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RAD 204 PathologyBasic Terminology
Week of 15.Septmeber.2013
College of Medical Sciences/ Radiological Sciences Department
Dr . Shai’ Lecture
2
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I. INTRODUCTION
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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
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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
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1. Aetiology
CauseKnown: primary aetiology {key to diagnosis and treatment development}Unknown: Idiopathic
ClassesGeneticAcquired
Infectious, Nutritional, Chemical, etc
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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
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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
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4. Functional derangements and clinical significance
There are different diagnosticmodalities used in pathology.
Most of these diagnostic techniques are based onmorphologic changes.
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5. Diagnostic techniques used in
pathologyHistopathology CytopathologyHaematopathology
Immunohistochemistry Microbiological Exam
Biochemical Exam Cytogenetics
Molecular Techniques Autopsy
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II. CELLULAR INJURY
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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
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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
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1. Cellular Adaptation
HYPERTROPHY
ATROPHY
HYPERPLASIA
METAPLASIA
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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
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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
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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.
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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.
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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
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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?
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4. Molecular Basis of Cancer
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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)
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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
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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
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https://www.youtube.com/watch?v=9KTDz-ZisZ0&list=PL88EDB2A96ED033AE
OVERVIEW (25 MIN)
https://www.youtube.com/watch?v=niBCqgM1Pb4