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Dr . Shai’
RAD 204 Pathology
Basic Terminology
Week of 15.Septmeber.2013
College of Medical Sciences/ Radiological Sciences Department
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
Cause
Known: primary aetiology {key to diagnosis
and treatment development}
Unknown: Idiopathic
Classes
Genetic
Acquired
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
Aetiology
Pathogenesis
Clinical
Features
Prognosis
There are different diagnostic
modalities used in pathology.
Most of these diagnostic techniques are based
on
morphologic changes.
5. Diagnostic techniques
used in pathology
Histopathology Cytopathology
Haematopathology
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 cells
Increased workload leads to increased protein
synthesis
Leads to increased size and number of intra cellular
organelles
Leads to increased cell size > increased ORGAN
size
Eg. LV enlargement in hypertensive heart dz
Eg. Increased skeletal muscle during strenuous
exercise
B. ATROPHY
Atrophy 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
Tumour
An 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
Proto Oncogenes
Tumour
Suppressor Genes
Cell proliferation and division regulated by 2 opposing functions
Proto oncogenes: genes expressed in normal cells
Code 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=9KTDzZisZ0&list=PL88EDB2A96ED033AE
OVERVIEW (25 MIN)
https://www.youtube.com/watch?v=niBCqgM1Pb4