
Answer:
Example. During my internship, I have examined a 40y female patient
who complained of a central chest pain radiating into the back. My first
impression was that this patient had an anginal pain. Therefore, I
requested ECG and laboratory tests for angina/myocardial infarction.
My senior colleague was not convinced that this is an ischaemic heart
disease. After discussion, he raised the possibility of GERD (gastro-
oesophageal reflux disease) because this patient's symptoms where
mild, the age and the pain characters. I asked the patient if she had
any reflux symptoms and surprisingly, he said that he is has GERD
since 10 years+ and she is under Barrett's oesophagus surveillance. I
learned that I should consider all the possibilities and to have a good
history taking.
66
77. GIVE AN EXAMPLE WHEN YOUR TEAM FAILED TO REACH

THE OBJECTIVES. GIVE REASONS FOR SUCH FAILURE.
Answer:
Example:
We planned to organise a pathology conference during August last
year, however, we could not finish on time due to many reasons.
Many of the contributors were away for summer holiday and the
budget was insufficient.
78. ONE OF THE CONSULTANTS REPORTED A CASE BY A WAY

THAT YOU THINK IS WRONG, HOW CAN YOU DEAL WITH SUCH
SITUATION?
Answer:
I will discuss this first with him and see how he explain such diagnosis.
If I am not convinced I will speak with a senior colleague and then
head of department.
79. HOW CAN YOU HANDLE COMPLAINTS FROM A SENIOR

COLLEAGUE?
Answer:
I will take this as a constructive criticism and don't take it personal. I
should be calm and try to improve myself.
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80. HOW CAN YOU BE SURE THAT YOU ARE PREPARING A

GOOD LECTURE/ PRESENTATION?
Answer:
I will see if there is good interaction, like questions from the students. I
may ask questions as well to be sure that they understood the lecture.
Feedback from the students can be helpful and the final exam result
can tell as well
81. HOW COULD YOU DEAL WITH CRITICISM FROM PATIENTS

REGARDING THE DIAGNOSIS OR PATHOLOGY SERVICE?
Answer:
As usually no direct contact between the pathologist and the patient,
all the explanation should go to the his/her clinical or GP. A review of
the slides also should be considered.
82. MENTION AN EXAMPLE WHEN YOU DISAGREED WITH THE

DIAGNOSIS OF A CASE THAT WAS REPORTED BY YOUR
CONSULTANT. HOW DID YOU MANAGE?
Answer:
Example
I had measured the tumour margin to be 1mm, but I found that the
report stated that the margin is 5mm. I went to the consultant to ask
and he convinced me that there was a split in the margin where the
ink tracked inside, therefore the proper distance should be measured
away from that split.
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Identification of a mislabelled specimen

 Phone the clinical colleague to confirm clinical details, check the
clinical request and match with the specimen, paraffin blocks and
slides.
 If a probable mix between 2 specimens do ABH blood group
antigen IHC
 PCR for HLA typing
 DNA typing
83. HOW TO DEAL WITH YOUR EDUCATIONAL SUPERVISOR-

CLINICAL TRAINER IF HE HAS A TOUGH PERSONALITY?
Answer:
Be calm, don't be confrontational, do things to the standard and get an
advice from a senior colleague
84. HOW TO HANDLE AN UNDERPERFORMING COLLEAGUE?

Answer:
In sequence:
Speak to him first and know what is behind his poor performance and
if you could advise and help. If not convinced, discuss with a senior
colleague or a consultant and finally the head of department.
85. WHAT CAN YOU DO IF YOUR CONSULTANT IS NOT HAPPY

WITH YOUR DISSECTION?
Answer:
I will take his opinion as a constructive criticism and start to improve
my knowledge and skills with the help of a senior colleague. After
reading and practicing, I will ask him to watch me while dissecting.
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86. YOU COME EARLY TO WORK DAILY; HOWEVER, YOUR

CONSULTANT THOUGHT THAT YOU COME TOO LATE. HOW
CAN YOU MANAGE THIS SITUATION?
Answer:
When I arrive to the hospital, I will knock on his door and say "Good
Morning"
87. IN A MDT MEETING, THE CLINICAL DIAGNOSIS WAS

DIFFERENT FROM THE PATHOLOGIC DIAGNOSIS, HOW
CAN YOU EXPLAIN THE PATHOLOGIST’S VIEW IN SUCH
SITUATION? CLINICOPATHOLOGIC DISAGREEMENT
How to answer this question?

General rules
 The case should be investigated aiming to reach the best for the
patient
 Do not blame the clinical colleague
 Start always thinking of something happened from your side
 This case could be a base for audit and research or as a part of
the MDT meeting
 Ask for help from senior colleagues if required
Procedures
1- Check the identification of the specimen/slide
2- Think of a possible swap incurred by the technician
3- Check all the demographic data, hospital number & clinical details
4- DNA typing may be needed
5- Review the case and the slides again
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6- Contact the clinical colleague

7- Express your opinion based on the received request, gross
examination and microscopic data
8- Ask for further information/ repeat biopsy if needed
9- If you did something wrong admit it immediately for the patient
sake
10- An addendum or reviewed report may be issued
11- Learn from errors and criticism
12- Take measures to prevent recurrence of errors
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72
CHAPTER 4
PRACTICAL PATHOLOGY
73
PRACTICAL PATHOLOGY SKILLS
The pathologist should have the following skills:
HISTOPATHOLOGY (SURGICAL PATHOLOGY)

Proper sampling/dissection of tissues to demonstrate pathologic
lesions
Basic principles of microscopy
Understand tissue fixation
Frozen sections
Able to interpret EM, immunofluorescence, immunohistochemistry and
special stains
Be familiar with recent surgical Pathology topics
Able to recognise lesion patterns microscopically and design a
differential diagnosis
Able to build a reasonable algorithm to reach the final diagnosis
Able to write a quality report including diagnosis, pathologic staging
and recommendations to clinicians when indicated
CYTOPATHOLOGY
Knows the common laboratory techniques for preparing Gynae and
non Gynae cytology materials
Knows the spectrum of normal cervical cytology at different
physiologic situations
Knows the morphology of non-neoplastic, pre-neoplastic and
neoplastic cervical cytopathology and the correlation with histology
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Knows the clinical follow-up of patients following different diagnosis

decisions
Understand the importance of quality control in cytology
Able to categorise the diagnosis into main categories of diagnosis
(example: unfit, benign, suspicious, malignant..etc)
AUTOPSY PATHOLOGY
Consent for an autopsy, regulations (hospital)
Confidentiality of patient information & respect for human remains
Coroner system understanding
Custody (ownership) of human body
Cause of death vs. mechanism of death vs. manner of death.
Careful handling of specimens & hazards control
Communication with clinicians
Complete dissection
Classify the cause of death including the underlying cause of death or
intervening causes of death and report writing
Spot artefactual findings of decomposition and embalming.
Specimen photography
Select specimens for microbiology, toxicology, EM or molecular
Sample representative tissues for histologic examination
Spot the urgent autopsy
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HISTOPATHOLOGY
88. WHAT IS THE DIFFERENCE BETWEEN STAGING AND

GRADING OF CANCER?
Answer:
Staging is the degree of tumour spread in the body.
Grading is the degree of differentiation of the tumour. Differentiation is
the degree of similarity of the tumour to normal tissue.
 Well differentiated: resembles normal tissue. Good prognosis
 Poorly differentiated: Does not resemble normal tissue. Poor
prognosis.
89. WHAT IS TNM?
Answer:
TNM is an abbreviation used to assess tumour staging at three levels:
T: Tumour size and/ or tumour spread locally
N: lymph node metastatsis regionally
M: Distant metastasis to other organs
90. WHAT IS THE COLORECTAL CANCER TNM?

Answer:
T1: Submucosa
T2: Muscularis propria
T3: Subserosa
T4: Perforates visceral peritoneum/ invades other organs locally
N1: Regional Lymph node metastasis
M1: Distant metastasis
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91. WHAT IS THE BREAST TNM?

Answer:
T1: Tumour < 2cm
T2: Tumour >2-5cm
T3: Tumour > 5cm
T4a: Chest wall invasion
T4b: Skin invasion
T4c:T4a+T4b,
T4d: Inflammatory carcinoma
N1a: 1-3 axillary lymph nodes metastasis

N1b: internal mammary lymph nodes metastasis
N1c: N1a + N1b.
92. WHAT ARE THE DIAGNOSTIC OUTCOMES OF BREAST FINE

NEEDLE ASPIRATION CYTOLOGY?
Answer:
C1- (Inadequate/unsatisfactory)
C2- (Benign)
C3 - (Uncertain), atypical probably benign
C4 - (Suspicious)
C5- (Malignant)
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93. WHAT ARE THE DIAGNOSTIC OUTCOMES OF BREAST

CORE BIOPSY?
Answer:
B1 (Normal)
B2 (Benign)
B3 (Uncertain malignant potential with or / without epithelial atypia).
B4 (Suspicious)
B5: Malignant
 B5a (Malignant in situ)
 B5b (Malignant invasive)
 B5c (Malignant not assessable)
94. WHAT ARE THE DIAGNOSTIC OUTCOMES OF THYROID FNA

CYTOLOGY?
Answer:
Thy 1 Non-diagnostic (blood only, artefact or inadequate (less thn 6
groups of 10 cells each)
Thy 1c Non-diagnostic– cystic lesion (no epithelial cells)
Thy 2 Benign (colloid nodule, goitre, Hashimoto’s..etc)
Thy 2c Benign, cystic lesion (benign epithelial cells present)
Thy 3a Neoplasm possible – atypia
Thy 3f Neoplasm possible – follicular /Hurthle cell neoplasm
Thy 4 Suspicious of malignancy
Thy 5 Malignant
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95. WHAT IS THE IMPORTANCE OF MOLECULAR TECHNIQUES

IN PATHOLOGY?
Answer:
Molecular techniques are used in the following areas in Pathology
1. More precise disease diagnosis
2. To identify specific infectious agents
3. Help to explain disease aetiology
4. Personalized patient therapy.
Examples of the molecular techniques are:
 In situ hybridization using Chromogen (CISH) or fluorescent dye
(FISH) to localise RNA or DNA
 Polymerase chain reaction (PCR).
 IHC (immunohistochemistry) is also used to localise certain
proteins including Her2 microsatellite instability (MSI).
96. DESCRIBE THE IMPORTANCE OF HEALTH AND SAFETY

MEASURES IN PATHOLOGY PRACTICE.
Answer:
Control of Substances Hazardous to Health Regulations 2002
(COSHH) provide instruction for health and safety in laboratories
The importance of health and safety measures in pathology
laboratories is to decrease the risk of infection to employees and
prevent the spread of infection in the hospital community.
In pathology laboratories, the health and safety should be sought in
the following areas:
 Handling of specimens: protective equipments
 Disinfection/Fixation
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 Cut up procedure
 Disposal and incineration of specimens
Key areas in health and safety include:

 Hazard group
 Risk assessment
 Containment levels
 Buildings and accommodation
 Standard operating procedures, including safe working
practices
 Health surveillance
 Monitoring, audit, review.
97. HOW CAN YOU DISINFECT TISSUE CONTAINING PRION

AGENT OR HCV?
Answer:
HCV can live in cotton for up to 2 days, on surfaces for 16 days, in
water for up to 21 days and in syringes for up to 63 days.
-HCV can be disinfected with bleach, heat and microwave
-Prion protein (the infective agent of mad cow disease) can be

disinfected by formic acid and heat
80
98. WHAT ARE THE VITAL/SUPRA-VITAL STAINS?

