Lecture 2

MD 406, 2022
 Causes of cell injury
 Mechanisms of cell injury
 Pathology of inflammation
 Cells of inflammatory exudates
 Types of inflammation
 Local changes in acute inflammation
 Mechanism of formation of inflammatory
exudates

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1- Decrease of oxygen supply
(hypoxia).

- Ischaemia as in arterial
occlusion
- Loss of oxygen carrying
capacity (anaemia)
- Inadequate oxygenation
of the blood

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2-Infectious agents
3-Physical agents
4-Chemical agents: acids, alkalis,
metals
5-Mechanical agents: trauma
6-Immunological reactions
(hypersensitivity)
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7-Nutritional imbalances
8-Genetic derangements

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1- ATP depletion and decreased ATP
synthesis (hypoxia, chemicals)
◦ Leads to loss of energy-dependent cellular
functions.
- Loss of ATP causes:
◦ Switch to anaerobic ATP synthesis, leading to
the accumulation of catabolites as lactic acid
& inorganic phosphates.

◦ Failure of the active cell membrane transport

(sodium pump)

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2- Intracellular toxic oxygen-derived radicals as
superoxide, hydrogen peroxide and hydroxyl
radicals.

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3- Increase intracellular calcium (hypoxia,
certain toxins).
 Influx of extracellular calcium ions or release
of calcium from mitochondria.
 Increased intracellular calcium activates the
enzymes:
◦ Phospholipases / degrade membrane
phospholipids.
◦ Proteases / break cellular proteins.
◦ ATPases / deplete ATP.
◦ Endonucleases/ cause DNA injury.

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 Normal cell is in a steady
state “Homeostasis”

 Change in Homeostasis
occurs due to – Injury

 Mild Injury / Reversible

(stress)/ Adaptation

 Severe injury/
Irreversible/ cell death

MD 406, 2022
 Adaptations (reversible):
◦ Hypertrophy/ increase size of cells
◦ Hyperplasia/ increase no of cells
◦ Atrophy/ decrease in size of cells
◦ Accumulations - protein, fat, etc.
◦ Extracellular calcium deposition

 Necrosis (irreversible): cell death

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 “In-flame” – to set fire. (red, hot, pain)

 Suffix itis to denote inflammation: colitis.

 Inflammation: is the dynamic response of
vascularized tissue to injury.

 Purpose:
- Important body's defense mechanism
- Serves to bring defense (White blood cells,
antibodies, chemicals) & healing mechanisms
to the site of injury.

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- Polymorphnuclear leukocytes
- Monocytes or histiocytes (macrophages)
- Lymphocytes
- Plasma cells

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1-Polymorphnuclear leukocytes:
(microphages)
Granulation in cytoplasm &
segmentation of the nucleus.
i-Neutrophils: 60- 70%, (pale pink
to blue )
-nucleus two, three or more lobes
-primary defense element
- motile & phagocytic

MD 406, 2022
 Neutrophils may die by bacterial toxins
(leukocidins) & become pus cells.

 Pus cells release proteolytic enzymes, that helps in

digestion (liquefaction) of necrotic tissue and
fibrin

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◦ ii- Eosinophils: 1-2%,
 N: two lobes, C: coarse granules
red
 neutralize histamine
 Have a role in allergic
inflammation

◦ iii-Basophils: 1%,
 Coarse granules dark blue
 Contain histamine and heparin
 Have role in allergic
inflammation

MD 406, 2021
2- Blood monocytes & macrophages: (4-
6%)
◦ Bean shaped nucleus, finely granular
gray cytoplasm
◦ monocytes macrophages
(blood) (tissues)
◦ Motile & phagocytic
◦ Macrophages fuse together
◦ forming giant cells.
◦ Giant cells engulf larger particles

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Inflammatory reaction

Dr. Manal M
Maher Hussein 3/7/2022
 3- Lymphocytes: 30%
◦ large dense nucleus & narrow non-granular
cytoplasm
i-B-lymphocytes / plasma cells/ secrete
antibodies
ii-T lymphocytes secrete lymphokines, which
activate macrophages
iii-Plasma cells:
◦ tissues
◦ basophilic cytoplasm & eccentric nucleus.

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 Redness – Vasodilatation
 Hotness– Increased blood flow
 Swelling – Fluid & cellular exudates
 Pain – Nerve, Chemical mediators
 Loss of function

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Hotness Redness Swelling Pain Loss of Function

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