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42 Cards in this Set
- Front
- Back
- 3rd side (hint)
Pathogenesis
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the pathogenesis of a disease is the sequence of events at the organ, cellular, ultrastructural, and molecular levels by which the disease develops
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Pathognomonic
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A particular abnormality that is found only in one condition.
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"Hearing the fetal heart tone is pathognomonic of pregnancy."
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Symptoms
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what the patients sees or feels
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Signs
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evidence of disease discovered by the physician or dentist - abnormalities on physical exam
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Findings
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physical, lab, or x-ray results
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Biopsy
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When tissues are removed from a live patient and sent to the pathologist for diagnosis.
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"Bios" means life.
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Autopsy/Necroscopy
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When tissue is removed from a dead patient and examined by the pathologist.
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Common causes of cell injury
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-O2 deprivation
-physical agents -chemical agents -immune rxns -genetic defects -infectious agents -nutritional imbalances -aging |
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Ischemia
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loss of arterial blood flow, "holding back the blood," includes no oxygen (hypoxia) AND no substrates for glycolysis.
*the most common cause of cell injury* |
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Hypoxia
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Insufficient oxygen. Cell loses the ability to carry on sufficient aerobic oxidative respiration --> reduced ATP generation.
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Reperfusion injury
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When the restoration of oxygen to a cell that was ischemic or hypoxic for a while causes more injury to the cell.
-extra Ca influx -increase in inflammatory cells --> release free radicals -damaged mitochondria --> free radicals |
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Free radicals
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Unstable compounds with unpaired electrons, i.e. H., HO., O2., hydrogen peroxide, superoxide
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Atrophy
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Cells get smaller in size (not number) to survive.
Causes: decreased use, decreased blood supply, decreased nutrition, hormones. |
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Hypertrophy
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Cells get larger in size (not number) in response to demand.
Causes: increased workload, hormones. |
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Hyperplasia
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Cells increase in number (not size).
Causes: hormones, GFs, etc. |
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Metaplasia
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Environmental stress causes one mature cell type to replace another.
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Smoking affects the epithelial cells of the larynx and trachea this way.
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Dysplasia
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Disorderly proliferation.
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Involution
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Decrease in cell number (not size) due to apoptosis.
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Cell Adaptations
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Adaptations that occur after prolonged exposure to adverse stimuli or exaggerated normal stimuli, which can include: atrophy, hypertrophy, involution, hyperplasia, metaplasia, dysplasia, or some combination.
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Subcellular responses to cell injury
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-lysosomal catabolism
-induction of sER -alterations in mitochondria -changes in the cytoskeleton -induction of stress proteins (heat shock proteins) |
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Heterophagy
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A type of lysosomal catabolism in which the secondary lysosome/phagolysosome contains engulfed material from outside the cell.
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"Hetero" means other.
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Autophagy
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A type of lysosomal catabolism in which an autophagic vacuole surrounds damaged organelles from within it's own cell.
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"Auto" means self.
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Lipofuscin granules
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A secondary lysosome/phagolysosome that contains undigested particles composed of oxidized lipids; it is often pigmented. Accumulates in aging tissues or can be a sign of chronic tissue damage.
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First site of cell injury
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mitochondria
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Dystrophic calcification
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Pathologic calcification with no calcium derangement; usually occurs in dead or dying tissues.
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Metastatic calcification
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Pathologic calcification that almost always reflects some derangement in calcium metabolism. Hypercalcemia causes calcium deposits in normal tissue.
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Cell swelling
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The first observable change when a cell is damaged. Reversible injury that reflects damage to water transport, mitochondrial damage, hydropic degeneration.
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Autolysis
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Enzymes from the cell itself digest the cell contents.
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Heterolysis
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Enzymes from arriving inflammatory cells digest the cell contents.
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Pyknosis
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Condensation of the nucleus (nuclei shrink).
Indicates cell is dead. |
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Karyorrhexis
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Fragmentation of the nucleus ("nuclear dust").
Indicates cell is dead. |
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Karyolysis
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Dissolution of nuclear structure (as a result of enzymatic digestion).
Indicates cell is dead. |
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How you know WHETHER the cell is dead or alive.
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Nuclear changes.
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How you know HOW the cell has died.
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Cytoplasmic changes.
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Necrosis
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Accidental cell death!
Localized death of cells or tissues in a living organism. Produces an inflammatory response. -Caused by exogenous injury and usually involves groups of cells -cells are swollen, show nuclear changes, and have ruptured cell membranes |
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Apoptosis
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Cell suicide!
Programmed death of single cells within a living organism. Does not produce an inflammatory response. -generally energy dependent -cell fragments ("apoptotic bodies")to be taken up by macrophages/adjacent parenchymal cells. |
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Coagulative necrosis
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-outline of cell preserved for days
-death is sudden: denatures structural proteins and destructive enzymes -hypoxic death (except in CNS) |
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Liquefactive necrosis
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-cells dissolve by enzymes: autolysis or heterolysis
-infiltrations of PMNs and dead cell components --> abscess! -seen in bacterial and fungal infections (ex. pneumonia) |
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Caseous necrosis
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-combination of coagulative and liquefactive necrosis
-gross appearance is white and cheesy -GRANULOMA: cells surrounded by lymphocytes and macrophages -typical of Mycobacterium tuberculosis (TB!), sarcoidosis, foreign body rxns, deep fungal infections |
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Gummatous necrosis
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Specific to SYPHILIS! (spirochete)
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Hemorrhagic necrosis
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-dead tissues contain many RBCs
-Usually due to blockage of a vein while the arterial supply continues to deliver blood. |
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Enzymatic fat necrosis
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-lipases digest fat cells
-triglycerides released from the cell bind with calcium to form soaps (saponification!) -most strongly asso. with damage to the PANCREAS, which has many digestive enzymes and is surrounded by fat. |
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