Pathanatomy Lecture - 02 Cell Injury

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 LECTURE ON PATHOLOGICAL ANATOMY IS PRESENTED BY AS.PROF. SERDOBINTSEVA T.S.

  m  à Structures of living systems are not constant à They are destructured and restored continuously à All living organisms absorb and extract proteins, lipids (fats), carbohydrates, and their components as well as water, ions, and pigments. |

  Ã All living systems including cells and extra cellular matrix absorb fresh substances and extract products of their metabolisms. Ã Polypeptides, polynucleotides and polysaccharides play the most significant role to metabolize. 

  à Every organism (body) consists of organs à Every organ consists of tissues à Tissue consists of cells à Cell consists of ultrastructures u

 

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à There are tissues: epithelium, derivations from mesenchymal tissue ( connective tissue, fatty tissues, bones, cartilages, muscles, vessels ) Nervous tissues Bone marrow tissues Lymphatic tissues ¬

  Ã The chain of changes develops under super normal (hyper normal) and pathological processes inside cells and extra cellular matrix

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 Ã ETIOLOGIC AGENT MAY BE EVERY ONE EXOGENIC OR INTRAGENIC Ã BUT CHAIN OF CELLULAR CHANGES CONSISTS OF STAGES AS FOLLOW: 1ADAPTATION | REVERSIBLE CHANGES  IRREVERSIBLE CHANGES as NECROSIS(CELLULAR DEATH) u autolysis and heterolysis

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 Ã Autolysis is termed self digestion by lysosomes enzymes . Ã Heterolysis is termed digestion by lysosomes of other cells

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 à Reversible changes or cellular degeneration or parenchymal dystrophy à According to metabolic disturbance there are protein, fatty, carbohydrate, and ion degenerations. According to localization there are parenchymal (cellular), mesenchymal (stromal(stromal-vascular), And mixed reversible changes or degenerations

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Causes or etiology: Hypoxia Ischemia Physic agents Chemical agents including medicine, drug Infective agents Immunologic reaction Genetic injury Nutrition disbalance

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 Mechanisms of reversible injury à Decomposition of membranes à Hyper infiltration of substances (intracellular accumulation) à Unnatural syntheses Disbalance of calcium metabolism à ATP depletion à Free radicalradical-induced injury 11

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 Cellular injury depends on cell: à 1 type (myocardial cells dies in |0|0-0 min. ,but epidermis cells dies in weeks, after cause (etiologic agents ) acted. à | genetic makeup à  adaptability ( hepatic cells are more adaptive cells, then neurons) à u status( normal or hypertrophic)

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 Cellular injury depends on injury: 1 type (ischemia or infective agent) | its duration  its severity

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m  Ã Myocardiac cell becomes no contractile in1 in1 to | minutes after ischemia stated. Ã It dies in |0 |0--0 minutes after ischemia started But ultra structural evaluation of changes appears in |- hours after ischemia started and light microscopical evaluation becomes possible in 0-1| hours after ischemia 1u started.

  
m  INTRACELLULAR RESPONSE INCLUDS 1 Aggregation of intramembranous particles | Endoplasmic reticulum swelling  Dispersion of ribosomes u Cell swelling ¬ Clumping of nuclear chromatin 0 Mitochondrial swelling G Small densities within mitochondrii 1¬

      

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m#  #%"  à 1classification according to location à Parenchymal (cellular) degeneration or dystrophy à Stromal vascular à Mixed 1G

m#  #%"  | classification according to type metabolism abnormality à Disproteinosis à Lipidosis à Carbohydrate abnormality

à Mineral abnormality à Pigment abnormality 1

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) LIPID METABOLISM ABNORMALITY

à INTRACELLULAR ACCUMULATION à STROMAL VASCULAR ACCUMULATION

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m  Intracellular accumulation 1 Cellular swelling or hydropic dystrophy | Lipid accumulation  Glycogen accumulation |0

  
m  Classification according to cellular disproteinosis 1 Cellular swelling or hydropic (vacuole) dystrophy or degeneration | Hyaline droplet dystrophy or degeneration  Hyper keratinization |1

m!   à Ions disbalance between sodium and potassium with water bubble formation à Protein infiltration within cells à Cellular membranes destruction ||

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Diseases: 1Infective diseases | Nephropathy  Chronic glomerulonephritis u Alcoholic disease Alzheimer disease |

m!   Organs are as follow: 1 Kidney | Liver  Skin (epidermis) u Brain (neurons)

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m!   The tubular vacuolization and tubular dilation here is a result of the toxic effect of ethylene glycol poisoning. The kidney |¬

(     Ã Here are Mallory bodies (the red globular material) composed of cytoskeletal filaments in liver cells chronically damaged from alcoholism

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m() +  , PARENCHYMAL LIPIDOSIS IS CHARACTERIZED BY ABNORMAL ACCUMULATION OF TRIGLYCERIDES WITHIN PARENCHYMAL CELLS ORGANS: THE LIVER, THE MYOCARDIUM, THE KIDNEYS. . |G

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  Ã ETIOLOGY IS TOXINS, PROTEIN MALNUTRITION, DIABETES MELLITUS, OBESITY AND ANOXIA. Ã PATHOGENESIS IS DISBALANCE BETWEEN REMOVE, UTILISATION AND EXCRETION OF LIPIDS BY HEPATOCYTES. |

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  à EXCESS ABSORPTION OF fatty acids and triglycerides à Reduced Utilization of them on mitochondrii à Decrease in apoprotein production

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'  &   ( Ã FIGURATIYE NAME IS GOOSE LIVER Ã DISEASES ARE 1 ALCOHOL ABUSE | DIADETES MELLITUS  OBESITY u STARVATION ¬ POISONING

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Micro sample stain is Sudan 

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 Ã REVERSE TO NORMAL STRUCTURE Ã HEPATITIS

à CIRRHOSIS |

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à ETIOLOGY HYPOXIA, INTOXICATION . à PATHOGENESIS LACK of OXYGEN LEAD TO decreasing oxidative phosphorylation anaerobic glycolysis decreasing ATP synthesis mitochondrion destruction inhibition of fatty acid oxidation toxins cause severe damage of membranes and enzyme systems u

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APPEARANT BANDS OF YELLOWED MYOCARDIUM ALTERNATING WITH BANDS OF DARKER, RED-BROWN UNINVOLVED HEART ³TIGERET ³EFFECT´ ± TIGER HEART´

Severe fatty change is produced by profound hypoxia with diffused yellow ±colored myocardium

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1Small droplets of lipid are found within myocardial cells. Prolonged moderate hypoxia results in local intracellular fat deposits according to venous blood collection

Micro sample stain is Sudan  0

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)   Ã 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.

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Stage of atherosclerosis is termed lipidosis micro

Foam cells within atherosclerotic plaque 

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 Ã Carbohydrate Parenchymal abnormality is divided into disorders of glycogen and glycoproteids. Diseases are diabetes mellitus and hereditary glycogen storage diseases named Glycogenoses or tezaurismosis tezaurismosis..

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"$ à Hyperglycosemia lead to glycogen accumulation within renal tubular epithelium à Best¶s stained by Carmine à Crimson ±colored granules of glycogen u0

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The end

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