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Transcript
Introduction of Pathology By: Dr Tarek Atia • Pathology is "Scientific study of disease“ Study of structural and functional changes in disease. • Diseases is an expression of "discomfort" due to structural or functional abnormality. • "Pathology deals with knowledge of what causes disease, how disease starts, progresses & it explains the reason for signs and symptoms of patient" Branches of Pathology: Histopathology / Anatomic Pathology : Pathologists specialising in anatomical changes in disease. Usually using a tissue biopsy. Cytopathology: Pathologists specialising in study of body fluids & Cells. Haematology: Study of blood and blood forming organs. Morbid Anatomy: Autopsy or Post mortem study for legal or educational purpose. • Factors causing disease could be :– Environmental or external factors \ and Genetic or Internal factors. • Diseases which present since birth are called Congenital diseases and all other diseases are known as Acquired diseases. • Diseases which occur in families are known as Familial diseases. Pathology of a disease is formally studied under four subdivisions. - Etiology - Study of cause / causative agent of disease - Pathogenesis- Study of disease progression or evolution. - Morphology - Study of structural changes in disease (Gross & microscopic) - Clinical Significance - Study of how clinical features are related to changes. Major groups of diseases are Inflammatory, Degenerative & Neoplastic. Inflammatory disorders are due to damage to tissues by various injuries (physical, chemical, infections etc.) Degenerative disorders are due to lack of growth or ageing. Neoplastic disorders are due to excess cell division forming tumours. Cell & Tissue Injury Principles • Human disease occurs because of injury to cells / tissue. • Most human disease results from injury to epithelium. • Injury to one tissue usually affects the adjacent or underlying tissue as well. • Cell injury produces morphologic changes. Cell Injury Damage or alteration of one or more cellular components 1. Many types of injury are tissue-specific because of anatomic relationships and tissue response to chemical and infectious agents. 2. Cell injury disrupt cell physiology; so the cell does not function at full capacity. Stages in the cellular response to stress and injurious stimuli Consequences of Injury 1. (Reversible): No long term effects- the cell damage is repaired, the effects of the injury are reversible. 2. The cell “adapts” to the damaging stimulus. 3. (Irreversible): The cell dies, undergoing necrosis. The damage is irreversible. Cell Injury Produces: 1. Signs: abnormal physical findings Objective 2. Symptoms : complaints experienced by the patient - Subjective Adaptation to injury 1. Atrophy: decrease in the size and functional capacity of the cell. after normal growth has been attained . ( O2, blood, nerve supply) 2. Hypertrophy: an increase in the size of the cell secondary to an increase in cell function. Increase in the number of mitochondria and ER, etc. 3. Hyperplasia: an increase in the number of cells of a tissue in response to a stimulus or injury. 4. Metaplasia: replacement of one type of tissue with another in response to an injury. Hypertrophy versus Necrosis Uterine hypertrophy Muscular hypertrophy Metaplasia Diagram of columnar to squamous metaplasia. Cell Atrophy Causes 1. 2. 3. 4. Loss of blood supply or innervations Loss of endocrine factors (eg. TSH) Decrease in the workload Aging, chronic illness A: Atrophy of the brain in an 82-year-old male with atherosclerotic disease. Note that loss of brain substance narrows the gyri and widens the sulci. B: Normal brain of a 36-year-old male. Outcomes from cell injury depend upon: 1. Type of injury 2. Severity of the injury 3. Duration of the injury 4. Type of cell being injured- Some cell types sustain injury better than others; some tissues (e.g. liver) have a capacity to regenerate. Reversible Cell Injury 1. Cell swelling– usually accompanies all types of injury. Results from an increase in water permeability degeneration. leading Reverses function is restored. to hydropic once or membrane 2. Fatty change in liver. Vacuoles of fat accumulate within the liver cell following many types of injury: alcohol intoxication, chronic illness, diabetes mellitus, etc. Vulnerable Sites of the Cell 1. 2. 3. 4. Cell membranes Mitochondria Endoplasmic reticulum Nucleus Cell Death • Apoptosis • Necrosis Apoptosis Morphology of Necrosis Pyknosis • Shrunken nucleus with dark staining • Seen in a necrotic (dead) cell Karyorrhexis • Fragmentation of pyknotic nucleus Karyolysis • Extensive hydrolysis of pyknotic nucleus with loss of staining • Represents breakdown of the denatured chromatin Karyolysis Types of Necrosis 1- Coagulative Necrosis • Dead cells remain as ghost-like remnants of their former self • Classically seen in an MI Cardiac muscle fibers 2- Liquefactive Necrosis • The dead cell undergoes extensive autolysis, caused by the release of lysosomal hydrolases (proteinases, DNases, RNases, lipases, etc.) • Seen classically in the spleen and brain following infarction. (A) Coagulative vs. (B) Liquefactive Necrosis 3- Caseous Necrosis (caseum - cheesy) • Resembles cottage cheese • Soft, friable, whitish-grey • Present within infected tissues • Seen in Tuberculosis (Mycobacterium tuberculosis) Caseous Necrosis Caseous Necrosis 4- Fat Necrosis •Leakage of lipases from dead cells attack triglycerides in surrounding fat tissue and generate free fatty acids and calcium soaps •These soaps have a chalky-white appearance •Seen in the pancreas following acute inflammation Causes of Cell and Tissue Injury 1. Physical agents 2. Chemicals and drugs 3. Infectious pathogens 4. Immunologic reactions 5. Genetic mutations 6. Nutritional imbalances 7. Hypoxia and Ischemia: cell injury resulting from inadequate levels of oxygen.