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Pathologic hyperplasia: Caused by excessive hormonal stimulation or growth factors. Used in wound healing where connective tissue cells (fibroblasts) and blood vessels aid in repair.
Pathologic hyperplasia: Caused by excessive hormonal stimulation or growth factors. Used in wound healing where connective tissue cells (fibroblasts) and blood vessels aid in repair.
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Pathologic hyperplasia: Caused by excessive hormonal stimulation or growth factors. Used in wound healing where connective tissue cells (fibroblasts) and blood vessels aid in repair.
Droits d'auteur :
Attribution Non-Commercial (BY-NC)
Formats disponibles
Téléchargez comme DOCX, PDF, TXT ou lisez en ligne sur Scribd
Reversible/ Irreversible Increased local production of GF, increased level of GF receptors, act of Cell death ʹ cell injury; ischemia, particular intracellular signaling pathways infection, toxins, and immune reactions. = cellular proliferation.
Necrosis- abnormal stresses; ischemia and Pathologic hyperplasia:
chemical injury Caused by excessive hormonal stimulation or growth factors. Apoptosis- controlled suicide; eliminate Useful in wound healing where connective unwanted cells tissue cells (fibroblasts) and blood vessels aid in repair. Cellular adaptations of growth and differentiation- for increased demand and external stimulation, reduced supple of Hyperthrophy nutrients and growth factors. Increase in size of cells resulting in increase in the size of organ; no new cells, Hyperplasia just larger cells. Cause by synthesis of An increase in the number of cells in an more structural components. Cells may be organ or tissue : increased volume. dividing and nondividing cells (where (hypertrophy may occur with hyperplasia nuclei have a higher dna content because as the same external stimulus triggers it is arrested in the cell cycle without both ie growth in uterus) mitosis). Requires cells to synthesize dna for For muscle; increased workload mitotic division. (heart/skeletal muscles) to permit at a higher level of activity. Balances demand Physiologic Hyperplasia and functional capacity. Hormonal hyperplasia: increases Hormone induced: during pregnancy by functional capacity (breasts at puberty estrogenic hormones increases muscle and pregnancy, and uterus) where cell size. Prolactin and estrogen increase hormones may acts as GF that trigger breasts for lact. transcription of various cell genes. Mechanisms: Compensatory hyperplasia: increases Genes the encode transcription factors; tissue mass after damage of partial growth factors; fibroblast growth factors; resection (liver regeneration) proliferation vasoactive agents. Reinduction of genes of remaining cells and devt of new cells expressed during early devt. from stem cells. Atrophy Irreversible /cell death: Shrinkage in cell size by loss of cell Structural changes and functional changes substance/structural components of the that are recognized as cell death. cell. Physiologic: fetal devt notochord and Causes of cell injury thyroglossal duct; uteral size decrease Oxygen deprivation: after parturition. Hypoxia- loss of oxygen carrying ability of Pathologic: the blood (CO poiso ning or anemia) Decreased workload Ischemia more sever as both nutrients Loss of innervation and metabolites are cut off from the Diminished blood supply (ischemia) tissue. Malnutrition Physical agents: Loss of endocrine stimulation (ie Mech trauma, temperature, pressure, menopause) radiation, shock. Aging (cell loss in brain and heart) Chemical agents: Pressure (ischemia to surrounding tissue Poisons, toxic chemicals from pressure from tumours, etc.) Infectious agents: Submicroscopic viruses to large Mechanisms: tapeworms, bacteria, fungi, etc. Increased protein degradation (ubiquitin - Immunologic reactions: proteasome pathway) -- glucocorticoids Hypersensitivity, anaphylactic shock, and thyroid hormone stimulation; TNF. autoimmune disease Increased autophagic vacuoles- vacuoles Genetic derangements: where cell fragments are digested. Malformations, etc. Nutritional imbalances: Metaplasia Anorexia, starvation, hyperlidiemia, etc. Reversible change where an adult cell type is replaced by another cell type Ie columnar to squamous in respiratory tract Mechanisms of cell injury: (barret esophagus from gastric reflux). Type of injury, duration, and severity. Type, state, and adaptability of injured Mechanisms: cell (vulnerability). Reprogamming of stem cells in normal Functional and biochemical abnormalities cells/undifferentiated mesenchymal cells in one or more of several essential cellular in connective tissue. components.
Cell injury and cell death: ATP depletion
Reversible: reduced oxidative mc NA accumulation in cell ʹ phosphorylation, atp depletion, and isosmotic gain of water ʹ cell cellular swelling (ion conc and water swelling and dilation of the er. influx. mc Anaerobic metabolism (glycolysis) Defect in membrane permeability ʹ glycogen stores depletion ʹ lactic mc Mitochondrial dysfunction ʹ acid and inorganic phosphate decreased phospholipid synthesis accumulation- reduction of ʹ faulty cell membrane intracell pH ʹ decreased cellular mc Loss of membrane phospholipids ʹ enzyme activity. activation of phopholipases by ca mc Ca pump failure- influx of Ca ʹ influx cellular component damage mc Cytoskeletal abnormality ʹ mc Prolonged depletion of ATP ʹ stretching nad rupture structural disruption of protein mc Reactive oxygen species synthetic apparatus ʹ ribosome mc Lipid breakdown products- detachment from rer ʹ reduction changes in permeability of protein synthesis. mc Protein misfolding. Reversible injury Cellular swelling, hydropi change/ Mitochondrial damage vacuolar degeneration. Swelling is Cytochrome c leakage into cytosol. reversible 1. c Plasma membrane alteration- Influx of Ca and loss of Ca homeostasis bebbing Increase in membrane permeability- 2. c Mitochondrial changes-swelling activates enzymes (ATPases, 3. c Dilation of er- detachment and phopholipases, proteases, and disaggregation of polysomes endonucleases. 4. c Nuclear alterations- granular and fibrillar elements Accumulation of O2 derived free radicals Reactive oxygen species from Necrosis mitochondrial respiration- oxidative Morphologic changes from progressive stress. Free radicals have a single degradative action of enzymes on cells. unpaired electron in the outer orbit which May elicit inflammation in surrounding may react with adjacent molecules. cells as contents leak out. mc Absorption of radiant energy (UV, xray) mc Dnzymatic metabolism of exogenous chemicals or drugs. mc Redox reaction occur during normal metabolic processes. (superoxide) mc Transition metals mc Nitric oxide