Pathology StudyGuide 2011 KAAU

PATHOLOGY
CORE COURSE 1

Study Guide
Faculty of Medicine

King Abdul-Aziz University

Phase II, MBBS

2011

TABLE OF CONTENTS

Topic
THE OUTCOMES OF THE UNDERGRADUATE CURRICULUM
CURRICULUM MAP
PHASE 2
STRUCTURE OF THE MODULE
INTRODUCTION
AIMS & OBJECTIVES
TEACHERS CONTACTS
ASSESSMENT
ICONS
TOPIC OUTLINES
NO. LECTURES (NAMES)

1. Introduction to pathology

2.
The Cell and the Environment

3.
Cellular Adaptation to Injury

4. Reversible and irreversible cell injury I (necrosis)

5. Irreversible cell injury II (Apoptosis) & Cellular Aging

6. Introduction to inflammation & Vascular Events

7. Leukocyte Cellular Events
8. Chemical Mediators of Acute Inflammation
9.
Outcome of Acute Inflammation & Chronic
Inflammation

10.
Morphologic Patterns in Acute Inflammation

11.
Repair by Regeneration and by connective tissue
replacement

12.
Wound Healing

13.
Edema, and Hemorrhage

14.
Venous Congestion and hyperaemia

15.
Thrombosis

16.
Embolism and infarction

17.
Nomenclature & characteristics of Benign &
Malignant neoplasm

KAAU Pathology-core course-1 study guide-2010-2011

3
18.
Epidemiology of cancer

19.
Carcinogenesis; The molecular basis of cancer

20.
Carcinogenesis; Fundamental changes in cells

21.
Carcinogenesis; Fundamental changes in cells

22.
Aetiology of cancer & cancer agent I

23.
Aetiology of cancer & cancer agent

24.
Aetiology of cancer & cancer agent II

25.
Clinical features of neoplasia

26.
Introduction to modes of spread of infectious agents,
tuberculosis

27.
Tuberculosis

28.
Bilharziasis

NO. PRACTICAL

1
Cell injury, necrosis

2
Cell adaptation

3
Acute Inflammation

4
Chronic Inflammation and tissue repair

5
Inflammation & repair

6
Hemodynamic Disorder

7
Hemodynamic Disorder

8
Benign tumours of epithelial origin

9
Benign tumours of mesenchymal origin

10
Malignant tumours

11
Malignant and benign tumours

12
Tuberculosis

13-15
General revision

TUTORIALS
1 Cell Injury
2
Inflammatory Reactions

3
Hemodynamic Disorders

KAAU Pathology-core course-1 study guide-2010-2011

4
4 Neoplasia

5 Infectious diseases
TOPICS STUDENT-DIRECTED LEARNING
SDL 1
Cell injury:

Cellular aging
Intracellular accumulation
Pathologic calcification

SDL2
Inflammation:
Defects in inflammatory response.
Systemic effects of inflammation
Leukocyte- induced tissue injury

SDL3:
Hemodynamic
disorders:

Non-thrombotic embolism
Disseminated intravascular coagulopathy

SDL4:
Neoplasia:

Tumour immunity and immunosurveillance.
How to diagnose a case of cancer breast.

SDL5:
Infectious
diseases:

The general features of infectious diseases.
The pathology of amebiasis.

KAAU Pathology core course study guide-2010-2011
5
INTRODUCTION
WELCOME to the pathology core course 1.
Pathology is the study of diseases.
It is the study of how the organs and tissues of a healthy body change to those of a sick
person.
Pathology involves the investigation of the pathophysiology of diseases at the cellular and
molecular levels as well as the study and characterization of diseases through the
morphologic and biochemical examination of organs, tissues, and body fluids. This focus
juxtaposes pathology between clinical medicine and the basic sciences.

CORE COURSE PRE- REQUISITES
Before the students begin the pathology core course (1), they should have knowledge
about:
1. Basic cell biology, including the cell cycle and processes of mitosis and meiosis
2. The basic anatomic and histological features of different body organ cells
3. The structure and function of the adult cell.
4. Cell homeostasis as regards; water, calcium, and electrolyte balance of the cell
5. The metabolic processes involved in the maintenance of metabolic fuel supplies
6. The basic morphology and function of white blood cells.
7. Biochemistry of chemical mediators of inflammation
8. Biochemistry of extra cellular matrix and how it interacts with cells.
9. Cell cycle and normal regulatory mechanisms.
10. The anatomy and physiology of microcirculation.
11. Normal blood vessel structure and function.
12. Physiology of haemostasis; interaction between the function of endothelial cells, platelets.
13. Physiology of coagulation cascade.
14. Biochemistry of tumor markers and growth factors.
15. The molecular mechanisms involved in target tissues
6

OUTCOMES OF THE MEDICAL UNDERGRADUATE
CURRICULUM

By the end of this course the student will utilize the basic science literature of cell
anatomic, histological, and physiologic normality to interpret clinical and morphological
changes. The student will recognize the mechanisms underlying disease processes, as
manifested by morphologic (gross, cellular, and ultrastructure), physiologic, and
biochemical changes in correlation to etiological factors, clinical features and
complications of diseases. The student will be able to describe the basic morphologic
changes of various disease processes, and formulate differential diagnosis using
morphologic appearance.
The student will Apply the knowledge and skill in solving clinical problems and interpret
the morphologic features and pathogenetic factors to the common clinical conditions as
well as he will develop concepts and sufficient understanding of the subject to be able to
pursue post-graduate studies and continuing medical education.

7

CURRICULUM MAP
YOU ARE HERE

Year 1 Year 2 Year 3 Year 4 Year 5 Year 6 Internship
Phase I Phase II Phase III

Module Code/No.
Module Units (Hours) Credit
Hours Theoretical Practical Tutorials SDL
PATHOLOGY
(I)
PATH 211 28 15 5 5 5

TEACHING
DEPARTMENTS:

PATHOLOGY

STRUCTURE OF THE MODULE
8

AIMS & OBJECTIVES

1) Knowledge

Graduate should have sufficient knowledge and understanding of:
1. Identify cell interaction with noxious agents in the environment.
2. Recognize causes and general principles of cell injury particularly ischemic and
hypoxic injury.
3. Identify the mechanisms, and conditions associated with cellular adaptations.
4. Overview on intracellular accumulations with regards to general pathways, types and
examples.
5. The basic concept of apoptosis with regards types, causes, clinical examples and
physiologic value.
6. Identify subsets of abnormal calcifications and their clinical associations.
7. Discuss aging process and its effect on body organs.
8. Overview on inflammation, its causes, different types, morphology, and different
events included in its pathogenesis, fate and complications.
9. Mechanism of tissue repair following injury and the conditions that favours repair by
regeneration, and those favours healing by connective tissue.
10. Process of fibrosis and wound healing , the mediators of this process and the enzymes
involved in scar remodelling.
11. Identify the different genetic and acquired defects in leukocytes function.
12. Discuss systemic and clinical presentations of inflammation.
13. The Pathophysiologic categories of oedema, haemorrhage, and congestion, in relation
to clinical associations, morphology, and effects.
14. Overview on haemostatic plug and thrombosis, the pathogenesis, different types and
fate of thrombosis.
15. The source, frequency and morphology of different types of emboli, and the factors
that influence the development of an infarct.
16. Discuss the various clinical setting and consequences of Disseminated Intravascular
Coagulopathy.
17. Recognize the terms given to different types of neoplasm in relation to the
histogenesis, clinical presentation and outcome of the tumour
9
18. Overview the benign and malignant neoplasms given the histogenetic origin,
morphology and the most common examples.
19. Discuss the general characteristics and biological behaviour of cancer cells.
20. Identify the molecular basis of multistep carcinogenesis and the main regulatory genes
involved in the growth and development of cancer.
21. Detect the host defence mechanisms against tumours as well as tumour immunity and
immunosurveillance.
22. Define infectious diseases, modes of infection of various microbial agents
23. Discuss different modes of spread of microbial agents with special reference to
haematological spread.
24. Discuss tuberculosis as example of infectious diseases, in relation to classification,
pathogenesis, clinical subsets ,morphology and complications
25. Recognize the pathogenesis of both urinary and intestinal Schistosomiasis , in relation
to pathogenesis , morphology and complications.
26. Identify the pathogenesis of amebiasis in relation to pathogenesis, clinical subsets,
morphology and complications.

