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Inflammation Jan Laco, MD, PhD. Inflammation complex protective reaction caused by various endo- and exogenous stimuli injurious agents are destroyed,

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Presentation on theme: "Inflammation Jan Laco, MD, PhD. Inflammation complex protective reaction caused by various endo- and exogenous stimuli injurious agents are destroyed,"— Presentation transcript:

1 Inflammation Jan Laco, MD, PhD

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 glossitis, not linguitis cheilitis, not labiitis

4 Mechanisms A) local - mild injury B) systemic – severe injury 3 major changes 1. alteration – tissue change 2. exudation - inflammatory exudate – liquid + proteins (exudate) – cellular (infiltrate) 3. proliferation – formation of granulation and fibrous tissue usually - all 3 components - not the same intensity

5 Classification several points of view according to length – acute × chronic (+ subacute, hyperacute) according to predominant component – 1. alterative – 2. exudative – 3. proliferative

6 Classification according to histological features – non-specific (not possible to trace etiology) - vast majority – specific / granulomatous (e.g. TBC) 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 early response important role in inflammation has microcirculation! supply of white blood cells, interleukins, fibrin, etc.

8 Local symptomatology classical 5 symptoms (Celsus, 1st c. BC) 1. calor – heat, warmth 2. rubor – redness, erythema 3. tumor – swelling, edema 4. dolor - pain 5. functio laesa – function loss/impairment

9 Systemic symptoms fever (irritation of thermoregulatory centre) – TNF, IL-1 – IL-6 – high RBCs sedimentation rate (via fibrinogen) leukocytosis - increased WBCs number – bacteria – neutrophils – parasites – eosinophils – viruses - lymphocytosis leukopenia - decreased WBCs number – viral infections, salmonella infections, rickettsioses immunologic reactions – “acute phase reactants“ – C-reactive protein, complement, SAA, fibrinogen,...

10 Vascular changes 1. arteriolar vasodilation (redness + warmth) 2. increased permeability of vessels – widened intercellular junctions – retraction of endothelial cells (histamin, VEGF, bradykinin) – protein-poor transudate (edema) – protein-rich exudate 3. endothelial injury – direct x leukocyte-dependent – proteolysis – protein leakage –  platelets adhesion  thrombosis

11 Cellular events leukocytes margination  rolling  adhesion  transmigration by diapedesis (in venules) transmigration – neutrophils (1-2 days) – monocytes (2-3 days) chemotaxis (along chemical gradient) – endogenous signaling molecules – ILs, LTs, C5a – exogenous – toxins, bacterial proteins,... phagocytosis (see below) passive migration of RBCs – no active role in inflammation - hemorrhagic inflammation

12 Phagocytosis 1. recognition and attachment – facilitated by opsonins (IgG, C3b) 2. engulfment – pseudopods formation  phagocytic vacuole + lysosome  phagolysosome 3. killing and degradation – oxidative burst – reactive oxygen metabolits – superoxide ion, hydrogen peroxide, hypochlorous radicals – lysosomal acid hydrolases in highly virulent microorganisms can die leukocyte and not the microbe in highly resistant microorganisms - persistence within macrophage - activation after many years (TBC)

13 Outcomes of acute inflammation 1. resolution - restoration to normal, in limited injury – chemical substances neutralization – normalization of vascular permeability – apoptosis of inflammatory cells – increased lymphatic drainage 2. healing by granulation tissue / fibrous scar – tissue destruction – fibrinous inflammation  adhesions, fibrosis – purulent inflammation  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 inflammations (otitis, rhinitis) – primary chronic inflammation - low virulence, sterile inflammations (silicosis) – autoimmune reactions (rheumatoid arthritis, glomerulonephritides, multiple sclerosis)

15 Chronic inflammation chronic inflammatory cells ("round cell" infiltrate) – lymphocytes (T and B), plasma cells – eosinophils – parasites, allergies – monocytes / macrophages activation by various mediators - fight against invaders B lymphocytes  plasma cells, Ig production NK cells monocytes-macrophages specialized cells (siderophages, gitter cells, mucophages)

16 Morphologic patterns of inflammation 1. alterative – poliomyelitis anterior acuta, diphtherial myocarditis 2. exudative – 2a. serous – 2b. fibrinous – 2c. suppurative – 2d. necrotizing, gangrenous – 2e. non-purulent 3. proliferative – primary (rare) x secondary (cholecystitis)

17 Morphologic patterns of inflammation 2a. serous – excessive accumulation of fluid, few proteins – e.g. skin blister, serous membranes - initial phases of inflammation, effusions – modification - catarrhal - accumulation of mucus on mucosas - larynx 2b. fibrinous – higher vascular permeability - exudation of fibrinogen -> fibrin – formation of pseudomembranes - fibrin, necrotic mucosa, etiologic agens, leukocytes – e.g. diphtheria - Corynebacterium, dysentery – Shigella spp., Cl. difficile – e.g. pericarditis (cor villosum, cor hirsutum - "hairy" heart) – e.g. lobar pneumonia – Str. pneumoniae – fibrinolysis  resolution – organization  fibrosis  scar, adhesions

18 2c. suppurative (purulent) - accumulation of neutrophillic leukocytes - formation of pus pyogenic bacteria - Staphylococci interstitial – phlegmone – diffuse – abscess - localized collection acute – border – surrounding tissue chronic – border - pyogenic membrane pseudoabscess – pus in lumen of hollow organ (epithelium) formation of suppurative fistule accumulation 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 bacteremia – septic fever, activation of spleen, septic shock thrombophlebitis – secondary inflammation of vein wall followed by thrombosis - embolization – pyemia - hematogenous abscesses (infected infarctions) lymphangiitis, lymphadenitis

20 2d. necrotizing inflammatory necrosis of the surface - ulcer (skin, stomach) gangrenous - secondary modification by bacteria - apendicitis, cholecystitis - risk of perforation – peritonitis 2e. non-purulent – round cell inflammatory infiltrate

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) lymphocytic rim NO agent elimination but walling off intracellulary agents (TBC) x inert foreign bodies

22 Granulomatous inflammation 1. Bacteria – TBC – leprosy – syphilis (3rd stage - gumma) 2. Parasites + Fungi 3. Inorganic metals or dust – silicosis – berylliosis 4. Foreign body – suture (Schloffer “tumor“), breast prosthesis, vascular graft 5. Unknown – – sarcoidosis, Wegener´s granulomatosis, Crohn disease

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 exudate – sero-fibrinous exudate (macrophages)

24 Leprosy M. leprae, Asia, Africa in dermal macrophages and Schwann cells air droplets + long contact rhinitis, eyelid destruction, facies leontina 1. lepromatous – contagious – skin lesion – foamy macrophages (Virchow cells) + viscera 2. tuberculoid – sterile – in peripheral nerves – tuberculoid granulomas - anesthesia death – secondary infections + amyloidosis

25 Syphilis Treponema pallidum (spirochete) STD + transplacental fetus infection acquired (3 stages) x congenital basic microscopic 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 (thoracic aorta) 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


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