Answer:
Definition: A stain applied on living cells. They could be used in
diagnostic and surgical techniques. Supravital stain applied on fresh
tissue after removal from the body, while intravital stain is done by
injecting the stain into the body.
Examples:
Propidium Iodide (PI): DNA stain used to differentiate necrotic from
normal tissue
Trypan (Toluidine) Blue: stains living cells for microscopic cell

counting (viable cells +, necrotic cells -). Also in mature cataract
surgery to stain the anterior capsule.
Janus Green: basic dye in histology
FROZEN SECTION
Frozen section, FS (intraoperative consultation) is a histopathological

technique used to perform a rapid microscopic examination of tissue
specimen, employing a cryostat to make a cryosection. This occurs by
o o
cooling/freezing the tissue to -20 C to -30 C
The quality of the FS slides is of lower quality than formalin fixed

paraffin embedded. The diagnosis may be deferred for paraffin
section if poor quality is a limiting factor or accurate diagnosis.
81
Questions:
99. DESCRIBE THE USES (INDICATIONS) OF FROZEN SECTION

DIAGNOSIS
Answer:
 Identification of tissue type (benign vs. Malignant). Example:
Incidental peritoneal nodule.
 Type of malignancy (e.g., lymphoma or carcinoma). Lymphoma
will not require further surgery and medical treatment would be the
target.
 Surgical margins (aiming to preserve the normal tissue).
Whether they are positive (contain malignant tissue) or negative (no
malignant tissue). Moh’s technique is used in dermatopathology where
thin layers of skin are sent for FS to examine the margin.
 Metastasis (present/or absent) in previously diagnosed cancer .
Either in a lymph node or other tissue. A positive sentinel lymph node
(breast cancer, melanoma), required further surgical procedure, e.g.
axillary clearance.
 Identification of normal tissue as parathyroid gland, ganglia
 Molecular techniques requires fresh tissue (e.g., PCR, flow
cytometry)
100. WHAT ARE THE ADVANTAGES OF FROZEN SECTION

DIAGNOSIS
Answer:
 If the diagnosis is malignant, the mass can be removed
immediately without a need for another operation
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 If more tissue is required for a precise diagnosis, the surgeon can

obtain an additional sample, avoiding a second operation.
 FS biopsy can ensure that the mass being removed is the intended
tissue for removal.
 It can help ensure that the entire mass and its surrounding margins
are removed.
 FS is essential for surgery of congenital megacolon; multiple
section levels may be done to reach the ganglionic segment
 IHC for certain antibodies can be more accurate using FS
 Fat stains can only be performed on FS (Oil-red)
 Fresh tissue can be used or further molecular studies and flow
cytometry
101. WHAT ARE THE DISADVANTAGES (PROBLEMS) OF

FROZEN SECTION DIAGNOSIS
Answer:
 Sampling error
 Lack of special studies (Rare special stains and IHC stains could
be used)
 Lack of consultation (time is too limited to ask for opinion).
Experienced pathologists are always required
 Artefacts: ice crystals, fat (does not freeze)
 Infection (risk of infection is high, no formalin)
 Poor quality, which may sometimes necessitate deferral for paraffin
section.
83
102. WHAT ARE THE CONTRAINDICATIONS OF FROZEN

SECTION USE?
Answer:
 Suspected tuberculosis and other communicable diseases
 Small lesions that may be destroyed during preparation
103. WHAT ARE OTHER METHODS THAT CAN BE USED TO

ENHANCE THE ACCURACY OF FS DIAGNOSIS?
Answer:
FS diagnosis can be enhanced (limited) by the use of:
- Imprints (Especially for lymphoid lesions) and
- Special stains (e.g., PAS stain can highlight the ITGCN
(intratubular germ cell neoplasia, in testis) which are glycogen
rich, fat stains in Sertoli-Leydig cell tumours)
84
AUTOPSY
104. WHAT IS THE ROLE OF AUTOPSY IN PATIENT

MANAGEMENT?
 Detection of cause of death ‘COD’ (if was not diagnosed clinically)

 Confirmation of COD (even if diagnosed clinically)
 Detection of a hidden COD (e.g., negligence)
 Clinical audit of the efficiency of clinical procedure/management
 Prognostic value
There are two types of autopsy: MEDICAL (patient died

immediately before, after, during a medical intervention); and
FORENSIC (suspicious death).
105. DOES THE AUTOPSY AT ALL TIMES GIVE A DEFINITIVE

ANSWER?
In most of cases, Yes, however 10% of medical (not forensic)

autopsies, a definitive cause of death cannot be reached.
106. WHAT ARE THE DIFFERENCES BETWEEN CAUSE,

MECHANISM AND MANNER OF DEATH?
Cause vs. mechanism of death

Cause of death (COD) is an initial occasion that started a chain of
events led to death, while mechanism of death is a chain of events
that were ignited by COD.
85
Example of cause of death: Acute myocardial infarction

Example of mechanism of death: Acute heart failure
Manner of death
 Natural Sudden death (see below)
 Unnatural: Accident, Suicide, Homicide (ASH)
 Undetermined
Causes of Natural Sudden Death
UNEXPLAINED: SIDS, SADS and SUDEP

- SIDS: sudden infant death syndrome (unexplained)
- SADS: sudden adult death syndrome (unexplained)
- SUDEP: sudden unexpected death in epilepsy (unexplained
EXPLAINED: Natural sudden deaths in adults

Cardiac
 Coronary Atherosclerosis
 Myocardial infarction (MI)
 Arrythmia and Ion channel defects e.g, Long QT syndrome
 Cardiomyopathy
 Pericarditis
 Myocarditis
 Mitral valve prolapsed, aortic stenosis
Lungs
 Pulmonary Embolism (PE)
 Pneumonia (infection, aspiration)
 Pneumothorax
 Asthma (status asthmaticus)
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Vascular
 Ruptured AAA (Abdominal Aortic Aneuryam)
 Dissecting aortic aneurysm
 Ruptured Berry aneurysm
Gastrointestinal
 Massive Haemorrhages (e.g., Oesophageal varices, Peptic
ulcer, AV malformation, Tumours)
 Gastroenteritis
 Pseudomembranous or fulminant colitis
CNS
 Cerebral stroke ( Cerebrovascular accident, CVA)
 Trauma
 Epilepsy
 Infection (Meningitis, Encephalitis)
 Colloid cyst of third ventricle
OTHERS:
Infections, anaphylaxis, Diabetic ketoacidosis
107. WHAT ARE THE DEATHS THAT SHOULD BE REPORTED

TO THE CORONER (UK) OR MEDICAL EXAMINER (US)?
Answer:
Any Accident, Suicide or Homicide (ASH) plus:

(a) Deaths at home if
• COD is uncertain
• The deceased was not attended by a doctor in last month
before death
• Death was sudden or unexpected
87
(b) Deaths in hospital if

• COD is uncertain
• Deceased died before diagnosis, pre or post operative
• Concern of negligence
• Industrial disease-related
• Death occurred in a Mental Hospital.
(c) Death reported by Police if
• Suspicious conditions
• Death is sudden or unexplained
• A dead body was found
(d) Death reported by a prison governor
(e) Others: sudden infant deaths (SIDs) & death of a child in care
Health and safety in Autopsy
108. IF YOU CAME ACROSS A NECROTIC LUNG LESION

UNEXPECTEDLY, WHAT THIS COULD BE? WHAT MEASURES DO
YOU TAKE?
Answer:
This lesion could be non infectious (cancer), but could also be
infectious like Tuberculosis (TB) or Aspergillosis. Therefore, measures
should immediately be done to minimise the risk of transmission,
including:
 Put lungs in formalin
 Mask
 Make others leave mortuary until lungs are in formalin
88
109. LIST HAZARD GROUPS PATHOGENS

Answer:
Hazard Group 1 – Biological agents that are unlikely to cause human
disease
Hazard Group 2 – Biological agents that cause human disease and

may be a hazard to laboratory workers, however they are unlikely to
spread to the community and there is usually effective prophylaxis or
treatment available.
Bacteria – Staphylococcus aureus, Streptococci, salmonella
Viruses – Adenovirus , CMV, EBV, HPV, Herpes, Hep A,
Coronavirus, mumps, measles, polio
Fungi - Aspergillus, candida, cryptococcus
Parasites– most are hazard group 2 (except Echinococcus, some
Leishmania spp, Plasmodium falciparum group 3)
Hazard Group 3 – Biological agents that can cause severe human

disease and present a serious hazard to laboratory workers, there is a
potential risk of spread to the community but effective prophylaxis or
treatment is usually available. Use triple sandwich gloves
(neoprene/latex/neoprene); fix brain 3 wks in formalin to disinfect
before cutting.
Bacteria – anthrax, brucella, E coli, TB
Viruses – Rabies, SARS, HIV, HCV, HBV, CJD, TB and VHFs-like
(viral Hemorrhagic fevers-like). VHFs-like include: Dengue, Yellow
Malaria, Leptospirosis and Nipah.
Fungi - Histoplasma
Parasites - Echinococcus, Some Leishmania spp, Plasmodium falciparum
89
Hazard Group 4 – Biological agents that can cause severe human

disease and present a serious hazard to laboratory workers, there is a
potential risk of spread to the community, but no effective
prophylaxis or treatment is available.
Absolute contraindication for autopsy
Bacteria – None
Viruses – Lassa fever, Ebola virus, Congo haemorrhagic fever
Fungi - None
110. WHAT SAFETY PRECAUTIONS DO YOU NEED TO TAKE BEFORE

DOING POST MORTEM EXAMINATION ON A PATIENT WHO IS
HCV+?
Answer:
 Notify mortuary staff
 Dedicated assistant (well trained mortuary technician assistant )
 Double glove, Kevlar/neoprene cut resistant gloves
 Surgical mask
 Eye visor
 Circulator
90
111. HOW DO YOU FORMULATE A CAUSE OF DEATH?

Answer:
Ia is the direct cause of death (e.g., pneumonia, multiorgan failure,
myocardial infarction, rupture of AAA (abdominal aortic aneurysm),
cerebral infarction, aspiration pneumonia...etc) caused by Ib (e.g.,
metastatic malignancy, atherosclerosis, chronic alcoholism...etc),
which is caused by Ic (e.g., immobility, multiple comorbidities...etc).
Note: Bottom line of I gets recorded by ONS. If two causes in bottom

line, the first one will only be recorded.
II is the contributing cause o death. Examples: Diabetes, morbid

obesity, hypertension..etc
112. WHEN ARE YOU ALLOWED TO RETAIN TISSUES WHEN

DOING A CORONER’S AUTOPSY?
Answer:
Tissue can be retained if this will be helpful in:
 Formulation of the cause of death by the pathologist
 Identification of the deceased
113. WHAT IS THE FUNCTION OF THE HUMAN TISSUE

AUTHORITY?
Answer:
The HTA regulates the removal, storage, use and disposal of human
bodies, organs and tissue for research, transplantation, education and
training, donation of solid organs and bone marrow from living donors
is also controlled by HTA.
91
Human Tissue Act 2004, is the main document in RCPath guidelines

to explain the instructions related to the use o human tissue.
114. WHAT IS PROHIBITED REGARDING TISSUE RETAINED AT

A CORONER’S AUTOPSY?
Answer:
No tissue should be retained after formulation of cause of death
The use of autopsy tissue for teaching or research is only allowed
after consent from next of kin.
115. ARE YOU ALLOWED TO UNDERGO RESEARCH ON

FRESH TISSUE FROM A COLECTOMY SPECIMEN IN THE
SURGICAL LABORATORY?
Answer:
Yes – if there is an ethical approval.
116. What are the stains that can be used to detect lesions
grossly (macroscopically)?
Answer:
Tetrazolium dye can be used to determine the extent of myocardial
infarct macroscopically (grossly)
117. WHAT CHANGES WOULD YOU SEE AFTER

