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CELLULAR RESPONSE TO
INJURY, ACUTE
INFLAMMATION,HEALING AND
REPAIR,CHRONIC
INFLAMMATION
BY;
JEGANATHAN.C
2ND YEAR M.SC
DEPT. OF BIOMEDICAL SCIENCE
CELL INJURY
● Cells actively control the composition of their immediate environment and
intracellular milieu within a narrow range of physiological
parameters(homeostasis)
CELL INJURY
Mechanisms of Cell Injury
● Depletion of ATP
● Mitochondrial Damage
● Influx of Intracellular Calcium and Loss of Calcium
Homeostasis
● Accumulation of Oxygen-Derived free radical
(Oxidative stress)
● Defects in Membrane Permeability
Morphology of Cell Injury and
Necrosis
● Cell Injury – Reversible
● – Irreversible
● Cell Death – Necrosis
● – Apoptosis
Cell Injury and Death
● Reversible Injury
o Cell swelling develops when cells are incapable of fluid an
ion homeostasis (↓ed function of ATP dependant pumps).
o Fatty change the accumulation of lipid vacuoles in the
cytoplasm.
● Irreversible injury (Necrosis)
o Two basic processes underlie the morphologic changes of
necrosis
▪ Denaturation of protein
▪ Enzymatic digestion of cell components
Reversible vs irreversible
cell injury
● Reversible injury
● * Decreased ATP levels
● * Ion imbalance
● * Swelling
● Decreased pH
● Fatty change (liver)
Irreversible injury
* Amorphous densities
in mitochondria
* Severe membrane
damage
* Lysosomal rupture
• Extensive DNA
damage
Morphology of Cell Injury
● Plasma membrane alteration
● Mitochondrial Changes
● Dilation of Endoplasmic reticulum
● Nuclear Alteration
Reversible Injury
Cellular swelling
Fatty change
HEALING AND REPAIR
REPAIR
● Process by which the cells in the body regenerate and repair to reduce the size of
the damage or necrotic area and replace it with new loiving tissue.
PROCESS
● Recall phase
● Resolution phase
● Regeneration phase
● Repair phase
Soft Tissue Healing
● Inflammatory Phase (0-6 days)
● Proliferation Phase (3-21 days)
● Regeneration and Maturation Phase (up to 1+ year)
Skin Tissue
● Epidermis
● Dermis
● Subcutaneous Layer
Skin Injury Classification
● Abrasions
● Blisters
● Skin Bruises
● Incisions
● Lacerations
● Avulsions
● Punctures
Muscles
● Epimysium
● Perimysium
● Endomysium
● Fasciculus
● Muscle Fibers
● Myofibrils
Bones
● Calcium Carbonate
● Calcium Phosphate
● Collagen
● Water
Bone Injury Classification
● Fractures
● Closed
● Compounded
● Transverse
● Comminuted
● Oblique
● Epiphyseal
● Spiral
● Greenstick
● Avulsion
● Impacted
● Depressed
Nerves
● Afferent Nerves (Affectors)
● Efferent Nerves (Effectors)
Nerve Injury Classification
● Tensile forces cause stretching of the nerve fibers.
● Grade I: Neurapraxia: temporary loss of sensation and/or motor function.
● Grade II: Axonotmesis: significant motor and mild sensory losses.
● Grade III: Neurotmesis: motor and sensory losses persisting for up to one year.
Acute & Chronic
Inflammation
INFLAMMATION
Inflammation:
Inflammation is the reaction of blood vessels, leading to the accumulation
of fluid (Serum) and leukocytes in extra vascular tissue.
Role of tissue and cells in
inflammation
The circulating cells are:
● Neutrophils.
● Monocytes.
● Eosinophils.
● Lymphocytes.
● Basophils.
● Platelets.
Sign & Symptoms Of Inflammation
These are:
● Fever (increase temperature).
● Pain.
● Tissue damage.
● Swelling of tissue.
● Redness of tissue.
● Loss of movements or restricted movement, if near joints.
Types Of Inflammation
Inflammation is divided into
I - Acute inflammation, which occurs over seconds, minutes, hours, and days.
