RAD 204 PathologyBasic Terminology

Week of 15.Septmeber.2013

College of Medical Sciences/ Radiological Sciences Department

Dr . Shai’ Lecture

2

I. INTRODUCTION

A. Objectives1. Define pathology2. Discuss the core aspects of disease in pathology 3. Know pathological manifestations of disease 4. Know the diagnostic techniques used in pathology

B. DefinitionsLatin, Patho: disease, Logy: study ofDiseases: Abnormal Variations in Structure or Function of Any Part of the BodyWE study the aetiology, pathogenesis, morphologic changes & functional derangements and clinical significance

1. AetiologyCause

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

ClassesGeneticAcquired

Infectious, Nutritional, Chemical, etc

2. PathogenesisMechanism through which the cause operates to produce the pathological and clinical manifestationsOccurs in latent or incubation periodLeads to morphological changes: visible by naked eye, microscopes and diagnostic visualization

3. MorphologyCell and Tissue StructureChanges: structural alterations subsequent to pathogenesisAllows pathologist to identify (diagnose) diseaseAnd 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 CytopathologyHaematopathologyImmunohistochemistry Microbiological ExamBiochemical Exam CytogeneticsMolecular 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 Terminology4. Molecular Basis of Cancer

B. DefinitionsCellular injury underlies ALL DISEASEINJURIOUS AGENT > CELL > OUTCOMES:

Cell adapts to situationCell acquires a reversible injuryCell acquires IRREVERSIBLE injury and dies by:

Necrosis (unprogrammed)Apoptosis (programmed)

Outcome depends on type of injurious agent & on cellular factorsIt depends on the Type, Severity, Duration of Injury & Type of cell

1. Cellular Adaptation

HYPERTROPHYATROPHYHYPERPLASIAMETAPLASIA

A. HYPERTROPHYIncrease in size of cells

Increased 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. Disuse2. Undernutrition3. Decreased endocrine stimulation4. Denervation5. Old age

C. HYPERPLASIAHyperplasia 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. METAPLASIAReplacement 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 swellingAnaplastic: poorly differentiatedBenign: localized cancers that do NOT invade other organsMalignant: capable of invasion and spread to distant organsDysplasia: 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 functionsProto 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 controlledUnhealthy cells: mutation produce onco protein which is functionally altered eg hyperactive mutant ras protein affects intracellular pathway signallingOr normal protein overproduced eg myc oncogene in neuroblastomasIncludes:

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 growthIf inactivated>>increased susceptibility to cancerEg. BRCA1 in breast cancer & ovarian cancer, located on chromosome 17qP53 protein on 17p (implicated in many cancers)RB1 in retinoblastoma, 17qTSGs 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 processSingle cell initiates own death under normal physiological conditionsOccurs 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