Pathology StudyGuide 2011 KAAU

8/12/2019 Pathology StudyGuide 2011 KAAU

1/83

PATHOLOGY

CORECOURSE1

Study Guide

Faculty of Medicine

King Abdul-Aziz University

Phase II, MBBS

2011


2/83

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 pathology2. The Cell and the Environment3. Cellular Adaptation to Injury4. Reversible and irreversible cell injury I (necrosis)5. Irreversible cell injury II (Apoptosis) & Cellular Aging6. Introduction to inflammation & Vascular Events7. Leukocyte Cellular Events8. Chemical Mediators of Acute Inflammation9. Outcome of Acute Inflammation & Chronic

Inflammation

10. Morphologic Patterns in Acute Inflammation11.

Repair by Regeneration and by connective tissuereplacement

12. Wound Healing13. Edema, and Hemorrhage14. Venous Congestion and hyperaemia15. Thrombosis16. Embolism and infarction17.Nomenclature & characteristics of Benign &Malignant neoplasm


3/83

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

3

18. Epidemiology of cancer19. Carcinogenesis; The molecular basis of cancer20. Carcinogenesis; Fundamental changes in cells21. Carcinogenesis; Fundamental changes in cells22. Aetiology of cancer & cancer agent I23. Aetiology of cancer & cancer agent24. Aetiology of cancer & cancer agent II25. Clinical features of neoplasia26. Introduction to modes of spread of infectious agents,

tuberculosis

27. Tuberculosis28. Bilharziasis

NO. PRACTICAL

1 Cell injury, necrosis

2 Cell adaptation

3 Acute Inflammation

4Chronic 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

10Malignant tumours

11 Malignant and benign tumours

12 Tuberculosis

13-15 General revision

TUTORIALS

1 Cell Injury

2 Inflammatory Reactions

3 Hemodynamic Disorders


4/83

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

4

4 Neoplasia

5 Infectious diseases

TOPICSSTUDENT-DIRECTED LEARNING

SDL1Cell injury: Cellular aging

Intracellular accumulation

Pathologic calcification

SDL2 Inflammation:Defects in inflammatory response.

Systemic effects of inflammationLeukocyte- induced tissue injury

SDL3:Hemodynamic

disorders:Non-thrombotic embolismDisseminated 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.


5/83

KAAU Pathology core course study guide-2010-2011

5

INTRODUCTION

WELCOMEto the pathology core course 1.

Pathologyis 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 cour se (1), they should have knowledge

about:

1. Basic cell biology, including the cell cycle and processes of mitosis and meiosis2. The basic anatomic and histological features of different body organ cells3. The structure and function of the adult cell.4. Cell homeostasis as regards; water, calcium, and electrolyte balance of the cell5. The metabolic processes involved in the maintenance of metabolic fuel supplies6. The basic morphology and function of white blood cells.7. Biochemistry of chemical mediators of inflammation8. 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


6/83


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.


7/83


7

CURRICULUM MAPYOUAREHERE

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

HoursTheoretical Practical Tutorials SDL

PATHOLOGY

(I)PATH 211 28 15 5 5 5

TEACHING

DEPARTMENTS:PATHOLOGY

STRUCTURE OF THE MODULE


8/83


8

AIMS &OBJECTIVES

1) KnowledgeGraduate should have suf fi cient 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 andphysiologic 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 byregeneration, and those favours healing by connective tissue.

10.Process of fibrosis and wound healing , the mediators of this process and the enzymesinvolved 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 andfate of thrombosis.

15.The source, frequency and morphology of different types of emboli, and the factorsthat influence the development of an infarct.

16.Discuss the various clinical setting and consequences of Disseminated IntravascularCoagulopathy.

17.Recognize the terms given to different types of neoplasm in relation to thehistogenesis, clinical presentation and outcome of the tumour


9/83


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 andimmunosurveillance.

22.Define infectious diseases, modes of infection of various microbial agents23.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 relationto pathogenesis , morphology and complications.

26.Identify the pathogenesis of amebiasis in relation to pathogenesis, clinical subsets,morphology and complications.

