Lec. 1

2ND CLASS / 2024-2025
DEPARTMENT OF PATHOLOGY
PROF. DR.NIHAD N. HILAL
Objectives: What are the
Objectives: What are the

 1. Components of normal cell
 2. Causes of cell injury
 3. General mechanism of cell injury
 4. Factors affecting cell response to injury
 5. types of cell injury
Components of normal cell
1.Essential for survival
• Cell membrane maintain intracellular environment

• Nucleus / nucleolus genetic code/ expression
• Mitochondria energy production/storage
• Endoplasmic reticulum/ribosomeprotein synthesis
• Golgi apparatustransport of products of protein
synthesis
• Lysosomesstorage of hydrolytic enzymes
Cell structure
2. Specialized components e.g.,
• Hemoglobin (RBC)
• Zymogen granules (exocrine cells)
• Neurofilaments (nerve cells)
* The causes of cell injury span a range
from gross physical trauma, such as after a
motor vehicle accident, to a single gene
defect that results in a nonfunctional
enzyme in a specific metabolic disease.
Causes of cell injury
1. Ischemia/hypoxia: any ↓ O2 / ↓ O2 transport (anemia),

COPD
2.Infection: viral, bacterial, fungal, parasitic
3.Physical: heat, cold, radiation, electricity
4.Chemical: acid, alkali, toxins, drugs.
5.Immunologic reaction:
- autoimmune reactions against one’s own tissues,
- allergic reactions against environmental substances,
- excessive or chronic immune responses to microbes..
6.Nutritional
7.Genetic: e.g. enzyme defect accumulation of toxic
product (iron in hemochromatosis)
8. Aging. Cellular senescence results in a diminished
ability of cells to respond to stress and eventually,
the death of cells and of the organism.
 Pathogenesis refers to the mechanisms of
development and progression of disease,
which account for the cellular and molecular
changes that give rise to the specific
functional and structural abnormalities that
characterize any particular disease.
 Thus, etiology refers to why a disease arises
and pathogenesis describes how a disease
develops (Fig. 2.1)
General mechanism of cell injury
1. Free radicalsDamage to DNA, proteins, lipid

2. ATP depletion
3. ↑ cell membrane permeability
4. Influx of calcium Activates enzymes
* Proteases  protein breakdown
* ATPaseATP depletion;
* Phospholipases  cell membrane injury;
* Endonudeases  DNA damage
5. Mitochondrial dysfunction
• ↓ Oxidative phosphorylation
• Release of cytochrome c which trigger apoptosis
Factors affecting cell response to injury
1.The type of injury

2.The duration of injury
3.The severity of injury
4.The type of injured cell
5.The cells metabolic state
6.The cell’s ability to adapt
Normal cell
Injurious agent
(ischemic, hypoxic, chemical, physical etc)
adaptation Irreversible changes

reversible changes
 Reversible Cell Injury : is the stage of cell injury at
which the deranged function and morphology of
the injured cells can return to normal if the
damaging stimulus is removed
 Irreversible injury, cells and intracellular organelles
typically become swollen because they take in
water as a result of the failure of energy-dependent
ion pumps in the plasma membrane, leading to an
inability to maintain ionic and fluid homeostasis.
In some forms of injury, degenerated organelles and
lipids may accumulate inside the injured cells
Reversible cell injury
Irreversible cell injury
1. Severe membrane damage (influx of Na/water etc)
2.Severe mitochondrial dysfunction: cessation of ATP

production
3. Rupture of lysosomes release of hydrolytic
enzymescell lyses
4. Nuclear changes
* pyknosis: condensation chromatin
* karyorhexis: fragmentation of nucleus
* karyolysis: disintegration of nucleus
Practical – cell injury 1
The two main morphologic correlates of
reversible cell injury are :
Cellular swelling:is commonly seen in cell injury associated

with increased permeability of the plasma membrane.
 It may be difficult to appreciate with the light microscope,
but it is often apparent at the level of the whole organ.
 When it affects many cells in an organ, it causes pallor (as a
result of compression of capillaries), increased turgor, and
an increase in organ weight.
 Microscopic examination may show small, clear vacuoles
within the cytoplasm.
 This pattern of nonlethal injury is sometimes called hydropic
change or vacuolar degeneration.
Fatty change
 is manifested by the appearance of
triglyceride containing lipid vacuoles in the
cytoplasm.
 It is principally encountered in organs that
are involved in lipid metabolism, such as
the liver.
Cut section of kidney showing cloudy swelling
note the pale swollen parenchyma
Hydropic degeneration
cells lining renal tubules distended with water,
cytoplasm eosinophilic & less granular than normal
Fatty degeneration: grossly liver enlarged, yellow & waxy
Fatty changes: liver: Some hepatocytes filled with fat
& looks empty due to removal of fat during processing
Dead cells: look to pyknotic faded nuclei
References
 Textbook: Kumar V, Abbas AK, Aster JC: Robbins

basic pathology. 10th edition, Elsevier, 2018.
 Currant's Atlas of Histopathology,4th Revised Edition

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2ND CLASS / 2024-2025

Objectives: What are the

1.Essential for survival

• Cell membrane maintain intracellular environment

1. Ischemia/hypoxia: any ↓ O2 / ↓ O2 transport (anemia),

1. Free radicalsDamage to DNA, proteins, lipid

1.The type of injury

(ischemic, hypoxic, chemical, physical etc)

adaptation Irreversible changes

2.Severe mitochondrial dysfunction: cessation of ATP

Cellular swelling:is commonly seen in cell injury associated

 Textbook: Kumar V, Abbas AK, Aster JC: Robbins

 Currant's Atlas of Histopathology,4th Revised Edition

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