cellular lesions i
DESCRIPTION
Cellular lesions I. Acute reversible injury : Hydropic degeneration From: Stevens A. J Lowe J. Pathology. Mosby 1995. Fig.1.1. Fig. 1.2. - PowerPoint PPT PresentationTRANSCRIPT
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