Your SlideShare is downloading. ×
0
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
cell injury
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

cell injury

4,130

Published on

Published in: Technology
0 Comments
1 Like
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total Views
4,130
On Slideshare
0
From Embeds
0
Number of Embeds
0
Actions
Shares
0
Downloads
821
Comments
0
Likes
1
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide

Transcript

  • 1. Cell & Tissue Injury
  • 2. Introduction     Every organism (body) consists of organs Every organ consists of tissues Tissue consists of cells Cell consists of ultrastructures
  • 3. Introduction      There are tissues: epithelial mesenchymal tissue ( connective tissue, fatty tissues, bones, cartilages, muscles, vessels ) Nervous tissues Bone marrow tissues Lymphatic tissues
  • 4. INTRODUCTION “All organ injuries start with structural or molecular alterations in cells” concept began by Virchow in 1800's •modern study of disease attempts to understand how cells react to injury, often at the subcellularor molecular level, and how this is manifested in the whole animal. Scanning Electron Micrograph of Blood Cells Caught in a Blood Clot •rbc’s -flattened discs with smooth surface. •white cells –spherical with roughened surface.
  • 5. INTRODUCTION Structures of living systems are not constant They are destructured and restored continuously All living organisms absorb and extract proteins, lipids (fats), carbohydrates, and their components as well as water, ions, and pigments
  • 6. definitions 1) Homeostasis •cells maintain normal structure & function in response to physiologic demands. 2) Cellular Adaptation •as cells encounter stresses they undergo functional or structural adaptations to maintain viability / homeostasis. •respond to some stimuli by increasing or decreasing specific organelle content. •adaptive processes: atrophy, hypertrophy, hyperplasia and metaplasia.
  • 7. definitions 3) Cell Injury •if limits of the adaptive response are exceeded or if adaptation not possible, a sequence of events called cell injury occurs. a) Reversible Cell Injury •removal of stress results in complete restoration of structural & functional integrity. b) Irreversible Cell Injury / Cell Death •if stimulus persists or is severe enough from the start, the cell suffers irreversible cell injury and death. • 2 main morphologic patterns: necrosis & apoptosis.
  • 8. CELLULAR INJURY ETIOLOGIC AGENT MAY BE EVERY ONE EXOGENIC OR INTRAGENIC    BUT CHAIN OF CELLULAR CHANGES CONSISTS OF STAGES AS FOLLOW: 1. ADAPTATION 2. REVERSIBLE CHANGES 3. IRREVERSIBLE CHANGES as NECROSIS(CELLULAR DEATH)  4. autolysis and heterolysis
  • 9. CELLULAR ADAPTATIONS  1)Atrophy  2)Hypertrophy  3)Hyperplasia  4)Hypoplasia / Aplasia  5)Metaplasia  6)Dysplasia
  • 10. Cell Membranes why so easily injured? 1. 2. 3. Membrane is in contact with the external environment: - sustains “trauma” - extracellular oxidants, proteases, etc. Requires a constant supply of ATP for normal function (ion pumps) Lipid molecules in the membrane are easily oxidized and support oxidative chain reaction called lipid peroxidation
  • 11. Cell Membrane Injury Epithelial cell proximal kidney tubule A. Normal B. Reversible ischemic changes C. Irreversible ischemic changes
  • 12. CELLULAR INJURY Reversible changes or cellular degeneration or parenchymal dystrophy  According to metabolic disturbance there are protein, fatty, carbohydrate, and ion degenerations.  According to localization there are parenchymal (cellular), mesenchymal (stromal- -vascular), and mixed reversible changes or degenerations
  • 13. CELLULAR INJURY Causes or etiology Hypoxia Ischemia Physic agents Chemical agents including medicine, drug Infective agents Immunologic reaction Genetic injury Nutrition disbalance
  • 14. CELLULAR INJURY        Mechanisms of reversible injury Decomposition of membranes Hyper infiltration of substances (intracellular accumulation) Unnatural syntheses Disbalance of calcium metabolism ATP depletion Free radical- induced injury induced injury