2) SkillsGraduate should acqui re the ski l ls of

1. Define a clinical problem2. Analysis a given clinical data3. Examination of specific organs or tissue slide showing particular disease process4. 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 andpathogenesis

8. Apply the knowledge and skill in solving clinical problems and interpret themorphologic 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


10/83


10

2. Peer communication3. Built up personal responsibility4. Acquire the skill of team work with peers, teaching staff and other health professionals5. Acquire the skill of respect colleagues and abide by relevant Islamic ethics6. 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 Jamal1714

Dr Eman Emam

(EE)

24025/ 3488

Dr. Layla Abdullah

(LA) 24021/ 3655

Dr. Rana Bokhary

(RB)24022/ 3528

Dr. Ghadeer Mokhtar

(GM)

17084/1645


11/83


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


12/83


12

ASSESSMENT

1. Summative:

This type of assessment is used for judgment or decisions to be made about yourperformance. It serves as:

a. Verification of achievement for the student satisfying requirementb. Motivation of the student to maintain or improve performancec. Certification of performanced. 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.

I n th is Course your performance wil l 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


13/83


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.


14/83


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 2ndfloor of the medical library,

building No. 7.

Independent learning from the Internet

Problem-Based Learning

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

The main concepts


15/83


15

Topic Outlines


16/83


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 terminology2. Identify various surgical procedures to obtain

a pathologic specimens

3. Identify variable types of pathologicspecimens

4. Recognize the value of obtaining skills indescribing pathological specimens.

5. Understand the relation between the biopsyand diagnosis of diseases

1. Definitionof:a. Incidenceb. Risk factorsc. Aetiologyd. Pathogenesise. Morphologyf. Complicationsg. Prognosish. Fate

2. Types of specimens;a. Autopsyb. Biopsyc. Exfoliative cytologyd. Fine needle aspirate specimense. Value of frozen section

3. Different techniques used in pathologicaldiagnosis:a. Routine H&Eb. Immunohistochemistryc. Utrastructural examinationsd. Immunofluorescencee. Molecular techniques.

Robbins Basic Pathology, 8thEdition (2007)

By: Kumar, Abbas, Fausto, Michel

Student Notes: .

(Insert here handouts and additionalpages for notes if needed)


17/83


17

www.google.comwww.studentconsult.com

Pathology is the science that breeches basic science

and clinical experience.
http://www.google.com/http://www.google.com/http://www.studentconsult.com/http://www.studentconsult.com/http://www.studentconsult.com/http://www.google.com/


18/83


18

Lecture 2:Cellular Adaptation To Stress


Lecturer: Dr.


1) Identify cellular response to stress and noxiousstimuli.

2) Discuss cell injury and cell death.3) Identify how the cells can adapt after exposure to

injurious agents.

4) Define different adaptation processes5) Differentiate between the mechanism, and causes of

each type of adaptation.

6) Relate the clinical associations with each type ofadaptation.

Cellular Adaptation to Injury:1) Definition of Atrophy, Hypertrophy, Hyperplasia,

and Metaplasia.2) The aetiology, pathogenesis of each.3) Classification into physiologic and pathologic

subtypes4) The Morphology of each adaptive response.5) Correlation between adaptation processes and some

clinical examples


By: Kumar, Abbas, Fausto, Michelwww.google.com

www.studentconsult.com

Hyperplasia is defined as:

a-Increase size of organ due to increase size of cellsb-Increase size of organ due to increase number of cells

c-Reduced size of organ due to increase size of cellsd-Increase size of organ due to decrease size of cells

Student Notes: .

(Insert here handouts and additional

pages for notes if needed)


19/83


19

Lecture 3:Reversibleand Irreversible cell injury (necrosis)


Lecturer: Dr.


1. List the causes of cell injury2. Discuss the General Principles of cell injury3. 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. Morphologyc. Examples

2-Irreversible Cell Injury

a. Necrosisb. Definitionc. Aetiology and pathogenesisd. Classificationse. Morphology of different typesf. Fate of necrosis


By: Kumar, Cotran, Robbinwww.google.comwww.studentconsult.com

Which of the following is not included among histological features of

necrosis?

a. Increased esinophiliab. Break down of plasma membranesc. Myelin figuresd. Fragmentation of cytoplasm

Student

Notes:

.

(Insert

here

handouts

and

additiona

l pages

for notes

if

needed)


20/83


20

Lecture 4:Mechanisms And Examples Of Irreversible Cell Injury


Lecturer: Dr.


1. Identify the subcellular responses to injury2. Discuss the mechanisms of cell injury3. 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 depletionb. Effect on mitochondriac. Effects on cell membranesd. DNA damagee. Role of calcium

3-

Examples of cell injury and necrosis:a. mechanism of cell injuryb. Application to clinical examples.


