1. - hemodynamic disorders - cellular adaptations
GENERAL PATHOLOGY
- hemodynamic disorders
- cellular adaptations
- cell injury and cell death
- inflammation
- healing, repair and regeneration
- neoplasia

2. MORPHOLOGICAL REACTIONSTO
ACUTE AND PERSISTENT
STRESS
CELLULAR ADAPTATIONS
CELL INJURY
CELL DEATH

3. Elements capable of causing cell injury
Chemical
Physical

4. Elements capable of causing cell injury
Biological

5. Cellular reaction varies
depending on the type
duration
and severity of injury eg

6. Adaptation
atrophy
hypertrophy
hyperplasia
metaplasia
dysplasia

7. Limits of adaptation

8. cell injury Subcellular alterations Reversible cell injury
“point of no return”
Irreversible cell injury

9. Subcellular responses to cell injury
Lysosomal catabolism

10. Subcellular responses to cell injury
Induction of smooth endoplasmic
reticulum
Mitochondrial alterations
Cytosceleton abnormalities

11. Reversible cell injury
e.g.
cellular swelling
fatty change

12. Cellular swelling
MACRO
MICRO

13. Intracellular and extracellular
accumulation (storage)

14. Normal cellular constituent accumulated in excess
e.g.
Abnormal substances
Pigments

15. LIPIDS
Steatosis (fatty change)
Liposis (obesity)

16. Cholesterol and cholesterol esters

17. PROTEINS

18. GLYCOGEN

19. PIGMENTS
-exogenous
-endogenous

20. CALCIFICATION
physiologic
pathologic

21. Dystrophic calcification

22. Metastatic calcification

23. HYALIN CHANGE
intracellular

24. HYALIN CHANGE
- extracellular

25. STAINING METHODS

26. metachromatic staining
One dye has the ability to produce different colors in various histological or cytological structures.

27. ATROPHY
Shrinkage in the size of the cells
by loss of cell substance

28. Cell death
necrosis
apoptosis

29. Necrosis-
„Death by injury”
cell death after exogenous stimuli
Apoptosis-
„Death by suicide”
cell death through activation of
an internally controlled
suicide program

30. Necrosis
morphologic changes following
cell death in living tissue largely
resulting from the action of enzymes
on the lethally injured cell
(live cells placed in fixative
are dead but not necrotic)

31. Morphology:

32. Two concurrent processes:
enzymic digestion
denaturation of proteins
Denaturation predominance
COAGULATIVE NECROSIS
Enzyme digestion predominance
LIQUEFACTIVE NECROSIS

33. Ulcer (ulceration)
Erosion

34. Caseous necrosis

35. Fat necrosis (Balser necrosis)

36. APOPTOSIS “falling off” - during development
- as a homeostatic mechanism
- as a defense mechanism
as a result of disease of noxious
agents action
- in aging

38. Programmed cell death
is as needed for proper development as mitosis is

39. Programmed cell death is needed to destroy cells
that represent a threat to the integrity of the organism

40. MORPHOLOGY:

41. Mechanisms
1. Signaling pathways

42. 2. Control and integration stage

43. 3. The execution phase

44. Apoptosis and cancer
some viruses associated with cancers act to prevent
apoptosis of the cells they have transformed

45. CELLULAR AGING

46. SUMMARY Cellular responses to injury Reversible injury
Irreversible cell injury
Cellular adaptations
atrophy
hypertrophy
hyperplasia
metaplasia
dysplasia
Intra- and extracellular storage
Cell death
apoptosis
necrosis
Cell aging