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

Cellular lesions I
Acute reversible injury: Hydropic degeneration
From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig.1.1
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
(clear degeneration).
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. 1.6
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).
Coagulative necrosis
From 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
Fig. 1.8
Fig. 1.8. Kidney-Necrotic cells: cell outlines are preserved, cytoplasm
becomes intense eosinophilic, nucleus and striations disappear.
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
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.
Caseous necrosis
From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig. 1.11
Fig. 1.11. Necrotic area is a homogenous pink area without structure.
Hemorrhagic necrosis
From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig. 1.12
Fig. 1.12. Necrotic area is suffused by blood from necrotic peripheral vessels
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 atrophy
From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig. 1.15.
Fig.1.16.
Fig. 1.16. Myocardial fiber atrophy
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 mass
From: Stevens A. J Lowe J. Pathology. Mosby 1995
- Intense functional demand / endocrin stimulation
- Tissue growth is maintained while stimulus
persists; after the cessation of stimulus action the
tissue returns to normal
Hipertrophy & Hyperplasia
Reversible injury/lesion
Fig. 1.17
Myocardial hypertrophy
From: Stevens A. J Lowe J. Pathology. Mosby 1995
From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi
Fig. 1.18
Myocardial fiber hypertrophy: large, hypercromatic, irregular nuclei
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
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 hyperplasia
From: Stevens A. J Lowe J. Pathology. Mosby 1995
Fig. 1. 22
Fig. 1.22. Increase in size of prostate