By: Kumar, Abbas, Fausto, Michelwww.google.com


Which of the following is not included among the mechanisms of cell injury?

a. ATP depletionb. Mitochondrial damagec. Reduced cytoplasmic calciumd. Cell membranes rupturee. DNA damage

Student

Notes:.

(Insert

here

handouts

and

additiona

l pages

for notes

if

needed)


21/83


21

Lecture 5:Irreversible cell injury (Apoptosis)Department: Pathology

Lecturer:


1. Define apoptosis.2. Identify the types and cause of apoptosis3. List clinical examples4. Explain the Biochemical and molecular

mechanisms of apoptosis

5. Describe the Morphology of apoptosis

1-Apoptosis

a. Physiologic Examples of Apoptosisb. Pathologic Examples of Apoptosisc. Morphology of Apoptosisd. Mechanism of Apoptosise. Physiologic value of apoptosis.

www.google.com



By: Kumar, Abbas,Fausto,Michel

Self-assessment

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

apoptosis.

Student Notes: .




22/83


22

Department: pathology

Lecture 6:Introduction to inflammation& VascularEvents


Lecturer: Dr.

..


1.Define inflammation2.Discuss the ultimate goal of inflammation3.List causes of inflammation4.List the potential harmful effects of inflammation5.Classify inflammation6.List the cardinal signs of acute inflammation7.Describe the vascular events in acute inflammation8.Describe changes in vascular flow and caliber9.Describe increased vascular permeability and its mechanisms10. Correlate the vascular changes to the cardinal signs of

inflammation.

1. Overview of inflammation

a. Definitionb. causesc. purpose of inflammationd. players of inflammatory responsee. types of inflammation2-Acute inflammationa. definitionb. local cardinal signsc. The two major components of the process of acute

inflammation:

A) Vascular events(mechanism & mediators)Changes in vascular calibre and flowIncreased vascular permeabilityB) 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)


23/83


23

Continue Lecture 6: Introduction to inflammation& Vascular Events


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

Briefly answer the following short question:

List the differences between exudate andtransudate

What are the chemical mediators ofinflammation that cause:-Vasodilation.

-Increased vascular permeability.

Student Notes: .
http://www.studentconsult.com/http://www.studentconsult.com/http://www.pathguy.com/http://www.pathguy.com/http://www.pathguy.com/http://www.studentconsult.com/


24/83


24

Lecture 7:Leukocyte Cellular Events

Department: PathologyLecturer: Dr.


1. List the steps in the cellular events of acuteinflammation

2. Describe the process of the leukocyte events in acuteinflammation:

- 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 rollingb.

Adhesion and transmigrationc. Chemotaxis and activation

d. Phagocytosis and degranulation

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


By: Kumar, Abbas, Fausto ,Michell


opportunity to see some useful web site :

www.fleshandbone.comwww.studentconsult.com

Self-assessment

Briefly answer the following short question:What is oxygen - dependant killing of organism?

Student Notes: .


http://www.fleshandbone.com/http://www.fleshandbone.com/http://www.studentconsult.com/http://www.studentconsult.com/http://www.studentconsult.com/http://www.fleshandbone.com/


25/83


25

Student Notes: .


26/83


26

Lecture 8:Chemical Mediators of AcuteInflammation 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 acuteinflammation

2. List mediators from plasma

3. List mediators from cells

4. Describe the role of different mediators in acuteinflammation.5. List the fate of acute inflammation and the conditionsthat leads to resolution or fibrosis6. Discuss abscess formation and its fate7. 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. resolutionb. scarring or fibrosisc. abscess formationd. chronic inflammation

resolution cannot occur after tissue loss.




27/83


27

Continue Lecture 8: Chemical Mediators of Acute Inflammation

Robbins Basic Pathology, 8thEdition

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


opportunity to see some useful web site about the

inflammatory process:

www.Fleshandbones.com

www.webpath.com

Self-assessment

Briefly answer the following short question:Enumerate the chemical mediators responsible for

chemotaxis

Student Notes: .

Student Notes: .
http://www.webpath.com/http://www.webpath.com/http://www.webpath.com/


28/83


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 nonsuppurative inflammation:

a. Catarrhal inflammationb. Pseudo-membranous inflammationc. Serous inflammationd. Fibrinous inflammatione. Hemorrhagic inflammationf. Gangrenous inflammation.2- Classification of Suppurative inflammation

a. Localized abscess.b. Diffuse cellulitis.

