Chapter 3: Cellular Adaptation Flashcards
REVERSIBLE cell injury
cells responds to stressors appropriately and can repair itself
IRREVERSIBLE cell injury
occurs when the stressor is prolonged, outlasting the adaptation capabilities of the cell
the cell dies
Atrophy
(without nourishment)
decrease in size and number of cells
Hypertrophy
(over nourishment)
increase in the SIZE of cells
Hyperplasia
(over formation)
increase in the NUMBER of cells
not seen in muscles, neurons, or cardiac cells
Metaplasia
change in formation
reversible change in which one adult cell type is replaced by another
Dysplasia
abnormal formation
deranged cell growth of a specific tissue that results in cells that vary in size, shape, and organization
Autophagia
starved cells eat their own cell components for survival
Expected atrophy
thymus (before puberty as levels of sex hormones increase)
uterus atrophy after delivery
breast tissue atrophy after lactation
DISUSE atrophy
having extremity in a cast
prolonged bed rest
DENERVATION atrophy
occurs in the muscles of paralyzed limbs due to loss of neural signals
LOSS OF ENDOCRINE STIMULATION atrophy
Menopause (loss of estrogen = atrophy of reproductive organs)
Hypopituitarism = atrophy of thyroid, gonads, and adrenal glands
Overuse of testosterone = testicular atrophy
Overuse of steroids = atrophy of the adrenal glands
INADEQUATE NUTRITION atrophy
Body depletes glycogen stores then fats then proteins (muscles)
Muscle wasting
cells being “eating” their own myosin and actin to stay alive
ISCHEMIA atrophy
atherosclerosis of cerebral blood vessels leads to brain atrophy
Labile and stable cells
capable of division
can undergo hypertrophy AND hyperplasia
Permanent cells
cardiac and skeletal muscle cells
can ONLY undergo hypertrophy
PHYSIOLOGIC hypertrophy
Physiologic conditions = increase in workload not caused by disease
Lifting weights, exercising
ADAPTIVE PATHOLOGIC hypertrophy
Responses are aimed at maintaining function
Hypertrophy of the myocardium d/t HTN
Hypertrophy of the stomach r/t pyloric stenosis
Hypertrophy of the bladder d/t BPH
COMPENSATORY PATHOLOGIC hypertrophy
One kidney is removed, the other will enlarge to compensate for the loss of its pair
HORMONAL-PHYSIOLOGIC hyperplasia
increase in # of cells to increase the functional capacity of the organ
Example: uterus response to increase in estrogen after ovulation
COMPENSATORY-PHYSIOLOGIC hyperplasia
increase in # of cells to increase the tissue mass after damage or partial removal
Regeneration of liver cells
Callus (hyperplasia of epithelial cells over over-worked area)
People living in high altitudes (hyperplasia of RBCs)
NONPHYSIOLOGIC (PATHOLOGIC) hyperplasia
response to either excessive hormonal stimulation or abnormal production of hormonal growth factors
Examples: BPH, acromegaly, endometrial hyperplasia, warts and cancers caused by HPV, psoriasis
EPITHELIAL metaplasia
Barrett’s esophagus - change in esophageal cells to columnar cells (found in the GI tract) that are better suited to exposure to acid
Smoking
Example of dysplasia
bronchopulmonary dysplasia (BPD) in preterm infants associated with prolonged supplemental oxygen concentration
Intracellular accumulations
represents to buildup of substances that cells cannot immediately use or eliminate
intracellular accumulation: NORMAL BODY SUBSTANCES
occurs when substances are produced at a rate that is higher than the body’s metabolism for removal
Examples: lipids, proteins, carbohydrates, melanin, bilirubin, fatty acids
intracellular accumulation: EXOGENOUS PRODUCTS
environmental agents (lead, mercury, coal dust) or ink (tattoos) that cannot be broken down by cells so they accumulate
intracellular accumulation: ENDOGENOUS PRODUCTS
can be related to inborn errors in metabolism and genetic disorders that can disrupt the metabolism of certain drugs
Example: Tay Sachs disease
Pathologic calcifications
involves abnormal tissue deposition of calcium salts along with smaller amounts of other minerals
DYSTROPHIC calcification
macroscopic deposition that occurs in dead/dying tissue - frequent cause of organ dysfunction
serum calcium levels will be NORMAL
Causes: infarcts, thrombi, tumors, and cysts
METASTATIC calcification
occurs in normal tissues in response to increased serum calcium levels (hypercalcemia)
Causes: hyperparathyroidism, prolonged immobilization, renal failure
