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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. • You need to have a basic knowledge of normal Anatomy (structure) and Physiology (function) to understand Pathology. Diseases is an expression of "discomfort" due to structural or functional abnormality. This abnormality can be caused by various agents Eg. Bacteria, virus, heat, radiation etc. collectively called 'etiology'. • Factors causing disease are mainly two types. 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. 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 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 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. Causes: A. Inadequate blood supply B. Lung disease C. Heart failure D. Shock Hypoxia and IschemiaWhy So Important? All cells in the body require a continuous supply of oxygen in order to produce ATP via oxidative phosphorylation in mitochondria. ATP is absolutely critical for life. Susceptibility of specific cells to ischemic injury • Neurons: 3 to 5 min. • Myocytes, hepatocytes, renal epithelium: 30 min. to 2 hr. • Cells of soft tissue, skin, skeletal muscle: many hours 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. 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. 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. 5. Hypoplasia: incomplete development or underdevelopment of an organ / tissue (less severe in degree than aplasia). 6. Aplasia: lack of development of an organ or tissue (may have a rudimentary organ). can also refer to lack of production of cells from an organ or tissue (eg aplastic anemia). Hypertrophy versus Necrosis Muscle hypertrophy Uterine hypertrophy Metaplasia Diagram of columnar to squamous metaplasia. Cell Atrophy Causes 1. Loss of blood supply or innervations 2. Loss of endocrine factors (eg. TSH) 3. Decrease in the workload 4. Aging, chronic illness Reversible Cell Injury 1. Cell swelling– usually accompanies all types of injury. Results from an increase in water permeability. Reverses once membrane function is restored 2. Increase in extracellular metabolite-- Because of a biochemical derangement. i.e.: Increase in extracellular glycogen in diabetes. 3. Fatty change in liver. Vacuoles of fat accumulate within the liver cell following many types of injury: alcohol intoxication, chronic illness, mellitus, etc. This may be due to: • An increase in entry of free fatty acids. • An increase in synthesis of free fatty acids. • A decrease in fatty acid oxidation. diabetes Vulnerable Sites of the Cell 1. 2. 3. 4. Cell membranes Mitochondria Endoplasmic reticulum Nucleus Cell Death • Apoptosis • Necrosis 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 Kidney (necrotic renal tubules) 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. Liquefactive Necrosis (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