Cell injury

• Intended learning objectives

• Define homeostasis and cell injury
• List causes of cell injury. What are types of cell
injury.
• Explain fatty change
• Analyze the mechanisms of hemochromatosis
and pathologic calcification
• Describe amyloidosis, necrosis and apoptosis
 Cell injury
•Homeostasis: is the ability of the cells to adjust their functions
with different environmental stress.
•Cell injury: is a condition when the changes in the
environmental stress exceed the ability of the cell to adapt.
•Causes of cell injury (Stress):
- Hypoxia: chronic heart failure and anemia.
- Physical agents: trauma and burns.
- Chemical agents: poisons and industrial chemicals.
- Inflammation: bacteria and viruses.
- Antigen-antibody reaction.
- Genetic abnormality: gene mutations.
- Nutritional imbalances: deficiencies of vitamins.
 Types of cell injury
- Reversible cell injury (degeneration): they are
pathological changes in which the cells can return to
normal state when the stimulus stops.
Degeneration: It is a reversible deterioration in the
cell function leads to change of tissue to less
functionally active one.
- Irreversible cell injury: The injury cannot adapt by
the cells and the cells cannot return to normal state.
Irreversible injuries lead to cell death either by
necrosis or apoptosis.
 Fatty change (steatosis)

•Definition: It is a reversible intra-cytoplasmic

accumulation of triglycerides either due to
excessive entry or defective metabolism and
release.
• Sites: liver, heart, muscles and kidney.
• Causes: Alcohol- Diabetes- Obesity
 Fatty change (steatosis)
•Gross picture:
The organ is enlarged, yellow, soft and greasy.
•Microscopically:
H&E stain: The affected cells appear
vacuolated. The fat droplets push the nucleus to
one side giving signet ring appearance.
•Complications: fatty change is a reversible
condition but it can lead to inflammation and
fibrosis.
Fatty change
 Primary hemochromatosis
(Bronzed diabetes)
Definition: iron overload due to an inborn error characterized by
increase absorption of dietary iron. It mainly affects males and is rare in
females (due to physiological loss of iron in menses and pregnancies).
Sites: The pigment is deposited in the cells of liver, pancreas, heart and
skin.
Gross: the organs appear enlarged, brown and hard.
Microscopically: the affected cells undergo necrosis and fibrosis.
Effects:
Liver: cirrhosis and liver cell carcinoma.
Pancreas: fibrosis replaces islet cells leads to diabetes mellitus.
Heart: fibrosis leads to heart failure.
Skin: bronzed color due to increased melanin and hemosiderin
deposition.
 Pathological calcification:
Abnormal soft tissue deposition of calcium salts.
1- Dystrophic calcification:
Definition: it is calcification of dead or damaged
tissues in spite of a normal blood calcium level.
Psammoma bodies: single necrotic cells around
which calcium is deposited. Psammos is Greek
for sand. Psammoma bodies are common in
papillary carcinomas of thyroid glands. 
2- Metastatic calcification:
Definition: it is calcification of normal tissues
due to hypercalcemia.  It occurs widely
throughout the body: (metastatic)
  Examples: gastric mucosa, kidney tubules
(nephrocalcinosis) and lung alveoli.
 Amyloidosis
•Definition: It is extracellular deposition of an
insoluble protein substance in between cells and
walls of blood vessels. Amyloid deposition leads
to pressure atrophy to adjacent tissue.
•Characters: Stains positively with Congo red.
•Causes: Multiple myeloma- Rheumatoid
arthritis
Congo red
 Necrosis
•Definition: it is a form of cell injury which
results in premature death of cells in a living
tissue by autolysis or heterolysis.
•Autolysis: digestion of cell by its own
lysosomal enzymes.
•Heterolysis: digestion of cell by lysosomal
enzymes of leukocytes.
 Types of necrosis
1- Coagulative necrosis: necrotic tissue remains firm.
Examples: Infarction of heart, kidney, and spleen
2- Liquefactive necrosis: digestion of tissues by
proteolytic enzymes.
Examples:
A) Infarction of brain: lysosomal enzymes from
microglial cells or necrotic cells liquefy the brain.
B) Abscess and cellulitis (proteolytic enzymes from
neutrophils liquefy infected tissues forming pus).
 Types of necrosis
3- Gangrenous necrosis: it starts as coagulation
necrosis due to cut of blood supply leads to dry
gangrene. By time, liquefaction of necrotic tissue
occurs due to the action of putrefactive bacteria
resulting in wet gangrene.
4- Caseation necrosis: the necrotic tissue is soft,
friable and cheesy.
Causes: reaction between macrophages and T
lymphocytes with bacterial antigen.
Example: Tuberculosis.
Gangrenous necrosis
Caseation necrosis
 Types of necrosis
5- Fat necrosis: it is seen in adipose tissue.
Examples:
1- Enzymatic necrosis of omental fat: In acute hemorrhagic
pancreatitis.
Causes: It is due to lipase enzyme released from injured pancreatic
cells.
2- Traumatic fat necrosis of female breast.
6- Fibrinoid necrosis: Pattern of necrosis occurs in:
A- Deposition of immune complex protein (Ag-Ab) and fibrin in
arterial wall
Examples: immune vasculitis as in SLE
B- Deposition of non-immune protein (plasma proteins).
Examples: malignant hypertension.
Fibrinoid necrosis
 Apoptosis
Definition: it is an energy dependent genetically
programmed cell death that involves single cells.
Characters:
1- Apoptosis is a cell suicide program.
2- This type of cell death is under the influence of
hormones, growth hormone and cytokines.
3- Apoptosis is not harmful to the host and doesn’t
result in inflammation.
The died cell doesn’t rupture and intracytoplasmic
granules are not released outside the cell.