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

Cellular lesions ICellular lesions I

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

Fig.1.1

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 (clear degeneration).

Fig. 1.2

Hydropic degeneration

From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi

Fig. 1.3

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 preserved and centrally located.

Irreversible cell injury: Necrosis

From: Stevens A. J Lowe J. Pathology. Mosby 1995

Fig. 1.5

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).

Fig. 1.6

Coagulative necrosisFrom cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi

Fig. 1.7. Myocardial infarction: preserved cell limits and lack of nuclei

Fig. 1.7

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

Fig. 1.8

Liquefactive necrosis Cerebral infarction

From: Stevens A. J Lowe J. Pathology. Mosby 1995

Fig. 1.9

Fig. 1.9. By liquefaction remain a swollen soft area.

Liquefactive necrosis

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.

Fig. 1.10

Caseous necrosisFrom: Stevens A. J Lowe J. Pathology. Mosby 1995

Fig. 1.11. Necrotic area is a homogenous pink area without structure.

Fig. 1.11

Hemorrhagic necrosis

From: Stevens A. J Lowe J. Pathology. Mosby 1995

Fig. 1.12. Necrotic area is suffused by blood from necrotic peripheral vessels

Fig. 1.12

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. 1.13 From: Stevens A. J Lowe J. Pathology. Mosby 1995

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.

Cardiac atrophyFrom: Stevens A. J Lowe J. Pathology. Mosby 1995

Fig. 1.15.

Fig. 1.16. Myocardial fiber atrophy

Fig.1.16.

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. 1.13. From: Stevens A. J Lowe J. Pathology. Mosby 1995

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

Myocardial hypertrophyFrom: Stevens A. J Lowe J. Pathology. Mosby 1995

From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi

Myocardial fiber hypertrophy: large, hypercromatic, irregular nuclei

Fig. 1.18

Fig. 1.19 Concentric hypertrophy of the left ventricle due to HTA –LV concentric thickening.

Fig.1.20 Myocardial fiber hypertrophy

Fig. 1.19-20

Hyperplasia and hypertrophy of the myometrium in pregnancy

From: Stevens A. J Lowe J. Pathology. Mosby 1995

Fig. 1.21

Fig. 1.21. Increase in size of uterus

Prostatic nodular hyperplasiaFrom: Stevens A. J Lowe J. Pathology. Mosby 1995

Fig. 1. 22

Fig. 1.22. Increase in size of prostate