Slide 1

Report
Cell injury
By
Staff members of pathology
Liquefaction necrosis
* Definition: necrosis with complete loss of cell
and tissue structure.
* Mechanism:
– Destruction of dead cells by hydrolytic enzymes.
– Enzymes derived from either:
• Cell’s own lysosomes (autolysis) or from
• Neutrophils and macrophages (heterolysis).
* Seen in:
– Suppurative bacterial infections: characterized by
formation of pus (liquefied tissue debris and
neutrophils).
– In ischemic injury to brain tissue: Enzymatic
destruction of brain tissue leaves behind a cystic
cavity.
* Gross appearance:
– Necrotic area: soft and filled with fluid.
* Microscopy:
– Structureless tissue debris (no cellular outlines).
– Neutrophils.
Lung Abscesses
Necrotic material
with loss of cellular
architecture
Neutrophils
Necrotic tissue
Coagulative vs. Liquefactive necrosis
Coagulative necrosis
Focus of liquefactive necrosis
Caseation necrosis
* Definition: a distinct form of necrosis without
preservation of cellular outlines and tissue architecture,
but firm in consistency.
• It is a combination of Coagulative and liquefaction
necrosis.
* Most commonly associated with:
– Granulomas like tuberculosis
– Fungal infection like histoplasmosis.
* GROSS:
– Yellowish white, “cheese-like” material.
– Cheese-like appearance
• Due to release of lipid from the cell walls of M.
tuberculosis and systemic fungi (histoplasma).
• (Latin “caseous” – cheese)
* MICRO:
– Eosinophilic material surrounded by activated
macrophages, multinucleated giant cells and
helper T cells (= a granuloma).
Caseous necrosis
B
Lymph node: histoplasmosis
Lung: tuberculosis
Caseous necrosis
Langhan’s giant cells
Granuloma
Epithelioid cell
Langhan’s
giant cell
Fat necrosis
1. Traumatic fat necrosis
Secondary to trauma to fatty tissue.
Trauma to fatty tissue  acute inflammatory
reaction (neutrophils)  healing by fibrous
tissue and dystrophic calcification.
Commonly seen in women with pendulous
breasts.
Clinical significance:
– Scar tissue feels firm, retracts the overlying skin and
shows calcifications on mammography.
– “These findings also seen in breast cancer”.
2. Enzymatic fat necrosis
• Focal areas of fat destruction due to the action
of pancreatic enzyme on fatty tissue located
around pancreas.
• Occurs as a complication of Acute pancreatitis.
• Acute pancreatitis:
– Release of lipases and amylase from pancreas.
– Lipases break triglycerides into fatty acids (FA).
– FA combine with Ca2+ via the process of
saponification to form chalky white calcified
deposits In the pancreas as well as in the omental
fat.
White nodules on the
surface of pancreas
Area of necrosis with
blue discoloration
Fibrinoid necrosis
• Is necrosis of immunologic injury.
• Is marked by deposition of Pink staining, fibrin-like
proteinaceous material within tissue.
• Examples:
– Rheumatic heart disease vegetations on mitral valve.
– Inflamed synovial tissue in rheumatoid arthritis.
– Malignant hypertension within vessel walls.
• Microscopy: fibrinoid material has
– Smudgy pink (Eosinophilic) appearance.
Fibrinoid
Necrosis
Gangrenous necrosis
- Most often occurs in lower limbs and bowel
secondary to loss of blood supply.
- Two types:
1. Dry gangrene:
– Is a form of infarction that results from
ischemia.
– Characterized primarily by coagulative
necrosis without liquefaction.
– Dead tissue has mummified appearance.
– Characteristic finding in diabetic foot.
Dry Gangrene
A
B
2. Wet gangrene:
– Refers to necrosis with superimposed
bacterial infection.
– Liquefactive necrosis is the primary type of
necrosis in wet gangrene.
Apoptosis
• Genetically, programmed single cell death.
* Morphologically:
• The cell membrane does not rupture.
• The cell contents are not released into the
extracellular space, and
• Inflammation does not occur.
• May be physiological or pathological.
* Physiologic examples of apoptosis:
1. Embryogenesis.
•
Development of lumen within hollow organs (e.g
bowel and heart).
2. Hormone-dependent involution in adults.
–
–
–
Endometrial breakdown in menstruation.
Post-lactational atrophy of breast.
Prostate atrophy following castration.
3. Involution of Thymus in the adult.
4. Cells that are programmed to die; for
example,
1. The cells of the outer layers of epidermis,
2. Cells in the gut epithelium.
* Pathologic examples of apoptosis:
1. Councilman bodies = dead hepatocytes in viral
hepatitis.
2. Psammoma bodies: apoptosis of neoplastic
cell with subsequent calcification.
3. Tumor cell death by cytotoxic T cells.
4. Neurons that are lost in Alzheimer's disease.
5. HIV-positive T-lymphocytes die by apoptosis.
* Morphologic appearance of apoptotic cells:
1.
2.
3.
4.
5.
Have deeply pink staining cytoplasm.
Have pyknotic nucleus which fragment.
Are smaller in size.
Formation of cytoplasmic buds.
Breaking off cytoplasmic buds to form apoptotic
bodies.
6. Phagocytosis of apoptotic bodies by adjacent cells or
macrophages.
7. A lack of inflammatory response.
Apoptosis of epidermal
cells
Apoptotic cell in liver
What if apoptosis is too little or too
much!! = dysregulated apoptosis:
• Two groups of disorders:
1. Decreased apoptosis with increased cell
survival can give rise to:
• Cancers
• Autoimmune disorders
2. Increased apoptosis with decreased cell
survival:
– Neurodegenerative diseases (Alzheimer’s)
– Death of virus infected cells: Lymphocyte depletion
as in AIDS
Apoptosis vs. Necrosis
Feature
Necrosis
Apoptosis
Cell size
Enlarged
(swelling)
Reduced
(shrinkage)
Nucleus
Pyknosis 
Fragmentation
karyorrhexis 
karyolysis
Cellular
contents
Enzymatic
digestion; may
leak out of
cell
Intact, may
be released in
apoptotic
bodies.
Feature
Necrosis
Apoptosis
Adjacent
inflammation
Frequent
No
Physiologic or
pathologic role
Always
pathologic
Often
physiologic, may
be pathologic
Good luck

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