2) Skills
Graduate should acquire the skills of
1. Define a clinical problem
2. Analysis a given clinical data
3. Examination of specific organs or tissue slide showing particular disease process
4. Identify variable morphologic abnormalities in disease processes by gross examination
and under the microscope.
5. Differentiate between morphology of various disease processes.
6. Acquire the skills to describe various morphologic abnormalities in different disease
processes.
7. Correlate the gross features and microscopic features to the underlying aetiology and
pathogenesis
8. Apply the knowledge and skill in solving clinical problems and interpret the
morphologic features and pathogenetic factors to the common clinical conditions.
9. Develop concepts and sufficient understanding of the subject to be able to pursue post-
graduate studies and continuing medical education.
10.
3) Attitudes
Graduate should have the attitude of:

1. Acquire the skill of self learning
10
2. Peer communication
3. Built up personal responsibility
4. Acquire the skill of team work with peers, teaching staff and other health professionals
5. Acquire the skill of respect colleagues and abide by relevant Islamic ethics
6. Responsibility to remain a life-long learner and maintain the highest ethical and
professional standard.

TEACHERS CONTACTS

Name Department
Tel/ pager
Dr. Jaudah Almaghrabi (JM)

21074/1735
Dr. Ali Sawan
(AS)

21076/ 1731
Dr. Osama Nassif
(ON)

21072/ 1716
Prof. Ahmad Ghanim
(AG)

21075/ 1715
Dr. Fadwa Altaf
(FA)

24015/ 1720
Dr. Sawsan Jalalah
(SJ)

24023/ 1742
Dr.Awatif Jamal
1714
Dr Eman Emam
(EE)
24025/ 3488

Dr. Layla Abdullah
(LA)

24021/ 3655
Dr. Rana Bokhary
(RB)

24022/ 3528
Dr. Ghadeer Mokhtar
(GM)
17084/1645
11
Dr. Ayman Naji
(AN)

21106/ 3607
Dr. Ayman Ghanim
(AM)

21109/ 1743
Dr. Shagufta Mufti
(SM)

24101/3513
Dr. Shabnum Sultana
(SS)

24020/ 3491
Dr. Sherin Ibrahim
(SI)
24024/ 3546

12

ASSESSMENT

1. Summative:

This type of assessment is used for judgment or decisions to be made about your
performance. It serves as:
a. Verification of achievement for the student satisfying requirement
b. Motivation of the student to maintain or improve performance
c. Certification of performance
d. Grades
A-Written Exams :
They will include multiple choice questions (MCQs).
MCQs will include topics covered in lectures, tutorials, and SDLs.
They will cover material presented in lecture, self-directed learning, and tutorials.
All exams must be taken on the date scheduled.
In case of an emergency, the coordinator must be notified.
No make-up exams will be provided if you fail to notify and discuss your situation
with the coordinator.
B- Practical Exam :
It will be in an OSPE (Objective Structured Practical Exam) format,
You will pass through a number of stations including jars and slides.
There will be 2 MCQ questions for each station.
In this Course your performance will be assessed according to the following:
Continuous assessment quizzes: (25%)
- Midterm examination 25
Summative assessment (final): (75%)
- Written Exams 50
- Practical Exam (OSPE) 20
- SDL 5

Total = 100 Marks

13

The following statement is TRUE regarding dystrophic calcification:

1. Associated with high serum calcium.
2. Calcium deposits occur also in healthy tissue.
3. Abnormal deposits of calcium in necrotic tissue.
4. It is considered as an adaptive cellular response.
5. Affects mainly old age group.

14

Icons (standards)
The following icons have been used to help you identify the various
experiences you will be exposed to.

Learning objectives

Content of the lecture

Independent learning from textbooks

Independent learning from the CD-ROM.
The computer cluster is in the 2
nd
floor of the medical library,
building No. 7.

Independent learning from the Internet

Problem-Based Learning

Self- Assessment (the answer to self-assessment exercises will
be discussed in tutorial sessions)

The main concepts
15

Topic Outlines

16

LECTURE # 01: Introduction to pathology

Department: Pathology
Lecturer: Dr.

At the end of the lecture you should be able to:

1. Define the important pathologic terminology
2. Identify various surgical procedures to obtain
a pathologic specimens
3. Identify variable types of pathologic
specimens
4. Recognize the value of obtaining skills in
describing pathological specimens.
5. Understand the relation between the biopsy
and diagnosis of diseases

1. Definition of:
a. Incidence
b. Risk factors
c. Aetiology
d. Pathogenesis
e. Morphology
f. Complications
g. Prognosis
h. Fate
2. Types of specimens;
a. Autopsy
b. Biopsy
c. Exfoliative cytology
d. Fine needle aspirate specimens
e. Value of frozen section
3. Different techniques used in pathological
diagnosis:
a. Routine H&E
b. Immunohistochemistry
c. Utrastructural examinations
d. Immunofluorescence
e. Molecular techniques.

Robbins Basic Pathology, 8
th
Edition (2007)
By: Kumar, Abbas, Fausto, Michel
Student Notes: .

(Insert here handouts and additional
pages for notes if needed)
17
www.google.com
www.studentconsult.com

Pathology is the science that breeches basic science
and clinical experience.
18

Lecture 2: Cellular Adaptation To Stress

Lecturer: Dr.


1) Identify cellular response to stress and noxious
stimuli.
2) Discuss cell injury and cell death.
3) Identify how the cells can adapt after exposure to
injurious agents.
4) Define different adaptation processes
5) Differentiate between the mechanism, and causes of
each type of adaptation.
6) Relate the clinical associations with each type of
adaptation.
1)

Cellular Adaptation to Injury:
1) Definition of Atrophy, Hypertrophy, Hyperplasia,
and Metaplasia.
2) The aetiology, pathogenesis of each.
3) Classification into physiologic and pathologic
subtypes
4) The Morphology of each adaptive response.
5) Correlation between adaptation processes and some
clinical examples

th
Edition (2007)
www.google.com

Hyperplasia is defined as:
a-Increase size of organ due to increase size of cells
b-Increase size of organ due to increase number of cells
c-Reduced size of organ due to increase size of cells
d-Increase size of organ due to decrease size of cells

Student Notes: .


19
Lecture 3: Reversible and Irreversible cell injury (necrosis)

Lecturer: Dr.


1. List the causes of cell injury
2. Discuss the General Principles of cell injury
3. Differentiate between reversible and irreversible cell injury.
4. Identify necrosis as an example of irreversible cell injury:
5. Relate data about necrosis to some clinical examples.

1-Reversible Cell Injury :
a. Mechanism
b. Morphology
c. Examples
2-Irreversible Cell Injury
a. Necrosis
b. Definition
c. Aetiology and pathogenesis
d. Classifications
e. Morphology of different types
f. Fate of necrosis

th
Edition (2007)
By: Kumar, Cotran, Robbin
www.google.com

Which of the following is not included among histological features of
necrosis?
a. Increased esinophilia
b. Break down of plasma membranes
c. Myelin figures
d. Fragmentation of cytoplasm

Student
Notes:
.

