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Cell injury for e-learning Dr. Faten Wagdi
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Cell injury Morphological +/- functional changes Of individual cells in response to any stress.
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PATHOLOGICAL STIMULI (Injurious agent/ stress) 1- Hypoxia 2- Chemical agents 3- Infectious agents 4- Physical agents 5- Immunological agents 6- Genetic agents
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Effect of these stimuli on cells ADAPTATION REVERSIBLE INJURY IRREVERSIBLE INJURY
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DEPENDING ON: Severity & Duration of stimulus AND Type of affected cell
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Cellular adaptation -No cell injury -Reversible -Change in ??? number/ size/ type/ function of the cell in response to ??? physiological or pathological changes Why???
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Forms of cell adaptation 1- Atrophy 2- Hypertrophy 3- Hyperplasia 4- Metaplasia
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Forms of cell adaptation
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A mother noticed empty right sided scrotal sac of her infant. Ultrasound revealed tiny right testicle few mms with normal sized left testicle. The right testicular condition is known: A- Atrophy B- Aplasia C- Agenesis
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The myocardial fibers of right ventricular wall In the arrowed heart Displays: A- Increase in number B- Decrease in number C- Increase in size D- Decrease in size E- A+C
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The increase in size Of this organ is Attributed to: A- Increase in number of its cells B- Increase in size of its cells C- A+B
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True or false ?? The lining urothelium of the renal pelvis may be ossified due to prolonged irritation by oxalate stones.
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Transformation of one cell type to another is known as: A- Hyperplasia B- Dysplasia C- Aplasia D- Metaplasia E- Neoplasia
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How injurious agents lead to cell injury ????
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Mechanisms of cell injury: 1- Depletion of ATP 2- Mitochondrial damage 3- Increased intracytoplasmic calcium 4- Accumulation of oxygen-derived free radicals 5- Membrane damage 6- Nuclear damage
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Which of these may be used as clinical parameter of cell death? A- Serum Calcium level B- Serum Ph C- Oxygen-derived free radicals D- Serum lysosomal enzymes
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Lowered intracellular p H in cell injury is attributed to: A- Calcium influx B- Accumulation of oxygen –derived free radicals C- Failure of Na pump D- Anaerobic glycolysis
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Reversible cell injury A- Cellular swelling (hydropic change) OR B- Intracellular accumulations of: Fat Proteins Glycogen Glycoproteins (mucin)
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REVERSIBLE CELL INJURY Cloudy swelling / Hydropic change/ vacuolar degeneration Accumulation of water within the cell cytoplasm. Represents the first manifestation of almost all forms of injury to the cell.
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Small cytoplasmic vacuoles in hydropic change represents: A- Distended mitochondria B- Distended endoplasmic reticulum C- Distended lysosomes D- Distended ribosomes
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NECROSIS -Definition -D.D. from autolysis -Pathogenesis -Morphology ( cytoplasm & nucleus) -Types - Assosiated pathological changes
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Types of necrosis ?? Type of necrosis depends on Balance between Protein denaturation & Lysosomal digestion
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Types of necrosis: 1- Coagulative 2- Liquefactive 3- Caseous 4- Fat 5- Fibrinoid
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Cut of blood supply leads to liquefactive necrosis in: A- Heart B- Spleen C- Spinal cord D- Kidney E- Intestine
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Case n= 1 A 40 yrs old female presents by a firm mass in the breast 2 weeks after she has been subjected to car accident. Needle biopsy reveals chronic inflammatory cellular infiltrate with granular basophilic deposits. A- What is your diagnosis? B- What is the clinical importance? C- Give another example to the same pathological condition.
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Renal infarction is suspected grossly by: A- Thin walled cystic lesion B- Cheesy yellowish lesion C- Hard chalky white foci D- Firm pale area
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APOPTOSIS -Definition -Morphology -Examples -Pathogenesis - D.D. from necrosis
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FAS FasL Bak p53 ??? Bcl-x1???
