Cell Injury, Adaptation, & Death

Cells

Tissues

Organs

Systems

Organism

 How is meiosis different?

 Tumor suppressor genes

synthesize growth inhibition proteins p53

Proto-oncogenes
stimulate cell growth

Proliferation of Cells
Labile
continuous reproduction

Stable
reproduce slowly until injured

Permanent
no division

Biologic Aging
Apoptosis
Programmed cell death

Necrosis
Death caused by disease

As cells age, functioning decreases Genetically, telomeres influence cell aging

 All disease occurs because of cell injury

Either because of the injury itself or the repair process that follows

Causes of Cell Injury

Hypoxia

Hypoxia
Inadequate oxygenation Most common cause of cell injury Usually due to ischemia Causes chemical & acidbase imbalances Reversible if O2 restored or death if not

Causes of Cell Injury

Hypoxia Direct physical action

Direct Physical Action

Major problems are hemorrhage & ischemia

Causes of Cell Injury

Hypoxia Direct physical action Ionizing radiation

Ionizing Radiation
Ionizes H2O into H+ & OH OH- attaches to DNA & prevents cell reproduction

DNA mutations

Causes of Cell Injury

Hypoxia Direct physical action Ionizing radiation Toxic molecular injury

Toxic Molecular Injury

Dose related

Causes of Cell Injury

Hypoxia Direct physical action Ionizing radiation Toxic molecular injury Microbes

Microbes
Toxins can interfere with protein synthesis or utilization of O2

Causes of Cell Injury

Hypoxia Direct physical action Ionizing radiation Toxic molecular injury Microbes Inflammatory & immune reactions

Inflammatory & Immune Reactions

Due to cell injury & then in turn causes injury

Causes of Cell Injury

Hypoxia Direct physical action Ionizing radiation Toxic molecular injury Microbes Inflammatory & immune reactions Nutritional imbalances Genetic defects Aging

Mild Cell Injury

Hydropic change
Na/K pump damaged so Na+ increases in the cell & H2O moves in causing swelling

Intracellular Accumulations
Some due to phagocytosis or other normal physiologic mechanisms

Fat

Cholesterol
Most extensive & damaging accumulation Atherosclerosis

Protein

Glycogen

Pigments

Adaptations
Change in size Change in number of cells

Change into another type of cell

Atrophy
Decreased size & function Metabolic processes shut down to conserve energy Due to
decreased demand ischemia lack of nerve or hormonal stimulation chronic inflammation

Hypertrophy
Increased size & functional capacity Due to
hormonal stimulation increased functional demand

Hyperplasia
Increase in number of cells Due to
hormonal stimulation increased functional demand chronic stress or injury

Dysplasia
Disorderly overgrowth of cells Premalignant Reversible

Metaplasia
One cell type to another Reversible

Necrosis
Pathologic cell death Usually in a collection of cells fed by a single artery

Coagulative Necrosis
Most common Dead cells form a gellike consistency No anatomic disruption so cells or tissues are left with a ghostly outline Infarction most common cause

Liquefactive Necrosis
Dead tissue dissolves into liquid Dead cells disrupted faster than it can be cleaned up

Caseous Necrosis
TB cheesy Cellular detail gone

Fat Necrosis
May due to trauma Triglycerides digested & free fatty acids precipitate as calcium salts One type of dystrophic calcification

Gangrene
Dry
part is dry & shrinks skin wrinkles dark brown or black slow spread line of demarcation form of coagulation necrosis extremities part cold, swollen, pulseless moist, black, & under tension liquefaction occurs foul odor no line of demarcation spreads rapidly death if not stopped organs & extremities

Wet (moist)