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Progressive Types Of Cell Injury & Response

Progressive Types Of Cell Injury & Response

Investigating disease includes collating a clinical history, examination, offering a provisional diagnosis and providing a confirmation of diagnosis via diagnostic or lab investigation.





Cell injury can be caused by:

  • Physical trauma
  • Extreme temperatures 
  • Electrical disturbance  
  • Chemical or radiation poisoning 
  • Biological agents
  • Nutritional issues
Most of the above cause radical production, a decrease in oxygen delivery or an increase in calcium intercellular release. They could be either reversible or irreversible causing necrosis (cell/ tissue injury) or apoptosis (normal physiological process).

Hypoxia conditions can include:

  • Stroke
  • Brain trauma
  • Arteriosclerosis 
  • Injury leading to hypoxia
  • A decrease in ATP production 
  • An increase in sodium and H2O into cells
  • An increase in potassium outside the cell
  • Increased osmotic pressure
  • Vacuoles formed
  • Increased vaculation
  • Increased hydropic degradation 

Progressive types of cell injury and response 

Cellular adaptation - atrophy, hypertrophy, hyperplasia and metaplasia
Active cell injury - immediate response of the cell
Reversible - decreased ATP, oedema, detachment of ribosomes, autophagy of lysosomes
Irreversible- severe vasculation, Calcium moved into the cell, mitochondrial damage
Apoptosis - normal pathological programmed cell death
Chronic cell injury- subcellular alterations
Accumulations - H2O, pigments, lipids, glycogen and proteins
Pathological calcification- dystrophic and metastatic calcification 
Inflammation - a reaction of vascularized tissue to local injury
Non-specific - a defence response of the body, response to tissue damage 
1st line of defence - skin, epithelial cells of the GI tract
2nd line of defence - inflammation 




Types of necrosis

Necrosis involves oedema and breakdown of organelles including tissue damage via lysosomal enzymes
Coagulative necrosis - tissue appears swollen and firm, no autolysis
Liquefaction necrosis - neurons rich in hydrologic enzymes 
Casseous necrosis - tuberculosis and granulomas

Vascular defence sequence 

  1. Immediately there are pattern recognition receptors 
  2. Mast cells
  3. Granulocytes (neutrophils, eosinophils, basophils)
  4. Monocytes/ macrophages 
  5. NK cells
  6. Platelets 
  7. Endothelial cells
  8. No memory involved
  9. Peptides (complement, clotting factors and kinins)
  10. Four physical symptoms (redness and heat due to hyperaemia, increased blood flow, pain due to chemicals (bradykinin),  nerve pressure and damage and swelling due to increased capillary permeability and filtration

3 basic stages of inflammation


  1. Vascular response, 
  2. Emigration of phagocytes from blood to interstitial fluid & 
  3. Tissue repair 

Vascular Response 

  • Changes that occur in the region of tissue injury include:
  • Blood vessel dilation
  • Increased permeability in capillaries 
  • Increased blood flow to remove toxin and dead cells
  • Adherence of white blood cells to inner walls of blood vessels
  • Immediate
  • Swelling
  • Plasma moves out and blood flow slows as blood increases in viscosity
  • Increased blood flow and RBC count leading to redness
  • WBC adhere to capillary walls, biochemical mediators e.g histamine stimulates endothelial cells to retract and more plasma enters leading to swelling.

What substances are involved?

  • Histamine (basophils, platelets and mast cells)
  • Neutrophils attracted to injured site stimulates release of histamine kinins
  • Prostaglandins (lipids are released from damaged cells)
  • Leukotrienes
  • Result in vasodilation and increased 

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