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Apoptosis vs Necrosis
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Apoptosis is characterised by being : A- Surrounded by inflammatory cells B- Always pathological C- Affect group of contiguous cells D- Active process E- Reversible cell injury
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Gangrene = Necrosis + putrefaction Necrosis : Ischaemia…… Putrefaction: Saprophytic organisms in soil & air/ in colon
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Types of gangrene I- Dry gangrene II- Wet gangrene III- Gaz gangrene
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Gangrene may affect all these sites except: A- Brain B- Vulva C- Lung D- Hand E- Intestine
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Complete: In dry gangrene …………………. Represents a zone of acute inflammation separating the …….. Part from the …… part.
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INTRACELLULAR ACCUMULATIONS A- Normal constituents: Lipids Proteins Carbohydrates B- Abnormal metabolic products C- Pigment: Endogenous or exogenous.
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Intracellular accumulation of fat: 1- Triglycerides in parenchymatous cells: Fatty change ( steatosis ) 2- Cholesterol in macrophages: Hges, cholesterolosis, xanthomas 3- Stromal fatty infiltration: Obesity (fat cells in stroma) 4- Abnormal lipids in reticulo endothelial cells : Lipid storage diseases
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Fatty change of liver occurs in the following conditions except: A- D.M. B- Cholesterolosis C- CHF D- Chronic alcoholism E- Starvation
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To stain intracellular fat the tissue must be: A- Formaline fixed B- Alcohol fixed C- Saline fixed D- Frozen E- Bouin’ s fixed
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Intracellular accumulation of proteins: Homogenous eosinophilic intracytoplasmic
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Russel bodies represent intracellular accumulation of: A- Proteins in lymphocytes B- Proteins in macrophages C- Proteins in plasma cells D- Glycogen in plasma cells E- Glycogen in macrophages
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Hyaline change ??? -Hyalos ??? -Descriptive non specific term??? -Protein or Not protein(secretion, degenerated collagen……) -Different pathological conditions -Intracellular (renal tubules/ russel bodies) or Extracellular (Wall of arterioles in hypertension)
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Intracellular accumulation of ( GLYCOGEN ) 1- D.M.?? : (renal tubules, cardiac myocytes, islets of langerhans) 2- Glycogen storage diseases?? ( cardiac and skeletal myocytes, hepatocytes) Hx & E ------ VACUOLATED CYTOPLASM
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Cell with vacuolated cytoplasm: -Fat----------- frozen, Sudan III or oil red -Glycogen-------- alcohol fixed, PAS before& after diastase - Water--------- No staining
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Mucoid (myxomatous)change: Glycoprotein (mucin) Produced normally by epithelial and mesenchymal cells?? Deposited under certain pathological conditions ?? Epithelial form---- mucoid Mesenchymal form---myxoid
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P.A.S. is used to stain: A- Fat B- Calcium C- Haemosiderin D- Proteins E- Glycogen
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Pathological pigmentation Endogenous Exogenous Melanin Skin Haemosiderin Inhalation Lipofuscin Ingestion Parasitic
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Pregnancy associated hyperpigmentation is known as: A- Freckles B- Vitiligo C- Chloasma D- Naevi
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Abnormal deposition of haemosiderin: A- Haemosiderosis: Deposition in phagocytes with no tissue damage. B- Haemochromatosis: Extensive deposition in parenchymatous cells with tissue damage.
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Some special stains -Fat : Sudan III and oil red on frozen -Glycogen : PAS before & after diastase -Mucin : PAS before & mucicarmine -Iron : Prussian blue reaction(Perl’s)
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All these conditions may result in secondary haemochromatosis except: 1- Repeated blood transfusion 2- Prolonged administration of iron 3- Fe deficiency anaemia 4- Chronic haemolytic anaemia
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All these are endogenous pigment except: 1- Melanin 2- Haemosiderin 3- Lipochrome 4- Lipofuscin 5- Porphyrin
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Pathological calcification Deposition of Ca salts in abnormal sites ??usually extracellular Where is the defect ?? Serum Ca level= Metastatic OR Site of deposition= Dystrophic
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The following are examples of dystrophic calcification except: A- Calcified bilharzial ova B- Calcified atheroma C- Renal stones D- Wall of chronic abscess E- Uterine fibroid
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Cellular aging Senescence
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Cellular aging
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Progressive shortening of telomeres leads to: A- Activation of apoptosis B- Initiation of necrosis C- Metaplastic changes D- Neoplastic changes E- Cell senescence
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