cell injury pathology for nursing students and undergraduate medical students

1. Detection of Cellular Changes After
Injury
By:
 Light microscopy or gross examination 
detect changes hours to days after injury
 Histochemical or ultrastructural techniques 
detect changes minutes to hours after injury

3. Patterns of Acute Cell Injury
 Reversible Injury
 Cellular swelling: Ultrastructural
changes
 plasma membrane blebbing,
blunting and distortion of microvilli
 mitochondrial swelling,
phospholipid-rich amorphous
densities
 dilation of endoplasmic reticulum
with detachment of ribosomes and
dissociation of polysomes
 disaggregation of granular and
fibrillar elements on nucleus

4.  Reversible Injury
2. Fatty change:
 Vacuolation of cells due to accumulation of lipid
droplets
 Results due to disturbance of ribosomal function
 The liver is commonly affected
 Occurs in hypoxic injury, toxic (alcohol), metabolic
(diabetes mellitus)
 Moderate fatty changes are reversible, but sever
changes may not be
Patterns of Acute Cell Injury

5. Patterns of Acute Cell Injury
Irreversible injury:
Cell death
 It is suggested that cell membrane is the central
factor in the pathogenesis of irreversible cell injury
 Also due to:
 sever mitochondrial dysfunction
 lysosomal rupture
 Two patterns of cell death:
 Necrosis
 Apoptosis

6. Patterns of Acute Cell Injury
 Irreversible injury: Cell death
1. Necrosis:
 Definition:
sequence of morphologic changes that follow cell death in living
tissue
 The morphologic appearance of necrosis is due to:
 Enzymatic digestion of cell:
 Autolysis: hydrolytic enzymes are derived from the dead cells
themselves
 Heterolysis: hydrolytic enzymes are derived from invading
inflammatory cells
 Denaturation of proteins

7. Patterns of Acute Cell Injury
 Microscopic appearance of Necrotic dead cells:
 Cytoplasmic changes
 eosinophilia (pink) increased  due to eosin binding to denatured
proteins
 Decreased basophilia (blue) – mainly imparted by RNA
 Glassy homogenous cytoplasm  due to loss of glycogen
 Clacification may occur late
 Nuclear changes  due to break down of DNA
 Karyolysis: decrease basophilia of chromatin
 Pyknosis: nuclear shrinkage and increased basophilia
 Karyorrhexis: fragmentation of pyknotic nucleus

9. Kidney, necrosis of tubular cells

10. Patterns of Acute Cell Injury
 Specific Morphologic Patterns of Necrosis
 Coagulative necrosis
 Liquefactive necrosis
 Gangrenous necrosis
 Caseous necrosis
 Fat necrosis
 Others (fibrinoid necrosis)

11. 1. Coagulative Necrosis:
 Preservation of the structural outline of the dead
(coagulated) cell for days
 The most common form of necrosis (particularly in
myocardium, liver, kidney)
 characteristic of hypoxic cell death in all tissues except in
the brain
 Myocardial infarction is a very good example
 Mechanism: denaturation of proteins and enzymes 
blocking cellular proteolysis  preserve cell outline
Specific Morphologic Patterns of
Necrosis

12. Specific Morphologic Patterns of
Necrosis
 Morphology of Coagulative Necrosis:
 Gross:
pale color, normal firm texture at the beginning  become soft later
due to digestion by macrophages (may lead to rupture of infarcted
myocardium)
 Microscopic:
first few hours  no abnormalities
later  progressive loss of nuclear staining,
with preservation of cell boundaries
finally  damaged cells are removed by macrophages
(the presence of necrotic tissue usually evokes inflammatory response
followed by repair)

13. Fate of Necrosis
 Most of necrotic tissue is removed by
leukocyte (Phagocytosis) combined with
extracellular enzyme digestion
 If necrotic tissue is not eliminated  it attracts
Ca++ salts  dystrophic calcification

14. Patterns of Acute Cell Injury
 Apoptosis
(a falling away from)
 Definition: Programmed cell death
 It is an active (energy-dependant) programmed single cell death to
delete the unwanted or defective cells
 It has an important role in physiological processes and
pathological conditions

15. Apoptosis
 Physiological processes:
 during embryogenesis (implantation, organogenesis, developmental involution,
separation of digits in limb development)
 hormone -dependent involution (endometrium during menstruation, lactating
breast after weaning)
 cell deletion in proliferating populations  intestinal crypt epithelium
 deletion of autoreactive T cells in thymus (failure might result in autoimmunity)
 Pathological conditions:
 pathologic atrophy-prostate after castration (hormone -dependent involution)
 Cell death in tumors
 Cell death induced by cytotoxic drugs and ionizing radiation
 Councilman’s bodies due to viral hepatitis

16. Apoptosis
Morphology:
 Involves single cells or small clusters
 Cells shrink rapidly, retain intact plasma membrane
 Formation of cytoplasmic buds
 Fragmentation into apoptotic bodies
 Apoptotic bodies phagocytosed or rapidly degraded
 No inflammatory response
 Entire process from 5 to 30 minutes

17. Apoptosis

18. Necrosis Vs Apoptosis
Necrosis
 Grp of cells or part of
tissue
 passive process
 Always pathologic
 Mechanism is ATP
depletion, mb damage
 Histology: coagulation.
liquefaction
 inflammation
Apoptosis:
 Single cell death in
living tissue
 Active process
 Physiologic or
pathologic
 Endonucleases
 Apoptotic bodies
 No inflammation