(Insert
here
handouts
and
additiona
l pages
for notes
if
needed)

20

Lecture 4: Mechanisms And Examples Of Irreversible Cell Injury

Lecturer: Dr.

1. Identify the subcellular responses to injury
2. Discuss the mechanisms of cell injury
3. Discuss examples of cell injury as:
Hypoxic cell injury
Ischemicreperfusion injury
Toxic cell injury

1- Effects of injurious agents on organelles and cellular components.
2- The general principals of cell injury:
a. ATP depletion
b. Effect on mitochondria
c. Effects on cell membranes
d. DNA damage
e. Role of calcium
3- Examples of cell injury and necrosis:
a. mechanism of cell injury
b. Application to clinical examples.

th
Edition (2007)
www.google.com

Which of the following is not included among the mechanisms of cell injury?
a. ATP depletion
b. Mitochondrial damage
c. Reduced cytoplasmic calcium
d. Cell membranes rupture
e. DNA damage

Student
Notes:
.

(Insert
here
handouts
and
additiona
l pages
for notes
if
needed)

21

Lecture 5: Irreversible cell injury (Apoptosis)
Lecturer:


1. Define apoptosis.
2. Identify the types and cause of apoptosis
3. List clinical examples
4. Explain the Biochemical and molecular
mechanisms of apoptosis
5. Describe the Morphology of apoptosis

1-Apoptosis
a. Physiologic Examples of Apoptosis
b. Pathologic Examples of Apoptosis
c. Morphology of Apoptosis
d. Mechanism of Apoptosis
e. Physiologic value of apoptosis.
www.google.com

th
Edition (2007)
By: Kumar, Abbas,Fausto,Michel
Self-assessment

Briefly answer the following short question:
Tabulate the Differences between necrosis and
apoptosis.

Student Notes: .


22

Department: pathology
Lecture 6: Introduction to inflammation& Vascular
Events
Lecturer: Dr.
..


1. Define inflammation
2. Discuss the ultimate goal of inflammation
3. List causes of inflammation
4. List the potential harmful effects of inflammation
5. Classify inflammation
6. List the cardinal signs of acute inflammation
7. Describe the vascular events in acute inflammation
8. Describe changes in vascular flow and caliber
9. Describe increased vascular permeability and its mechanisms
10. Correlate the vascular changes to the cardinal signs of
inflammation.

1. Overview of inflammation
a. Definition
b. causes
c. purpose of inflammation
d. players of inflammatory response
e. types of inflammation
2-Acute inflammation
a. definition
b. local cardinal signs
c. The two major components of the process of acute
inflammation:
A) Vascular events
(mechanism & mediators)
Changes in vascular calibre and flow
Increased vascular permeability
B) Cellular events

Don't forget!! The local cardinal signs of acute
inflammation are caused by the process of inflammation.

Student Notes:
.

(Insert here handouts and
additional pages for notes if
needed)

23

Continue Lecture 6: Introduction to inflammation& Vascular Events

th
Edition (2007)
By: Kumar, Abbas, Fausto , Michel

In the computer cluster also you have the
opportunity to see some useful web site.

www.pathguy.com
http//library.med.utah.edu/webpath/webpath.html

Self-assessment


List the differences between exudate and
transudate
What are the chemical mediators of
inflammation that cause:
-Vasodilation.
-Increased vascular permeability.

Student Notes: .
24

Lecture 7: Leukocyte Cellular Events
Lecturer: Dr.

1. List the steps in the cellular events of acute
inflammation
2. Describe the process of the leukocyte events in acute
inflammation:
- Margination and rolling.
- Adhesion and transmigration.
- Chemotaxis.
- Activation.
- Phagocytosis and degradation
3. List the chemical mediators involved in each step.

Acute inflammation:
Cellular Events;
a. Margination and rolling
b. Adhesion and transmigration
c. Chemotaxis and activation
d. Phagocytosis and degranulation

Don't forget!! The cellular events in acute inflammation are
essential to kill and degrade the causative agent.

th
Edition (2007)
By: Kumar, Abbas, Fausto ,Michell

opportunity to see some useful web site :
www.fleshandbone.com

Self-assessment

What is oxygen - dependant killing of organism?
Student Notes: .


25

Student Notes: .
26
Lecture 8: Chemical Mediators of Acute
Inflammation and outcome of acute inflammation

Lecturer: Dr

At the end of the lecture the student should be
able to:

1. List the major groups of mediators of acute
inflammation
2. List mediators from plasma
3. List mediators from cells
4. Describe the role of different mediators in acute
inflammation.
5. List the fate of acute inflammation and the conditions
that leads to resolution or fibrosis
6. Discuss abscess formation and its fate
7. Discuss how chronic inflammation follows acute
inflammation

The nature and role of the chemical mediators of
inflammation
1) Chemical mediators classification.
2) Outcomes of acute inflammation:
a. resolution
b. scarring or fibrosis
c. abscess formation
d. chronic inflammation

resolution cannot occur after tissue loss.


27

Continue Lecture 8: Chemical Mediators of Acute Inflammation

th
Edition
(2007)

opportunity to see some useful web site about the
inflammatory process:
www.Fleshandbones.com
www.webpath.com

Self-assessment

Enumerate the chemical mediators responsible for
chemotaxis

Student Notes: .
Student Notes: .
28
Lecture 9: - Outcome of Acute Inflammation
- Morphologic Patterns in Acute
Inflammation
Lecturer:


1. List the morphologic patterns of acute inflammation.
2. Define: abscess, furuncle, carbuncle, and cellulitis
and identify their aetiology and morphology

1-Classification of non suppurative inflammation:
a. Catarrhal inflammation
b. Pseudo-membranous inflammation
c. Serous inflammation
d. Fibrinous inflammation
e. Hemorrhagic inflammation
f. Gangrenous inflammation.
2- Classification of Suppurative inflammation
a. Localized abscess.
b. Diffuse cellulitis.

To be given in the lecture


29
Continue Lecture 9: - Morphologic Patterns in Acute Inflammation

th
Edition (2007)

In the computer cluster also you
have the opportunity to see some useful web site
about the
www.webpath.com
www.robbinspathology.com

Self-assessment

Which of the following is NOT included among types of
acute inflammation:
a. Granulomatous inflammation
b. Serous inflammation
c. Gangrenous inflammation
d. abscess formation
e. hemorrhagic inflammation

Student Notes: .

30
Lecture 10: Chronic Inflammation

Lecturer: Dr.

At the end of the lecture you
should be able to:

1. Define chronic inflammation
2. Describe the characteristic features of chronic
inflammation.
3. Describe the mechanism of chronic
inflammation.
4. List the cells of chronic inflammation.
5. List the biologically active products secreted by
activated macrophage
6. Define granulomatous inflammation

1-Chronic inflammation:
a. Definition
b. The causes of chronic inflammation
c. Mechanism
d. Types of chronic inflammation.
2-Granulomatous inflammation
a. definition
b. causes
c. morphology
d. examples of granulomatous inflammation

Remember, however, that granulomatous
inflammation is a specific type of inflammation
Student Notes: .


31

Continue Lecture 10: Chronic Inflammation

th
Edition (2007)
By: Kumar, Abbas, Fausto ,Miche


Self-assessment


List differences between acute and chronic
inflammation

Student Notes: .

32
Lecture 11: Repair by Regeneration
- Repair by Connective tissue

Lecturer: Dr


1. classify cell types according to their regenerative
ability
2. Identify the conditions that favours repair by
regeneration
3. List molecular events involved in cell growth
4. List the components of repair by connective tissue
5. Identify the factors which favours healing by
connective tissue.
6. Define granulation tissue and describe how it is
formed
7. Describe the process of angiogenesis and enumerate
its mediators
8. Describe the process of fibrosis, identify the cells
involved and enumerate the mediators of this process
9. List the enzymes involved in scar remodelling and
identify their function, and their inhibitors.

