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43 Cards in this Set
- Front
- Back
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homeostasis
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dynamic state of normal cell, handles normal physiologic demands
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cellular adaptation
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response to stress or pathologic stimuli
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cellular injury
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failure to adapt;
reversible and irreversible |
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reversible injury
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can return to normal up to a certain point
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irreversible injury
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ultimately results in cell death
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cell death
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necrosis & apoptosis
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necrosis
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manifestations of cell death in living tissue - enzyme degradation mainly -
always pathological |
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apoptosis
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programmed cell death -
genetically controlled - eliminates unwanted cells - physiological or pathological |
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agent: altered physiologic stimuli
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response: cell adaptations
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agent: reduced O2 supply, chemicals, microbes, etc
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response: cell injury
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agent: mild chronic injury
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response: subcellular alterations
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agent: metabolic alteration
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response: intracellular accumulations/calcification
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agent: cumulative sub-lethal injury
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response: cellular aging
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cellular adaptation types
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hypertrophy,
hyperplasia, atrophy, metaplasia, "dysplasia" |
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hypertrophy
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increase in cell SIZE
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hyperplasia
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increase in cell NUMBER
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atrophy
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decrease in size and function of cells
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metaplasia
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replacement of one cell type with another: squamous,
glandular, connective, myeloid |
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dysplasia
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disorderly growth
mixture of hyperplasia and hypertrophy |
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hypertrophy causes
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increased workload (skeletal muscle, LV, uterus), organ removal
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labile cells
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mainly undergo hyperplasia (i.e. bone marrow stem cells)
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stable cells
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undergo hyperplasia/hypertrophy only if stimulated (i.e. liver)
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permanent cells
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undergo hypertrophy only (i.e. skeletal & heart muscle fibers)
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stenosis
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narrowed opening
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physiologic hyperplasia
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hormonal stimulation (breasts, uterus), compensatory (liver regeneration)
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pathologic hyperplasia
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excessive hormonal stimulation
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hyperplasia effects
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increase in organ size and functions;
potential to develop cancer |
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equal hyperplasia and hypertrophy
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uterine smooth muscle (pregnancy),
iodine deficiency (goiter) |
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physiologic atrophy
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during early development (notochord, thyroglossal duct),
uterus after parturition |
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pathologic atrophy
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decreased workload,
loss of innervation, reduced blood supply, inadequate nutrition, decreased hormonal stimulation, aging, occlusion of secretory ducts, pressure/compression |
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atrophy effects
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autophagy --> lipofuscin
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autophagy
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destruction of organelles and structural proteins without cell death;
vacuoles form around organelles -> degraded -> leave behind lipofuscin |
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lipofuscin
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yellow brown pigment,
"wear and tear", brown atrophy |
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agenesis
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absence of an organ, primordial tissue failed to develop
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aplasia
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primordium present but no further development occurred
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hypoplasia
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incomplete or partial development of organ/tissue
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metaplasia occurrence
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adaptive response to chronic irritation, often reversible:
bronchial epithelium + tobacco smoke --> squamous metaplasia |
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squamous metaplasia
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replace columnar epithelium with squamous epithelium:
bronchial, cervical, bladder, corneal cells |
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glandular metaplasia
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replace squamous epithelium with glandular epithelium: barrett's esophagus, intestinal
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connective tissue metaplasia
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formation of cartilage, bone, adipose tissue in tissues without these cells normally (i.e. bone in muscle = myositis ossificans)
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myeloid metaplasia
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proliferation of hematopoietic tissue outside bone marrow (i.e. spleen, liver)
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dysplasia
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not a true adaptation,
atypical hyper/metaplasia with cancer-potential, reversible if irritant is removed: change in cell size/shape, loss of organization, increased mitotic activity |
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dysplasia causes
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hyperplasia, metaplasia, infection, UV light
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