II - Chronic inflammation, which occurs over longer times, days & months.
Acute Inflammation
● Acute inflammation, begins within seconds to minutes following the injury of
tissues.
● The damage may be purely physical, or it may involve the activation of an
immune response.
Chronic Inflammation
Chronic inflammation is of longer duration and is associated histologically with the
presence of:
● Lymphocytes and macrophages.
● The proliferation of blood vessels.
● Fibrosis and tissue necrosis.
Response Of Inflammation
The main processes are:
I - Increased blood flow.
II - Increased permeability.
III - Migration of neutrophils.
IV - Chemotaxis.
V - Leucocytes recruitment & activation.
Response of Acute Inflammation
● Increased Blood Flow, increased permeability and Edema in Inflammation:
● The increased blood flow & increased permeability are readily visible within a few
minutes following a scratch that does not break the skin.
Response of Acute Inflammation
● At first, there is pale red line of scratch.
● Later on there is accumulation of inflammatory cells lead swelling, (inflammation).
● Finally, there is accumulation of interstitial fluid cause edema.
Acute Inflammation
Acute Inflammation
(Acute Bronchitis)
Chronic inflammation
● It is the inflammation of prolong duration (weeks or months).
● It is occurred as:
● Following acute inflammation.
● Occurs, incidentally as active inflammation.
● With tissue destruction.
With repair process.
Chronic Inflammation
(Chronic Bronchitis)
Chronic Bronchitis
Causes of Chronic inflammation
I - Persistent infection:
● Bacteria.
● Viruses.
● Fungi.
● Parasites
Chronic Inflammation
Causes of Chronic inflammation
II - Prolonged exposure to potentially toxic agents:
● Endogenous, (atherosclerosis).
● Exogenous, ( particulate silica-Silicosis).
Causes of Chronic inflammation
III - Autoimmunity:
Occurs in:
● Rheumatoid arthritis.
● Lupus erythmatosus.
Chronic Inflammation
(Rheumatoid arthritis)
THANK YOU

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Cellular response to injury, acute inflammation,healing and jeganathan

  • 1. CELLULAR RESPONSE TO INJURY, ACUTE INFLAMMATION,HEALING AND REPAIR,CHRONIC INFLAMMATION BY; JEGANATHAN.C 2ND YEAR M.SC DEPT. OF BIOMEDICAL SCIENCE
  • 2. CELL INJURY ● Cells actively control the composition of their immediate environment and intracellular milieu within a narrow range of physiological parameters(homeostasis)
  • 4. Mechanisms of Cell Injury ● Depletion of ATP ● Mitochondrial Damage ● Influx of Intracellular Calcium and Loss of Calcium Homeostasis ● Accumulation of Oxygen-Derived free radical (Oxidative stress) ● Defects in Membrane Permeability
  • 5. Morphology of Cell Injury and Necrosis ● Cell Injury – Reversible ● – Irreversible ● Cell Death – Necrosis ● – Apoptosis
  • 6. Cell Injury and Death ● Reversible Injury o Cell swelling develops when cells are incapable of fluid an ion homeostasis (↓ed function of ATP dependant pumps). o Fatty change the accumulation of lipid vacuoles in the cytoplasm. ● Irreversible injury (Necrosis) o Two basic processes underlie the morphologic changes of necrosis ▪ Denaturation of protein ▪ Enzymatic digestion of cell components
  • 7.
  • 8. Reversible vs irreversible cell injury ● Reversible injury ● * Decreased ATP levels ● * Ion imbalance ● * Swelling ● Decreased pH ● Fatty change (liver) Irreversible injury * Amorphous densities in mitochondria * Severe membrane damage * Lysosomal rupture • Extensive DNA damage
  • 9. Morphology of Cell Injury ● Plasma membrane alteration ● Mitochondrial Changes ● Dilation of Endoplasmic reticulum ● Nuclear Alteration Reversible Injury Cellular swelling Fatty change
  • 10.
  • 11.
  • 13. REPAIR ● Process by which the cells in the body regenerate and repair to reduce the size of the damage or necrotic area and replace it with new loiving tissue.
