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1 inflammation Presentation Transcript

  • 1. Inflammation Jan Laco, M.D., Ph.D.
  • 2. Inflammation
    • complex protective reaction
    • caused by various endo- and exogenous stimuli
    • injurious agents are destroyed, diluted or walled-off
    • without inflammation and mechanism of healing could organism not survive
    • can be potentially harmfull
  • 3. Terminology
    • Greek root + -itis
    • metritis, not uteritis
    • kolpitis, not vaginitis
    • nephritis, not renitis
  • 4. Mechanisms
    • local - in cases of mild injury
    • systemic
    • 3 major:
    • 1. alteration
    • 2. exsudation - inflammatory exsudate
      • liquid (exsudate)
      • cellular (infiltrate)
    • 3. proliferation (formation of granulation and fibrous tissue)
    • usualy - all 3 components - not the same intensity
  • 5. Classification
    • several points of view
    • length:
      • acute × chronic (+ subacute, hyperacute)
    • according to predominant component
      • 1. alterative (predominance of necrosis - diphtheria)
      • 2. exsudative (pleuritis)
      • 3. proliferative (cholecystitis - thickening of the wall by fibrous tissue)
  • 6. Classification
    • according to histological features
      • nonspecific (not possible to trace the etiology) - vast majority
      • specific (e.g. TB)
    • according to causative agent
      • aseptic (sterile) - chemical substances, congelation, radiation - inflammation has a reparative character
      • septic (caused by living organisms) - inflammation has a protective character
  • 7. Acute inflammation
    • important role in inflammation has microcirculation!
    • supply of white blood cells, interleukins, fibrin, etc.
  • 8. Local symptomatology
    • classical 5 symptoms (Celsus 1st c. B.C., Virchow 19th c. A.D.)
    • 1. calor - heat
    • 2. rubor - redness
    • 3. tumor - swelling
    • 4. dolor - pain
    • 5. functio laesa - loss (or impairment) of function
  • 9. Systemic symptomatology
    • fever (irritation of centre of thermoregulation)
      • TNF, IL-1
      • IL-6 – high erythrocyte sedimentation rate
    • leucocytosis - increased number of WBC
      • bacteria – neutrophils
      • parasites – eosinophils
      • viruses - lymphocytosis
    • leucopenia - decreased " "
      • viral infections, salmonella infections, rickettsiosis
    • immunologic reactions - increased level of some substances (C-reactive protein)
  • 10. Vascular changes
    • vasodilation
      • increased permeability of vessels due to widened intercell. junctions and contraction of endothelial cells (histamin, VEGF, bradykinin)
    • protein poor transudate (edema)
    • protein rich exsudate
    • leukocyte-dependent endothelial injury
      • proteolysis – protein leakage
    •  platelet adhesion  thrombosis
  • 11. Cellular events
    • leukocytes margination  rolling  adhesion  transmigration
    • emigration of:
      • neutrophils (1-2 days)
      • monocytes (2-3 days)
    • chemotaxis
      • endogenous signaling molecules - lymphokines
      • exogenous - toxins
    • phagocytosis - lysosomal enzymes, free radicals, oxidative burst
    • passive emigration of RBC - no active role in inflamm. - hemorrhagic inflammation
  • 12. Phagocytosis
    • adhesion and invagination into cytoplasm
    • engulfment
    • lysosomes - destruction
    • in highly virulent microorganisms can die leucocyte and not the microbe
    • in highly resistant microorganisms - persistence within macrophage - activation after many years
  • 13. Outcomes of acute inflammation
    • 1. resolution - restoration to normal, limited injury
      • chemical substances neutralization
      • normalization of vasc. permeability
      • apoptosis of inflammatory cells
      • lymphatic drainage
    • 2. healing by scar
      • tissue destruction
      • fibrinous inflammtion
      • purulent infl.  abscess formation (pus, pyogenic membrane, resorption - pseudoxanthoma cells - weeks to months)
    • 3. progression into chronic inflammation
  • 14. Chronic inflammation
    • reasons:
      • persisting infection or prolonged exposure to irritants (intracell. surviving of agents - TBC)
      • repeated acute inflamations (otitis, rhinitis)
      • primary chronic inflammation - low virulence, sterile inflammations (silicosis)
      • autoimmune reactions (rheumatoid arthritis, glomerulonephritis, multiple sclerosis)
  • 15. Chronic inflammation
    • chronic inflammatory cells ("round cell" infiltrate)
      • lymphocytes
      • plasma cells
      • monocytes/macrophages activation of macrophages by various mediators - fight against invaders
    • lymphocytes  plasma cells, cytotoxic (NK) cells, coordination with other parts of immune system
    • plasma cells - production of Ig
    • monocytes-macrophages-specialized cells (siderophages, gitter cells, mucophages)
  • 16. Morphologic patterns of inflammation
    • 1. alterative
    • 2. exsudative
      • 2a. serous
      • 2b. fibrinous
      • 2c. suppurative
      • 2d. pseudomembranous
      • 2e. necrotizing, gangrenous
    • 3. proliferative
      • primary (rare) x secondary (cholecystitis)
  • 17. Morphologic patterns of inflammation
    • 2a. serous - excessive accumulation of fluid, few proteins - skin blister, serous membranes - initial phases of inflamm.
