General Pathology Assignment

Cellular Injury
The effect of variety of stress due to etiological agents a cell encounters resulting in its internal
and external environment. Cellular response to stress varies and depends upon
1. Host factors: Type of cell and tissue involved

2. Factors pertaining to injurious agents: Extent and type of injury
Cell injury results when cells are under stress and can no longer adapt. Injury may progress
through a reversible stage.
Stages in the cellular response to stress and injurious stimuli

Reversible Cell Injury:
Reduced oxidative phosphorylation with resultant depletion of energy stores in the form of
adenosine triphosphate (ATP).
Cellular swelling caused by changes in ion concentrations and water influx.
Types of cell injury

There are two types of cell injury
1. Necrosis ( lethal)
2. Apoptosis (non lethal)
Apoptosis or non lethal (cell degeneration):

DNA or proteins are damaged beyond repair; the cell kills itself characterized by nuclear
dissolution, fragmentation of the cell without complete loss of membrane integrity.
 Impairment or loss of the function and structure of cells or tissues, as by disease or

injury.
 Its reversible but may become irreversible (necrosis/apoptosis)
 Nonlethal injury may produce cell degeneration
 Manifested as a abnormality of biochemical function, structural changes or
combination.
 May produce clinical disease.
Necrosis or lethal injury:

Damage to membranes is severe, lysosomal enzymes enter the cytoplasm and digest the cell,
and cellular contents leak out.
 UN programmed cell death and living tissues. (opposite to apoptosis).

 Irreversible.
 Accompanied with by biochemical and morphological changes.
 Due to hypoxia, chemical substances, free radical, immunologic response, infections etc.
Stages of Necrosis:
1. Early changes : Morphologically normal
2. Nuclear changes : Pyknosis – chromatin clumps into coarse strands, nucleus
become shrunken
3. Cytoplasmic changes : Denaturation of cytoplasmic protein and lost of
ribosomes, swelling of mitochondria and disruption of organelle membranes and
autolysis occur via lysosomes.
Type of Necrosis
Different cells show different morphologic changes after they undergo necrosis. Base on that
necrosis can be classified into:
1. Coagulative necrosis
2. Liquefactive necrosis
3. Caseous / gummatous necrosis
4. Fat necrosis
5. Gangrenous Necrosis
Coagulative Necrosis:
 Typically occur in solidorgan; heart, kidney, adrenal glands
 Due to hypoxia (maybe from severe ischemia or chemical)
 Normally, this necrotic cells retains its cellular outline.
 Denaturation of protein albumin causes coagulation.
Liquefactive Necrosis:
 Normally occurs in CNS which affects neuronand neuroglia cells
 Associated with focal bacterial and fungus infections
 The affected cells completely digest by hydrolytic enzymes thus changes the tissue into
liquid viscous mass.
Caseous Necrosis:
 Caseous – cheese like appearance
 Associated with tuberculous pulmonary (TB) infection, esp by Mycobacterium
Tuberculosis.
Fat Necrosis:
 Occur in pancreas, breast and other abdominal structures.
 Caused by lipases enzymes which break down triglycerides (lipid) into fatty acids
andglycerol.
 Fatty acids and glycerol then combine with Ca, Mg, Na to form Calcium Soaps
(Saponification).
 The necrotic tissue appears opaque and chalk white.
Gangrenous Necrosis (gangrene)

 Extensive tissue necrosis.
 Divide into two; dry andwet.
 Dry – occurs in extremities as a results of ischemic coagulative necrosis due to
arterialobstruction.
 Wet – occurs in extremities and internal organ as a results of liquefactive necrosis due
to bacterial infection.
 Gas – necrotic tissue infectedby clostridium perfringes.
Gangrene
Causes of Cell Injury:
The can be
1. Genetics causes
2. Acquired causes
Genetics causes:
Genetic defects may cause cell injury because of deficiency of functional proteins, such as
enzyme defects in inborn errors of metabolism, or accumulation of damaged DNA or misfolded
proteins, both of which trigger cell death when they are beyond repair.
Acquired causes:
They include
1. Oxygen deprivation
2. Chemical agents
3. Infectious agents
4. Immunologic reactions
5. Genetic defects
6. Nutritional imbalances
7. Physical agents
8. Aging
Oxygen deprivation:
- Hypoxia – oxygen deficiency
- Due to ischemia – lost/lack of blood supply (due to arterial blockage or reduce venous
drainage)
- Hypoxia also can occurs via:
- Lack of oxygen inside blood
- Reduction in oxygen carrying capacity in RBC(anemia)
- Carbon monoxide poisoning
Chemical agents:
- Most of the chemical substances can cause cell injury
- For example : poisons, air pollutants, insecticides, CO, asbestos, ethanol, therapeutics
drugsetc
- This agents can cause cell death by:
- Altering membrane permeability’
- Altering osmotic homeostasis
- Altering integrity of an enzyme
Infectious agent:
- Viruses, bacteria, fungi, parasites, helminthes.
Immunologic Reactions:
- Autoimmune disease – immunity against its own tissues . For examples SLE, Rheumatoid
Arthritis etc.
Genetic Defects:
- Abnormalities to the genomes – mutation.
- This chromosome anomaly is associated with missing, or Irregularities or extra in portion
of chromosomal DNA.
- Syndrome Down, Alzheimer's disease, Huntington’s Disease etc.
Nutritional Imbalance:
- Cause by directly or indirectly lack of essentialnutrients (malnutrition)
- Or it maybe related to excessive of food intake (Diabetic Mellitus)
- For example protein deficiency– Kwashiorkor, Marasmus
- Calcium deficiency – osteoporosis
- Vitamin C – Scurvy
Physical Agents:
- Trauma, extremes of temperature, radiation, electrical shock all have wide ranging
effects on cells.
Aging:
- Aged cells become larger, less able to divide and multiply.
- Lose their ability to functions, or function abnormally.
Features of necrosis and apoptosis:

Cellular adaptation:
For the sake of survival on exposure to stress, the cells make an adjustment with the changes in
their environment or adapt
 To physiological need (physiological adaptation)

 To non lethal injury (pathological adaptation)
Under stress cell can go or adopt the following
1. Hyperplasia: it is in increase in the number of parenchyma cells resulting in

enlargement of the organ or tissue.
Physiologic hyperplasia: hyperplasia of female breast at puberty, during pregnancy and

lactation.
Pathologic hyperplasia: endometrial hyperplasia following estrogen excess.
2. Metaplasia: a reversible change of one type of epithelial or mesenchymal adult

cells to another type of adult epithelial or mesenchymal cell.
Physiologic metaplasia: metaplasia of endocervix: columnar epithelial into squamous epithelial.
Pathologic metaplasia: respiratory epithelium in smokers.
Ciliated columnar epithelium to squamous epithelium.

3. Hypertrophy: increase tissue size via enlargement of cells caused by an increase
in organelles, and structural protein.
Physiologic hypertrophy: increased muscle mass through sports, uterus enlargement during
the pregnancy.
Pathologic hypertrophy: hypertrophy of cardiac muscle.

Atrophy: reduction of number and size of parenchymal cells of an organ.
Physiologic atrophy: atrophy of gonads after menopause , atrophy of braing with aging.
Pathologic atrophy: starvation atrophy, ischemic atrophy.
Dysplasia: it means disordered cell cellular development, often accompanied with

mataplasia and hyperplasia. It is therefore also referred to as atypical hyperplasia. Dysplasia
occurs most often in epithelial cells. Epithelial hyperplasia is characterized by cellular
proliferation and cytologic changes.
1. Increased number of layers of epithelial cells
2. Disorderly arrangement of cells from basal layer to the surface layer.
Dysplastic changes often occur due to chronic irritation or prolonged inflammation.
Different types of cellular adaptation shown in picture.

References:
 Cellular injury.pdf
 Cellular injury slide share
 Slides provided by Teacher
 Group member collected data from different sites.

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Cellular Injury

1. Host factors: Type of cell and tissue involved

Stages in the cellular response to stress and injurious stimuli

Cellular swelling caused by changes in ion concentrations and water influx.

Types of cell injury

Apoptosis or non lethal (cell degeneration):

 Impairment or loss of the function and structure of cells or tissues, as by disease or

Necrosis or lethal injury:

 UN programmed cell death and living tissues. (opposite to apoptosis).

3. Caseous / gummatous necrosis

Gangrenous Necrosis (gangrene)

Features of necrosis and apoptosis:

 To physiological need (physiological adaptation)

Under stress cell can go or adopt the following

1. Hyperplasia: it is in increase in the number of parenchyma cells resulting in

Physiologic hyperplasia: hyperplasia of female breast at puberty, during pregnancy and

Pathologic hyperplasia: endometrial hyperplasia following estrogen excess.

2. Metaplasia: a reversible change of one type of epithelial or mesenchymal adult

Physiologic metaplasia: metaplasia of endocervix: columnar epithelial into squamous epithelial.

Pathologic metaplasia: respiratory epithelium in smokers.

Ciliated columnar epithelium to squamous epithelium.

Pathologic hypertrophy: hypertrophy of cardiac muscle.

Pathologic atrophy: starvation atrophy, ischemic atrophy.

Dysplasia: it means disordered cell cellular development, often accompanied with

Dysplastic changes often occur due to chronic irritation or prolonged inflammation.

Different types of cellular adaptation shown in picture.

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