To be given in the lecture




29/83


29

Continue Lecture 9: - Morphologic Patterns in Acute Inflammation



In the computer cluster also you

have the opportunity to see some useful web site

about thewww.webpath.com

www.robbinspathology.com

Self-assessment


Which of the following is NOT included among types ofacute inflammation:a. Granulomatous inflammationb. Serous inflammationc. Gangrenous inflammationd. abscess formatione. hemorrhagic inflammation

Student Notes: .
http://www.webpath.com/http://www.webpath.com/http://www.robbinspathology.com/http://www.robbinspathology.com/http://www.robbinspathology.com/http://www.webpath.com/


30/83


30

Lecture 10:Chronic Inflammation


Lecturer: Dr.

At the end of the lecture you

should be able to:

1. Define chronic inflammation2. 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 macrophage6. Define granulomatous inflammation

1-Chronic inflammation:a. Definition

b. The causes of chronic inflammationc. Mechanismd. Types of chronic inflammation.2-Granulomatous inflammation

a. definitionb. causesc. morphologyd. examples of granulomatous inflammation

Remember, however, that granulomatous

inflammation is a specific type of inflammation

Student Notes: .




31/83


31

Continue Lecture 10: Chronic Inflammation


By: Kumar, Abbas, Fausto ,Miche




Self-assessment


List differences between acute and chronic

inflammation

Student Notes: .
http://www.studentconsult.com/http://www.studentconsult.com/http://www.studentconsult.com/


32/83


32

Lecture 11:Repair by Regeneration- Repair by Connective tissue


Lecturer: Dr


1. classify cell types according to their regenerativeability

2. Identify the conditions that favours repair byregeneration

3. List molecular events involved in cell growth4. List the components of repair by connective tissue5. Identify the factors which favours healing by

connective tissue.6. Define granulation tissue and describe how it is

formed7. Describe the process of angiogenesis and enumerate

its mediators8. Describe the process of fibrosis, identify the cells

involved and enumerate the mediators of this process9. List the enzymes involved in scar remodelling and

identify their function, and their inhibitors.

-Tissue repairA) Cell regeneration:a. The cell cycle.b. Proliferative capacity of tissue.c. Growth factors that regulate cell growthd. 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: .




33/83


33

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





modes of healing.

www.infoseek.com

Self-assessment


What is the difference between granulation tissueand granuloma?

Epithelial cells and haematological cells are labile

cells, nerve and cardiac cells are permanent cells.

Student Notes: .

Student Notes: .
http://www.infoseek.com/http://www.infoseek.com/http://www.infoseek.com/


34/83


34

Lecture 12:Wound HealingDepartment: pathology

Lecturer: Dr.


1. Describe the process of wound healing by firstintention, and the timed sequence till healing is

completed

2. Define tensile strength and identify the timingand strength of the scar.

3. Describe the process of healing by secondintention, and list the differences from first

intension

4. List factors influencing wound healing5. List complications of wound healing

1-Wound healing:A. Healing by first intention

Conditions that favour this process

Sequence of eventsB. Healing by second intention

Conditions that favour this process Difference between primary and secondary

healingC. Wound strength

2-Pathologic aspects of repair:a. Factors that influence wound healing

b. Complications of wound healing




35/83


35

Continue Lecture 12: Wound Healing



In the computer cluster also you have theopportunity 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 firstintention

Student Notes: .


36/83


36

Lecture 13:Edema and HemorrhageDepartment: pathology

Lecturer: Dr.


1. Identify the Pathophysiologic categories ofedema

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 ofeach type and cause of edema.

5. Identify different types of Hemorrhage incorrelation to size and site.

6. List the effects and consequences of differentsites of Hemorrhage.

1-Edema:1. Definition of edema and different nomenclatures

body cavities.

2. The main Pathophysiologic categories of edemaand 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 differenttypes 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: .




37/83


37

Continue Lecture 13: Edema, and Hemorrhage




opportunity to see some useful web site

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: .
http://www.webpath.com/http://www.webpath.com/http://www.robbinspathology.com/http://www.robbinspathology.com/http://www.robbinspathology.com/http://www.robbinspathology.com/http://www.webpath.com/


38/83


38

Lecture 14:Venous Congestion andhyperaemia


Lecturer: Dr.


1. Define hyperaemia and congestion.2. Differentiate between hyperaemia and

congestion, as regards to the pathophysiologycauses.

3. Recognize the morphology of acute and chronicpulmonary congestion also acute and chronichepatic congestion.

4. List the different causes of chronic venouscongestion (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 thepathological 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: .