Cell injury from MECHANICAL FORCES
physical agents
occurs as a result of body impact with another object
direct damage to cells - tears tissues, fractures bones, disrupts blood flow
Cell injury from EXTREMES OF TEMPERATURE
physical agents
Intense heat = coagulation of blood and tissue proteins
Extreme cold = increases blood viscosity, causes vasoconstriction (capillary stasis, thrombosis, edema)
Cell injury from ELECTRICAL INJURY
physical agents
causes extensive tissue injury and disruption of neural and cardiac impulses
effect on the body is affected by VOLTAGE, TYPE OF CURRENT, PATHWAY of the current, RESISTANCE of the tissue, and DURATION of exposure
VOLTAGE
lightning and high voltage wires produce the most severe damage
ELECTRICAL CURRENT
AC (alternating current) is more dangerous than DC (direct current) due to violent muscle contractions, causing the person to be unable to release the electrical source
PATHWAY and RESISTANCE of electrical current
tissues with higher electrical resistance will suffer more damage
Thick, dry skin will have higher resistance = localized injury (skin burns)
Wet, thin skin has less resistance = deeper, systemic effects
Cell injury from CHEMICAL INJURY
chemicals can injure cells when they come into contact with the body or injure cells in the process of metabolism or elimination (excretion)
Examples: pollution, tobacco smoke, processed/preserved foods, carbon monoxide, insecticides, drugs (alcohol, antineoplastics, acetaminophen), and lead (esp in infants and children)
Lead toxicity
absorbed through GI tract or lungs and stored in bone and excreted by kidneys
Effects: inactivates enzymes
competes with calcium
interferes with nerve transmission and brain development
Major targets of lead toxicity
RBCs
GI tract
Kidneys
Nervous system
Cell injury from BIOLOGIC AGENTS
Viruses - incorporate into DNA of cell and use up its resources
Bacteria - damage cells through exotoxins or endotoxins
Parasites
Cell injury from NUTRITIONAL IMBALANCES
nutritional excesses and nutritional deficiencies predispose cells to injury
Obesity and high-fat diets = atherosclerosis
Starvation = protein and calorie deficiencies = widespread tissue damage
Selective deficiencies: iron, vitamin C, thiamine, niacin, folic acid, vitamin B12
HYPOXIC Cell Injury
mechanism of cell injury
Hypoxia deprives the cell of oxygen and interrupts oxidative metabolism and the generation of ATP = “power failure”
Leads to anaerobic metabolism = lactic acid production = cell damage
Brain is the first to deteriorate in hypoxic injury d/t high oxygen demand
IMPAIRED CALCIUM HOMEOSTASIS
mechanism of cell injury
calcium functions as a messenger for the release of many intracellular enzymes
normally, extracellular Ca > intracellular Ca
certain toxins can lead to the increase in intracellular metabolism
Patterns of REVERSIBLE cell injury
impairs cell function but does not result in cell death Cellular swelling (impairment of the Na/K-ATPase pump) Fatty change (intracellular accumulation of fat)
APOPTOSIS (programmed cell death)
highly selective, controlled autodigestion of cell components
normal physiologic process in the body
once apoptosis begins, it cannot be stopped - energy dependent
NECROTIC cell death
unregulated death caused by injuries to cells
cells swell and rupture - inflammation results
damage to one cell can have a snowball effect on other/surrounding cells
not energy dependent
LIQUEFACTIVE necrosis
liquefies necrotic cells - softened center of an abscess
common in brain (rich supply of enzymes)
wet gangrene
COAGULATIVE necrosis
looks like a firm gray mass
related to hypoxia and seen in infarcted areas (cardiac and muscle tissue)
dry gangrene
CASEOUS necrosis
soft, cheesy appearance
mainly found in center of tuberculous granulomas (pulmonary tuberculosis)
DRY Gangrene
form of coagulative necrosis
spreads very slowly
line of demarcation exists
interference of arterial blood supply
WET Gangrene
form of liquefactive necrosis area is cold, swollen, pulseless, moist, often with a foul odor spreads rapidly (can have severe systemic symptoms) interferes with venous return
GAS Gangrene
severe trauma introduces bacteria that release toxins
affected muscle cells release gas bubble (hydrogen sulfide gas)
spreads rapidly - can cause widespread edema
can be fatal