RESUSCITATION ATTEMPTS?
Answer:
OUTSIDE
 Bruising on anterior chest wall (CPR), or mouth
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 Burns on anterior chest from defibrillation pads

 Holes for vascular access, chest drains or pericardiocentesis, or
pneumothorax decompression
 Endotracheal tube. Examine if it is in place (may be obstructed
or not inside the larynx lumen)
INSIDE
 Rib fractures/haemorrhages, anteriorly or laterally (Posterior
fractures are not resuscitation-related)
 Lung bruises
MICROSCOPIC EXAMINATION
 Bone marrow emboli (fat, haemopoeitic cells) in lungs
 Myocardial necrosis from adrenaline injection
118. ON CHECKING THE BODY ID, THERE ARE

DISCREPANCIES IN DATE OF BIRTH OR ADDRESS – WHAT
YOU SHOULD DO?
Answer:
Contact coroner’s office before starting the autopsy procedure (if
Coroner’s PM) or hospital registration and clinical department (if
Hospital PM)
119. HOW HISTOLOGY EXAMINATION WOULD BE USEFUL IN

DEFINING THE CAUSE OF DEATH?
Answer:
- To confirm the macroscopic diagnosis. Example; pneumonia
(always require a histologic confirmation), fatty change of the liver,
myocardial infarction, coronary atherosclerosis, tumours...etc
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- Macroscopically normal heart, in a suspected cardiac cause of

death.
- In SIDS, SUDEP and SADS. As these entities a diagnosis of
exclusion, normal tissue should be confirmed before using any o
these terms as COD.
- When medicolegal issues need confirmation.
120. SHOULD AUTOPSY BE A MUST IN PATHOLOGY

TRAINING?
Answer:
WITH AUTOPSY
- Widens your medical knowledge and skills
- Helps in clinicopathologic correlation
- Allows you to apply your academic pathology into practice
AGAINST AUTOPSY
- Autopsies complicates the training and requires extra time for
training
- Coroner’s autopsies are not part of the NHS
- Not of public interest
121. WHEN TOXICOLOGY SPECIMEN SHOULD BE TAKEN IN

AN AUTOPSY CASE?
Answer:
- When there is a history or suspicion of drug/alcohol abuse
- If there is a suspicion of intoxication
- In SIDS, SADS, SUDEP
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122. WHAT ARE THE COMPONENTS OF AN AUTOPSY REPORT

Answer:
Components of Autopsy report
Demographic data, clinical history, external examination, internal
examination, summary of findings, cause of death, COD (ONS
format), histology and further investigation
123. HOW THE CAUSE OF DEATH (COD) IS FORMULATED

ACCORDING TO ONS FORMAT?
Answer:
ONS format of COD
 Ia: direct cause of death due to Ib

 Ib: caused Ia and it is due to: Ic
 Ic: caused Ib
 II: contributing cause to death
124. GIVE THE CAUSE OF DEATH ACCORDING TO THE ONS

FORMAT?
JK, 90 year old, diabetic woman has died in the hospital. She had
dropped at home a few weeks earlier and got her right leg
broken. An internal fixation was done. She had lung
consolidation by X-ray few weeks later that was diagnosed as
lobar pneumonia. How can you certify the COD?
95
Answer:
This case should be discussed with the coroner, as death was
preceded by an accident, i.e., the fall resulting in a broken leg,
immobility and pneumonia.
Cause of death:
– Ia: pneumonia
– Ib: prolonged immobility
– Ic: leg fracture
– II: Diabetes Mellitus
96
CHAPTER 5
OSPES EXAMPLES
97
EXAMPLE NUMBER 1
STATION 1: clinical scenario – male, 50y complained of

haemoptysis, cough and weight loss over 4/52
 What is the differential diagnosis?
 What investigations would you recommend?
 What are the precautions needed when dealing with infected
sample like tuberculosis (TB)?
STATION 2: presentation:
Describe the role of the pathologist in management of a patient with
cervical cancer’ in layperson format to the general population (cervical
screening)
STATION 3: risk & management

 What is considered a clinical risk in NHS?
 How would you manage as a head of pathology department if
suddenly two consultants were absent due to unforeseen events?
 Poor clinical requests are used to arrive with tissue sample to the
pathology department. These requests are missing important clinical
information. What would you do to audit such clinical request?
STATION 4: portfolio/CV
 Do you consider yourself a good doctor? What shows this in your
portfolio?
 What is your greatest achievement?
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STATION 5: Clinicopathological Correlation

Examples include lung cancer, tuberculosis, pneumonia, heart
failure..etc
 What is the definition of Heart failure? Answer: Inability to
maintain normal cardiac output.
 What clinical signs do you find in an autopsy of a patient with
heart failure? Answer: generalised oedema, heart disease.
 What symptoms do patients with heart failure have? Answer:
fainting/syncope, fatigue, oedema, dyspnoea
 What is the main mechanism of such symptoms? Answer: Low
cardiac output and decreased venous return (congestion, increased
intravascular hydrostatic pressure oedema)
STATION 6: role of histopathologist

 How histopathologist differ from basic medical scientist (BMS)?
Answer: A histopathologist would have a clinical background
 Describe the role of the pathologist as a part of clinical team?
Answer: see team player
Written exam – 20 mins.

Example
An 80y old man died suddenly with past medical history of angina,
hypertension and diabetes
Questions:
 Describe possible autopsy findings. Answer: myocardial
infarction, cardiac enlargement, leg gangrene (DM), kidney
enlargement or atrophy (Hypertension, DM), cerebral
haemorrhage
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 What are the different causes of death in this case? Answer:

remember complications of atherosclerosis, hypertension and
diabetes.
 If this patient found to have in addition a massive cerebral
haemorrhage. How would you formulate the cause of death?
Answer: Ia: massive cerebral haemorrhage, Ib: due to
hypertension. II. Diabetes.
EXAMPLE NUMBER 2
STATION 1: Clinical governance

 What are the errors that may cause no harm, minor harm and
major harm to the patient?
 How to identify errors and how to deal with them?
 What a clinical audit means?
 How could you perform an audit?
 Why clinical audit is important?
 Describe audit cycle.
STATION 2: Management- Work Prioritisation

How to organise and prioritize the work in Pathology laboratory in
case of sudden shortage in consultant histopathologists?
STATION 3: Presentation Station

What is the role of the pathologist in breast/cervical screening?
STATION 4: Portfolio Station

- What items in your CV would support you as a pathologist?
100
- What are your best achievements?
STATION 5. Clinicopathological Correlation

Lung cancer
 Why shortness of breath (dyspnoea) is a common symptom in
patient with lung cancer? Answer: Mechanical obstruction of
bronchi, lung collapse, or pleural effusion.
 How lung cancer can cause pleural effusions? Answer: Tumour
penetration into pleura (haemothorax), tumour metastasis to
pleural cavity
101
102
CHAPTER 6
APPENDIX
103
PATHOLOGICAL STAGING AND GRADING
I. PATHOLOGICAL STAGING
 Non tumour staging: e.g., fibrosis staging in liver inflammation

 Tumour staging: Detailed below
Definition: Tumour Staging is the assessment of the degree of the spread of the
tumour. The staging could be clinical (cTNM) or pathological (pTNM).
Malignant tumours have the inherent ability to expand to nearby anatomical

planes (direct spread) and/ or to involve remote anatomical structures/organs
away from the original tumour (metastasis). This innate behaviour of
malignant tumours explains their deadly effect on the body.
The ability of the malignant tumour to metastasise has attracted a countless
research labour.
Tumour staging is the most important prognostic factor. Therefore, the

accuracy of staging procedure is crucial for determining the treatment options
VALUE OF STAGING
 Staging helps plan a person’s treatment.

 The stage can be used to estimate the person’s prognosis
 Linking the stage to histological grade
 Knowing the stage is important in identifying clinical trials that may be
suitable for a particular patient.
LIMITATIONS TO PATHOLOGICAL STAGING:
Anatomical site limitation:

Spleen: splenic biopsy is unknown in surgery. The only method to biopsy the
spleen is to do splenectomy, because of the extensive haemorrhage following
even a minute rupture of the capsule induced by the biopsy needle
Procedure limitation
Brain stem is non-accessible to surgery because the current procedure is
highly destructive in such location. The biopsy procedures have a high
percentage of complications, some of which could be fatal. Such
complications are currently hindered by the use of radiology-guided
procedures
104
Patient condition limitation:

Critically-ill patients are not amenable for biopsy, which may contribute to
deterioration of the patient condition and therefore other non-invasive staging
procedures may be employed.
Clinical staging used in the following cases

No surgical treatment
Adjuvant treatment done before surgery
Deficient data to stage pathologically
Sites Usually Staged Clinically:

Cervix
Head and neck, tumours
Lymphomas
Discrepancy in tumour staging between pathologic, clinical and

radiologic staging:
In some instances, there is difference between the tumour size evaluated

clinically/radiologically and the pathologic macroscopic staging. The possible
causes include:
Time elapsed between the clinical/radiologic assessment and the sampling of
the lesion for pathologic. This is a true difference and the pathologic
assessment should be considered the most accurate
Measurement discrepancy: maximum dimension of the lesion is the most
important and hence, the comparison should be done at this level or the three
dimensions of the lesion should be mentioned
Reaction surrounding the tumour, including fibrosis, necrosis, inflammation ,
haemorrhage and calcification may hinder the accuracy of Clinical/ radiologic
assessment compared to pathologic examination
Discrepancy between macroscopic and microscopic pathologic

staging:
Microscopic measurements are the most accurate, because it can precisely

exclude the peritumoural tissues, including fibrosis and deduct it from the
lesion size. However, the shrinkage of tissue following formalin fixation,
limitation of the size of the cassette and being chiefly a 2D measurement
implies some modification to improve it. These modifications include:
Composite blocks
Combination of microscopic examination and macroscopic measurement (3D
measurements)
Addition of 10% to the microscopic measurement, which equal the percentage
of tissue shrinkage as a result of formalin fixation.
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METHODS OF TUMOUR SPREAD

DIRECT SPREAD (T)
Direct spread means increase of the tumour size with subsequent invasion of
the surrounding normal structures. Direct spread is a preliminary step before
metastasis. The size of the tumour and the depth of invasion correlate with the
tumour ability to metastasise.
Steps of direct spread:
 Detachment: the tumour cells start to lose the adhesive substances and
molecules, like E-cadherin. Therefore, the cells will set free to move
away.
 Attachment: once the cells have lost their adhesive molecules, they
attach to the underlying basement membrane by new adhesion
molecules that recognises the basement membrane components
including laminin and collagen type IV.
 Penetration of basement membrane: the tumour cells start to secrete
lytic enzymes to destroy the basement membrane and underlying tissue,
to create more spaces for more free movements with the extracellular
matrix.
 Motility: acquiring motility in epithelial cells is a behavioural sign of
malignancy, that can be better observed in tumour culture. The cells
move towards the lymphatic and blood vessels.
Effects:
Direct spread of the tumour corresponds clinically to the local manifestations
of the tumour. These include:
 Perforation of a hollow organ wall, with subsequent loss of its content
within the nearby cavity, causing severe irritations like peritonitis, pleuritis
and effusions
 Penetration to the nearby organ, causing adhesions and fistulae formation
 Ulcer of the lining epithelium with subsequent haemorrhage. bleeding per
rectum in colorectal cancer or hematemesis in gastric cancer
 Haemorrhage: examples include fatal haemorrhage from lingual artery in
cancer tongue, haemoptysis in lung cancer due to erosion of
peribronchial vessels, haematuria in renal cancer and epistaxis in
nasopharyngeal tumours.
 Compression and Obstruction: examples include intestinal obstruction
(Chin, Wang et al.), superior vena cava (mediastinal) syndrome,
Pancoast tumour (apical lung carcinoma). Bilateral compression on both
ureters by retroperitoneal neoplasm or cervical carcinoma can lead to
bilateral hydronephrosis and renal failure
Mediastinal syndrome: compression of mediastinal structures by a growing

tumour mass, usually from central lung carcinoma. The manifestations are
summarised in Ds:
106
 Dysphagia: due to compression on the oesophagus