39/83


39

Continue Lecture 14: Venous Congestion and hyperaemia



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

www.google.com

Self-assessment


Pooling of blood in capillary beds and venules dueto impaired blood flow is

known as:

a. Congestion.b. Hyperemia.

c. Hypovolemia.

d. Shock.

e. Vasoconstriction.

Student Notes: .
http://www.google.com/http://www.google.com/http://www.google.com/


40/83


40

Lecture 15:ThrombosisDepartment: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 thrombiformation.

4. Describe the fate of thrombus5. Correlate clinically between the types and effects

of thrombi

1-Thrombosis:

1-The definition of thrombosis and the differencebetween thrombosis and blood clot

2-The pathogenesis of thrombosis (Virchow triad).a. Endothelial injury

b. Abnormal blood flowc. Hypercoagulability3-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:




41/83


41

Continue Lecture 15: Thrombosis




opportunity to see some useful web site

www.webpath.com


Self-assessment

Briefly answer the following short question: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: .


42/83


43/83


43

Continue Lecture 16: Embolism andinfarction



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

www.studentconsult.comwww.robbinspathology.com

Self-assessment


The term paradoxical "embolism" is defined as:

a. Death in a healthy person from a Saddle-typepulmonary 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.
http://www.studentconsult.com/http://www.studentconsult.com/http://www.robbinspathology.com/http://www.robbinspathology.com/http://www.robbinspathology.com/http://www.studentconsult.com/


44/83


44

Lecture17:Nomenclature & characteristics of Benign &Malignant neoplasms


Lecturer: Dr

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


By: Kumar, Abbas, Fausto, Michel

On the website you will find many interactive cases for discussion, MCQs and images.www.studentconsult.comwww.robbinspathology.comSelf-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.


45/83


45

Lecture 18:Epidemiology of cancerDepartment: Pathology

Lecturer: Dr


1. List the most common types of cancer in both males and females locally andinternationally.

2. List the different types of cancer in different geographic areas in the world andthe influencing factors.

3. Discuss the effect of environmental factors on the incidence and spread ofcancer.

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. Frequency2. Aetiology3. Incidence of cancer death4. Geographic and environmental factors5. Age differences.6. Hereditary and acquired preneoplastic disorders.

To be announced in the lecture.


By: Kumar, Abbas, Fausto, Michell

On the website you will find many interactive cases for discussion, MCQs and images.www.studentconsult.comwww.robbinspathology.com

Self-assessment

Which of the following cancers is most common in males?

a. Cancer prostateb. Cancer lungc. Cancer urinary bladderd. Cancer kidneye. Sarcoma bone


46/83


47/83


47

LECTURE 20: CARCINOGENESIS

The seven fundamental phenotypic changes in carcinogenesis

Department:PathologyLecturer: Dr


1-Discuss the seven fundamental changes in cell physiology that together dictate the malignant

phenotype in details relevant to his practice2- 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 andtumour 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.



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

www.studentconsult.comwww.pathguy.com

Self-assessment

P53 is considered as:1. Oncogene2.

Proto-oncogene3. Growth factor

4. Tumour suppressor gene
http://www.studentconsult.com/http://www.studentconsult.com/http://www.pathguy.com/http://www.pathguy.com/http://www.pathguy.com/http://www.studentconsult.com/


48/83


48





1. Discuss the role of evasion of apoptosis in carcinogenesis2. Identify the genes that control apoptosis3. Discuss the limitless replicative potential of cells4. 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





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

www.google.com

www.nature.com
http://www.studentconsult.com/http://www.studentconsult.com/http://www.pathguy.com/http://www.pathguy.com/http://www.google.com/http://www.google.com/http://www.nature.com/http://www.nature.com/http://www.nature.com/http://www.google.com/http://www.pathguy.com/http://www.pathguy.com/http://www.studentconsult.com/


49/83


49





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 cells3-Genomic instability;

The role of mutations of DNA repair-genes in the predisposition to cancer andits role in hereditary types of cancer.

4-The molecular model of evolution of colorectal carcinoma through the adenoma-

carcinoma sequence.





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.brain3. Ovary 4. Liver 5. Spleen
http://www.studentconsult.com/http://www.studentconsult.com/http://www.pathguy.com/http://www.pathguy.com/http://www.pathguy.com/http://www.pathguy.com/http://www.pathguy.com/http://www.pathguy.com/http://www.pathguy.com/http://www.studentconsult.com/


50/83


50

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


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 radiations5. Discuss the role in chromosomal abnormalities..

