1. Cellular lesions I

2. Acute reversible injury: Hydropic degeneration From: Stevens A
Acute reversible injury: Hydropic degeneration From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig.1.1

3. Fig. 1.2
Fig Hydropic cells: cell balooning; cell nucleus has a normal appearance and a central position; cytoplasm appearance varies from a fine vacuolization (vacuolar degeneration) to extreme degrees, in which the cytoplasm is completely unstained
(clear degeneration). 3

4. Hydropic degeneration From cases of the Pathology Department - U. M. F
Hydropic degeneration From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi
Fig. 1.3

5. Fig. 1.4
Fig Hepatocytes are swelled due to various degrees of cellular hyperhydration, and have a vacuolated cytoplasm. Hepatocyte nuclei are preserved and centrally located.

6. Irreversible cell injury: Necrosis From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig. 1.5

7. Fig. 1.6
Fig Cytoplasm Changes. Cytoplasm becomes homogeneous and deeply acidophilic. Cytoplasm vacuolation by swelling of mitochondria. Finally, cell lysis is caused by enzymatic digestion. Nuclear Changes. In pyknosis, the nucleus becomes a shrunken, dense, and deeply basophilic mass.The nucleus may break up into numerous small basophilic particles (karyorrhexis).The nucleus undergoes lysis by enzymatic digestion (karyolysis).

8. Coagulative necrosis From cases of the Pathology Department - U. M. F
Coagulative necrosis From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi
Fig. 1.7
Fig Myocardial infarction: preserved cell limits and lack of nuclei

9. Fig. 1.8
Fig Kidney-Necrotic cells: cell outlines are preserved, cytoplasm becomes intense eosinophilic, nucleus and striations disappear.

10. Liquefactive necrosis Cerebral infarction From: Stevens A. J Lowe J
Liquefactive necrosis Cerebral infarction From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig. 1.9
Fig By liquefaction remain a swollen soft area.

11. Liquefactive necrosis
Fig. 1.10
Fig Necrotic cells are totally digested: the nucleus and cellular limits disappear early and in the place of dead cells remain a blank space filled with macrophages.

12. Caseous necrosis From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig. 1.11
Fig Necrotic area is a homogenous pink area without structure.

13. Hemorrhagic necrosis From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig. 1.12
Fig Necrotic area is suffused by blood from necrotic peripheral vessels

14. Types of cellular adaptive reactions Changes in cell growth and differentiation
Changes in cell size
Atrophy
Reduction in the cell size
Hipertrophy
Increase in the cell size
Changes in cell number
Involution
Decrease in the cell number
Hyperplasia
Increasing in the cell number
Changes in cell differentiation
Metaplasia
Cell change to another cell type
(transformation of a mature cell type into another mature cell type)
Fig From: Stevens A. J Lowe J. Pathology. Mosby 1995 14

15. Adaptative reaction with decreased tissular masses
Abnormal stimuli (reduced functional demand, decreased trophical stimuli / nutritional substances)
Atrophy (involution)
Adaptation is maintained as long as the stimulus persists; by removing it allows the return to normal
Reversible injury
Fig.1.14. 15

16. Cardiac atrophy From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig

17. Fig. 1.16. Myocardial fiber atrophy

18. Types of cellular adaptive reactions Changes in cell growth and differentiation
Changes in cell size
Atrophy
Reduction in the cell size
Hipertrophy
Increase in the cell size
Changes in cell number
Involution
Decrease in the cell number
Hyperplasia
Increasing in the cell number
Changes in cell differentiation
Metaplasia
Cell change to another cell type
(transformation of a mature cell type into another mature cell type)
Fig From: Stevens A. J Lowe J. Pathology. Mosby 1995 18

19. Adaptative responses with increased tissue mass From: Stevens A
Adaptative responses with increased tissue mass From: Stevens A. J Lowe J. Pathology. Mosby 1995
- Intense functional demand / endocrin stimulation
Hipertrophy & Hyperplasia
- Tissue growth is maintained while stimulus persists; after the cessation of stimulus action the tissue returns to normal
Reversible injury/lesion
Fig. 1.17

20. Myocardial hypertrophy From: Stevens A. J Lowe J. Pathology
Myocardial hypertrophy From: Stevens A. J Lowe J. Pathology. Mosby From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi
Fig. 1.18
Myocardial fiber hypertrophy: large, hypercromatic, irregular nuclei

21. Fig
Fig Concentric hypertrophy of the left ventricle due to HTA –LV concentric thickening.
Fig.1.20 Myocardial fiber hypertrophy

22. Hyperplasia and hypertrophy of the myometrium in pregnancy From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig. 1.21
Fig Increase in size of uterus

23. Prostatic nodular hyperplasia From: Stevens A. J Lowe J. Pathology
Prostatic nodular hyperplasia From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig
Fig Increase in size of prostate