PrepBank · বিষয়ভিত্তিক প্রশ্ন
Cell Injury & Adaptation
Cell Injury & Adaptation
PrepBank · পাতা ১ / ১ · ১–৬৬ / ৬৬
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Coagulative necrosis is a form of necrosis in which the architecture of dead tissue is preserved for a span of at least some days .
The affected tissue has a firm texture. Presumably, the injury denatures not only structural proteins but also enzymes and so blocks the proteolysis of the dead cells; as a result, intensely eosinophilic cells with indistinct or reddish nuclei may persist for days or weeks.
Ultimately, the necrotic cells are broken down by the action of lysosomal enzymes derived from infiltrating leukocytes, which also remove the debris of the dead cells by phagocytosis. Ischemia caused by obstruction in a vessel may lead to coagulative necrosis of the supplied tissue in all organs except the brain (see next paragraph for explanation).
A localized area of coagulative necrosis is called an infarct.
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• Hyperplasia is defined as an increase in the number of cells in an organ or tissue in response to a stimulus.
• Hyperplasia is the result of growth factor-driven proliferation of mature cells and, in some cases, by increased output of new cells from tissue stem cells.
• Physiological hyperplasia occurs in – breast during puberty, liver after hepatectomy
• Pathological hyperplasia occurs in – BPH, wart & endometrial tumour
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• Physiologic atrophy is common during normal development. Some embryonic structures, such as the notochord and thyroglossal duct, undergo atrophy during fetal development. The decrease in the size of the uterus that occurs shortly after parturition is another form of physiologic atrophy.
• Pathologic atrophy occurs due to – disuse atrophy, denervation atrophy, pressure atrophy, senile atrophy, nutritional deficiency atrophy
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• Coagulative: ischemic necrosis of heart, kidney, liver, adrenal gland & other solid organs; gumma of tertiary syphilis
• Liquefactive: boil, abscess & ischemic necrosis of brain
• Caseous: Granuloma of TB
• Fat: Enzymatic-pancreas, Traumatic- breast
• Fibrinioid: in collagen disease
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Avuscular necrosis seen in :
Head of femur
Talas
Scaphoid
Radiation therapy
Sickle cell crisis
Trauma
Tumor
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Metastatic calcification :
Metastatic calcification may occur in normal tissues whenever there is hypercalcemia. Hypercalcemia also accentuates dystrophic calcification. There are four principal causes of hypercalcemia: (1) increased secretion of parathyroid hormone (PTH) with subsequent bone resorption, as in hyperparathyroidism due to parathyroid tumors, and ectopic secretion of PTH-related protein by malignant tumors (2) resorption of bone tissue, secondary to primary tumors of bone marrow (e.g., multiple myeloma, leukemia) or diffuse skeletal metastasis (e.g., breast cancer), accelerated bone turnover (e.g., Paget disease), or immobilization; (3) vitamin D–related disorders, including vitamin D intoxication, sarcoidosis (in which macrophages activate a vitamin D precursor), and idiopathic hypercalcemia of infancy (Williams syndrome), characterized by abnormal sensitivity to vitamin D; and (4) renal failure, which causes retention of phosphate, leading to secondary hyperparathyroidism. Less common causes include aluminum intoxication, which occurs in patients on chronic renal dialysis, and milk-alkali syndrome, which is due to excessive ingestion of calcium and absorbable antacids such as milk or calcium carbonate.
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Coagulative necrosis :
Occurs in solid organ except brain
Example - Infract of heart ( MI),Kidney,Spleen,Gumma of tertiary syphilis.
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Features of irreversible cell injury -
Membrane injury
Intracellular release and activation of lysosomal enzyme
Increase calcium influx
Decreased basophilia
Phagocytosis.
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• Atrophy is defined as a reduction in the size of an organ or tissue due to a decrease in cell size and number.
• Atrophy results from decreased protein synthesis and increased protein degradation in cells. Protein synthesis decreases because of reduced metabolic activity. The degradation of cellular proteins occurs mainly by the ubiquitin-proteasome pathway.
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Site of traumatic fat necrosis -
Mostly breast
Then- salivary gland
Pancreas
Neonates after delivery.