  • 14. PROCESS ● Recall phase ● Resolution phase ● Regeneration phase ● Repair phase
  • 15. Soft Tissue Healing ● Inflammatory Phase (0-6 days) ● Proliferation Phase (3-21 days) ● Regeneration and Maturation Phase (up to 1+ year)
  • 16. Skin Tissue ● Epidermis ● Dermis ● Subcutaneous Layer
  • 17. Skin Injury Classification ● Abrasions ● Blisters ● Skin Bruises ● Incisions ● Lacerations ● Avulsions ● Punctures
  • 18. Muscles ● Epimysium ● Perimysium ● Endomysium ● Fasciculus ● Muscle Fibers ● Myofibrils
  • 19. Bones ● Calcium Carbonate ● Calcium Phosphate ● Collagen ● Water
  • 20. Bone Injury Classification ● Fractures ● Closed ● Compounded ● Transverse ● Comminuted ● Oblique ● Epiphyseal ● Spiral ● Greenstick ● Avulsion ● Impacted ● Depressed
  • 21. Nerves ● Afferent Nerves (Affectors) ● Efferent Nerves (Effectors)
  • 22. Nerve Injury Classification ● Tensile forces cause stretching of the nerve fibers. ● Grade I: Neurapraxia: temporary loss of sensation and/or motor function. ● Grade II: Axonotmesis: significant motor and mild sensory losses. ● Grade III: Neurotmesis: motor and sensory losses persisting for up to one year.
  • 24. INFLAMMATION Inflammation: Inflammation is the reaction of blood vessels, leading to the accumulation of fluid (Serum) and leukocytes in extra vascular tissue.
  • 25. Role of tissue and cells in inflammation The circulating cells are: ● Neutrophils. ● Monocytes. ● Eosinophils. ● Lymphocytes. ● Basophils. ● Platelets.
  • 26. Sign & Symptoms Of Inflammation These are: ● Fever (increase temperature). ● Pain. ● Tissue damage. ● Swelling of tissue. ● Redness of tissue. ● Loss of movements or restricted movement, if near joints.
  • 27. Types Of Inflammation Inflammation is divided into I - Acute inflammation, which occurs over seconds, minutes, hours, and days. II - Chronic inflammation, which occurs over longer times, days & months.
  • 28. Acute Inflammation ● Acute inflammation, begins within seconds to minutes following the injury of tissues. ● The damage may be purely physical, or it may involve the activation of an immune response.
  • 29. Chronic Inflammation Chronic inflammation is of longer duration and is associated histologically with the presence of: ● Lymphocytes and macrophages. ● The proliferation of blood vessels. ● Fibrosis and tissue necrosis.
  • 30. Response Of Inflammation The main processes are: I - Increased blood flow. II - Increased permeability. III - Migration of neutrophils. IV - Chemotaxis. V - Leucocytes recruitment & activation.
  • 31. Response of Acute Inflammation ● Increased Blood Flow, increased permeability and Edema in Inflammation: ● The increased blood flow & increased permeability are readily visible within a few minutes following a scratch that does not break the skin.
  • 32. Response of Acute Inflammation ● At first, there is pale red line of scratch. ● Later on there is accumulation of inflammatory cells lead swelling, (inflammation). ● Finally, there is accumulation of interstitial fluid cause edema.
  • 35. Chronic inflammation ● It is the inflammation of prolong duration (weeks or months). ● It is occurred as: ● Following acute inflammation. ● Occurs, incidentally as active inflammation. ● With tissue destruction. With repair process.
  • 38. Causes of Chronic inflammation I - Persistent infection: ● Bacteria. ● Viruses. ● Fungi. ● Parasites
  • 40. Causes of Chronic inflammation II - Prolonged exposure to potentially toxic agents: ● Endogenous, (atherosclerosis). ● Exogenous, ( particulate silica-Silicosis).
  • 41. Causes of Chronic inflammation III - Autoimmunity: Occurs in: ● Rheumatoid arthritis. ● Lupus erythmatosus.