  • 15. CELLULAR INJURY Cellular injury depends on cell:  1. type (myocardial cells dies in20- 30 min. ,but epidermis cells dies in weeks, after cause (etiologic agents ) acted.  2.genetic makeup  3.adaptability ( hepatic cells are more adaptive cells, then neurons)  4.status( normal or hypertrophic)
  • 16. CELLULAR INJURY Cellular injury depends on injury:  1. type (ischemia or infective agent)  2.its duration  3.its severity
  • 17. REVERSIBLE Cellular injury        INTRACELLULAR RESPONSE INCLUDS Aggregation of intramembranous particles Endoplasmic reticulum swelling Dispersion of ribosomes Cell swelling Clumping of nuclear chromatin Mitochondrial swelling Small densities within mitocondria
  • 18. Mitochondrial Injury
  • 19. Endoplasmic Reticulum Injury
  • 20. Classifications of reversible injury      classification according to type metabolism abnormality Disproteinosis Lipidosis Carbohydrate abnormality Mineral abnormality Pigment abnormality
  • 21. ACCUMULATION PATHOLOGY    LIPID METABOLISM ABNORMALITY INTRACELLULAR ACCUMULATION STROMAL VASCULAR ACCUMULATION
  • 22. REVERSIBLE Cellular injury    Intracellular accumulation Cellular swelling or hydropic dystrophy Lipid accumulation Glycogen accumulation
  • 23. REVERSIBLE Cellular injury Classification according to cellular disproteinosis Cellular swelling or hydropic (vacuole) dystrophy or degeneration  Hyaline droplet dystrophy or degeneration  Hyper keratinization 
  • 24. Cellular swelling or hydropic dystrophy Ions disbalance between sodium and potassium with water bubble formation   Protein infiltration within cells  Cellular membranes destruction
  • 25. Renal tubular epithelium – reversible ischemic injury Loss of microvilli Surface blebbing Slight swelling of mitochondriaClum ping of nuclear chromatin
  • 26. Cellular swelling or hydropic dystrophy Diseases:  Infective diseases  Nephropathy  Chronic glomerulonephritis  Alcoholic disease  Alzheimer disease
  • 27. Cellular swelling or hydropic dystrophy Organs are as follow:     Kidney Liver Skin (epidermis) Brain (neurons)
  • 28. Cellular Swelling •organ swollen with rounded edges. •cut surface: tissue bulges and wet / heavy.
  • 29. Cellular swelling or hydropic dystrophy The tubular vacuolization and tubular dilation here is a result of the toxic effect of ethyleneglycol poisoning
  • 30. Hyaline droplets dystrophy or degeneration Here are Mallory bodies (the red globular material) composed of cytoskeletal filaments in liver cells chronically damaged from alcoholism
  • 31. INTRACELLULAR ACCUMULATION FATTY CHANGE (STEATOSIS) PARENCHYMAL LIPIDOSIS IS CHARACTERIZED BY ABNORMAL ACCUMULATION OF TRIGLYCERIDES WITHIN PARENCHYMAL CELLS ORGANS:  THE LIVER,  THE MYOCARDIUM,  THE KIDNEYS.
  • 32. FATTY CHANGES IN THE LIVER - ETIOLOGY IS TOXINS, PROTEIN MALNUTRITION, DIABETES MELLITUS, OBESITY AND ANOXIA. - PATHOGENESISIS IS DISBALANCE BETWEEN REMOVE, UTILISATION AND EXCRETION OF LIPIDS BY HEPATOCYTES.
  • 33. PATHOGENESIS OF FATTY LIVER EXCESS ABSORPTION OF fatty acids and triglycerides Reduced Utilization of them on mitochondrii Decrease in apoprotein production
  • 34. THE STAIN FOR LIPIDS IS NAMED SUDAN THREE Gross sample Micro sample h/e stained
  • 35. FATTY LIVER Hepatic liposis, higher magnification. The well-delineated lipid filled cytoplasmicvacuoles causing swelling of the hepatocytes, usually pushing nucleus to the periphery of the cell. Note, how the vacuoles can be single and large or multiple and small.
  • 36. FATTY CHANGES IN THE HEART ETIOLOGY HYPOXIA, INTOXICATION . PATHOGENESIS LACK of OXYGEN LEAD TO decreasing oxidative phosphorylation anaerobic glycolysis decreasing ATP synthesis mitochondria destruction inhibition of fatty acid oxidation toxins cause severe damage of membranes and enzyme systems
  • 37. Prolonged moderate hypoxia results in focal intracellular fat deposits APPEARANT BANDS OF YELLOWED MYOCARDIUM ALTERNATING WITH BANDS OF DARKER, RED BROWN UNINVOLVED HEART TIGERET EFFECT´ ± TIGER HEART Severe fatty change is produced by profound hypoxia with diffused yellow±colored myocardium
