Cellular lesions I

1. Cellular lesions I

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

3. Fig. 1.2 Fig.1.1-2.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 (cleardegeneration).

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

5. Fig. 1.4 Fig. 1.3-4.Hepatocytes are swelled due to various degrees of cellular hyperhydration, and have a vacuolated cytoplasm. Hepatocyte nuclei are preservedand centrally located.

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

7. Fig. 1.6 Fig. 1.5-6.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 necrosisFrom cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi Fig. 1.7 Fig. 1.7. Myocardial infarction: preserved cell limits and lack of nuclei

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

10. Liquefactive necrosisCerebral infarctionFrom: Stevens A. J Lowe J. Pathology. Mosby 1995 Fig. 1.9 Fig. 1.9. By liquefaction remain a swollen soft area.

11. Liquefactive necrosis Fig. 1.10 Fig. 1.10. 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 necrosisFrom: Stevens A. J Lowe J. Pathology. Mosby 1995 Fig. 1.11 Fig. 1.11. Necrotic area is a homogenous pink area without structure.

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

14. Types of cellular adaptive reactionsChanges in cell growth and differentiation Fig. 1.13 From: Stevens A. J Lowe J. Pathology. Mosby 1995

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.

16. Cardiac atrophyFrom: Stevens A. J Lowe J. Pathology. Mosby 1995 Fig. 1.15.

17. Fig.1.16. Fig. 1.16. Myocardial fiber atrophy

18. Types of cellular adaptive reactionsChanges in cell growth and differentiation Fig. 1.13. From: Stevens A. J Lowe J. Pathology. Mosby 1995

19. Adaptative responses with increased tissue massFrom: 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 hypertrophyFrom: Stevens A. J Lowe J. Pathology. Mosby 1995From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi Fig. 1.18 Myocardial fiber hypertrophy: large, hypercromatic, irregular nuclei

21. Fig. 1.19-20 Fig. 1.19 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 pregnancyFrom: Stevens A. J Lowe J. Pathology. Mosby 1995 Fig. 1.21 Fig. 1.21. Increase in size of uterus

23. Prostatic nodular hyperplasiaFrom: Stevens A. J Lowe J. Pathology. Mosby 1995 Fig. 1. 22 Fig. 1.22. Increase in size of prostate