1. Cell injury, death and adaptation
Dr Heyam Awad
FRCPath

2. Pathology 1 for dentistry
Coordinator : Dr Heyam Awad
Lectures will be available on my university website on the day they are given.
Office hours: Monday and Wednesday Office in hospital 3rd floor.

3. Course structure CELL DAMAGE 4 LECTURES Dr HEYAM AWAD INFLAMMATION
DR MAHA SHOMAF
AMYLOIDOSIS
I LECTURE
DR FATIMA OBAIDAT
HEALING AND REPAIR
2 LECTURES
DR TAREK AL ODALY
NEOPLASIA
5 LECTURES
RESPIRATORY SYSTEM
DR FATIMA OBEIDAT
CIRCULATORY SYSTEM
3 LECTURES
DR NISREEN ABU SHAHIN
BLOOD VESSELES
HEART
BLOOD

4. EVALUATION 2 EXAMS: 40 MARKS FOR THE MIDTERM AND 60 FOR THE FINAL.
THEORY AND PRACTICAL.
MIDTERM IN THE WEEK STARTING 8/11
8/11 – 12/11 NO LECTURES.. MIDTERM WEEK
LAST LECTURE 22/12

5. What is pathology? Patho… disease Logy… study
Pathology = study of disease
involves: causes of disease.. Etiology
: mechanisms.. pathogenesis
:morphological changes.

6. Etiology: Origin of disease , underlying causes.
Pathogenesis: steps in the development of disease…… cellular and molecular changes .
Morphology: macroscopic and microscopic changes.

7. Why to study pathology???

8. Cellular adaptations and cell injury
Cells maintain a steady state.. Homeostasis.
Stresses .. Adaptation….. New homeostatic state with preservation of function.
Stress beyond capability of adaptation.. Cell injury.
Cell injury… reversible within certain limits
Then .. Irreversible…. Ends in cell death.
Two types of cell death: necrosis and apoptosis.

12. Adaptation
Hyertrophy
Hyperplasia
Atrophy
metaplasia

13. Adaptation Adaptive changes are reversible.
Can be physiologic or pathologic.

14. Hypertrophy: Increased cell size.
Hyperplasia: increased number of cells.. Cell division.
Metaplasia: change from one adult cell type to another
Atrophy: decreased size.

15. Hypertrophy versus hyperplasia

16. Hypertrophy Increased cell size.
Due to increased organelles and proteins.
Increased intracellular synthesis..
Caused by: increased demands, hormones or growth factors.

17. Physiologic hypertrophy
Uterus during pregnancy… due to estrogen
Skeletal muscle… due to increased demand

18. Physiologic hypertrophy

19. Pathologic hypertrophy
Cardiac.. Hypertensive heart disease
Pathogenesis.. Two types of signals: mechanical: stretch and trophic: growth factors and androgenic hormones

20. Pathologic hypertrophy

21. Pathologic hypertrophy

22. hyperplasia Only in tissues that can replicate.
Can be physiologic or pathologic.

23. Physiologic hyperplasia
Hormonal: uterus, breast.
Compensatory: after removal or loss of part of tissue.

24. Gingival hyperplasia

25. Pathologic hyperplasia
Due to excess in hormones or growth factors.
E:g endometrial hyperplasia.
Controlled.. Responds to decreased stimulation. This differentiates it from cancer

26. Normal endometrium

27. Endometrial hyperplasia

28. atrophy Shrinkage in cell size due to loss of cell substance. Causes
decreased work load.
Loss of innervation
Loss of endocrine stimulation.
Aging

29. Muscle atrophy

30. Brain atrophy

31. Atrophy Physiologic: endometrial atrophy during menopause
Pathologic: loss of innervation.

32. atrophy Mechanisms: Decreased protein synthesis.
Degradation of cellular proteins.
Autophagy…. Literally means self eating.

33. metaplasia Adult cell type replaced by another adult cell type.
Arise in reprogrammed stem cells to differentiate along a new pathway.

34. Epithelial metaplasia
Respiratory epithelium to squamous.
Barrett's mucosa.. Esophegeal squamous to columnar

35. Barrett’s mucosa

36. Normal esophegeal mucosa

37. Metaplastic, Barrett’s mucosa

38. Metaplasia in mesenchymal tissue
Usually pathologic
Ossification of soft tissue due to injury.