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pathology intro.pptx
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- 3. Importance of pathology •Understanding cause of disease • Progression of disease • Early and effective diagnosis • Prevention of diseases • Management of disease conditions
- 4. • pathos =suffering, logos = study • foundation of modern pathology is understanding the cellular and molecular abnormalities that give rise to disease
- 6. Cellular adaptation • cellularadaptation refers to changes made by a cell in response to adverse or varying environmental changes • physiologic (normal) or pathologic (abnormal).
- 7. Cellular Adaptation • Atrophy– decrease in the size of the cells-thymus • Hypertrophy – increase in the size of the cells- skeletal muscle • Hyperplasia-increase in the number of cells- endometrium • Metaplasia –change of one cell type to another- esophagus • Dysplasia-abnormal changes in cell size, shape or organisation
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- 16. CAUSES OF CELLINJURY • Hypoxia and ischemia. • Toxins • Infectious agents. • Immunologic reactions. • Genetic abnormalities. • Nutritional imbalances. • Physical agents. • Aging
- 17. Reversible Cell Injury •Cellular swelling • Fatty change • Hyaline change • Myxoid or mucoid change
- 19. Irreversible cell injury •Autolysis – cell digested by enzymes of lysosomes • Necrosis • Apoptosis
- 20. Cell Death • Necrosis •Apoptosis
- 21. NECROSIS • is aform of cell death in which cellular membranes fall apart, and cellular enzymes leak out and ultimately digest the cell • Always abnormal • Always accompanied by Inflammation
- 22. • Coagulative necrosis •Liquefactive necrosis • Caseous necrosis • Fat necros • Fibrinoid necrosisis
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- 25. GANGRENE • Necrosis withputrefaction • Dry gangrene • Wet gangrene • Gas gangrene
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- 29. APOPTOSIS • Programmed celldeath. • Distinctive pattern of cell death to eliminate unwanted cells • Physiological or pathological (abnormal) • No inflammation
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- 31. • Physiological –embryogenesis, endometrial shedding during menstruation • Pathological – viral infection, destruction of cells by cancer drugs
- 32. Steps of apoptosis •Initiation – trigger of FAS or lack of hormones or heat or radiation • Execution – activation of enzymes
- 34. • Caspases –cleave cytoskeletal proteins • Nucleases – hromatin condensation • Flipping out of phosphatidyl serine for phagocytosis • Appearance of thrombospondin bodies
- 36. Pathological calcification • Dystrophiccalcification – calcium depositd in dead tissues • Post TB lesion with calcification • Metastatic calcification – deposition of calcium in living tissue • Hyperparathyroidism and hypervitaminosis D
- 37. INFLAMMATION • Inflammation isa response of vascularized tissues • to infections and tissue damage that brings cells and molecules of host defense • from the circulation to the sites where they are needed, • to eliminate the offending agents.
- 38. Signs of Inflammation •SWELLING • REDNESS • PAIN • HEAT • LOSS OF FUNCTION
- 39. Types of nflammation •Acute inflammation • Chronic inflammation
- 40. Acute inflammation • Suddenand Short lived • Neutrophils • Mild and self limiting • Signs and symptoms are prominent
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- 42. Changes in acuteinflammation • Vascular – dilation of blood vessel, increase in microvasculature permeability • Cellular – extravasation of neutrophils
- 43. Mediators of inflammation •Cell derived – histamine, serotinin • Plasma derived – kinin system, complement system
- 44. Effects of acuteinflammation • Beneficial - Dilution of toxins, entry of antibodies, drugs and nutrients • Harmful – digestion of normal tissue, swelling, allergic response
- 45. What does itlook like • Ulcer • Abscess • cellulitis
- 47. Result of acuteinflammation • Resolution • Fibrosis • Abscess • Chronic inflammation
- 48. Chronic inflammation • Slowonset and progressive • Lymphocytes and monocytes/macrophges • Severe tissue destruction • Less local signs and synptoms
- 49. Monocyte and macrophagelymphocyte
- 50. What does itlook like? • Peptic ulcer • Osteomyelitis • Tuberculosis (chronic granulomatous inflammation)
- 52. Systemic effects ofchronic inflammation • Fever • Anemia • ESR elevetaed • leucocytosis
- 53. PHAGOCYTOSIS • Process ofengulfment of solid material by cells • Phagocytes - Neutrophils and macrophages • Steps – recognition and attachment, engulfment, killing or degradation
- 55. Regeneration • Replacement ofinjured cells by the same type cell • Stem cells / labile cells
- 56. Wound healing • Orderlyand timely reparative process that results in durable restoration of the anatomy and functionality of the organ • Healing by primary intention • Healing by secondary intention
- 57. Healing by primaryintention
- 59. Factors influencing woundhealing • Local – infection, size, apposition of edges, blood supply, mobility, presence of foreign body, cellular hypoxia, ioniisng radiation. • Systemic factors – age, nutritional status, diabetes, immune status, innadequate circulation, hormones.
- 60. Complications of woundhealing • Secondary Infection • Deficient scar formation • Keloids • Contractures
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