1. Cell Injury, Adaptation, & Death

2. Cells
Tissues
Organs
Systems
Organism

8. How is meiosis different?

9. Tumor suppressor genes
synthesize growth inhibition proteins
p53
Proto-oncogenes
stimulate cell growth

10. Proliferation of Cells
Labile
continuous reproduction
Stable
reproduce slowly until injured
Permanent
no division

12. 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

13. All disease occurs because of cell injury
Either because of the injury itself or the repair process that follows

14. Causes of Cell Injury
Hypoxia

15. 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

16. Causes of Cell Injury
Hypoxia
Direct physical action

17. Direct Physical Action
Major problems are hemorrhage & ischemia

18. Causes of Cell Injury Hypoxia Direct physical action
Ionizing radiation

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

20. Causes of Cell Injury Hypoxia Direct physical action
Ionizing radiation
Toxic molecular injury

21. Toxic Molecular Injury
Dose related

22. Causes of Cell Injury Hypoxia Direct physical action
Ionizing radiation
Toxic molecular injury
Microbes

23. Microbes
Toxins can interfere with protein synthesis or utilization of O2

24. Causes of Cell Injury Hypoxia Direct physical action
Ionizing radiation
Toxic molecular injury
Microbes
Inflammatory & immune reactions

25. Inflammatory & Immune Reactions
Due to cell injury & then in turn causes injury

26. Causes of Cell Injury Hypoxia Direct physical action
Ionizing radiation
Toxic molecular injury
Microbes
Inflammatory & immune reactions
Nutritional imbalances
Genetic defects
Aging

27. Mild Cell Injury Hydropic change
Na/K pump damaged so Na+ increases in the cell & H2O moves in causing swelling

28. Intracellular Accumulations
Some due to phagocytosis or other normal physiologic mechanisms

29. Fat

31. Cholesterol
Most extensive & damaging accumulation
Atherosclerosis

32. Protein

33. Glycogen

34. Pigments

35. Adaptations Change in size Change in number of cells
Change into another type of cell

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

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

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

39. Dysplasia
Disorderly overgrowth of cells
Premalignant
Reversible

40. Metaplasia
One cell type to another
Reversible

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

42. 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

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

45. Caseous Necrosis TB
“cheesy”
Cellular detail gone

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

47. 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