Cell stress

Cell stress

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

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