    • modification - catarrhal - accumulation of mucus
    • 2b. fibrinous - higher vascular permeability - exsudation of fibrinogen -> fibrin - e.g. pericarditis (cor villosum, cor hirsutum - "hairy" heart
    • fibrinolysis  resolution; organization  fibrosis  scar
  • 18.
    • 2c. suppurative (purulent) - accumulation of neutrophillic leucocytes - formation of pus (pyogenic bacteria)
    • interstitial
      • phlegmone – diffuse soft tissue
      • abscess - localized collection
        • acute – border – surrounding tissue
        • chronic – border - pyogenic membrane
        • Pseudoabscess – pus in lumen of hollow organ
    • formation of suppurative fistule
    • accumulation of pus in preformed cavities - empyema (gallbladder, thoracic)
  • 19.
    • complications of suppurative inflamm.:
    • bacteremia (no clinical symptoms!; danger of formation of secondary foci of inflamm. (endocarditis, meningitis)
    • sepsis (= massive bacteremia) - septic fever, activation of spleen, septic shock
    • thrombophlebitis - secondary inflammation of wall of the vein with subsequent thrombosis - embolization - pyemia - hematogenous abscesses (infected infarctions)
    • lymphangiitis, lymphadenitis
  • 20.
    • 2d. pseudomembranous - fibrinous pseudomembrane (diphtheria - Corynebacterium, dysentery - Shigella) - fibrin, necrotic mucosa, etiologic agens, leucocytes
    • 2e. necrotizing - inflammatory necrosis of the surface - ulcer (skin, gastric)
      • gangrenous - secondary modification by bacteria - wet gangrene - apendicitis, cholecystitis - risk of perforation - peritonitis
  • 21. Granulomatous inflammation
    • distinctive chronic inflammation type
    • cell mediated immune reaction (delayed)
    • aggregates of activated macrophages  epithelioid cell  multinucleated giant cells (of Langhans type x of foreign body type)
    • NO agent elimination but walling off
    • intracellulary agents (TBC)
  • 22. Granulomatous inflammation
    • 1. Bacteria
      • TBC
      • leprosy
      • syphilis (3rd stage)
    • 2. Parasites + Fungi
    • 3. Inorganic metals or dust
      • silicosis
      • berylliosis
    • 4. Foreign body
      • suture (Schloffer „tumor“), breast prosthesis
    • 5. Unknown - sarcoidosis
  • 23. Tuberculosis – general pathology
    • 1. TBC nodule – proliferative
    • Gross: grayish, firm, 1-2 mm (milium)  central soft yellow necrosis (cheese-like – caseous)  calcification
    • Mi: central caseous necrosis (amorphous homogenous + karyorrhectic powder) + macrophages  epithelioid cells  multinucleated giant cells of Langhans type + lymphocytic rim
    • 2. TBC exsudate – sero-fibrinous exsudate (macrophages)
  • 24. Leprosy
    • M. leprae, Asia, Africa
    • in dermal macrophages and Schwann cells
    • air droplets + long contact
    • rhinitis, eyelid destruction, facies leontina
    • 1. lepromatous – infectious
      • skin lesion – foamy macrophages (Virchow cells) + viscera
    • 2. tuberculoid – steril
      • in peripheral nerves – tuberculoid granulomas - anesthesia
    • death – secondary infections + amyloidosis
  • 25. Syphilis
    • Treponema pallidum (spichochete)
    • STD + transplacental fetus infection
    • acquired (3 stages) x congenital
    • basic microspical appearance:
      • 1. proliferative endarteritis (endothelial hypertrophy  intimal fibrosis  local ischemia) + inflammation (plasma cells)
      • 2. gumma – central coagulative necrosis + specific granulation tissue + fibrous tissue
  • 26. Syphilis
    • 1. primary syphilis - contagious
    • chancre (ulcus durum, hard chancre)
    • M: penis x F: vagina, cervix
    • painless, firm ulceration + regional painless lymphadenopathy
    • spontaneous resolve (weeks)  scar
  • 27. Syphilis
    • 2. secondary syphilis - contagious
    • after 2 months
    • generalized lymphadenopathy + various mucocutaneous lesions
    • condylomata lata - anogenital region, inner thighs, oral cavity
  • 28. Syphilis
    • 3. tertiary syphilis
    • after long time (5 years)
    • 1) cardiovascular - syphilitic aortitis (proximal a.)
      • endarteritis of vasa vasorum  scaring of media  dilation  aneurysm
    • 2) neurosyphilis – tabes dorsalis + general paresis
      • degeneration of posterior columns of spinal cord  sensory + gait abnormality
      • cortical atrophy  psychic deterioration
    • 3) gumma – ulcerative lesions of bone, skin, mucosa – oral cavity
  • 29. Congenital syphilis
    • 1) abortus
      • hepatomegaly + pancreatitis + pneumonia alba
    • 2) infantile syphilis
      • chronic rhinitis (snuffles) + mucocutaneous lesions
    • 3) late (tardive, congenital) syphilis
      • > 2 years duration
      • Hutchinson triad – notched central incisors + keratitis (blindness) + deafness (injury of n. VIII)
      • mulberry molars + saddle nose