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BIOL4344-CH 2
Chapter 2 terms Pathophysiology
Question | Answer |
---|---|
How do normals cells respond to changes in environment, both internal or externally? | Cellular Adaptation |
Term that describes cell shrinkage due to fewer organelles (Rough ER, mitochondria, cytoskeleton) that causes decreased protein synthesis | Atrophy |
Normal cellular atrophy | Physiologic Atrophy e.g. shrinkage of thymus gland, shinkage of cells from aging, shinkage of muscle cells fromvoluntary disuse |
Abnormal cellular atrophy | Pathologic atrophy caused by forced disuse (broken bone cause muscle cell atrophy) or from disease like Alzheimers |
Term describing cell growth by increase in organelles through production or by decreases in the degradation cycle of a cell. Not caused by increase in fluid. | Hypertrophy |
Normal cellular Hypertophy | Physiologic hypertrophy caused by increased load on muscle cells (working out) |
Abnormal cellular Hypertrophy | Pathologic hypertrophy e.g. cellular damage to lungs increases the load on the heart causing Hypertrophy of the cardiac cells to obtain proper oxygen levels |
Increase in the number of cells, either by increased cellular proliferation or decrease in cell death, can be caused by injury that is severe enough to cause cell death | Hyperplasia |
Normal Hyperplasia | Physiologic Hyperplasia like development of the endometrium during mensturation (Hormonal hyperplasia) or regeneration of the liver (compensatory hyperplasia) |
Normal adaptive mechanism that enables certain organs to regenerate. e.g. liver, but can NOT happen in the nerve, skeletal muscle, mycardial cells or lens cells of eyes | Compensatory hyperplasia |
Normal adaptive mechanism that occurs in cheifly estrogen dependent organs (uterus or breast) | Hormonal Hyperplasia, e.g. build up of the endometrium (normal unless caused by estrogen and progesterone secretion imbalances) |
Abnormal proliferation of normal cells in response to excessive hormonal stimulation or the effects of groth factors on target cells | Pathologic Hyperplasia e.g. excessive build up of the endometrium from hormonal imbalances which cause hyperplastic endometrial cells that can transform into malignant cells "pre-cancerous" |
Abnormal changes to the size, shape, & orgaization of mature cells. Not considered a true adaptive cellular response | Dysplasia aka atypical hyperplasia e.g. \can be indicated in an abnormal PAP smear. Also can frequently occur in the epithelial tissue of the respiratory tract |
Reversible replacement of one mature cell type by another. | Metaplasia |
Reversible replacement of the normal columnar ciliated epithelial cells of the bronchials with squamous epithelial cells | Bronchial Metaplasia - can be caused by smoking and is reversible if the perso stops smoking. |
Occurs if when a cell is unable to maintain homeostasis, either i a normal or an adaptive steady state- in the face of injurous stimuli e.g. exposure to toxic chemicals, infections & hypoxia | Cellular injury |
Type of cellular injury from which cells can recover. Loss of ATP, cellular swelling, detachment of ribosomes, autophagy of lysosomes | Reversible cellular injury |
Type of cellular injury in which cells die. Point of no return structurally when severe vacuolization of the mitochondria occures & Ca++ moves into the cell | Irreversible injury |
Decreased level of oxygen delivery to tissue. most commonly caused by ischemia | Hypoxia |
An electrically uncharged atom or molecule that has an unpaired electron | Free Radical, includes Hydroxy radicals, |
Common type of cell death with severe swelling & breakdown of organelles | Necrosis |
Cellular celf-destruction for elimination of unwanted cell populations, a type of programmed cell death | Apoptosis |
Catalytic enzymes (proteins) that breakdown cell components by breaking down cytoskeleton causing release of apoptic bodies | Casphases |
Cellular self digestion that does not cause immune reaction because it remains in a membrane, causes production of autolysosomes, no casphases are produced | Autophagy |