 Dyspepsia
 Dyspnoea: due to compression on the trachea
 Destruction of the Aorta
 Dysphonia/ Dysphasia: compression on the recurrent laryngeal nerve
 Dilated congested jugular veins, non-pulsating
Primary tumour
TX Primary tumor cannot be evaluated
T0 No evidence of primary tumor
Tis Carcinoma in situ
Ta: malignant tumour that is exophytic like non invasive papillary carcinoma
and verrucal carcinoma
T1, T2, T3, T4 Size and/or extent of the primary tumor
Size does not matted in hollow organ tumours in general including GI
adenocarcinomas, urothelial carcinoma, uterine adenocarcinoma and ovarian
tumours in addition to thymic carcinoma
Size is crucial in carcinoid tumours, renal cell carcinoma, cervical carcinoma,
Maximum extension of all tumours is the main representative of the tumour

except in cervical carcinoma where both transverse and longitudinal
diameters are needed.
Metastasis (N, M):
Metastasis (Greek = displacement, plural: metastases), occasionally

shortened as mets
Metastasis is the single most important difference between benign and

malignant tumours.
The ability of the malignant tumours to metastasise varies from one tumour
type to the other. Sarcomas in general are more frequently metastasise than
carcinomas. On the other hand, some malignant tumours do not have
capacity to metastasise and therefore recognised as “locally malignant
tumours”. Examples of the last category include gliomas, basal cell
carcinoma, ameloblastoma, most of giant cell tumours of bone and
craniopharyngeoma.
o
When tumour cells metastasize, the new tumour is called a secondary, 2 ,
metastatic tumour implants, deposits, or mets, while the original tumour called
o
primary tumour or 1
Methods of tumour metastasis
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Lymphatic spread: the prefered method of metastasis by carcinoma.

However, some sarcomas may give lymph node deposits. Examples include
synovial sarcoma and rhabdomyosarcoma.
Tumour Emboli
Permeation: continuous cord of tumour cells travel through the lymphatics to
LN
Retrograde lymphatic spread: tumour emboli travel to a common sharing
tissue like skin
Haematogenous (blood) spread: the preferred method of metastasis by

sarcomas. However, some carcinomas are recognised by their propensity for
hematogenous spread. Of these, follicular thyroid carcinoma,
choriocarcinoma, hepatocellular carcinoma, renal cell carcinoma
Perineural spread: preferred mean of spread in prostatic adenocarcinoma

and pancreatic adenocarcinoma
Implantation: tract of fine needle biopsy, or dislodged malignant cells during

surgical operation
Inoculation (contact metastasis): a tumour of one labia or lip transmitted to
the normal facing side
Transluminal spread: tumour cells drop off and form another tumour in a
luminal structure like bronchus or intestine
Transcoelomic spread: tumour cells separate from the original tumour and
become lodged on the surface of another organ. Kruckenberg tumour of the
ovary is an example, however there is a debate that kruckenberg tumour may
represent a lymphatic spread
Note : mimics of metastasis in malignant tumours

Field effect: urothelial tumours are known to be multifocal, in the background
of multifocal CIS
Synchronous/ metachronous tumours: incidental two tumours arise
separately at same time (synchronous) or within a period of time
(metachronous)
Effects of metastasis
Metastasis is the most important negative prognostic factor in tumours
Failure of vital organs
Pathological Fracture
All the local effects of the primary tumour but in other organs, examples:
In lymph nodes, a common symptom is lymphadenopathy
Lungs: cough, hemoptysis and dyspnea (shortness of breath)
Liver: hepatomegaly (enlarged liver) and jaundice
Bones: bone pain, fracture of affected bones
Brain: neurological symptoms such as headaches, seizures, and vertigo
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GENERAL RULES OF PATHOLOGICAL TNM STAGING FOR CANCER
 For gynaecological tumours, there is in addition the FIGO classification

 For colon carcinoma there is Duke’s in addition to TNM
 Ipsilateral =same side
 Contra lateral = opposite side
 Midline nodes are considered ipsilateral nodes.
 Radical neck dissection specimen usually yield 10 or more LNs
 12 pericolic LNs is median number for colectomy specimen
 New staging following radio-chemotherapy will be assigned “ y”. This could be
pathological (yp) or clinical (yc) staging
 No TNM staging for thymic carcinoma, phyllodes or brain tumours in
TNM7.
 No T1 or T2 in mucosal melanoma. Not T1, T2 or T3 in anaplastic thyroid
ca. No T1 in radical prostatectomy for adenocarcinoma as T1 is reserved
for prostatic biopsies
 Multiple synchronous tumours of same type in one organ, stage using
highest T stage and add (m) for multiple, e.g., T3 (m) or number of
tumours , e.g., T3 (3)
 Synchronous bilateral tumours, classify individually, e.g. in both ovaries,
both adrenals, both thyroid lobes or both liver lobes
 T4 generally (and specifically head and neck) indicates an advanced disease
where:
T4a: Moderately advanced local disease = deep local invasion or skin
over
T4b: Very advanced local disease = adjacent, vital or remote tissue
invasion
 Microscopic features included in staging in certain tumours, e.g., necrosis
in soft tissue, grade in soft tissue, bone and penile tumours, mitosis in
melanoma, histological subtype in thyroid carcinoma
 Regional LNs differ according to anatomical site.
 Size for pN is the size of metastatic deposit, not of the entire LN.
 Number of LNs is lower in post-neoadjuvant cancer resections
 No “MX” or “pM0” in in TNM7. If a biopsy is negative for metastasis, it is
cM0 or consider no pM stage in this case.
 Completeness of Resection (R): this is required in many tumour resection
staging and considered an important prognostic factor; however, it is not
always possible to comment on. This is divided into:
R0: T completely excised locally
R1: microscopic involvement of margin by T (to within 1mm)
R2: macroscopic T left behind or gross involvement of margin
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Completeness of resection also includes circumferential (non peritonealised)

margins of the oesophagus and rectum (also ascending and descending
colon), vascular and bronchial margins of the lung, vascular and ureteric
margins of the kidney.
Grossly the comment of total mesorectal excision (TME) grading in rectal
cancer and total mesocolic resection (TMC) in colon cancer are
complementary to the degree of perfection of removal of the tumour
Note: Completeness of resection is an independent prognostic factor.
 Perineural Invasion “Pn”, essential to be assessed in prostate and pancreas
 After radio/chemotherapy, new staging will be assigned yTNM.
Retreatment staging, following recurrence will be assigned rTNM.
Tumour regression grading (TRG) = tumour response to therapy.
 Stage grouping: different combinations of T+N+M that yield the final
stage of the disease. This varies according to tumour type. In all TNM
stage grouping, the final stage is IV, which indicates an advanced
disease except in nephroblastoma-Wilms tumour- where there is stage V
in bilateral disease
 Micromets: diagnosed after SLNB and lymphadenectomy (clinically
occult)
 Macromets: clinical LN mets confirmed by bx or LN mets + extensive
ECE (clinically apparent). Note: clinically detected = detected by imaging
(not lymphoscintigraphy) or by clinical exam.
 N1, N2, N3: Involvement of regional LNs (size, side, number or anatomical
site)
Abbreviations:
T: Tumour,
LN: Lymph node,
SLNB or (sn): sentinel LN Bx,
(i): LN metastasis detected by IHC,
LVI: lymphovascular invasion,
LP: Lamina propria,
SM: Submucosa,
MP: Muscularis propria,
MM: Muscularis mucosa,
SS: Subserosa,
ECE: extracapsular extension
Note:
 When M not mentioned in the text, M1= distant mets
 When N not mentioned in the text, N1= regional LNs mets
TNM grouping
Stage grouping:
• Anatomical extent of disease, composed of T, N, and M categories alone in
different combinations. Any M1= Stage IV
Prognostic Grouping:
• T, N, and M plus other prognostic factors, e.g., serum hormone level,
mutations…etc
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SUMMARY OF PATHOLOGICAL TNM, 7TH EDITION

HEAD AND NECK TUMOURS
 Head & neck carcinomas only included. Other tumours like lymphoma or
soft issue tumours staged differently.
 T size not considered in mucosal melanoma, nasal sinuses, nasopharynx
and larynx
 Extracapsular Extension (ECE), histologic grade, LVI and resection
margins status are important prognostic factors
 Carotid involvement is by encasing not by invading it
 Cervical LN dissection includes levels I-VII
 Cervical Lymph nodes (neck block dissection specimen):
Level 1: submental & submandibular , Level 2: Upper jugular , Level 3: Mid-
jugular, Level 4: Lower jugular, Level 5: Posterior triangle LNs, Level 6:
Prelaryngeal , Pretracheal & Paratracheal, Level 7: Upper mediastinal
Lip, Oral Cavity, Oropharynx, Hypopharynx
T1: ≤2cm
T2: > 2 - 4 cm
T3: > 4cm
T4 differs according to the anatomical site:
 T4a (lip): skin of nose/chin, inferior alveolar nerve, mouth floor or through
cortical bone
 T4a (oral cavity): skin of face, deep tongue muscles, maxillary sinus or
through cortical bone.
 T4b (lip+oral): masticular space, pterygoid plates, skull base or carotid.
 T4a (oropharynx): larynx, medial pterygoid, deep tongue muscles
 T4b (oropharynx): lateral pterygoid muscle, skull base, carotid
 T4a (hypopharynx): cricoid, hyoid , thyroid cartilage, or central soft tissue
 T4b( hypopharynx): prevertebral fascia, carotid, or mediastinum
Notes:
Oral cavity involves the tongue, floor of the mouth
Superficial bone erosion ≠T4
Lip has three compartments, each staged differently:
-Vermilion surface and commissures, staged under the lip as above
-Hair bearing area of the lip is staged under skin cancer
-Inner mucosal surface of the lip, staged under oral cavity
Mucosal Melanoma
No T1 or T2 in mucosal melanoma staging, due to their aggressiveness
T3: Epithelium/ submucosa
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T4a: Deep local invasion (soft tissue, cartilage, bone) or overlying skin
T4b: Adjacent (skull base, carotid, masticator or prevertebral space), vital
(skull contents: brain, dura or cranial nerves) or remote structures
(mediastinum)
Salivary gland
T1: ≤ 2 cm, inside gland
T2: >2 - 4 cm, inside gland
T3: >4 and/or outside gland (extraparenchymal extension)
T4a: Deep local invasion (mandible, ear, facial nerve) or overlying skin
T4b: Adjacent ( skull, pterygoid plates) or vital (carotid)
Note: extraparenchymal extension evaluated clinically or macroscopic NOT
microscopic.
N for all previous (lip, oro-hypopharynx, larynx, nose/paranasal salivary
and oesophagus:
N1: Ipsilateral single ≤3 cm
N2: ipsilateral 3 - 6 cm (single/multiple) or any size (bilateral/contralateral)
N2a: Ipsilateral single >3 - 6 cm
N2b: Ipsilateral multiple, any ≤6 cm
N2c: Bilateral or contralateral, any ≤6 cm
N3: any >6 cm
THYROID
Papillary/follicular/medullary/Hurthle:
T1: ≤ 2cm, intrathyroid
T2: >2-4cm, intrathyroid
T3: > 4cm or minimal extrathyroid extension
T4a: larynx, trachea, oesophagus, recurrent laryngeal nerve or subcutaneous
T4b: prevertebral fascia, carotid or mediastinal vessels
Anaplastic/undifferentiated: (no T1,T2 or T3. Any size)
T4a: intrathyroid
T4b: extrathyroid
N1a: cervical level VI (pre/paratracheal, prelaryngeal)

