Chapter 2: Cellular Injury, Adaptations, and Maladaptive Changes
Adaptations: Atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia —> stress removed—> normal cell restored
Reversible cell injury: degenerations, sub-cellular alterations, intracellular accumulations —> stress removed—> repair and healing
Irreversible cell injury —> cell death
The cell either adapts or compensates
cells develop maladaptive changes resulting in changes to cell function/ structure
cells can de
Cellular adaptation and maladaptive changes occur as a result of specific disease processes, altered cell function or environmental factors
Causes of cellular adaptation
damage to cell membrane
reduced levels of ATP
changes in metabolic processes
change in pH
Cellular changes: Aging
Decrease in cellular function
cell structure changes
mitosis slows down
increased accumulation of waste
altered protein syntheses and ATP production
decreased collagen and elastin fibers
inability to adapt to change or exposure
alteration in nucleus-free radicals
alterations in DNA during mitosis
Causes of cellular change
ischemia or cellular hypoxia - decreased oxygen
inflammation or immunological runs (autoimmune)
nutrition imbalance
fluid and electrolyte disturbances
microorganisms
free radical injury
physical agents
genetic defects
Normal alterations - hypertrophy or atrophy
Hypertrophy- enlargement of tissue mass due to the increased size of cells
normal physiologic hypertrophy- increased stimuli (workload)
Pathologic hypertrophy- cardiomyopathy
atrophy- decreased tissue mass- cells become smaller
disuse or decreased metabolic need
decrease in blood flow- ischemia
lack of nerve stimulation
loss of hormonal stimulation
aging
Abnormal alterations (pathologic) leads to cell death
DNA changes- ionizing radiation
Trauma or chemical exposure
hyperplasia- overproduction of cells (pregnancy)
metaplasia- mature cell replaced by another mature cell
dysplasia- cells vary in size and shape within a tissue type, increased rate of mitosis; often due to chronic irritation, infection, or precancerous change
neoplasia- new growth, tumor
Endothelial Cell Injury
Endothelium= lining of arterial blood vessels
Body larges organ → injury causes widespread effects
Causes
Hypertension (HTN → shearing injury, weakening of vessel walls
Diabetes mellitus (DM)→ hyperglycemia causes chemical damage to endothelial cells but also narrowing of the arteries (vasoconstriction)
smoking→ arteriosclerosis and vasoconstriction
angiotensin II → vasoconstriction
Effects: atherogenesis (deposition of plaque within arteries)
Hypoxia- Most common cause of cell injury
due to ischemia or reduced blood supply to the issue
Causes- inadequate oxygen intake(high altitude, pulmonary disease), anemia, cardiac arrest, poor circulation, or obstruction of blood flow(arteriosclerosis, thrombosis)
Results of cellular Hypoxia
inability to produce ATP
failure of NA+ and K+ pump
Ca++ flooding of cell
cellular swelling
protein synthesis slows/stops
cellular hypoxia→ anaerobic metabolism → 2 ATP and pyruvic acid (lactic acid)
cell dies
Impact on tissue from hypoxia
Infarction = death of tissue due to prolonged ischemia (ischemic necrosis
individual cell types have varying tolerance levels to ischemia
brain & heart cells infarct within minutes
skeletal muscles can last for hours
Apoptosis: cell death; programmed cell death
eliminated unwanted, unnecessary, or damaged cells without any adverse effects
can be either normal or due to disease
if doesn’t occur at approximate times, can lead to excess accumulation or excessive distraction
Necrosis= cell death caused by injury
cell degraded by autolysis(break apart)
Complications of necrosis
gangrene= infection of necrotic tissue
caused by Clostridium perfringens
most commonly occurs in necrotic tissues of lower extremities caused by PAD
emits a gas within the tissues
often requires amputation