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Adaptation
Mechanism to survive – maintain homeostasis meet demand of the stress. Physiologic/morphologic changes. It is Reversible
5 types of cellular adaptation
Hypertrophy, Atrophy, Hyperplasia, Metaplasia, Dysplasia
Hypertrophy
increase in cell size
Atrophy
decrease in cell size
Hyperplasia
increase in number of cells. Physiologic response during puberty and pregnancy. Excessive hormonal signaling can cause
Metaplasia
Change in cell type. Reversible change/replacement of one cell type to another. Usually caused by chronic irritation and inflammation. Always pathologic but not cancer.
Dysplasia
Deranged or disorganized overgrowth of cells. Prolonged metaplasia can turn into dysplasia. Still not cancer. Not organized.
Intracellular accumulations
Buildup of substances that cells cannot immediately use or dispose of. Leads to metabolic derangement. Can be harmless and reversible. Can also be toxic and irreversible.
Alpha 1 antitrypsin deficiency (intracellular accumulation example)
Mutation in gene for AAT causes abnormal folding of the protein in the endoplasmic reticulum. Prevents it from being exported from liver AND accumulation. Causes lung and liver damage sometimes referred to as “genetic COPD”
5 types of injury that can damage cells.
Deficit, physical, endogenous, exogenous, and immune injuries
Deficit injury
Hypoxia, Ischemia, Malnutrition, Dehydration
Physical Injuries
Mechanical, Thermal
Endogenous Injuries
Genetic errors, Metabolic errors
Exogenous Injuries
Radiation/UV, Chemical, Toxins
Immune Injuries
Immune response, Infection
Dystrophic calcification
NON-REVERSIBLE. Abnormal deposits of calcium salts in aging or previously damaged tissue. Can cause organ dysfunction. Pt has normal calcium level. Atheromatous plaque in blood vessels. Heart valve & aorta (aortic stenosis)
Metastatic calcification
Occurs in normal tissue but in inappropriate sites (lung, renal tubules, blood vessels). Usually due to increased calcium levels.
Apoptosis
programmed and controlled destruction of a cell. Bodies way of removing damaged or aged cells. Non-inflammatory. Pathological or physiological. A way the body maintains homeostasis.
Necrosis
uncontrolled destruction of a cell. Cell membrane destroyed and inflammatory response activated. Always pathologic.
Dry gangrene
loss of blood supply, typically arterial flow issue. The affected area becomes cold, black, and numb. Common in extremities. Associated with diabetes and autoimmune diseases.
Wet gangrene
bacterial infection after injury/wound. The infected area is swollen and painful. Common in bowels. The tissue is wet and malodorous. Poor prognosis.
Gas gangrene
Caused by bacteria Clostridium perfringens after trauma. Gas in the affected area causes swelling and crepitus. Can occur on any site. Discoloration of affected skin and swelling. Life threatening if not treated.
Effects of aging on body systems
Reduces oxidative phosphorylation by mitochondria. Reduced synthesis of nucleic acids. Reduced synthesis of structural proteins. Reduced synthesis of cell receptors and transcription factors.
Functional effects of aging
Decline in muscle strength. Drop in cardiac reserve. Nerve conduction time increases. Glomerular filtration rate drops. Vascular elasticity decreases. Vital capacity is reduced
Aging Theories
that there are a finite number of times a cell can divide. Cells stop dividing and functionality is impaired. Telomere (compound structure at end of chromosome) shortening is associated with aging. Telomeres are the ends of chromosomes – padding for the genes