N1b: cervical other levels (uni-, bi-, or contralateral), retropharyngeal or
mediastinal
Stage grouping differs according to age (<45 or >45), histological type
(papillary/follicular vs. medullary vs. anaplastic). Note: follicular/papillary <45
staged I or II only, no stage III or IV, while anaplastic is stage IV by definition.
GASTROINTESTINAL TRACT
Stomach
Tis: CIS/ high grade dysplasia
T1: LP or SM ( T1a: LP, T1b: SM )
T2: MP
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T3: SS (also extension to lesser /greater omentum without perforation)

T4a: Perforates serosa
T4b: invades adjacent structures
N1: 1 - 2 LNs, N2: 3 -6 LNs, N3a: 7 - 15 LNs, N3b: ≥ 16 LNs
M1: distant mets, positive peritoneal cytology or peritoneal bx
Pancreas
Both exocrine (adenocarcinoma) and neuroendocrine tumours
Tis: CIS (high grade PanIN)
T1: limited to pancreas, ≤ 2cm
T2: limited to pancreas, >2cm
T3: beyond pancreas, but not T4
T4: celiac axis or SMA
Prognostic factors:
Exocrine: Preoperative CA 19-9 & CEA
Endocrine: Preoperative plasma chromogranin A level (CgA) + Mitotic count
N1: Regional lymph node metastasis
Colon-Rectum
T1: SM
T2: MP
T3: SS, non-peritonealized pericolic/perirectal tissues
T4a: perforates visceral peritoneum
T4b: invades other organs
N1: 1 -3 LNs (N1a: 1 LN, N1b: 2 – 3 LNs, N1c: Satellites in SS, without LN
mets)
N2: ≥ 4 LNs ( N2a: 4 – 6 LNs, N2b:≥ 7 LNs)
M1: Distant mets, 1 organ (M1a), > 1 organ or peritoneum (M1b)
Dukes' staging:
A: Inv. into but not through bowel wall
B: Inv. through bowel wall
C: LN mets
D: systemic mets
Modified Dukes' (Astler-Coller)
A: Limited to mucosa
B1: Inv into but not penetrating through MP
B2: Penetrating through MP
C1: B1+ LN mets
C2: B2 + LN mets
D: systemic mets
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Note: Neuroendocrine tumours (NET) Staging

GI tract:
• Carcinoid of stomach, SI, LI and appendix: individual staging according to
site
• Mucinous (goblet) carcinoid staged as carcinoma
Pancreas and Lung: any NET staged as carcinoma
Skin: Merkel cell carcinoma staged differently from Non-Merkel
Small cell or large cell NET of any site: staged as carcinoma
Carcinoids (NET) of Gastrointestinal Tract

The ENETS and UICC TNM staging of neuroendocrine tumours
Appendix (classic carcinoid)
T1= ≤ 2 cm, (T1a: ≤1cm, T1b: >1-2cm)
T2= > 2 – 4 cm or involves caecum,
T3= > 4 cm or involves ileum,
T4= Perforates peritoneum or other organs
Small intestine
T1: LP/SM & ≤1 cm, T2: MP or > 1 cm, T3: SS or pancreas/retroperitoneum
(ampullary), T4: Perforates serosa or other organs
Stomach
Tis: < 0.5 mm (in situ, confined to mucosa),
T1: LP/SM & ≤ 1 cm,
T2: MP or > 1 cm
T3: SS,
T4: Perforates serosa or other organs
Large intestine
T1: LP/SM & ≤2cm (T1a: < 1 cm, T1b: 1 - 2 cm)
T2: MP or > 2 cm
T3: SS
T4: Perforates serosa or other organs
ENETS introduced the grading of carcinoid (NET) based on the Ki-67 index.
Ki-67 index = % of Ki-67 (+) cells/2000 cells. Grade 1= <2%, Grade 2= 2-20%,
Grade 3= >20%
Liver, bile ducts & Gall bladder
HEPATOCELLULAR CARCINOMA
T1: single, No LVI,
T2: single + LVI or multiple + any < 5 cm,
T3a: Multiple + any >5 cm T3b: invades major branch of portal/hepatic vein,
T4: other organs (not gall bladder) or perforation of visceral peritoneum
RESPIRATORY TRACT (lower)

114
Lung, NSCC, SCC and carcinoid

T1: ≤3 cm (T1a: ≤ 2 cm, T1b: > 2 - 3 cm) – not in main bronchus
T2: >3 -7cm or T in main bronchus ≥ 2 cm from carina or invades visceral
pleura or partial atelectasis
T2a: >3 - 5 cm
T2b: >5 -7 cm
T3: > 7 cm or T in main bronchus <2 cm from carina or invades parietal
pleura, chest wall, diaphragm, pericardium, mediastinal pleura or total
atelectasis or separate nodule(s) in same lobe
T4: Mediastinum (heart, carina...) or separate nodules in ipsilat lobe
N1: Ipsilateral peribronchial/ hilar nodes
N2: Ipsilateral mediastinal/ subcarinal
N3: Contralateral mediastinal, hilar, scalene or supraclav
Regional lymph nodes
N1 nodes: 10= Hilar, 11= Interlobar (peribronchial), Intrapulmonary including
12= Lobar, 13= Segmental, 14= Subsegmental)
N2 nodes: 1= Highest mediastinal, 2 =Upper paratracheal, 3 =Prevascular
and retrotracheal, 4 =Lower paratracheal, 5= Subaortic, 6= Para-aortic, 7=
Subcarinal, 8= Paraesophageal, 9= Pulmonary ligament
N3 nodes: any contralateral LNs
M1a: T nodule(s) in contralat lung, pleural nodules or malignant

pleural/pericardial effusion
M1b: Distant mets
Note: pleural invasion known after H&E combined with elastic stain
FEMALE ORGANS
A-Breast
Tis (DCIS / LCIS/Paget’s)

T1: T in mm (T1mi :≤ 1mm, T1a: >1- 5mm, T1b: >5 -10mm, T1c: >10 -20mm)
T2: > 2-5cm,
T3: > 5cm
T4a: Chest wall (not pectoralis), T4b: Skin (ulcer, nodules or edema “peau d’
orange”. Note: Dermis only ≠ T4), T4c: T4a + T4b, T4d: Inflammatory
carcinoma (clinically= erythema + oedema “peau d’ orange” ≥1/3 breast skin,
pathologically dermal lymphatic emboli + invasive tumour)
N1mi: micromets = >0.2 or >200cells, but any <2mm. Note: ITCs (isolated
tumour cells): < 0.2 mm or < 200 cells in one section (considered N0, or
=N0(i+) if detected only by IHC)
N1a: 1-3 axillary, >2mm (macromets)

N1b: int. mamm mets by SLNB, not clinically
N1c: 1-3 axillary + int. mamm mets by SLNB, occult clinically
N2a: 4-9 axillary
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N2b: Int mamm, clinically

N3a: ≥10 axillary, or infraclav
N3b: int. mamm, clinically or >3 axillary + Int. mamm, by SLNB, occult
clinically
N3c: supraclav
Breast regional LNs (all ipsilateral) :
1. Axillary (intramammary LNs counted as axillary):
Level1 (low axilla)
Level2 (mid axilla) include Rotter [interpectoral LN]
Level3 (apical axilla), include infraclav
2. Internal mammary LNs
3. Supraclav LN
Any other LNs, including cervical or contralateral LNs = M1
Definitions:
N1& N2: Level1& 2 axillary, N3: Level3, infraclav, supraclav, Internal mamm.
cM0(i+): Molecularly/micro-detected T cells in circulating blood, bone marrow
or other non-regional nodal tissue < 0.2 mm in patient without symptoms or
signs of metastases
M1: mets detected clinically/ radiographic or histologically > 0.2 mm
Intramammary LNs are staged under axillary
B- Female genital tract

Cervix
Tis: In situ
T1: Confined to uterus
T1a: microscopic only (clinically occult)
T1a1: Depth <3 mm, horizontal <7 mm
T1a2: Depth >3-5 mm, horizontal <7mm
T1b: Depth> T1a2, or clinically detected
T1b1 <4cm
T1b2: >4 cm
T2: Beyond uterus but not pelvic wall or lower 1/3 vagina
T2a: No parametrium
T2b: Parametrium
T3: Lower 1/3 vagina/pelvic wall/hydronephrosis
T3a: Lower 1/3 vagina
T3b: Pelvic wall/hydronephrosis
T4: Mucosa of bladder/rectum; beyond true pelvis
Note: FIGO follows TNM exactly, e.g., T1b2 = IB2, except T4=IVA
IVB= M1
Corpus
Adenocarcinoma and carcinosarcoma

Tis: In situ
T1: within corpus
T1a: endometrium or < ½ myometrium
116
T1b: ≥ ½ myometrium
T2: cervical stroma (glandular invasion only = T1)
T3: Local or regional
T3a: serosa or adnexa
T3b: vagina or parametrium
T4: mucosa of bladder/rectum
N1: pelvic LNs
N2: para-aortic LNs
M1: Inguinal LNs, peritoneuml or distant organs e.g., lung, liver
Grading of Endometrioid adenocarcinomas:

 G1= ≤5% , G2= 6-50% , G3= > 50% (of non-squamous or non-morular -NS/NM-
solid growth pattern)
 Marked nuclear atypia increases the grade by 1.
 Serous, clear cell, and mixed mesodermal tumors = Grade 3.
Ovary
T1: Limited to the ovaries
T1a: 1 ovary, capsule intact
T1b: 2 ovaries, capsule intact
T1c: Capsule ruptured, T on surface, malignant cells in ascites/wash
T2: Pelvic extension
T2a: Uterus, tube(s)
T2b: Other pelvic tissues
T2c: Malignant cells in ascites or peritoneal washings
T3: Peritoneal mets outside pelvis
T3a: Microscopic mets
T3b: Macroscopic mets ≤2cm
T3c: Macroscopic mets >2 cm
N1: Regional LN mets
M1: Distant mets (excludes peritoneal mets)
Note: FIGO staging like cervix
MALE ORGANS
Prostate
T1: Not palpable or visible by imaging
T1a: incidental, ≤5% of tissue resected (prostate TURP)
T1b: incidental, >5% of tissue resected (prostate TURP)
T1c: detected by needle bx, after high PSA
T2: Confined within prostate (or apex involvement but intact capsule)
T2a: ≤ ½ of 1 lobe
T2b: > ½ of 1 lobe
T2c: Both lobes
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T3: Extraprostatic extension (Note: Invasion into apex or into-but not beyond-
prostatic capsule = T2)
T3a: Extracapsular/bladder neck extension (base)
T3b: Seminal vesicle (SV)
T4: Fixed or invades adjacent structures, not SV
N1: Regional LN(s)
M1a: Non-regional LNs
M1b: Bone
M1c: Other sites
Note:
 Positive inked (intra/extracapsular) margin = R1
 Stage grouping involves PSA level and Gleason score
 Clinically important parameters: Gleason 1ry, 2ry and 3ry patterns and
No. of (+) /examined bx cores
 Differentiation grade:
 Gleason ≤ 6 Well differentiated, G1
 Gleason 7 Moderately differentiated, G2
 Gleason 8-10 Poorly differentiated/undifferentiated, G3
Testis
Tis: Intratubular (ITGCN)
T1: within testis & epididymis, no LVI
T2: within testis & epididymis + LVI or T. vaginalis invasion (If T. albuginea
only= T1)
T3: Spermatic cord ± LVI
T4: Scrotum ± LVI
N1: ≤ 2 cm and or ≤ 5 LNs, none >2cm
N2: >2 -5 cm or >5 LNs, none >5cm or or extranodal extension
N3: > 5 cm
M1a: Non-regional LNs or lung
M1b: Other sites
Serum tumour markers level (S) included in the stage grouping.
Serum Tumour Markers (S)
S0 = normal
S1 : LDH < 1.5 X N and hCG : < 5K and AFP : < 1K
S2 : LDH 1.5 –10 x N or hCG: 5K–50K or AFP: 1K–10K
S3: LDH > 10 x N or hCG : > 50K or AFP : > 10K
URINARY SYSTEM / ADRENAL
Kidney
T1: ≤7 cm, within the kidney (T1a: ≤4 cm, T1b:>4cm )
T2: >7 cm, within the kidney (T2a: >7-10cm, T2b: >10cm)
T3: major veins or perinephric/peripelvic fat (grossly)
T3a: Renal vein or perinephric/peripelvic fat
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T3b: extends to Vena cava < diaphragm