  • 38. FATTY CHANGES IN THE HEART
  • 39. FATTY CHANGES IN THE AORTAAND LARGE ARTERY Atherosclerotic plaque contains cholesterol and its esters within macrophages and smooth muscle cells (foam cells). After cell death, cholesterol and its esters are seen out of cells.
  • 40. CARBOHYDRATE ABNORMALITY Carbohydrate Parenchymal abnormality is divided into disorders of glycogen and glycoproteids. Diseases are diabetes mellitus and hereditary glycogen storage diseases named Glycogenoses or tezaurismosis
  • 41. Diabetes mellitus Hyperglycosemia lead to glycogen accumulation within renal tubular epithelium Best is stained by Carmine Crimson ± ±colored granules of glycogen
  • 42. Consequences of Injury 1. 2. 3. No long term effects- - the cell damage is repaired, the effects of the injury are reversible. The cell “adapts” to the damaging stimulus. The cell dies, undergoing necrosis. The damage is irreversible.
  • 43. IRREVERSIBLE CELL INJURY the morphologic appearance is due to 2 concurrent processes: 1. denaturation of proteins 2. enzymatic digestion
  • 44. Necrosis      Coagulation Necrosis Liquefactive Necrosis Caseous Necrosis Gangrenous Necrosis Fat Necrosis
  • 45. Coagulation Necrosis •most common manifestation of cell death. •characteristic of hypoxic / ischemic death of cells in all tissues (except brain). •on LM, basic outline of the coagulated cell persists at least a few days. - protein denaturation predominates over enzymatic digestion. •necrotic cells eventually removed by leukocyte proteolysis & phagocytosis.
  • 46. Coagulation Necrosis Gross Appearance •architecture resembles normal tissue, but colorant texture are different. •lighter in color (pale) -due to coagulation of cytoplasmic proteins and decreased blood flow (eg infarcts). •usually firm. •tissue may be swollen or shrunken. •may see a local vascular / inflammatory reaction to necrotic tissue.
  • 47. Coagulation Necrosis Microscopic Appearance •original cell shape & tissue architecture is Preserve die dead cells resemble an eosinophilic "shadow" of the original cells. •cytoplasm: increased eosinophilia (H&E stain)usually hyalinized (homogeneous glassy appearance) may be mineralized. a) Coagulation Necrosis •nucleus: 1. karyolysi 2. pyknosis 3. karyorrhexis
  • 48. Karyorrhexis, lymphocytes, Lymphocyte nuclei have fragmented (arrow). H&E stain.
  • 49. Skeletal muscle note coagulation necrosis of myofibers characterized by fragmentation and hyalinization; also note extensive mineralization (blue-purple staining)
  • 50. Liquefactive Necrosis •when enzymatic digestion of necrotic cells predominates. •esp bacterial infections; neutrophils contain potent hydrolases. •in hypoxic damage (and other types of damage) of the CNS. •affected tissue is liquefied to a soft, viscous, fluid mass. •in acute inflammation, the liquid is often mostly dead WBC’s (pus). •may see degenerate neutrophils and/or amorphous necrotic material.
  • 51. Liquefactive Necrosis
  • 52. Caseous Necrosis •typical seen with specific bacterial diseases, eg TB, caseous lymphadenitis.  Gross appearance• grey-white, dry and friable to pasty (caseous = cheese like).  Microscopic appearance• dead cells persist as amorphous, coarsely granular, eosinophilic debris.• don’t retain cellular outline but don’t undergo complete dissolution either.
  • 53. Caseous Necrosis
  • 54. Gangrenous Necrosis •definition= necrosis (usually ischemic) of extremities, eg digits, ear tips. •dry gangrene= coagulation necrosis of an extremity. •wet gangrene= when the coagulative necrosis of dry gangrene is modified by liquefactive action of saprophytic/putrefactive bacteria.
  • 55. Fat Necrosis •distinguished by its location in body fat stores. •etiology: inflammation (eg pancreatitis), Vit E deficiency, trauma, idiopathic
  • 56. Fat Necrosis
  • 57. Summary     All human disease occur because of cell/tissue injury Membranes-outer and mitochondrial are key targets Many early steps are reversible Cell death follows going beyond a point of no return -drop in pH, rise in Ca2+
  • 58. Thank you for your kind attention.

×