1inflammation

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1inflammation

  1. 1. Inflammation Jan Laco, M.D., Ph.D.
  2. 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. 3. Terminology  Greek root + -itis  metritis, not uteritis  kolpitis, not vaginitis  nephritis, not renitis
  4. 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. 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. 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. 7. Acute inflammation  important role in inflammation has microcirculation!  supply of white blood cells, interleukins, fibrin, etc.
  8. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 27. Syphilis  2. secondary syphilis - contagious  after 2 months  generalized lymphadenopathy + various mucocutaneous lesions  condylomata lata - anogenital region, inner thighs, oral cavity
  28. 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. 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

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