T3c: extends to Vena cava > diaphragm or invades vena cava wall
T4: Beyond Gerota fascia or adrenal (ipsilateral)
N1: 1 LN
N2: >1 LN
Urinary bladder TCC
Tis: In situ: "flat T"
Ta: Non-invasive papillary
T1: Subepithelial CT
T2: MP
T2a: Inner ½,
T2b: Outer ½
T3: perivesical (beyond muscularis)
T3a: microscopic
T3b: macroscopic
T4: Extravesical organs/structures
T4a: prostatic stroma, uterus, vagina
T4b: pelvic wall, abdominal wall
N1: 1 LN mets in true pelvis (hypogastric, obturator, external iliac or presacral
LN)
N2: >1 LN mets in the true pelvis
N3: mets in common iliac LN
SOFT TISSUE SARCOMA (STS)

As a part of the staging, histological diagnosis and grading into low/high grade
is essential. Some tumours are high grade by definition. Examples include
MFH, synovial sarcoma, soft part alveolar sarcoma
T1: ≤ cm (T1a: Superficial, T1b: Deep)
T2: >5 cm ( T2a: Superficial, T2b: Deep)
Notes:
 Superficial = all the tumour above superficial facia without invasion to the
fascia. Muscle involvement = deep location.
 Stage grouping includes grade.
 STS not included in TNM: Kaposi, angiosarcoma, DFSP, fibromatosis,
GIST and STS of viscra (hollow or parenchymatous) or brain
BONE TUMOURS
The staging applies to all primary malignant bone tumours except lymphomas,
multiple myeloma, juxtacortical osteosarcoma/chondrosarcoma.
T1:≤ 8cm, T2: >8cm, T3: Discontinuous Ts in primary site
N1: Regional
M1a: Lung (no. of mets clinically important), M1b: Other sites
Grade: Low grade, High grade
Stage grouping includes grade (high grade tumours include Ewing’s)
Percentage of necrosis following Tx should be included in the report
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SKIN TUMOURS
Squamous cell carcinoma ‘SCC’
T1: ≤2 cm + <2 high-risk factors

T2: >2 cm or any size + ≥2 high-risk factors
T3: Deep structures (muscle, cartilage, bone)
T4: Skull base, axial skeleton
N1: 1 LN ≤ 3 cm
N2: 1 LN >3 -6 cm, or multiple ≤6 cm
N3: Any > 6 cm
High risk factors:
Depth/invasion: >2mm (AJCC) or >4mm (UICC), Clark IV, Perineural inv or
LVI
Site: ear, hair-bearing lip
Differentiation: poorly or undiff
Melanoma
Tis: in situ, lentigo maligna melanoma
T1: ≤1.0 mm in thickness
2
T1a: ≤ 1mm, Clark 2/3, no ulcer + mitosis <1/mm
2
T1b: ≤ 1mm Clark 4/ 5 + ulcer or mitoses ≥ 1/mm
T2: > 1-2mm (T2a: no ulcer, T2b: + ulcer)
T3: >2-4mm (T3a: no ulcer, T3b: + ulcer)
T4: >4mm (T4a: no ulcer, T4b: + ulcer)
N1: 1LN (N1a: micro, N1b: macro)
N2: 2-3 LNs (N2a: micro, N2b: macro, N2c: satellite/in-transit + no LN mets)
N3: ≥4LN or matted or satellite/in-transit + LN mets
M1a: distant skin/subcutaneous tissues, or distant LNs
M1b: lung
M1c: other viscera or any site + elevated serum LDH
Prognostic factors:
Depth, ulcer, serum LDH, mitosis, tumour infiltrating lymphocytes (TIL), Clark
level, vertical growth pattern, regression
II. PATHOLOGICAL GRADING

Pathological grading includes:
A. Tumour grading
B. Tumour responce grading (following radio, chemotherapy)
C. Non-Tumour grading: examples;
 Hepatitis activity index (HAI): grading of necoinflammatory reaction in
liver inflammation.
 Lupus nephritis grading
 Grading of graft (transplant) rejection
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TUMOUR GRADING
Grading of a tumour is done based on tumour differentiation (differentiation =

resmbelence of the tumour to tissue of origin)
Grading includes assessment of both the architectural and cytologic features

of the tumour.
Combined architecture and cytology: most of tumours
Pure architecture grading: Gleason’s in prostate
Nuclear grading: RCC, DCIS
Grading is included in tumour staging in brain tumours

High-grade tumours require wider excision, has high rate of recurrence and
poor prognosis
Low grade = well differentiated= grade 1
High grade = poorly differentiated= grade 3
ADENOCARCINOMA
Grade 1: >95% of tumour composed of glands

Grade 2: 50% to 95% of tumour composed of glands
Grade 3: 5% to 49% of tumour composed of glands
Grade 4: <5% of glands
SQUAMOUS CELL CARCINOMA
Sites: oral, skin, oesophagus
• G1, Well differentiated, low grade: nests of squamous + prominent cell

borders+ keratin pearl formation. (in keratinizing type)
• G2, Moderately diferentaiated, intermediate grade, small nests of squamous
C. + moderate pleomorphism
• G3, Poorly differentiated, high grade: sheets of anaplastic cells + severe
pleomorphism+ ill-defined cell borders.
NEUROENDOCRINE TUMOURS
Neuroendocrine markers used to define neuroendocrine markers

(Synaptophysin, Chromogranin and CD56), however Ki67 proliferation index
is required for grading (in addition to morphology) for pancreatic and GI
neuroendocrine tumours (NETs)
G1: (well differentiated, low grade, carcinoid): Ki-67 index <2%

G2: (intermediate grade, atypical carcinoid): Ki-67 index 2- 20%
G3: (poorly differentiated, high grade, NE carcinoma): Ki-67 index >20%
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PROSTATE GLEASON GRADING AND GLEASON SCORE
Gleason score is between 2 -10 and it is the sum of primary (most prevalent
grade) and secondary pattern (worst grade)
Gleason patterns (grades)

Gleason grade 1: well circumscribed nodules of single, separate glands. Not
diagnosed in needle biopsies
Gleason grade 2: as grade 1 but some variabilities in gland size. Not
diagnosed in needle biopsies
Gleason grade 3: Single, separate, variable glands, irregularly separated,
ragged, poorly defined edge.
Gleason grade 4 : fused/cribriform glands. Ductal carcinoma is grade 4
Gleason grade 5: either single cells with no glands or comedo pattern
BREAST CARCINOMA GRADING

Elston / Nottingham modification of Bloom-Richardson system. The system
assess three parameters:
Tumor tubule formation:

1 point: > 75% of tumor
2 points: 10 - 75% of tumor
3 points: < 10% of tumor
Mitotic count/10hpf
1 point: 0 - 9
2 points: 10 - 19
3 points: 20+
Nuclear pleomorphism:
1 point: mild
2 points: moderate
3 points: severe
Final Scoring
3 - 5 points: Grade 1
6 - 7 points; Grade 2
8 - 9 points: Grade 3
RENAL CELL CARCINOMA
Fuhrman grading system is a nuclear grading system uses the low

magnification power to grade the nuclei in the worst area of the tumour
Fuhrman’s grading system is used for clear cell and papillary renal cell
carcinomas
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Grade 1: Nucleoli are absent or inconspicuous and basophilic at 400x

magnification
Grade 2: Nucleoli are conspicuous and eosinophilic at 400x and visible but
not prominent at 100x
Grade 3: Nucleoli are conspicuous and eosinophilic at 100x
Grade 4: Extreme nuclear pleomorphism, multinucleate giant cells, and/or
rhabdoid and/or sarcomatoid differentiation
CERVICAL INTRAEPITHELIAL NEOPLSIA (CIN)
CIN 1, mild squamous dysplasia, +/-HPV related changes (koilocytic changes,

arisainoid nuclei)
CIN 2, moderate squamous dysplasia, lower 2/3
CIN 3, severe squamous dysplasia, full thickness, may involve the squamous
metaplastic crypts.
TUMOUR RESPONCE GRADING

Tumour regression grading (TRG) evaluates the response of a malignant
tumour to preoperative chemo/radiotherapy in colorectal cancer
TRG4: total regression of the tumour, no viable tumour cells (tumour ablation).
The tumour mass becomes totally necrotic or fibrosed.
TRG3: fibrosis/necrosis occupies most of the residual tumour mass (>50%
tumour regression)
TRG2: dominant tumour with fibrosis/necrosis in 25-50% of the tumour mass
TRG1: minor regression, fibrosis/necrosis in <25% of the tumour mass
TRG0: no regression (chemo/radio-resistant tumour)
NON TUMOUR GRADING
METHOTREXATE INDUCED LIVER DISEASE
Grade 1: mild fatty change + mild portal inflammation

Grade 2: G1 + focal necrosis
Grade 3a: G2 + Mild portal fibrosis
Grade 3b: interface hepatitis or bridging fibrosis
Grade 4: cirrhosis
BANFF SCORES FOR ACUTE HEPATIC CELLULAR REJECTION:
Portal inflammation:
Score 1: lymphocytes in some portal tracts
Score 2: lymphocytes+ neutrophils + eosinophils in most portal tracts
Score 3: Score 2 + spillover into peripotal hepatocytes
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Bile duct:
Score1: few bile ducts inflitrated by inflammatory cells
Score 2: all bile ducts infiltrated by inflammatory cells + cellular atypia in some
bile ducts
Score 3: cellular atypis in all bile ducts
Endothelial inflammation:
Score 1: subendotheial lymphocytic infiltrate in venules in some portal tracts
Score 2: score 1 but in most portal tracts
Score 3: as score 2 + perivascular inflammation and necrosis
Final score
<3 not diagnostic of rejection
4-5 mild
6-7 moderate
8-9 severe
MISCELLANEOUS SUBJECTS
Diseases caused by hyperestrinism:
 Senile prostatic hyperplasia

 Gynecomastia
 Cancer breast
 Leiomyoma
 Cancer body
 Cancer cervix
 Endometrial hyperplasia
 Endometriosis
 Hypertension
 Fibrocystic disease
 Fibroadenoma
 Some manifestation of liver cell failure ( spider nevi and palmar erythema)
Pseudo in pathology
Pseudo means false. The following are common terms in pathology which
include (pseudo):
 Pseudo-membranous inflammation
 pseudo ( false) aneurysm (not a part of arterial wall e.g A-V fistula)
 pseudo ( false) diverticulum ( its wall = mucosa + s.mucosa only e.g
pulsion div of oesophagus)
 Pseudo-rosette (cells arranged around a Bl.v not a lumen e.g
Neuroblastoma)
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 Pseudo-cyst (no lining e.g. pancreatic)