1-The chemical carcinogenesis:a. General features of chemical carcinogens

b. Directacting genesc. Indirectlyacting genesd. 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


By: Kumar, Abbas, Fausto,Michell

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

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

Self-assessment


.
http://www.studentconsult.com/http://www.studentconsult.com/http://www.library.med.utah.edu/WebPath.comhttp://www.library.med.utah.edu/WebPath.comhttp://www.library.med.utah.edu/WebPath.comhttp://www.studentconsult.com/


51/83


51

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


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


By: Kumar, Abbas, Fausto,

Michell




Self-assessment


Epstein barr virus is associated with:a. Mammary carcinoma

b. Hepatocellular carcinomac. Prostatic carcinomad. Gastric carcinomae.

Nasopharyngeal carcinoma.


52/83


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 cachexcia3. discuss Paraneoplastic syndromes4. 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, whilestaging of the tumours is the role of the Surgeon

Robbins Basic Pathology, 8thEdition (2007)By: Kumar, Abbas,Fausto,Michel


www.studentconsult.comwww.robbinspathology.com


53/83


53

Self-assessment

Briefly answer the following short question:1-Tabulate the difference between preneoplastic conditions and paraneoplastic syndrome?

2-Which tumour is most commonly associated with paraneoplastic manifestations?


54/83


54

Lecture 26:Introduction to infectious diseases and tuberculosisDepartment: Pathology

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 agents3. Discuss different modes of spread of microbial agents.4. Define and classify pyemia, bacteremia, toxaemia, and septicaemia.5. List the causative agents of TB6. Identify route of infection by the agent7. Classify TB into primary and secondary subtypes8. 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


By: Kumar, Abbas, Fausto,Michell

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


Self-assessment


Bacteremia is defined as presence of:

a. Small number of low virulence bacteria in the bloodb. Big number of highly virulence rapidly multiplying bacteria in the bloodc. Small number of viruses in the bloodd. Circulating toxins


55/83


55

Lecture 27:TuberculosisDepartment: Pathology

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) p516-532Robbins Basic Pathology, 8thEdition (2007)





www.google.com

Self-assessment

Briefly answer the following short question:Primary tuberculosis is characterized by:

1. Occurs in previously sensitized persons2.

Lesion in upper lung zone3. Hilar lymph nodes are sometimes enlarged

4. More than 90% of cases heal by fibrosis5. Kidney is site for primary complex
http://www.studentconsult.com/http://www.studentconsult.com/http://www.library.med.utah.edu/WebPath.comhttp://www.library.med.utah.edu/WebPath.comhttp://www.google.com/http://www.google.com/http://www.google.com/http://www.library.med.utah.edu/WebPath.comhttp://www.studentconsult.com/


56/83


56

1. Lecture 28:SchistosomiasisDepartment: Pathology

Lecturer: Dr


1. List the different types of causative agents and mode of transmission ofSchistosomiasis

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 Schistosomiasis5. 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 Schistosomiasis6. Complications

Robbins and Cotran Pathologic Basis of diseases, 7th

Edition (2005)

P406-409.



www.studentconsult.comwww.Robbinspathology.com

Self-assessment

Briefly answer the following short question:1. Which of the following conditions is not included among complications of bilharziasis?2. Portal hypertension3. Hepatic fibrosis4. colonic carcinoma5. intestinal obstruction


57/83


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 onpathologic gross specimens.

2. 75 minutes of illustration of digital images and/or gross ORhistological 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 ofnormal 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.


58/83


58

Practical 1: Cell injury, necrosis;

TUTOR: Department: pathology

OBJECTIVES:

1. Identify the morphological changes in the necrotic cells2. 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 Change2. T. B. Lymphadenitis3. Myocardial Infarction4. Infarction brain (Liquefactive)5. Gangrenous intestine

READING: Robbins Basic Pathology, 8thEdition (2007)



59/83


59

Practical 2: Cell adaptationgross specimensTUTOR: Department: pathology

.

