RAD 204 PathologyBasic Terminology

Week of 15.Septmeber.2013

College of Medical Sciences/ Radiological Sciences Department

Dr . Shai’ Lecture

2

I. INTRODUCTION

A. Objectives

1. Define pathology

2. Discuss the core aspects of disease in pathology

3. Know pathological manifestations of disease

4. Know the diagnostic techniques used in pathology

B. Definitions

Latin, Patho: disease, Logy: study of

Diseases: Abnormal Variations in Structure or Function of Any Part of the Body

WE study the aetiology, pathogenesis, morphologic changes & functional derangements and clinical significance

1. Aetiology

CauseKnown: primary aetiology {key to diagnosis and treatment development}Unknown: Idiopathic

ClassesGeneticAcquired

Infectious, Nutritional, Chemical, etc

2. Pathogenesis

Mechanism through which the cause operates to produce the pathological and clinical manifestations

Occurs in latent or incubation period

Leads to morphological changes: visible by naked eye, microscopes and diagnostic visualization

3. Morphology

Cell and Tissue Structure

Changes: structural alterations subsequent to pathogenesis

Allows pathologist to identify (diagnose) disease

And will lead to understanding of clinical signs and symptoms of disease

4. Functional derangements and clinical significance

There are different diagnosticmodalities used in pathology.

Most of these diagnostic techniques are based onmorphologic changes.

5. Diagnostic techniques used in

pathologyHistopathology CytopathologyHaematopathology

Immunohistochemistry Microbiological Exam

Biochemical Exam Cytogenetics

Molecular Techniques Autopsy

II. CELLULAR INJURY

A. Objectives

1. Define hyperplasia, hypertrophy, atrophy, hyperplasia, metaplasia & list some of their causes.

2. Know the differences between reversible & irreversible forms of cell injury.

3. Oncology Terminology

4. Molecular Basis of Cancer

B. Definitions

Cellular injury underlies ALL DISEASE

INJURIOUS AGENT > CELL > OUTCOMES:Cell adapts to situation

Cell acquires a reversible injury

Cell acquires IRREVERSIBLE injury and dies by:Necrosis (unprogrammed)

Apoptosis (programmed)

Outcome depends on type of injurious agent & on cellular factors

It depends on the Type, Severity, Duration of Injury & Type of cell

1. Cellular Adaptation

HYPERTROPHY

ATROPHY

HYPERPLASIA

METAPLASIA

A. HYPERTROPHY

Increase in size of cellsIncreased workload leads to increased protein synthesisLeads to increased size and number of intra cellular organellesLeads to increased cell size > increased ORGAN size

Eg. LV enlargement in hypertensive heart dzEg. Increased skeletal muscle during strenuous exercise

B. ATROPHYAtrophy is a decrease in the size of a cell. This can lead to decreased size of the organ.

The atrophic cell shows autophagic vacuoles which contain cellular debris from degraded organelles.

Atrophy can be caused by:

1. Disuse

2. Undernutrition

3. Decreased endocrine stimulation

4. Denervation

5. Old age

C. HYPERPLASIA

Hyperplasia is an increase in the number of cells. It can lead to an increase in the size of the organ.

It is usually caused by hormonal stimulation. It can be physiological as in enlargement of the breast during pregnancy or it can pathological as in endometrial hyperplasia.

D. METAPLASIA

Replacement of one differentiated tissue by another differentiated tissue.

Examples include:

1. Squamous metaplasia: replacement of another type of epithelium by squamous epithelium. Eg. columnar epithelium of bronchus replaced by squamous epithelium in cigarette smokers

2. Osseous metaplasia: replacement of a connective tissue by bone, for example at sites of injury.

3. Oncology Terminology

TumourAn abnormal mass of tissue, resulting from autonomous disordered growth that persists after the initiating stimulus has been removed.

Results from genetic alteration and deregulated growth control mechanisms

-oma: means swelling

Anaplastic: poorly differentiated

Benign: localized cancers that do NOT invade other organs

Malignant: capable of invasion and spread to distant organs

Dysplasia: Disordered development of cells resulting in an alteration in size, shape and organization

https://www.youtube.com/watch?v=rrMq8uA_6iA&list=PL88EDB2A96ED033AE

Carcinoma in situ: Epithelial neoplasm with cellular features associated with malignancy, but not yet invaded through epithelial basement membrane

DID YOU KNOW?

Japan: gastric carcinoma is 30 times more common than UK

? Why do you think this is?

4. Molecular Basis of Cancer

Cell proliferation and division regulated by 2 opposing functions

Proto oncogenes: genes expressed in normal cellsCode for onco proteins, which positively regulate cell growth differentiation {growth factors, transcription factors, receptor molecules}

Healthy cells: tightly controlled

Unhealthy cells: mutation produce onco protein which is functionally altered eg hyperactive mutant ras protein affects intracellular pathway signalling

Or normal protein overproduced eg myc oncogene in neuroblastomas

Includes:Nuclear binding proteins (eg c-myc)

Tyrosine kinase proetins (eg src)

Growth factors (eg platelet derived growth factor)

Receptors for growth ( eg c-erb, HER 2), GTP binding proetins (eg ras)

Tumour Suppressor Genes (TSG)

Encode proteins that prevent or suppress tumour growth

If inactivated>>increased susceptibility to cancer

Eg. BRCA1 in breast cancer & ovarian cancer, located on chromosome 17q

P53 protein on 17p (implicated in many cancers)

RB1 in retinoblastoma, 17q

TSGs lose normal function by:Mutations (hereditary / acquired)

Binding of TSG protein to viral gene proteins (HPV E6/7)

Complexing TSG protein to mutatnt TSG protein

If DNA damaged, TSG will promote cell apoptosis

5. Definitions …Apoptosis: PROGRAMMED CELL DEATH

Active process

Single cell initiates own death under normal physiological conditions

Occurs in tissue modelling, embryogenesis, immune regulation, and deregulated in tumours

https://www.youtube.com/watch?v=9KTDz-ZisZ0&list=PL88EDB2A96ED033AE

OVERVIEW (25 MIN)

https://www.youtube.com/watch?v=niBCqgM1Pb4