 Pseudo-myxoma peritonii (rupture of mucin containing cavity into
peritoneum)
 Pseudo-Meig’s syndrome (if ovarian tumour is not a fibroma)
 Pseudo-fungi (Actinomyces)
 Pseudo-tumour (inflammatory mass)
 Pseudo-epitheliomatous hyperplasia (marked hypeplasia of epidermis in
severe inflammation, looks like squamous cell carcinoma)
Mass in Right iliac fossa (RIF)

Intestinal causes:
 Ileocecal crohn’s
 Ileocecal intususception
 Ileocecal actinomycosis
 Ileocecal TB
 Ileocecal lymphoma
 Ameboma ( amebic pericolic mass)
 Appendicular mass ( ruptured appendix+ peritoneum+fibrosis+intestinal
loops)
 Cancer cecum
Extraintestinal causes:
 Ptosed (dropped) kidney due to loss of fat in strict diet
 Ovarian mass (tumour, cyst , Abscess)
 Huge splenomegally
Mass In Left Iliac fossa (LIF)
Intestinal causes:
 Volvulous of Sigmoid
 Cancer sigmoid
 Bilharzioma ( Bilharzial pericolic mass)
Extra-Intestinal causes:
The same as RIF
ulcers of small intestine

 Peptic ulcers : duodenum , jejunum, ileum
 Malignant ulcer
 Crohn’s
 TB
 Typhoid
 Uraemic
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Ulcers of large intestine

 Malignant
 Bilharzial
 Amebic
 Bacillary
 Crohn’s
 Ulcerative colitis
 Traumatic
 Stercoral
 Uraemic
GIT ulcers with undermined edges ( Flask shaped ulcer)= destruction

superficially < deeply
Small intestine:
 Typhoid ( axis parallel to intestine)
 TB
Large intestine:
 Amebic
Leg ulcers:
 Varicose ulcer
 Trophic ulcer ( loss of sensation as in DM, leprosy)
 Fungus infection
 Malignant ulcer Marjoline ulcer ( Squamous cell carcinoma on top of
varicose ulcer or burn )
Autoimmune diseases
Organ- specific
 Thyroid: Hashimoto & Graves
 Pancreas: type I DM
 Stomach: autoimmune atrophic gastritis: type A gastritis
 Liver: 1ry biliary cirrhosis
Non organ specific ( generalized)
Collagen vascular diseases

 Systemic Lupus Erythematosis (SLE)
 Rheumatoid arthritis
 Polyarteritis Nodosa (PAN)
Paget’s diseases:
 Mammary (Nipple) Paget’s disease (carcinoma in situ of the nipple,
usually associated with invasive ductal carcinoma of the breast)
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 Paget’s disease of Bone. Disarray and deformity of bone.

 Extramammary (genital) Paget’s, carcinoma in situ. Usually associated
with genital or intestinal invasive tumour.
Functioning (hormone secreting) ovarian tumours:

Sex cord tumours:
 Granulosa-theca
 Sertoli – Leydig
 Gyn-andro-blastoma
Ovarian cysts:
Neoplastic:
 Serous cysts
 Mucinous ysts
 Teratoma
Non neoplastic
 Follicular cyst
 Chocolate cyst
 Corpus leuteum cysts
 Polycystic ovary
Hormone dependent tumours:

 Cancer breast
 Cancer prostate
 Leiomyoma
Role of 2 in Meckle’s diverticulum

2% of general population show this anomaly
2 inches long
2 feet from ileocecal valve
2 types of tissue may be seen: intestinal & gastric ( ectopic) peptic ulcer
DDx of Multinodular Lesion in the Lung (Radiology)
 Multiple cysts: congenital, acquired

 Nodules+ necrosis: necrotizing granulomas
 Solid rounded lesions: pneumoconiosis, cannon-ball mets, TB, sarcoidosis,
lymphoma/lymphoid hyperplasia, leukaemia, histiocytosis (bilateral)
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Benign Tumours of the Lung
 Epithelial
o Squamous papilloma
o Alveolar adenoma
o Adenomas- salivary gland type: pleomorphic adenoma
o Mucinous cystadenoma
o Clear cell tumour “sugar tumour”
 Mesenchymal
o Chondroma
o pulmonary hamartoma, sclerosing haemangioma
o Inflammatory myofibroblastic tumour
o Thymoma, meningioma
Localized Pleural Tumours

 Fibrous plaque
 Lipoma
 Localized mesothelioma
 Localized sarcoma
 Solitary fibrous tumour: patternless pattern, CD34(+)
 Malignant solitary fibrous tumour ( invasion, > 10 cm, haemorrhage + necrosis, M/E:
cellular, atypia, mitoses > 4/hpf, sarcomatous areas)
 Schwannoma
DDx of Abdominal Enlargement = Fs + Lumps + Megalys

 Fat
 Foetus
 Flatulence /Flatus as in cholecystitis
 Faecal impaction
 Full stomach
 Full bladder
 Fatigued muscles (weak abdominal muscles)
 False pancreatic cyst (pseudocyst)
 Fluid (ascites)
 Fibroid (leiomyomata)
 Fluid filled cavities (encysted effusion, ovarian cysts)
 Lumps (tumours of ovary, colon, liver, spleen, kidney, stomach, bladder,
neuroblastoma)
 Megalys (hepatomegaly, splenomegaly, megacolon)
DDx of Acute Abdomen (medical and surgical forms)

 Acute appendicitis, cholecystitis, diverticulitis, pancreatitis
 Intestinal obstruction (paralytic ileus, intussusception, strangulated hernia, volvulus)
 Perforated peptic ulcer (leads to chemical peritonitis)
 Mesenteric infarction (thrombosis, embolism)
 Twisted ovarian cyst
 Ectopic pregnancy
 Peritonitis (chemical or infective)
128
 Meconium Ileus in neonates

 Necrotizing enterocolitis in neonates
 Ischemic colitis in elderly (often painless, associated with fresh blood and mucous in
the stool)
 Mediterranean fever (medical acute abdomen)
DDx of Leg Ulcers:

 Burn
 Fungus infection
 Ischemic : atherosclerosis, anterior tibial syndrome
 Malignant ulcer (Marjoline ulcer; a squamous cell carcinoma on top of varicose
ulcer or burn)
 Radiation
 Trauma and decubitus ulcer (prolonged immobilisation, bony prominences)
 Trophic ulcer (loss of sensation due to peripheral neuropathy as in DM, leprosy):
occur on bony prominences and toes bases.
 Necrobiosis lipoidica, pyoderma gangeronosum
 Varicose ulcer: on medial malleolus
Granuloma
 Granuloma containing eosinophils parasitic granuloma as Bilharzial
 Granuloma containing degeneration collagen diseases as Rheumatic
fever ( fibrinoid degeneration)
 Granuloma containing neutrophils ( suppurative granuloma)
actinomycosis
 Granuloma containing caseation TB & $
 Non caseating granuloma Sarcoidosis
 Granuloma of unknown cause Sarcoidosis
 Granuloma with metastatic calcification Sarcoidosis
 Naked granuloma (no lymphocytes)  sarcoidosis
 Allergic granuloma collagen vascular diseases as Rheumatic,
rheumatoid and SLE
 Non infective granuloma Allergic and FB granulomas
Reactions in all types of dysentry

 Amebic liquifactive necrosis
 Bacillary pseudomembranous inflammation
 Bilharzial Granulomatous
Role of 80% in salivary gland tumours

80%: of salivary tumours are in Parotid gland
80%: of parotid gland tumours are benign
80%: of benign Parotid gland tumours are pleomorphic adenoma (mixed
salivary gland tumour)
129
Epstein Barr Virus (EBV) induced tumours:

 Hodgkin’s
 Burkitt’s
 Nasopharyngeal carcinoma
Krukenberge tumour
Transcoelomic spread to both ovaries from cancer stomach or colon
Microscopically: signet ring cell carcinoma
Locally malignant tumours (tumours with restricted ability to

metastasise)
A: Adamantinoma
B: Basal cell carcinoma
Brain tumour
Bronchial adenomas
C: Craniopharyngioma
G: Giant cell tumour
F: fibromatosis
Tumours containing giant cells:

 Hodgkin’s
 Giant cell tumour of bone
 Any high grade carcinoma or sarcoma: Mg giant cell formation
Capsulated malignant tumours

 Renal cell carcinoma (kidney capsule)
 Seminoma (testicular capsule)
 Thyroid carcinoma (Thyroid capsule)
non capsulated benign tumours

 Papillomas
 Some mesenchymal tumours : osteoma, enchondroma
Metastasizing benign tumours:

 Invasive mole
 Metastasizing leiomyoma
Testicular tumours:
 Child…4 ys old with a testicular tumour yolk sac tumour
 Old man …65 ys old with a testicular tumour lymphoma
 A tumour with pregnancy test positive in male : Choriocarcinoma
Tumours which are AFP positive

 Heptocellular carcinoma
130
 Yolk sac tumour

 Undifferentiated teratoma
Tumours which can produce cannon ball metastasis in lung (radiology):

 Seminoma
 Renal cell carcinoma
Malignant tumours containing benign lymphocytes

 Hodgkin’s disease
 Seminoma
 Medullary carcinoma in Thyroid & breast
Commonest
Commonest malignant tumour::

Bronchogenic carcinoma
Commonest Malignant tumour in Females : Cancer breast, bronchogenic
carcinoma
Commonest Malignant tumour in males: Prostate cancer, Bronchogenic

carcinoma
Commonest brain tumour:

Glomas
Commonest gliomas
Astrocytoma
Commonest astrocytoma:
Glioblastoma multiforme
Commonest adult brain tumour:

Glioblastoma of Cerebrum
Commonest child brain tumour:

Medulloblastoma of cerebellum
Commonest tumour at cerebello-pontine angle

th
Acoustic ( 8 ) Neuroma
Commonest malignant tumours in children:

 Leukemia
 Brain tumours
 Neuroblastoma
131
 Nephroblastoma
Commonest bone tumour:

Secondaries (metastasis)
Commonest 1ry bone tumour

 Of bone itselfOsteosarcoma
 Of bone marrow Multiple myeloma
Commonest tumours caused by radiation:

 Leukemia
 Osteosarcoma
 Papillary thyroid carcinoma in children
Metastasis are commonest tumours in

L: Lung
L: Liver
B: Bone
B: Brain
L.N: Lymph nodes
Carcinomas usually metastasise to lymph nodes, but rare sarcomas

metastasise to lymph nodes. Examples are
 Rhabdomyosarcoma
 Synovial sarcoma
Single most important predisposing factor in cancer breast

 Age
Single most important prognostic factor in cancer breast

 LN metastasis
Which is most important in prognosis of any cancer?