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The ultrastructural changes of reversible cell injury, visible by
electron microscopy, include the following:
1. Plasma membrane alterations, such as blebbing, blunting, and loss of microvilli
2. Mitochondrial changes, including swelling and the appearance of small amorphous densities
3. Accumulation of “myelin figures” in the cytosol composed of phospholipids derived from damaged cellular membranes
4. Dilation of the ER, with detachment of polysomes 5. Nuclear alterations, with disaggregation of granular and fibrilar elements.
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Ischemia reperfusion injury causes cell injury by :
Reactive oxygen species
IgM complement
Intracellular calcium deposition
Cytokine
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Physiological giant cell -
Osteoclast
Megakaryocytes
Syncytiotrophoblast of placenta
Pathological giant cell-
Anaplastic tumors
Hodgkin's disease
Choriocarcinoma
Poorly differentiated astrocytoma
Primary billiary cirrhosis
Giant cell of herpes simplex virus
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• Hyperplasia is defined as an increase in the number of cells in an organ or tissue in response to a stimulus.
• Hyperplasia is the result of growth factor-driven proliferation of mature cells and, in some cases, by increased output of new cells from tissue stem cells.
• Physiological hyperplasia occurs in – breast during puberty, liver after hepatectomy
• Pathological hyperplasia occurs in – BPH, wart & endometrial tumour
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Necroptosis -is a hybrid that shares aspects of both necrosis and apoptosis. Morphologically, and to some extent biochemically, it resembles necrosis, as both are characterized by loss of ATP, swelling of the cell and organelles, generation of reactive oxygen species (ROS), release of lysosomal enzymes, and ultimately rupture of the plasma membrane.
Mechanistically, it is triggered by signal transduction pathways that culminate in cell death, a feature similar to apoptosis. Because of these overlapping features, necroptosis is sometimes called programmed necrosis to distinguish it from forms of necrosis driven passively by toxic or ischemic injury to the cell.
Can occur both physiology and pathological condition.
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• The reduction-oxidation reactions that occur during normal metabolic processes.
• Absorption of radiant energy (e.g., ultraviolet light, x-rays).
• Rapid bursts of ROS are produced in activated leukocytes during inflammation.
•. Defects in leukocytic
superoxide production lead to chronic granulomatous disease.
• Enzymatic metabolism of exogenous chemicals or drugs can generate free radicals
• Transition metals such as iron and copper donate or accept free electrons during intracellular reactions and catalyze free radical formation
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The removal of supernumerary cells (in excess of the required number) during development.
• Involution of hormone-dependent tissues on hormone withdrawal, such as endometrial cell breakdown during the menstrual cycle, ovarian follicular atresia in menopause, and regression of the lactating breast after weaning.
• Cell turnover in proliferating cell populations, such as immature lymphocytes in the bone marrow and thymus, B lymphocytes in germinal centers that fail to express useful antigen receptors and epithelial cells in intestinal crypts, to maintain a constant cell number (homeostasis).
• Elimination of potentially harmful self-reactive lymphocytes to prevent immune reactions against one’s own tissues.
• Death of host cells that have served their useful purpose, such as neutrophils in an acute inflammatory response, and lymphocytes at the end of an immune response.
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• Metaplasia is a reversible change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another cell type.
• Epithelial metaplasia is a double-edged sword
• It’s of 2 types. Epithelial & connective tissue metaplasia
• The most common epithelial metaplasia is columnar to squamous as occurs in the respiratory tract in response to chronic irritation.
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Decreased workload or disuse atrophy is seen in skeletal muscle in a patient with restricted to bed rest,or when immobilised in plaster cast.
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• Hypertrophy refers to an increase in the size of cells that result in an increase in the size of the affected organ.
• The hypertrophied organ has no new cells, just larger cells.
• The most common stimulus for hypertrophy of muscle is increased workload.
• Hypertrophy is the result of increased production of cellular proteins.
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• Metaplasia from squamous to columnar type may also occur, as in Barrett oesophagus
• Connective tissue metaplasia is the formation of cartilage, bone, or adipose tissue (mesenchymal tissues) in tissues that normally do not contain these elements
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Morphology of apoptotic cell -
Cell shrinkage
Chromatin condensation
Formation of cytoplasmic blebs and apoptotic body
Phagocytosis