Goal of cellular adaptation
Maintain a STEADY STATE despite adverse conditions. Survivial depends on changes in size or shape without affecting function
A decrease in cell SIZE Reduce oxygen consumption and other cell funtions. Most common in skeletal muscle, heart, sex organs, brain. Physiologic, disuse, pathologic examples
Increase in cell SIZE and amount of functioning tissue. Cells increase oxygen and cell functions. Physiologic, pathologic, compensatory examples
Increase in NUMBER of cells of organ or tissue with cells that are capable of mitotic division. Epidermis, intestinal, epithelium and glandular tissues capable. (often occurs with hypertrophy)Physiologic (hormonal, compensatory), pathologic examples
Stimulates RBC production through erythropoeitin
Reversible replacement of one cell type by another cell type. Occurs from chronic irritation and inflammation. (smoking)
Atyppical hyperplasia. Deranged cell growth resuling in change of cells size, shape and organization. May return to normal or concern it is cancer precursor
Plasia -- Trophic--
Number ; Size
Injurious Agents leading to cell injury
Physical forces, Radiation, Biologic agents and nutritional imbalances, chemical agents.
Lead filtered in kidneys and leads to hypertension. Enters brain and causes demyelination to cause acute encephalopathy and decreased intelligence. Competes with enzymes that decrease RBC which can lead to ANEMIA (cardinal sign)
Three outcomes of cell injury
1. Reversible injury
Mechanism causing cell injury. It's a by product of natural body function and too much can cause injury to DNA.
Mechanism causing cell injury. Most common cause of cell injury where decrease oxygen causes damage to mitochondia and decreased ATP. Cell swelling is sign and there's lactic acid build up. Results from COPD, anemia, edema, ichemia
Mechanism causing cell injury. It's activated due to injury and causes damage to cell.
Three types of intracellular accumulations
1. Normal - fat build up
2. Abnormal endogenous products - Genetic disorders like Tay-Sachs and jaundice from bilirubin
3. Exogenous - environmental agents
Involves abnormal calcification deposits. Occurs in DEAD OR DYING TISSUE. Found in the lesions of atherosclerosis and leads to myocardial infarction (heart valves, aorta)
Involves abnormal calcification deposits. Consists of mineral deposits that occurs in NORMAL TISSUE as a result of hypercalcemia. Causes could be hyperparathyroidism, cancer with bone lesions, Vit B intox.
Impairs cell function. Manifestations of injury are cell swelling due to impaired Na/K pump; and fatty changes due to decrease in protein synthesis (liver, kidney, heart susceptible)
aka Cellular dissolution. Cell DEATH in organ/tissue that is part of living person (burn, heart attack). Loss of cell membrane integrity with release of products of cell death in intracellular space. Leads to inflammatory response.
4 types of necrosis
1. Liquefactive - bacterial infection. Cells become soft and liquid
2. Coagulative - result from hypoxia from severe ichemia or chemical injury (kidneys, heart, adrenal glands).
3. Caseous - results from TB - cheese-like debris
4, Fat - Caused by lipases (breast, pancreas, abdominal structutres)
Three types of gangrene
1. Dry - Slow spread, see line of demarcation, color to dark brown/black (result of coagulative necrosis)
2. Wet - Rapid tissue destruction. No line of demarcation. Foul odor, affects internal organs or extremities
3. Gas - Clostridium bacteria produces toxin that dissolves cell membranes, serious and amputation required. Bubbles of hydrogen sulfide gas from muscle tissue
"Dropping off or programmed death". Controlled cellular autodigestion. Physiological or pathologic. Eliminates cells that are worn out, too many, genetic damage
Three mechanisms of cell injury
1. Free Radical
2. Hypoxic/Ischemic (ATP depletion)
3. Intracellular calcoium