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1inflammation (2)

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  • 1. InflammationInflammation Jan Laco, M.D., Ph.D.
  • 2. InflammationInflammation 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. TerminologyTerminology Greek root + -itis metritis, not uteritis kolpitis, not vaginitis nephritis, not renitis
  • 4. MechanismsMechanisms  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. ClassificationClassification  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. ClassificationClassification  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 inflammationAcute inflammation important role in inflammation has microcirculation! supply of white blood cells, interleukins, fibrin, etc.
  • 8. Local symptomatologyLocal 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 symptomatologySystemic 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 changesVascular 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 eventsCellular 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. PhagocytosisPhagocytosis 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 inflammationOutcomes 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 inflammationChronic 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 inflammationChronic 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 ofMorphologic patterns of inflammationinflammation  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 ofMorphologic patterns of inflammationinflammation  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 inflammationGranulomatous 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 inflammationGranulomatous 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 – generalTuberculosis – general pathologypathology  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. LeprosyLeprosy  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. SyphilisSyphilis  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. SyphilisSyphilis 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. SyphilisSyphilis 2. secondary syphilis - contagious after 2 months generalized lymphadenopathy + various mucocutaneous lesions condylomata lata - anogenital region, inner thighs, oral cavity
  • 28. SyphilisSyphilis  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 syphilisCongenital 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