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.4. Write a comprehensive description of different lesions.5. Name the pathological diagnosis or related differential diagnosis.6. Answer simple applied questions related to disease process

Teaching material of different gross specimens and electronic images demonstrating thefollowing lesions:

1. Brown atrophy heart2. Hypertrophy LV3. Nodular colloid goitre4. Benign prostatic hyperplasia.

READING:Robbins Basic Pathology, 8th

Edition (2007)



60/83


60

Practical 3: Acute Inflammationgross specimens


OBJECTIVES:

1. Identify the components of inflammatory exudates2. Identify some morphologic patterns of acute inflammation;

fibrinous inflammation suppurative inflammation localized abscess

3. Write a comprehensive description of different lesions.4. Name the pathological diagnosis or related differential diagnosis.5. Answer simple applied questions related to disease process

Gross specimens showing examples of acute inflammation:

1. Pericarditis (Ox Heart)2. Lobar Pneumonia3. Acute Suppurative Appendicitis4. Lung Abscess

READING:Robbins Basic Pathology, 8thEdition (2007)

By: Kumar, Abbas, Fausto,michell


61/83


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 Cholecystitis2. Different examples of T.B. Lung (Caseating)3. Healed Myocardial Infarction

READING:Robbins Basic Pathology, 8thEdition (2007)

By: Kumar, Abbas, Fausto


62/83


62

Practical 5: Inflammation & repairmicroscopic slide


OBJECTIVES:

By the end this session the student should be able to:

1. Describe the component cells of acute inflammation2. 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 lesion6. Answer simple applied question

Different electronic images and microscopic slides showing examples of acute and

chronic inflammation: and healed necrosis:

1. Acute Appendicitis2. Lobar Pneumonia3. TB Granuloma4. Healed Infarction

Robbins Basic Pathology, 8thEdition (2007)By: Kumar, Abbas, Fausto, Michell


63/83


63

Practical 6: Hemodynamic Disorder gross specimenTUTOR: \ 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 gangrenousnecrosis 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 Hemorrhage2. Subarachnoid hemorrhage3. Myocardial infarction (recent)4. Chronic Venous Congestion (Nutmeg liver)5. Coronary Thrombus6. Mesenteric Vein Thrombosis (Infarcted gangrenous intestine)7. Massive Pulmonary Embolism




64/83


64

Practical 7Hemodynamic DisordersTUTOR: Department: pathology

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 factors4. State the different fate of thrombi as resolution, Organization, recanalization, and

embolization5. Correlate theoretical data to practical examples

Digital images for the following will be explained:

a. Chronic Venous Congestion Liverb. Organized Thrombusc. Organized Thrombus with calcification in the wall

READING:Robbins Basic Pathology, 8th

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


65/83


65

Practical 8: Benign tumours of epithelial origin-TUTOR: Department: pathology

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 tumors3. Describe a cystic structure.4. Differentiate between benign and malignant tumors5. Correlate theoretical data to practical examples

Teaching material of different specimen with benign lesion includes:

1. Thyroid Adenoma2. Familial Polyposis3. Familial Multiple polyps Colon4. Fibroadenoma Breast5. Dermoid Cyst Ovary (Cystic Teratoma)

Teaching material of different digital images showing examples of

1. Squamous Papilloma (oral)2. Fibroadenoma Breast




66/83


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.4. Correlate theoretical data to practical examples

Teaching material of different gross specimens demonstrating the following lesions:

1. Lipoma2. Leiomyoma Uterus3. Osteochondroma Bone




67/83


67

Practical 10: Malignant tumoursTUTOR: Department: pathology

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

tumours:

1. Examine different examples of malignant tumours2. Describe a malignant epithelial tumour3. Diagnosis lesions in given specimens4. Differentiate between different tumours in different organs.5. Correlate theoretical data to practical examples

The teaching material of different specimens with gross specimen and images ofmalignant diseases:

1. Carcinoma Colon2. Carcinoma oesophagus (Fungating)3. Cancer Breast4. Cancer Stomach5. Osteosarcoma6. Chondrosarcoma7. Chondrosarcoma (Lt. Distal Radius)




68/83


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 tumours2. Describe a malignant epithelial tumour3. Diagnosis lesions in given specimens4. Differentiate between different tumours in different organs5. Correlate theoretical data to practical examples

Teaching material of different gross specimens demonstrating:

1. Metastasis Lymph node2. Metastasis Lung3. Metastasis Liver4. Metastasis Brain

Teaching material of different digital images demonstrating:1. Adenocarcinoma Colon2. Infiltrating Duct Carcinoma Breast3. Osteosarcoma




69/83


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 TB3. Identify the basic histological feature of the granulomatous inflammation in any tissue.4. Correlate theoretical data to practical examples

Teaching material of different specimens and digital images for both histologic and gross featuresdemonstrating:

1. Primary complex of tuberculosis2. Secondary pulmonary TB3. TB lymphadenitis4. TB small intestine

Robbins Basic Pathology, 8th

Edition (2007),chapter 13By: Kumar, Abbas, Fausto


70/83


70

STUDENT GUIDE TO

TUTORIALThe 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 hisreading.