 Staging ( tumour spread, metastasis)
Oseoblastic -bone forming- metastasis are seen with the following

cancers
 Prostate cancer
 Breast cancer
 Lymphoma
Note: Most of tumour metastasis are osteolytic (bone destructive)
132
Causes of Contracted kidneys (small kidneys)

1ry contracted kidney: Benign nephrosclerosis (hypertension-associated)
2ry contracted kidneys:
 Chronic glomerulonephritis
 Chronic pyelonephritis
 Tb kidney with patent ureter
 Following infarction
 Following amyloidosis
 Partial nephrectomy
Contracted Kidneys with fine granular surface

 Bg nephrosclerosis
 chronic glomerulonephritis
Contracted Kidney with Coarse granular surface

Chronic suppurative conditions of kidney

 Pyonephrosis
Causes of shrunken (small) liver:

 Bilharzial periportal fibrosis
 Cirrhosis ( except biliary cirrhosis, the liver enlarges due to bile duct
obstruction)
 Massive and submassive necrosis
 Partial hepatectomy
Enlarged nodular liver

 Biliary cirrhosis
 Multiple metastasis
 Multifocal hepatocellular carcinoma
 Pyemic abscesses
 Ascending cholangitis
 Multiple Amoebic abscesses
Causes of huge spleen ( > 1.5 Kg)

 Bilharziasis
 Chronic myeloid leukemia
 Malaria
 Leishmania ( Kalazar)
 Storage disease ( lipid & glycogen)
 Hodgkin’s lymphoma
 Amyloidosis ( diffuse)
Pure clinical definitions:

133
 Angina : central retrosternal pain

 Chronic bronchitis: cough + expectoration for 3 months/year for 2 years
 Chronic hepatitis: elevated serum enzymes for > 6 months
Acute conditions that never turn chronic

 Acute heart failure
 Acute leukaemia
 Acute peptic ulcer
Chronic conditions that can become acute
Chronic ischemia of atheroma can transform to acute ischemia when

 A thrombus forms on top of an atheroma
 Haemorrhage occurs inside ian atheroma
Skin manifestations of cancer breast]
 Peu d’ orange
 Cancer en cuirase
 Nipple retraction
 Paget’s disease of nipple
 Puckering
 Malignant ulcer
 Fungating mass
 Dilated veins
 Skin nodules
Chronic inflammation denovo ( not preceded by acute inflammation )

 Granulomas
 Crohn’s
Causes of Macroglossia ( large tongue)

 Amyloidosis
 Tumours
 Hamartomas ( hemangioma & lymphangioma)
 Parenchymatous glossitis ($ & TB)
 Congenital : cretinism = Hypothyroidism)
134
SYNDROMES:
definition: combination of symptoms and signs that cannot be explained by

single event
Genetic syndromes:
Turner's: XO
Down: trisomy 21
Kilnefelter's: XXY  gynecomastia + seminoma
Immunological syndrome
Chediak-Higashi: autosomal recessive defects in leukocytes, including
impaired chemotaxis;
Endocrine syndromes
Conn's: 1ry hyperaldosteronism  salt & H2O retention 2ry hypertension
Cushing's: increased adrenocortical secretion of cortisol caused by elevated
ACTH levels; moon facies, acne, abdominal striae, hypertension, amenorrhea,
and hirsutism; when associated with pituitary adenoma, called Cushing's
disease
Sheehan's: postpartum pituitary infarction and necrosis
Lung syndrome
 Kartagener's: congenital absence of cilia includes : dextrocardia (heart is
on the right side) chronic sinusitis and bronchiectasis
Kidney syndromes
 Nephrotic syndrome: massive proteinuria + hypoproteinemia + edema +
hypercholestrolemia
 Nephritic syndrome : Oliguria + hypertension + edema + hematuria
Cardiovascular syndromes
 Marfan's syndrome: myxoid degeneration of CT Aortic dissection
Gastrointestinal syndromes
zollinger-Ellison: gastric hyperplasia secondary to a gastrin secreting tumour
Plummer-Vinson: Iron deficiency anemia, atrophic glossitis, dysphagia
post-cricoid carcinoma liable
Carcinoid: combination of symptoms produced by serotonin release from
carcinoid tumours that have metastasized to the liver: flushing of face,
carcinoid endocarditis (affect Rt side of Ht only), diarrhea, bronchospasm,
mental aberration
BODIES
Liver
 Councilman bodies: apoptotic, eosinophilic hepatocytes extruded into the
sinuses
135
 Mallory bodies: alcoholic hyalin-eosinophilic intracytoplasmic prekeratin

inclusions in hepatocytes
CNS:
 Cowdry: acidophilic intranuclear inclusion typical of herpes-infected cells
 Lewy bodies: round, concentric eosinophilic cytoplasmic inclusions in
neurons in Parkinson's disease
 Negri bodies: bullet-shaped cytoplasmic inclusions in neurons (esp.
Purkinje cells); pathognomonic for rabies infection
 Neurofibrillary tangles: in Alzheimer's disease
 Rosenthal fibers: intracytoplasmic corkscrew shaped, found in (GI)
pilocytic astrocytoma
 Verocay bodies: palisades of nuclei in a schwannoma (neurilemoma)
136
Index
34BE12, 16 governance, 3, 4, 31, 32, 38, 39, 40,
accreditation, 21, 39, 46, 50 51, 60, 100
assurance, 3, 38, 45 haemangioma, 108
ASSURANCE, 44 Hazard group, 80
Audit, 3, 34, 41, 43 Hazard Group, 89, 90
AUDIT, 40, 41, 42, 43, 44 Helicobacter pylori, 16
Autopsy, 3, 24, 27, 28, 56, 88, 95 HER-2, 35
Basic research, 30, 57 HERCEPTIN, 35
BIOPSY, 29, 78 HLA typing, 69
BMS, 28, 57, 99 HTA, 21, 23, 91
BREAST, 77, 78 Image analysis, 19
Chain of custody, 29 Immunohistochemistry, 16
challenges, 3, 22, 23 INFORMATION TECHNOLOGY,
CHALLENGES, 21, 23 19
CHI, 39, 59 IQA, 21, 45
Circumferential margin, 65 IT advancement, 23
Clinical management, 25, 56 laboratory information
clinicopathologic, 53, 57, 59, 61, 94 management system, 17
Clinicopathologic correlation, 3, 33 leader, 3, 58, 62
Closing the loop, 42, 44 low priority, 28
CME, 23, 39, 50, 61 lymphoma, 15, 16, 21, 22, 24, 82
COMPLAINTS, 67 Management, 3, 25, 100
CPD, 20, 21, 39, 44, 50, 58, 60, 61 MANAGEMENT, 25, 31, 35, 56, 85
CYTOLOGY, 77, 78 Marjoline ulcer, 109
DCIS, 130, 136 MDT, 3, 21, 40, 50, 52, 53, 70
Digital pathology, 17, 24 mesothelioma, 108, 129
DNA typing, 69, 70 Metastasis, 82
EBP, 32, 33, 34 MODERNISATION, 19, 20
EQA, 21, 45, 50, 58, 60, 61 Molecular, 16, 79, 82
Error, 21, 49, 50, 51 MOLECULAR TECHNIQUES, 79
errors, 6, 20, 47, 48, 49, 50, 71, 100 MULTIDISCIPLINARY TEAM, 52
Errors, 3 NEQAS, 45, 46
ERRORS IN PATHOLOGY, 47 Neuroendocrine, 128, 137
EVIDENCE-BASED NHS, 19, 20, 38, 40, 94, 98
PATHOLOGY, 33 NICE, 39, 41, 59
FNAB, 26 oestrogen receptor, 35
Frozen section, 3, 81 ONS, 91, 95
FROZEN SECTION, 81, 82, 83, 84 OSPE, 8
Frozen sections, 26, 74 papilloma, 108
GOOD MEDICAL PRACTICE, 58, PCR, 69, 79, 82
59 performance, 32, 37, 38, 41, 45, 46,
48, 60, 61, 69
137
Portfolio, 3, 63, 100 SIDS, 86, 94

PPPI, 32, 60 SPECIFICITY, 37
problem, 3, 9, 41, 51 Staffing and workload, 40
Prognosis, 18 staging, 15, 18, 19, 33, 74, 76
Quality Control, 3 SUDEP, 86, 94
QUALITY CONTROL, 44 teaching, 17, 19, 23, 56, 58, 60, 92
Racemase, 16 team, 3, 9, 52, 58, 62, 63, 99
Report, 17, 19, 44, 47, 49 team player, 3, 58, 63, 99
RESEARCH, 30, 31, 32, 34, 35, 36, Team player, 62
92 telepathology, 17, 19, 22
RESUSCITATION ATTEMPTS, 92 Telepathology, 17
review, 10, 39, 40, 45, 51, 68, 80 THYROID FNA, 78
Risk assessment, 40 TNM, 15, 76, 77, 123, 124, 125, 128,
risk management, 51 131, 134
Risk management, 38, 39 UKAS, 46
SADS, 86, 94 WHO, 29, 30, 36, 53, 90
Sarcomatoid, 133 Workload, 24
SENSITIVITY, 37
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Pathology Interviews

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THE SKILFUL PATHOLOGIST

Copyright © 2017 by Osama Sharaf Eldin, MBBCh, MSc, PhD

All Rights Reserved. No part of this publication may be reproduced or

Library of Congress Control Number:

CHAPTER4: PRACTICAL PATHOLOGY

CHAPTER 5: OSPES EXAMPLES

This book is the second edition of the only published Pathology

In this book, I highlighted the hot topics in Pathology interviews in the

Osama Sharaf Eldin, South Wales, 2017

I dedicate this work to the soul of my father, to my mother, my wife

I would like to thank the supervisors, colleagues and friends who

 Mansoura Faculty of Medicine – Egypt

This is a study guidebook, designed in the Power Point (bullet) format,

The interview is an essential tool for selecting the appropriate

The new trend of Pathology interviews is to be a panel interview in

Currently a combination of panel interview and OSPE (Objective

OSPE EXAM COMPONENTS

 The interview panel includes 5-7 interviewers.

PURPOSES OF THE INTERVIEWS

The interviews test the following:

Examples “What would you do if …….?” Such questions may be built

The interviewer will ask more questions based on the interviewee’s

HOW TO GET PREPARED?

 Read this book!

 Create a question bank

GENERAL RULES DURING ANY INTERVIEW

WHAT WILL YOU DO AFTER THE INTERVIEW?

 Write down all the questions and your answers

GENERAL PATHOLOGY OVERVIEW

3. WHAT ATTRACTS YOU TO THE HISTOPATHOLOGY

-I am interested in histopathology since I was a medical student.

4. WHAT ARE THE MOST INTERESTING ADVANCES IN

C- Advances in Auxiliary techniques:

-Molecular techniques: These are useful adjuncts to

D-Clinical advances that are linked with Histopathology

- Advances of other laboratory tests:

In the future, I expect that there will be more introduction of molecular

5. WHAT ELECTRONIC TOOLS ARE USED IN PATHOLOGY?

-Digital pathology, where the glass slide is scanned by a high

-Telepathology, in which a pathologist in one location looks at

6. WHAT IS THE VALUE OF PATHOLOGY REPORT?

INPUT (Request +specimen)……….OUTPUT (Report + slides)

7. WHAT ARE THE COMPONENTS OF THE PATHOLOGY

8. WHAT IS IT (INFORMATION TECHNOLOGY)? HOW IT CAN

9. WHAT IS PATHOLOGY MODERNISATION/REFORMING?

Pathology reforming is a part of the NHS modernisation. The NHS

Summary of goals of Pathology Modernisation

10. WHAT ARE THE CURRENT PROBLEMS/CHALLENGES IN

 Changes in the accuracy of other diagnostic techniques including

11. IF YOU ARE ASKED TO ADVISE A FIRST YEAR MEDICAL

Pathology as a clinical practice faces many problems. Pathology is a

12. WHAT ARE THE MOST IMPORTANT ISSUES IN PATHOLOGY

MANAGEMENT AND PATHOLOGY

13. WHAT IS CLINICAL MANAGEMENT?

Management means goal-oriented planning.

Steps of time management:

A- High priority work in Pathology

B- Low priority work

18. EXAMPLE QUESTION OF WORK PRIORITIZATION:

D. Send work away (specific companies who employ other

19. GIVE AN EXAMPLE WHEN BIOPSY FROM NON-NEOPLASTIC

20. HOW CAN YOU DETERMINE THE SEVERITY OF SYSTEMIC

21. DEFINE RESEARCH. WHAT IS THE DIFFERENCE BETWEEN

Types of research: Basic research is to detect a fact or to