-Tissue repair
A) Cell regeneration:
a. The cell cycle.
b. Proliferative capacity of tissue.
c. Growth factors that regulate cell growth
d. Extracellular matrix components and role.

B) Repair by connective tissue (Fibrosis):
- Four sequential processes:
a- Angiogenesis.
b- Scar formation.
c- ECM and tissue remodelling.
- Examples of chemical factors influencing each
process.

Student Notes: .

33

Continue Lecture 11: Repair by Regeneration
- Repair by Connective tissue replacement

th
Edition (2007)

modes of healing.
www.infoseek.com

Self-assessment

What is the difference between granulation tissue
and granuloma?

Epithelial cells and haematological cells are labile
cells, nerve and cardiac cells are permanent cells.

Student Notes: .

Student Notes: .
34
Lecture 12: Wound Healing
Lecturer: Dr.


1. Describe the process of wound healing by first
intention, and the timed sequence till healing is
completed
2. Define tensile strength and identify the timing
and strength of the scar.
3. Describe the process of healing by second
intention, and list the differences from first
intension
4. List factors influencing wound healing
5. List complications of wound healing

1-Wound healing:
A. Healing by first intention
Conditions that favour this process
Sequence of events
B. Healing by second intention
Conditions that favour this process
Difference between primary and secondary
healing
C. Wound strength
2-Pathologic aspects of repair:
a. Factors that influence wound healing
b. Complications of wound healing


35
Continue Lecture 12: Wound Healing

th
Edition (2007)

opportunity to see some useful web site
www.webpath.com

Self-assessment


Tabulate the differences between the process of
healing by second intention and healing by first
intention

Student Notes: .

36

Lecture 13: Edema and Hemorrhage
Lecturer: Dr.


1. Identify the Pathophysiologic categories of
edema
2. Identify the causes of edema in each category.
3. Correlate the type of edema in relation to site and
morphology.
4. Discuss the clinical correlation and effects of
each type and cause of edema.
5. Identify different types of Hemorrhage in
correlation to size and site.
6. List the effects and consequences of different
sites of Hemorrhage.

1-Edema:
1. Definition of edema and different nomenclatures
body cavities.
2. The main Pathophysiologic categories of edema
and examples for each will be discussed.
a. Edema due to increased hydrostatic pressure.
b. Edema due to reduced plasma osmotic
pressure.
c. Edema due to Lymphatic obstruction:
d. Edema due to Sodium retention and
inflammation.
3. The morphology of subcutaneous edema,
pulmonary edema and brain edema will be
explained.
4. Clinical correlation and effects of the different
types of edema will be discussed.
2- Hemorrhage:
1. The different types of hemorrhage.
2. Morphology and effect of hemorrhage in
different sites. Will be discussed.
3. Fate and complications of hemorrhage.

Student Notes: .


37

Continue Lecture 13: Edema, and Hemorrhage

th
Edition (2007)

www.webpath.com

The development of oedema would be expected in:
a. Decreased intravascular hydrostatic pressure.
b. Increased oncotic pressure of blood.
c. Increase interstitial pressure.
d. Increase negative pressure in the pleura.
e. Lymphatic obstruction

Student Notes: .
38

Lecture 14: Venous Congestion and
hyperaemia
Lecturer: Dr.


1. Define hyperaemia and congestion.
2. Differentiate between hyperaemia and
congestion, as regards to the pathophysiology
causes.
3. Recognize the morphology of acute and chronic
pulmonary congestion also acute and chronic
hepatic congestion.
4. List the different causes of chronic venous
congestion (C.V.C.)
5. Describe the morphology of C.V.C. of the liver,
spleen, lung and intestine.
6. Correlate the clinical pictures of CVC to the
pathological findings of C.V.C.

1-Hyperemia:
1. Definition of hyperaemia,
2. Associated clinical settings such as inflammation.
2-Congestion:
1. Definition of acute and chronic congestion.
2. Different clinical settings associated with each type
of congestion.
3. Morphology of acute pulmonary and hepatic
congestion.
4. The different causes of C.V.C. will be listed:
5. Effect of Right side heart failure on the liver.
6. Effects of Left side heart failure on the lung.
7. The morphology of acute and chronic pulmonary and
hepatic congestions.
8. The clinical picture of C.V.C. will be explained and
correlated with the pathology of C.V.C.

To be announced in lecture
Student Notes: .


39

Continue Lecture 14: Venous Congestion and hyperaemia

th
Edition (2007)

www.google.com

Self-assessment

Pooling of blood in capillary beds and venules due
to impaired blood flow is
known as:
a. Congestion.
b. Hyperemia.
c. Hypovolemia.
d. Shock.
e. Vasoconstriction.

Student Notes: .
40

Lecture 15: Thrombosis
Department:pathology
Lecturer:


1. Discuss the pathogenesis of thrombosis.
2. List the conditions associated with an increased
risk of thrombosis.
3. List the different types and sites of thrombi
formation.
4. Describe the fate of thrombus
5. Correlate clinically between the types and effects
of thrombi

1-Thrombosis:
1-The definition of thrombosis and the difference
between thrombosis and blood clot
2-The pathogenesis of thrombosis (Virchow triad).
a. Endothelial injury
b. Abnormal blood flow
c. Hypercoagulability
3-The morphology of different types and sites of
thrombi; Mural, arterial and venous thrombi.
4-The clinicopathological correlation of venous and
arterial thrombosis.

Remember, the difference between venous and
arterial thrombi, as regards the underlying
mechanisms, aetiology, and complications.
.
Student Notes:


41

Continue Lecture 15: Thrombosis

th
Edition (2007)

www.webpath.com

Self-assessment

Which of the following disorder does not predispose
to thrombosis:
a. Pancreatic carcinoma.
b. Pregnancy.
c. Vit K deficiency.
d. Sickle cell anemia.
e. Severe burns.

Student Notes: .
42

Lecture 16: Embolism and infarction
Lecturer: Dr.


1. Define embolism
2. Discuss the different types of emboli.
3. Discuss the source, frequency and morphology of
each type of emboli.
4. Correlate the fate and of emboli in relation to site and
size of original thrombus.
5. Define infarction and know the main causes of
infarction.
6. Describe the morphology of infarction.
7. List the factors that influence the development of an
infarct.

1- Embolism:
a. The types, incidence, origin and morphology of
different emboli
b. The fate of emboli will be correlated with the site
of the emboli.
Pulmonary embolism:
a. Incidence and Source
b. Effect of pulmonary embolism in relation to
embolus size and status of the lung.
c. Saddle embolus and paradoxical emboli and their
effects.
Infarction:
a. The definition of infarcts.
b. Main causes and different factors that influence
the infarction.
c. The morphology and different types of infarction;
Red and pale (white) infarction.
d. Morphology of pulmonary red infarct and
development of heart and renal pale infarct.
e. Correlation between the different types of
infarctions in different organs.
f. Fate of infarct.

Remember, however, that not all pulmonary emboli
are thrombotic in origin, and there are many other
types of emboli.
Student Notes: .

43

Continue Lecture 16: Embolism and
infarction

th
Edition (2007)

On the website you will find many interactive cases
for discussion, MCQs and images.


Self-assessment

The term paradoxical "embolism" is defined as:
a. Death in a healthy person from a Saddle-type
pulmonary embolism.
b. An embolism that does not cause an infarct.
c. An organized embolus.
d. A venous embolus that gain access to the arterial
side through a heart wall defect.
e. Emboli from deep venous thrombosis.

