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Cell stress
Descripción
? Pathology Mapa Mental sobre Cell stress, creado por Lindie Metz el 18/03/2016.
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pathology
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Mapa Mental por
Lindie Metz
, actualizado hace más de 1 año
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Creado por
Lindie Metz
hace más de 8 años
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Resumen del Recurso
Cell stress
Inability to adapt to new environment
Adaptation
reversible changes = restoration of normal conditions = restoration of normal cell function
Stimuli ↑ demand
Hypertrophy
↑ in cell size = ↑ in organ size
↑ size of organelles, proteins and membranes, membrane synthesis, ATP & enzyme
Seen in cells that can't divide, permanent cell populations
PHYS: (1) ↑ functional demand, (2) Hormone stimulation
PATH: (1) ↑ resistance (art P > LV pump ↑ > size ↑), (2) Physical obstruction (resistance = ↑ work)
Ltd: Can lead to injury > ↑ mass ≠ nutrient supply
Hyperplasia
↑ in # of cells = ↑ in size of organ
Occurs with hypertrophy with cells that can divide
PHYS: (1) Hormonal (puberty/pregnancy), (2) Cell loss (skin injury being repaired)
PATH: (1) Hormonal (eg tumor in pituitary), (2) Cell destruction (ulcerated colon, HPV, Keloid)
Controlled ↑ in # cells (will subside when stimulation subsides)
vs Neoplasia = uncontrolled growth (hyperplasia can predispose to ca)
Stimuli ↓ demand
Atrophy
↓ in cell size and function = ↓ in organ size
Loss of substance = loss in function and diffirentiation
↓ mitochondria, ER, myofilaments
↓ metabolism = ↓ amino acid uptake, O2 consumption, protein synthesis
PHYS: (1) senile, (2) uterine
PATH: (1) Denervation, (2) Ischemia, (3) ↓ Nutrition, (4) ↓ functional demand, (5) ↓ Endocrine stimulation, (6) Pressure
Hypoplasia
Tissue fails to reach normal size, congenital
Metaplasia
Replacement of one adult cell type with another > normal epithelium in abnormal location
Usually in squamous/columnar epithelium, CT where stem cell diffirentiate due to stress
Usually reversible, but predisposes to neoplasia
PATH: (1) Smoking, (2) Barret's esophagus, (3) Chronic infection
Disorders
Dysplasia
(1) ↑ Cell growth (mitosis, bulk) (2) Atypical morphology (pleomorphism, hyperchromatism) (3) Altered differentiation (immaturity, location)
Disorderly proliferation = possible early sign of neoplasia
Mild = reversible, Severe = malignant neoplasm
PATH: Chronic inflammation, Viral infection (HPV) UV radiation
LOC: Squamous mucosa (smokers), Squamous EP (cervix), Barret's EP, Intestinal EP (H.pylori)
Carcinoma in situ: severe dysplasia covering entire depth of EP, just before BM > pre-invasive ca
Anaplasia
Lack of structural and functional differentiation = hallmark of malignancy
Cells of malignancies so poorly differentiated origin is unknown
Growth with tissue of unknown origin = malignancy
Neoplasia
Abnormal, uncoordinated, excessive tissue growth and proliferation after withdrawal of initiating cause
PATH: Genetic changes, deregulated growth control mechanisms
Can influence normal cells through hormonal and growth factor production
Benign/malignant
Death
Irreversible injury
(1) Duration of stimulus, (2) Dose of chemical agent, (3) Tx type/metabolic activity, (4) Health of tx
Necrosis
Pathological + uncontrolled cell death in living organism, noxious stimuli
PATH: (1) Ischemia, (2) Metabolic disorders, (3) Trauma, (4) Toxins, (5) Infections, (6) Drugs
Cells digested by lysosomal enzymes
Intracellular
Lysosomal membrane damage (leak out)
Cell membrane damage > lysE + cell components leak out > inflammation
Coagulative, Liquefaction, Gangrenous, Caseous, Gummatous, Suppuration, Fat, Fibrinoid
Apoptosis
Programmed cell death, packaged in membranes, tagged for collection by phagocytes
Cell used during growth and development, then removed
Embryonic development, DNA damage that cannot be repaired
No cell damage, no leakage, no inflammation
PHYS: Eliminate necessary cells (1) Embryogenesis, (2) Hormone dependent tissue (menstruation etc), (3) Cell loss in proliferating populations, (4) Elimination of harmful lymphocytes, (5) Induced by cytotoxic T-cells
PATH: still beneficial (1) DNA damage, (2) Cell injury d/t infections
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