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44. Inflammation stages, main signs and types.

Main signs:

  1. oedema – tumor; 2) reddish (rubor); 3) heat, ardour, fever –calor; 4) pain – dolor; 5) dysfunction – functio laesa. These features are known as pentade of Cels-Galen.

Stages:

  1. alteration;

  2. microcirculation disorders with exsudation and emigration;

  3. proliferation.

Doctor must remember that these stages are not always consequent and can interfere one another.

Inflammation types (continuation).

I. Dependently on exsudate character:

  1. haemorhagic;

  2. purulent;

  3. decoy;

  4. serose et al.

II. Dependently on sepsis development:

    1. septic;

    2. aseptic.

45. Primary and secondary alteration.

Primary alteration – tissue injury due to flogogenic agents direct action.

Secondary alteration – tissue injury which occurs due to action of factors being formed as primary alteration result.

Secondary alteration developmental factors:

  1. Inflammation mediators (lyzosomal factors, activated complement, lymphokines-lymphotoxins).

  2. Free radicals and peroxides.

  3. Hypoxy occurring as a result of circulation local disorders.

  4. Local acidosis.

  5. Osmotic and oncotic pressure increasing in inflammation locus (as a result of protein level increasing, its dispersity and hydrophyly).

  6. Hyperiony – accumulation such ions as K+, Cl-, HPO4-, Na+.

  7. Dysiony.

46. Mediators and antimediators.

According to the source:

    1. Cellular:

    1. From polymorphic-nuclear leucocytes, mainly neutrophils and basophils:

      1. highly-active lysosomal hydrolases;

      2. cationic proteins;

      3. prostaglandines;

      4. leucotriens;

      5. interleukines;

      6. biogenic amines.

Eosinophils participate in oxidants and leucotriens detoxication. They play essential role in inflammation allergy component.

  1. From mononuclears (lymphocytes, monocytes, tissular macrophags):

      1. lymphokines;

      2. monokines;

      3. neutral proteases;

      4. estherases;

      5. acid phosphatases and others.

  2. From platelets:

      1. adhesive proteins;

      2. ADP;

      3. serotonine;

      4. lysosomal enzymes;

      5. Willebrand’s factor.

  3. From labrocytes (adipocytes):

      1. biogenic amines;

      2. platelet activation factor;

      3. leucotriens (C4 and D4) are compounds of anaphylaxy slow-reacting substance (ASRS);

      4. eosinophilic chemotactic factor;

      5. neutrophilic chemotactic factor;

      6. heparine and others.

  4. Other cells of injured tissue:

      1. lysosomal enzymes;

      2. prostaglandines;

      3. lipids peroxidative oxidation products et al.

    1. Plasmic – from blood:

      1. complement system components;

      2. kinines;

      3. blood coagulation system factors.

According to mediators nature:

  1. Biogenic amines:

    1. histamine;

    2. serotonine and others.

  2. Active polypeptides and proteins:

    1. kinines (bradykinine, kallydine, methyonyl-lysyl-bradykinine);

    2. complement system components;

    3. enzymes (mainly lysosomal);

    4. leucocytic proteinic factors (cationic proteins, interleukine-1, monokines, lymphokines).

  3. Polysaturated fatty acids (arahidonic, linolic) derivates:

    1. prostaglandines (E, I2 or prostacycline);

    2. thromboxanes;

    3. leucotrienes;

    4. lipids free-radical peroxidative oxidation products.

Antimediators – 1) glucocorticoids decrease alteration, arachidonic acid and its derivation synthesis (decreasing of exsudation and leucocytes emigration, microcirculation disorders weakening); cellular division and protein biosynthesis inhibiting by glucocorticoids leads to proliferation decreasing in inflammation focus;

    1. proteases inhibitors;

    2. histaminase – it is in eosinophils (it decomposes histamine released from basophils)…

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