44

Lecture17: Nomenclature & characteristics of Benign &
Malignant neoplasms
Lecturer: Dr

1. Define the different terminology given to different types of neoplasm and refer them
accordingly to the cell of origin.
2. Relate the histogenesis of the tumour as applied to its clinical presentation and outcome.
3. Differentiate between benign and malignant tumours.
4. Identify the difference between dysplasia and invasive carcinoma.

1. Definition of neoplasm.
2. Categorization of tumours into benign and malignant with giving the most common
examples.
3. Differentiating criteria between benign and malignant neoplasm in terms of;
4. Differentiation vs. Anaplasia,
Rate of growth
Local invasion
Metastasis
5. Differences between
Adenoma vs. adenocarcinoma
Papilloma vs. squamous cell carcinoma
Hamartoma, teratoma, fibroadenoma and their malignant counter parts
6. Definition of dysplasia.
7. Classification of dysplasia into low and high grade.

Remember, however, the most characteristic feature of malignant tumour is local
invasion and distant metastasis.

th
Edition (2007)

On the website you will find many interactive cases for discussion, MCQs and images.
Self-assessment
Which of the following features best distinguishes a malignant tumour from a benign
tumour?
1. Presence of necrosis. 3-Increased mitotic rate.
2. Lack of encapsulation. 4. Nuclear pleomorphism.
5. Presence of metastasis.
45
Lecture 18: Epidemiology of cancer
Lecturer: Dr


1. List the most common types of cancer in both males and females locally and
internationally.
2. List the different types of cancer in different geographic areas in the world and
the influencing factors.
3. Discuss the effect of environmental factors on the incidence and spread of
cancer.
4. Discuss the distribution of cancer in relation to age.
5. Define the hereditary form of cancer with e.g. of most common types.
6. Discuss the most acquired preneoplastic disorders.

Vital statistics of different tumours incidence in different part of the world with regard to:
1. Frequency
2. Aetiology
3. Incidence of cancer death
4. Geographic and environmental factors
5. Age differences.
6. Hereditary and acquired preneoplastic disorders.

To be announced in the lecture.

th
Edition (2007)
By: Kumar, Abbas, Fausto, Michell

Self-assessment
Which of the following cancers is most common in males?
a. Cancer prostate
b. Cancer lung
c. Cancer urinary bladder
d. Cancer kidney
e. Sarcoma bone
46
Lecture 19:CARCINOGENESIS: THE MOLECULAR BASIS OF CANCER
Lecturer: Dr

1. Discuss the non-lethal carcinogenic agents that inflict genetic damage.
2. Identify the four classes of regulatory genes.
3. Discuss the multistep process of Carcinogenesis;
At phenotypic level
At genetic level
4. LIST the seven fundamental changes in cell physiology that together dictate the malignant
phenotype.

1-The four classes of regulatory genes;
oncogenes
tumour suppressor genes
apoptosis genes
DNA repair genes
2-The fundamental phenotypic changes in carcinogenesis:
Self-sufficiency in growth signals
Insensitivity to growth-inhibitory signals
Evasion of apoptosis
Limitless replicative potential (i.e., overcoming cellular senescence and avoiding mitotic
catastrophe)
Development of sustained angiogenesis
Ability to invade and metastasize
Genomic instability resulting from defects in DNA repair.
3-The molecular basis of multistep theory:
Karyotypic changes.
Epigenetic changes.

th
Edition (2007)

Which of the following is included among phenotypic changes of cancer cell?
1. Reduction in growth signals
2. Sensitivity to growth-inhibitory signals
3. Stimulation of apoptosis
4. Limited replicative potential
5. Development of sustained angiogenesis
47
LECTURE 20: CARCINOGENESIS
The seven fundamental phenotypic changes in carcinogenesis
Lecturer: Dr


1-Discuss the seven fundamental changes in cell physiology that together dictate the malignant
phenotype in details relevant to his practice
2- Discuss Self-sufficiency in growth signals.
3- Discuss insensitivity to growth inhibitory signals

1-Self-sufficiency in growth signals:
1-Defintion and function of proto-oncogene, oncogene, and oncoproteins.
2-Types of oncogenes; with special emphasis on one subtype as regards its importance and
tumour association.
Growth factors.
Growth factor receptors;HER2/NEU
Signal-transducing proteins; RAS
Nuclear transcription factors.
Cyclins.
3-The effect of oncogene overexpression or mutations on cell cycle, and neoplasm progression.
2-Insensitivity to growth inhibitory signals
Definition of tumour suppressor genes
Effect of their mutation on cell cycle
Examples of tumour suppressor genes; P53,RB gene, and APC gene
Their effect on cell cycle and example of one associated tumour.

th
Edition (2007)

www.pathguy.com
Self-assessment
P53 is considered as:
1. Oncogene
2. Proto-oncogene
3. Growth factor
4. Tumour suppressor gene
48

Lecturer: Dr

1. Discuss the role of evasion of apoptosis in carcinogenesis
2. Identify the genes that control apoptosis
3. Discuss the limitless replicative potential of cells
4. Discuss the role of angiogenesis on tumorigenesis

cont, The seven fundamental..
3-Genes controlling apoptosis;
Proapoptosis genes (BAX)
Anti-apoptosis genes (BCL-2)
Relation of p53 to apoptosis.
4- Limitless replicative potential of cells;
The importance of telomeres in cell aging
Role of mutated telomeres in carcinogenesis
5-Development of angiogenesis;
How growing tumour develop its own blood supply
Role of VEGF in angiogenesis

th
Edition (2007)

www.pathguy.comwww.Library.med.utah.edu/WebPath.com
www.google.com
www.nature.com
49

Lecturer: Dr

1. Discuss the ability of cancer cells to invade and metastasize.
2. Discuss the different steps of metastasis that include invasion of extracellular matrix,
vascular dissemination and honing of tumour cells.
3. Identify the effect of genomic instability in cancer cells-enabler of malignancy.
4. Discuss the effect of accumulations of multiple mutations of different regulatory
genes in the behaviours of cancer cells (the basis of multistep carcinogenesis).

1-Theory of metastasis
2-Steps of invasion and metastasis;
Detachment
Degradation
Attachment to ECM
Migration
Vascular dissemination
Homing of tumour cells
3-Genomic instability;
The role of mutations of DNA repair-genes in the predisposition to cancer and
its role in hereditary types of cancer.
4-The molecular model of evolution of colorectal carcinoma through the adenoma-
carcinoma sequence.

th
Edition (2007)

www.pathguy.com
www.pathguy.comwww.Library.med.utah.edu/WebPath.com

Self-assessment
A 40 year-old female complaining of cancer colonone year ago.The expected site
for metastasis is:
1. lung 2.brain
3. Ovary 4. Liver 5. Spleen

50
LECTURE 23: The Etiology of Cancer: The carcinogenic agents.

Lecturer: Dr

At the end of the lecture the student should be able to:
1. Identify the effect of chemical substances on the cell.
2. Discuss mechanism of action of carcinogenic substances.
3. Explain the initiator-promoter action of chemical carcinogenesis.
4. Identify source and types of radiations
5. Discuss the role in chromosomal abnormalities..

1-The chemical carcinogenesis:
a. General features of chemical carcinogens
b. Direct acting genes
c. Indirectly acting genes
d. Effect on DNA and different regulatory genes.
e. Examples, and associated cancer:
Direct-acting alkylating agents; and leukaemia
Procarcinogens; hydrocarbon and lung cancer
Natural plant and microbial products; Afla toxins and hepatocellular
carcinoma
2-Radiation carcinogenesis:
Solar UV ray and their relation to carcinoma of the skin

th
Edition (2007)
By: Kumar, Abbas, Fausto,
Michell

www.Library.med.utah.edu/WebPath.com
Self-assessment

.
51
LECTURE 24: The Etiology of Cancer: The carcinogenic agents.

