2 Inflammation complex protective reaction caused by various endo- and exogenous stimuliinjurious agents are destroyed, diluted or walled-offwithout inflammation and mechanism of healing could organism not survivecan be potentially harmfull
3 Terminology Greek root + -itis metritis, not uteritis kolpitis, not vaginitisnephritis, not renitisglossitis, not linguitischeilitis, not labiitis
4 Mechanisms A) local - mild injury B) systemic – severe injury 3 major changes1. alteration – tissue change2. exudation - inflammatory exudateliquid + proteins (exudate)cellular (infiltrate)3. proliferationformation of granulation and fibrous tissueusually - all 3 components - not the same intensity
5 Classification several points of view according to length acute × chronic (+ subacute, hyperacute)according to predominant component1. alterative2. exudative3. proliferative
6 Classification according to histological features non-specific (not possible to trace etiology) - vast majorityspecific / granulomatous (e.g. TBC)according to causative agentaseptic (sterile) - chemical substances, congelation, radiation - inflammation has a reparative characterseptic (caused by living organisms) - inflammation has a protective character
7 Acute inflammation early response important role in inflammation has microcirculation!supply of white blood cells, interleukins, fibrin, etc.
10 Vascular changes 1. arteriolar vasodilation (redness + warmth) 2. increased permeability of vesselswidened intercellular junctionsretraction of endothelial cells (histamin, VEGF, bradykinin)protein-poor transudate (edema)protein-rich exudate3. endothelial injury – direct x leukocyte-dependentproteolysis – protein leakage platelets adhesion thrombosis
11 Cellular eventsleukocytes margination rolling adhesion transmigration by diapedesis (in venules)transmigrationneutrophils (1-2 days)monocytes (2-3 days)chemotaxis (along chemical gradient)endogenous signaling molecules – ILs, LTs, C5aexogenous – toxins, bacterial proteins, ...phagocytosis (see below)passive migration of RBCsno active role in inflammation - hemorrhagic inflammation
12 Phagocytosis 1. recognition and attachment 2. engulfment facilitated by opsonins (IgG, C3b)2. engulfmentpseudopods formation phagocytic vacuole + lysosome phagolysosome3. killing and degradationoxidative burst – reactive oxygen metabolits – superoxide ion, hydrogen peroxide, hypochlorous radicalslysosomal acid hydrolasesin highly virulent microorganisms can die leukocyte and not the microbein highly resistant microorganisms - persistence within macrophage - activation after many years (TBC)
13 Outcomes of acute inflammation 1. resolution - restoration to normal, in limited injurychemical substances neutralizationnormalization of vascular permeabilityapoptosis of inflammatory cellsincreased lymphatic drainage2. healing by granulation tissue / fibrous scartissue destructionfibrinous inflammation adhesions, fibrosispurulent inflammation abscess formation (pus, pyogenic membrane, resorption - pseudoxanthoma cells - weeks to months)3. progression into chronic inflammation
17 Morphologic patterns of inflammation 2a. serousexcessive accumulation of fluid, few proteinse.g. skin blister, serous membranes - initial phases of inflammation, effusionsmodification - catarrhal - accumulation of mucus on mucosas - larynx2b. fibrinoushigher vascular permeability - exudation of fibrinogen -> fibrinformation of pseudomembranes - fibrin, necrotic mucosa, etiologic agens, leukocytese.g. diphtheria - Corynebacterium, dysentery – Shigella spp., Cl. difficilee.g. pericarditis (cor villosum, cor hirsutum - "hairy" heart)e.g. lobar pneumonia – Str. pneumoniaefibrinolysis resolutionorganization fibrosis scar, adhesions
18 pyogenic bacteria - Staphylococci interstitial 2c. suppurative (purulent) - accumulation of neutrophillic leukocytes - formation of puspyogenic bacteria - Staphylococciinterstitialphlegmone – diffuseabscess - localized collectionacute – border – surrounding tissuechronic – border - pyogenic membranepseudoabscess – pus in lumen of hollow organ (epithelium)formation of suppurative fistuleaccumulation of pus in preformed cavities - empyema (gallbladder, thoracic cavity)
19 complications of suppurative inflammation bacteremia no clinical symptoms!formation of secondary foci of inflamm. (endocarditis, meningitis)sepsis = massive bacteremiaseptic fever, activation of spleen, septic shockthrombophlebitissecondary inflammation of vein wall followed by thrombosis - embolizationpyemia - hematogenous abscesses (infected infarctions)lymphangiitis, lymphadenitis
20 inflammatory necrosis of the surface - ulcer (skin, stomach) 2d. necrotizinginflammatory necrosis of the surface - ulcer (skin, stomach)gangrenous - secondary modification by bacteria - apendicitis, cholecystitis - risk of perforation – peritonitis2e. non-purulentround cell inflammatory infiltrate
21 Granulomatous inflammation distinctive chronic inflammation typecell mediated immune reaction (delayed)aggregates of activated macrophages epithelioid cell multinucleated giant cells (of Langhans type x of foreign body type)lymphocytic rimNO agent elimination but walling offintracellulary agents (TBC) x inert foreign bodies
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