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.


71/83


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 thepractical 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




72/83


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 thepathogenesis and mechanism of these types

2. Discuss the clinical signs and symptoms of inflammation3. Relate clinical signs and symptoms of inflammation to the chemical mediators4. Discuss the harmful effects of inflammation and its clinical implications.5. Differentiate between types of healing processes6. Correlate between type of wound and healing process7. Identify factors that delay healing8. Discuss how to improve healing process

1- The morphologic patterns of inflammation2- The clinical signs and symptoms of inflammation3- The harmful effects of inflammation and its clinical implications 4- wound and healing process


By: Kumar, Cotran, Robbins


73/83


73

TUTORIAL # 03: hemodynamic disorders


OBJECTIVES:

- The student should be able to:

1. Correlate between chronic congestion and edema2. Identify the clinical signs and symptoms of thrombophlebitis3. Correlate between clinical settings and embolus formation

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

1. Congestion and edema2. Clinical signs and symptoms of thrombophlebitis3. Cinical settings of emboli




74/83


74

TUTORIAL # 4: A case of neoplasm for diagnosis


OBJECTIVES:


1. Differentiate between benign and malignant tumours.2. Discuss the biological behaviour of malignant tumours3. Identify clinical manifestation of malignant tumours

1- Difference between benign and malignant tumours2- biological behaviour of malignant tumours3- Clinical manifestation of malignant tumours4- Groups are assigned cases of benign tumour.

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




75/83


75

TUTORIAL # 5: Infectious diseases


OBJECTIVES:


1. Correlate the clinical presentation of each infectious disease to the histologicalappearance of its different stages.

2. Discussion on TB vaccination, Mantoux test3. Discuss the epidemiology of TB around the world and in Saudi Arabia.

1. Histological and clinical presentation of infectious disease2. TB vaccination, Mantoux test .Wider discussion is encouraged among all the students guided by the tutor




76/83


76

Student Guide toIndependent learning

Independent learning is a very essential skill for tomorrows doctors.

We will train you to gain this important skill by asking you to readindependently 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 inhis 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 30minutes), 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 subtractedfrom the discussed SDL material.

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

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


77/83


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.


78/83


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.




79/83


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 inflammation4. List the chemical mediators involved5. Describe the circumstances under which leukocyte induce injury.

A-Defects in leukocytes function:

1. Defects in adhesion2. Defects in microbicidal activity3. Defect in phagosome formation

B- Systemic effects of inflammation.C- Leukocyte- induced tissue injury.




80/83


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 types2. 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 causesb. Clinical featuresc. Pathogenesis

2- Disseminated intravascular coagulation:

a. Definitionb. Various clinical settings underlying the condition.c. Consequences




81/83


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 antigensb. Tumour associated antigens.c. Products of mutated oncogenes and tumor suppressor genesd. Aberrantly expressed cellular proteinse. Oncofetal proteins

2-Mechanism of how the tumour cells escape immunosurveillance.3-Laboratory diagnosis of cancer:-Morphological methods;

1- frozen section2- fine needle aspiration3- cytological smears4- immunohistochemistry5- flow cytometry

-Biochemical assays:The value of serum tumour markers as, CEA, AFP, and PSA




82/83


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 infectionc. Know to barriers can breakdown infectiond. Enumerate methods of spread of infectione. Identify the inflammatory mechanism against infectious agents

2-Understand the pathology of amebiasis.

a. Identify modes of transmissionb. List common sites of infectionc. Correlation between morphology and complications.

2.

A- Barriers of the body to infection:

B-Spread of microbes:

1. Direct spread2. Lymphatic spread3. Blood spreadC-Types of inflammation against infections:

1. Suppurative inflammation,2. Chronic inflammation3. Granulomatous InflammationD-Amebiasis:4. The route of infection of amebiasis.5. Pathologic lesions in the large bowel6. Complications with special emphasis of liver abscess.


83/83


FurtherReading

1.Robbins and Cotran Pathologic Basis of diseases, 7thEditionby: Kumar, Abbas, Fausto, (2005)

2.Robin Reid, Fiona Roberts. Pathology Illustrated. 6thEd,Elsevier, Churchill Livingston. 2005.

3. Ivan Damjan

Pathology StudyGuide 2011 KAAU

Documents

Transcript of Pathology StudyGuide 2011 KAAU