Lecturer: Dr

1. Discuss the relation between viruses and microbes and carcinogenesis.
2. Identify the microbial agent that will inflect damages on DNA leading to cancer.
3. List the oncogenic RNA and DNA viruses.
4. Identify the associated types of cancers.

1- Classification of common viruses resulted in DNA damage.
2- The effect of common virus on DNA damage and development
of different cancers.
3- Oncogenic RNA virus (HTLV) and its association with leukaemia
4- Oncogenic DNA viruses
HPV and cervical carcinoma
EBV and Burkitt lymphoma and nasopharyngeal carcinoma
HBV, HCV and hepatocellular carcinoma.
5-The effect of bacteria (Helicobacter pylori) on DNA damage and development of
gastric malignancy.

th
Edition (2007)
Michell

Self-assessment
Epstein barr virus is associated with:
a. Mammary carcinoma
b. Hepatocellular carcinoma
c. Prostatic carcinoma
d. Gastric carcinoma
e. Nasopharyngeal carcinoma.
52
Lecture 25: Clinical aspects of neoplasia

Lecturer: Dr


1. Identify the different effects of tumour on the host including local and systemic effect.
2. Identify cancer cachexcia
3. discuss Paraneoplastic syndromes
4. Recognize the importance of tumour grading and clinical staging in the management of
malignant tumours.
5. Discuss Diagnosis of malignant tumour.

1-Cancer cachexcia;
definition
clinical manifestations
2-Paraneoplastic syndrome;
definition
clinical examples
the most commonly associated tumours
3- Tumour grading:
Definition
Classification into 4 grades
The most common methods used in histological grading.
4-Clinical staging;
Definition
The TNM staging system
Examples for Stage 0 to stage 4 carcinoma (breast and colon)
Clinical value of staging.
5-Diagnosis of malignant tumour:
Morphological examination
Value of Tumour markers; CEA, AFP, and PSA.

Remember, that grading of malignant tumour is the role of the histopathologist, while
staging of the tumours is the role of the Surgeon

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Edition (2007)


53
Self-assessment
1-Tabulate the difference between preneoplastic conditions and paraneoplastic syndrome?
2-Which tumour is most commonly associated with paraneoplastic manifestations?

54

Lecture 26: Introduction to infectious diseases and tuberculosis
Lecturer: Dr

By the end of the lecture the student will know
1. Define infectious diseases and subclinical infection.
2. Identify mode of infection of various microbial agents
3. Discuss different modes of spread of microbial agents.
4. Define and classify pyemia, bacteremia, toxaemia, and septicaemia.
5. List the causative agents of TB
6. Identify route of infection by the agent
7. Classify TB into primary and secondary subtypes
8. Identify the aetiology and pathogenesis of TB

Different etiological bacilli of T.B. and their mode of transmission
Differences between primary & secondary pulmonary TB from the point of view
of
- immune status of the patients
- location of the infection
- characteristic appearance (clinical and morphological)
- progression of the disease
- fate of the disease
Other forms of TB such as intestinal TB

th
Edition (2007)
Michell

Self-assessment
Bacteremia is defined as presence of:
a. Small number of low virulence bacteria in the blood
b. Big number of highly virulence rapidly multiplying bacteria in the blood
c. Small number of viruses in the blood
d. Circulating toxins
55

Lecture 27: Tuberculosis
Lecturer: Dr

1. Identify components of primary complex of TB.
2. Identify the source of secondary TB.
3. Identify sites and morphology of secondary TB.
4. Correlation between pathogenesis, clinical presentation of T.B.
5. List complications of secondary TB.
6. Identify the relation between TB and HIV.

A- Primary complex of TB
Different sites for primary complex of TB.
Morphology of primary complex of TB
The Outcomes of primary TB infection
B- Secondary TB:
Morphology in lungs
Routes of spread and effects on or organs
miliary TB
solitary organ TB
Secondary TB of small intestine
Clinical presentations
Complication
c-TB in immunocompromized patients.
Respiratory system (chapter 13) p516-532
th
Edition (2007)

www.google.com
Self-assessment
Primary tuberculosis is characterized by:
1. Occurs in previously sensitized persons
2. Lesion in upper lung zone
3. Hilar lymph nodes are sometimes enlarged
4. More than 90% of cases heal by fibrosis
5. Kidney is site for primary complex
56
1. Lecture 28: Schistosomiasis
Lecturer: Dr


1. List the different types of causative agents and mode of transmission of
Schistosomiasis
2. Discuss the pathogenesis of both urinary and intestinal Schistosomiasis.
3. List the complications of both urinary and intestinal Schistosomiasis.
4. Discuss the relation between malignancy and urinary Schistosomiasis
5. Discuss Diagnosis of Schistosomiasis

1. The aetiology of urinary and intestinal Schistosomiasis.
2. Morphology of colonic and urinary types; (sandy patches, polyps, ulcer, cystitis, cystic
cystitis, glandularis, Brunns nests.
3. Relation of squamous metaplasia in urinary Schistosomiasis to development of carcinoma.
4. Clinical effects of bilharzial hepatic fibrosis.
5. The clinical presentation and complications of Schistosomiasis
6. Complications

Robbins and Cotran Pathologic Basis of diseases, 7
th
Edition (2005)
P406-409.

www.Robbinspathology.com
Self-assessment
1. Which of the following conditions is not included among complications of bilharziasis?
2. Portal hypertension
3. Hepatic fibrosis
4. colonic carcinoma
5. intestinal obstruction
57

STUDENT GUIDE TO
PRACTICALS

The duration of each practical is not less than 100 minutes distributed as
follows:
The main objectives of practicals are:

1. First 15 minutes are directed for inquiry learning by students on
pathologic gross specimens.

2. 75 minutes of illustration of digital images and/or gross OR
histological specimen with discussion of ;
- Name of the organ.
- Description of the gross morphology of the lesion, as regard to:
Site, size, shape, colour, surface, consistency and cut surface.
- Comparison of morphology of diseased organ to morphology of
normal organ if available and needed.
- Correlation and discussion of the disease process.
- Correlation of gross features with microscopic features.

3. Illustration of the examples of the practical examination.
58

Practical 1: Cell injury, necrosis ;

TUTOR: Department: pathology

OBJECTIVES:
1. Identify the morphological changes in the necrotic cells
2. Distinguish between morphology of necrosis as caseous and coagulative, and fat
necrosis.
3. State the different clinical settings associated with each type of necrosis.
4. Differentiate between apoptosis and necrosis.
5. Write a comprehensive description of different lesions.
6. State the pathological diagnosis different disease diagnosis.
7. Answer simple applied questions related to disease process

Teaching material of different gross specimens and electronic images demonstrating the
following lesions:
1. Liver Fatty Change
2. T. B. Lymphadenitis
3. Myocardial Infarction
4. Infarction brain (Liquefactive)
5. Gangrenous intestine

READING: Robbins Basic Pathology, 8
th
Edition (2007)

59

Practical 2: Cell adaptation gross specimens

.

1. Identify the differences between hyperplasia, and hypertrophy.
2. Identify the effects of these adaptation reactions on different organs and the
different clinical associations.
3. State examples of intracellular accumulations, both exogenous and endogenous.
5. Name the pathological diagnosis or related differential diagnosis.

Teaching material of different gross specimens and electronic images demonstrating the
following lesions:
1. Brown atrophy heart
2. Hypertrophy LV
3. Nodular colloid goitre
4. Benign prostatic hyperplasia.

READING:Robbins Basic Pathology, 8
th
Edition (2007)

60
Practical 3: Acute Inflammation gross specimens


OBJECTIVES:

1. Identify the components of inflammatory exudates
2. Identify some morphologic patterns of acute inflammation;
fibrinous inflammation
suppurative inflammation
localized abscess
4. Name the pathological diagnosis or related differential diagnosis.

