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 Necrosis As cells age, functioning decreases 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 & acid-base 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- DNA mutations 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 gel-like 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 Wet (moist) part is dry & shrinks skin wrinkles dark brown or black slow spread line of demarcation form of coagulation necrosis extremities Wet (moist) part cold, swollen, pulseless moist, black, & under tension liquefaction occurs foul odor no line of demarcation spreads rapidly death if not stopped organs & extremities