Gross specimens showing examples of acute inflammation:
1. Pericarditis (Ox Heart)
2. Lobar Pneumonia
3. Acute Suppurative Appendicitis
4. Lung Abscess

th
Edition (2007)
By: Kumar, Abbas, Fausto,michell

61
Practical 4: Chronic Inflammation and repair

TUTOR: Department: PATHOLOGY

OBJECTIVES:

Describe the component cells of diffuse non-specific chronic inflammation.
Identify the components of different types of granuloma.
Differentiate between inflammatory component in case of acute suppurative
inflammation, chronic inflammation and granulomatous reactions.
Describe the morphology of scar

Gross specimens and electronic images demonstrating chronic inflammation:
1. Different examples of Chronic Cholecystitis
2. Different examples of T.B. Lung (Caseating)
3. Healed Myocardial Infarction
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Edition (2007)
By: Kumar, Abbas, Fausto

62
Practical 5: Inflammation & repair microscopic slide


OBJECTIVES:

By the end this session the student should be able to:
1. Describe the component cells of acute inflammation
2. List the component cells of chronic inflammation.
3. Describe the morphology of cells in case of granulomatous reaction.
4. Identify the morphology of healed process.
5. State the correct diagnosis of each lesion
6. Answer simple applied question

Different electronic images and microscopic slides showing examples of acute and
chronic inflammation: and healed necrosis:

1. Acute Appendicitis
2. Lobar Pneumonia
3. TB Granuloma
4. Healed Infarction
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Edition (2007)

63
Practical 6: Hemodynamic Disorder gross specimen
TUTOR: \ Department: pathology

OBJECTIVES:
By the end of the practical session, the student will be able to
1. Identify and describe the gross appearance of C.V.C. of the liver and the lung.
2. Compare between the gross appearance of intracranial hemorrhage and
subarachnoid hemorrhage.
3. Describe the gross appearance of mesenteric vein thrombosis and gangrenous
necrosis of the small intestine.
4. Describe the gross appearance of myocardial infarction (recent).
5. Describe the gross appearance healed myocardial infarction.
6. Correlate theoretical data to practical examples

Jars and digital images will be explained for the following conditions:
1. Cerebral Intraventricular Hemorrhage
2. Subarachnoid hemorrhage
3. Myocardial infarction (recent)
4. Chronic Venous Congestion (Nutmeg liver)
5. Coronary Thrombus
6. Mesenteric Vein Thrombosis (Infarcted gangrenous intestine)
7. Massive Pulmonary Embolism

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Edition (2007)

64
Practical 7 Hemodynamic Disorders

OBJECTIVES:

By the end of the practical session, the student will be able to :
1. Identify the microscopic features of chronic venous congestion of the liver,
2. Identify the microscopic features of chronic venous congestion of the lung .
3. Correlate between morphologic features and etiologic factors
4. State the different fate of thrombi as resolution, Organization, recanalization, and
embolization

Digital images for the following will be explained:
a. Chronic Venous Congestion Liver
b. Organized Thrombus
c. Organized Thrombus with calcification in the wall
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Edition (2007)

65
Practical 8: Benign tumours of epithelial origin-

OBJECTIVES:

The student will be given number of jars that contain different types of benign tumours:

1. Describe of the benign epithelial lesions.
2. Differentiate between epithelial and mesenchymal benign tumors
3. Describe a cystic structure.
4. Differentiate between benign and malignant tumors

Teaching material of different specimen with benign lesion includes:
1. Thyroid Adenoma
2. Familial Polyposis
3. Familial Multiple polyps Colon
4. Fibroadenoma Breast
5. Dermoid Cyst Ovary (Cystic Teratoma)
Teaching material of different digital images showing examples of
1. Squamous Papilloma (oral)
2. Fibroadenoma Breast

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Edition (2007)

66
Practical 9: Benign tumours of mesenchymal origin-


OBJECTIVES:

The student will achieve the ability to examine the tumour under the microscope, and
they are able to identify the histological criteria present in the sections:
1. Describe the gross and histological features of benign tumours.
2. List the criteria of benignity.
3. Examine the adjacent tissue.

Teaching material of different gross specimens demonstrating the following lesions:
1. Lipoma
2. Leiomyoma Uterus
3. Osteochondroma Bone

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Edition (2007)

67
Practical 10: Malignant tumours

The student will be given number of jars that contain different types of malignant
tumours:

1. Examine different examples of malignant tumours
2. Describe a malignant epithelial tumour
3. Diagnosis lesions in given specimens
4. Differentiate between different tumours in different organs.

The teaching material of different specimens with gross specimen and images of
malignant diseases:
1. Carcinoma Colon
2. Carcinoma oesophagus (Fungating)
3. Cancer Breast
4. Cancer Stomach
5. Osteosarcoma
6. Chondrosarcoma
7. Chondrosarcoma (Lt. Distal Radius)

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Edition (2007)

68
Practical 11: Features of malignant neoplasm


OBJECTIVES:
The student will achieve the ability to examine the tumour in gross specimens and under
the microscope, and they are able to:
1. Examine different examples of malignant tumours
2. Describe a malignant epithelial tumour
3. Diagnosis lesions in given specimens
4. Differentiate between different tumours in different organs

Teaching material of different gross specimens demonstrating:
1. Metastasis Lymph node
2. Metastasis Lung
3. Metastasis Liver
4. Metastasis Brain
Teaching material of different digital images demonstrating:
1. Adenocarcinoma Colon
2. Infiltrating Duct Carcinoma Breast
3. Osteosarcoma

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Edition (2007)

69
Practical 12: Tuberculosis


OBJECTIVES:
The student will achieve the ability to examine the pathology in gross specimens and under the
microscope, and they are able to:
1. Differentiate the primary from secondary TB as regards morphological changes.
2. Describe the gross appearance of the various forms of TB
3. Identify the basic histological feature of the granulomatous inflammation in any tissue.

Teaching material of different specimens and digital images for both histologic and gross features
demonstrating:
1. Primary complex of tuberculosis
2. Secondary pulmonary TB
3. TB lymphadenitis
4. TB small intestine

th
Edition (2007),chapter 13

70
STUDENT GUIDE TO
TUTORIAL
The main Aims of tutorial are:

1. Conducting an interactive learning.
2. Discussing disease process facilitated by the tutor.
3. Emphasizing on student-centred Learning type.

CONTENTS:

1. The students should come prepared to the tutorial and be involved in:
Answering MCQs provided by the tutor.
Constructing their own MCQs
Participate and engaged with his peers in various discussions and
activity.
Diagram and summarize his understanding form lecture and his
reading.

2. The student should seek further classification of the different topics
covered in the lectures by:
Asking questions.
By involving in smaller group discussion about specific topics.
By solving specific clinical case scenario.

4. Attendance and participation activity in the tutorials is mandatory.

Student marks will be determined according to it.
71
Details of Tutorials
TUTORIAL # 01: Cell Injury and Adaptation

DEPARTMENT: Pathology TUTOR:

OBJECTIVES:
-By the end of this session the student will be able to:

1. Relate the morphologic patterns of different types of necrosis as learned in the
practical with the pathogenesis and mechanism of these types
2. Discuss the difference between apoptosis and necrosis.
Additional readings and solving examples of MCQ will be discussed during the tutorial

Difference between reversible and irreversible cell injury
Coagulative necrosis, and related diseases
Liquefactive necrosis
Traumatic fat necrosis

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Edition (2007)

72
TUTORIAL # 02: Inflammatory reactions, Repair and wound healing


- The student should be able to:
1. Relate the morphologic patterns of inflammation as learned in the practical with the
pathogenesis and mechanism of these types

2. Discuss the clinical signs and symptoms of inflammation

3. Relate clinical signs and symptoms of inflammation to the chemical mediators

4. Discuss the harmful effects of inflammation and its clinical implications.
5. Differentiate between types of healing processes
6. Correlate between type of wound and healing process
7. Identify factors that delay healing
8. Discuss how to improve healing process

1- The morphologic patterns of inflammation
2- The clinical signs and symptoms of inflammation
3- The harmful effects of inflammation and its clinical implications
4- wound and healing process

th
Edition (2007)
By: Kumar, Cotran, Robbins

73
TUTORIAL # 03: hemodynamic disorders


OBJECTIVES:
- The student should be able to:
1. Correlate between chronic congestion and edema
2. Identify the clinical signs and symptoms of thrombophlebitis
3. Correlate between clinical settings and embolus formation

-Additional readings and solving examples of MCQ will be discussed during the tutorial.

1. Congestion and edema
2. Clinical signs and symptoms of thrombophlebitis
3. Cinical settings of emboli

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Edition (2007)

74
TUTORIAL # 4: A case of neoplasm for diagnosis


OBJECTIVES:

1. Differentiate between benign and malignant tumours.
2. Discuss the biological behaviour of malignant tumours
3. Identify clinical manifestation of malignant tumours

1- Difference between benign and malignant tumours
2- biological behaviour of malignant tumours
3- Clinical manifestation of malignant tumours
4- Groups are assigned cases of benign tumour.

Wider discussion is encouraged among all the students guided by the tutor

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Edition (2007)

75

TUTORIAL # 5: Infectious diseases

OBJECTIVES:

1. Correlate the clinical presentation of each infectious disease to the histological
appearance of its different stages.
2. Discussion on TB vaccination, Mantoux test
3. Discuss the epidemiology of TB around the world and in Saudi Arabia.

1. Histological and clinical presentation of infectious disease

2. TB vaccination, Mantoux test .

Wider discussion is encouraged among all the students guided by the tutor

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Edition (2007)

76

Student Guide to
Independent learning

Independent learning is a very essential skill for tomorrows doctors.
We will train you to gain this important skill by asking you to read
independently about specific topics in pathology

The main objectives of student-directed learning (SDL) are:

1. The student is responsible to enhance his knowledge in the assigned in
his study guide for the topics selected for his SDL.

2. The student should obtain material for reading from different sources
(text book, article, and internet) and bring them to the SDL session.

3. During the session, the students should read the material (in 30
minutes), then they should participate in small group discussions
(small groups will be divided accordingly in the session).

4. The student should understand that exam questions will be subtracted
from the discussed SDL material.

5. This format of SDL is to be followed by all faculty staff in the male
and female sections.

6. The goals for the SDL is included in the final exam of the pathology
core one.

77

List of Core Course student directed learning:
SDL 1: CELL INJURY:
Cellular aging
Intracellular accumulation
Pathologic calcification
SDL 2: INFLAMMATION AND REPAIR:
Defects in inflammatory response.
Systemic effects of inflammation
Leukocyte- induced tissue injury
SDL 3: HEMODYNAMIC DISORDERS:
Non-thrombotic embolism
Disseminated intravascular coagulopathy.
SDL 4: NEOPLASIA:
Tumour immunity and immunosurveillance.
How to diagnose a case of cancer breast.
SDL 5: INFECTIOUS DISEASES:
The general features of infectious diseases.
The pathology of amebiasis.

78
SDL 1#: CELL INJURY

OBJECTIVES:

1. Discuss the general pathways of intracellular accumulations.
2. Identify different types of intracellular accumulations.
3. Apply intracellular accumulation to various clinical conditions.
4. Identify subsets of abnormal calcification.
5. Differentiate between metastatic and dystrophic types as regards, serum calcium level,
underlying conditions, and distribution.
6. Identify the process of aging.

A-Examples of intracellular accumulation:
Fatty changes,
Glycogen,
Pigments as hemosedrin, melanin, and Lipofuscin.
Aetiology, pathogenesis and morphology of each type.
B-Pathologic calcification:
-Dystrophic Calcification
examples
sites
morphology; intracellular or extracellular
serum calcium level
-Metastatic Calcification
conditions associated with high calcium levels
sites of abnormal calcium deposition
complications
C-aging:
Value of telomeres.

th
Edition (2007)
79
SDL 2#: Inflammation

OBJECTIVES:


1. Identify the different defects in leukocytes function.
2. Classify defects into genetic and acquired.
3. List the clinical signs and symptoms associated with inflammation
4. List the chemical mediators involved
5. Describe the circumstances under which leukocyte induce injury.

A-Defects in leukocytes function:
1. Defects in adhesion
2. Defects in microbicidal activity
3. Defect in phagosome formation
B- Systemic effects of inflammation.
C- Leukocyte- induced tissue injury.

th
Edition (2007)
80
SDL 3#: Non-thrombotic embolism

OBJECTIVES:
The students should enhance his knowledge and be able to :
1- Discuss the various types of emboli other than thromboembolism.
2- Identify their sources, pathogenesis, and consequences.
3- Define DIC.
4- Discuss the various clinical setting of this condition.
5- Discuss The consequences of this condition.

1-Embolism:
1. Classify emboli into solid, gaseous and liquid types
2. Identify the source, associated clinical conditions of fat, amniotic fluid and air
emboli.
3. Fat embolism, Air embolism, and Amniotic fluid embolism:
a. Source and causes
b. Clinical features
c. Pathogenesis
2- Disseminated intravascular coagulation:
a. Definition
b. Various clinical settings underlying the condition.
c. Consequences

th
Edition (2007)
81
SDL 4#: Neoplasia

OBJECTIVES:


1. Tumour immunity:
Identify the different types of tumour antigens and their influences on
immune system.
Recognize the antitumor effector mechanism.
Identify how would cancer cells escape immunosurveillance?
2. Identify the value of morphological and biological methods in cancer diagnosis.
Apply methods of diagnosis on a case breast cancer.
3.

1-Different tumour antigens:
a. Tumour specific antigens
b. Tumour associated antigens.
c. Products of mutated oncogenes and tumor suppressor genes
d. Aberrantly expressed cellular proteins
e. Oncofetal proteins
2-Mechanism of how the tumour cells escape immunosurveillance.
3-Laboratory diagnosis of cancer:
-Morphological methods;
1- frozen section
2- fine needle aspiration
3- cytological smears
4- immunohistochemistry
5- flow cytometry
-Biochemical assays:
The value of serum tumour markers as, CEA, AFP, and PSA

th
Edition (2007)
82
SDL 5 #: INFECTIOUS DISEASES

OBJECTIVES:

1. Identify the general features of infectious diseases.
a. Categories of infectious agents
b. List the host barriers to infection
c. Know to barriers can breakdown infection
d. Enumerate methods of spread of infection
e. Identify the inflammatory mechanism against infectious agents
2-Understand the pathology of amebiasis.
a. Identify modes of transmission
b. List common sites of infection
c. Correlation between morphology and complications.

2.

A- Barriers of the body to infection:
B-Spread of microbes:
1. Direct spread
2. Lymphatic spread
3. Blood spread
C-Types of inflammation against infections:
1. Suppurative inflammation,
2. Chronic inflammation
3. Granulomatous Inflammation
D-Amebiasis:
4. The route of infection of amebiasis.
5. Pathologic lesions in the large bowel
6. Complications with special emphasis of liver abscess.

83

Further
Reading

1. Robbins and Cotran Pathologic Basis of diseases, 7
th
Edition
by: Kumar, Abbas, Fausto, (2005)
2. Robin Reid, Fiona Roberts. Pathology Illustrated. 6
th
Ed,
Elsevier, Churchill Livingston. 2005.
3. Ivan Damjanov. Pathology secrets. 2
nd
ed. Elsevier
Mosby.2005

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