1 inflammation
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Transcript of 1 inflammation
InflammationInflammation
Jan Laco, M.D., Ph.D.
InflammationInflammation
complex protective reactioncaused 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
TerminologyTerminology
Greek root + -itismetritis, not uteritiskolpitis, not vaginitisnephritis, not renitis
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
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)
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
Acute inflammationAcute inflammation
important role in inflammation has microcirculation!
supply of white blood cells, interleukins, fibrin, etc.
Local symptomatologyLocal symptomatology
classical 5 symptoms (Celsus 1st c. B.C., Virchow 19th c. A.D.)
1. calor - heat2. rubor - redness3. tumor - swelling4. dolor - pain5. functio laesa - loss (or impairment) of
function
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)
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
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
PhagocytosisPhagocytosis
adhesion and invagination into cytoplasmengulfmentlysosomes - destructionin highly virulent microorganisms can die
leucocyte and not the microbein highly resistant microorganisms -
persistence within macrophage - activation after many years
Outcomes of acute Outcomes of acute inflammationinflammation
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
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)
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)
Morphologic patterns of Morphologic 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)
Morphologic patterns of Morphologic 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
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)
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
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
Granulomatous inflammationGranulomatous 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)
NO agent elimination but walling offintracellulary agents (TBC)
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
Tuberculosis – general Tuberculosis – 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)
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
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
SyphilisSyphilis
1. primary syphilis - contagiouschancre (ulcus durum, hard chancre)M: penis x F: vagina, cervixpainless, firm ulceration + regional painless
lymphadenopathyspontaneous resolve (weeks) scar
SyphilisSyphilis
2. secondary syphilis - contagiousafter 2 monthsgeneralized lymphadenopathy + various
mucocutaneous lesionscondylomata lata - anogenital region, inner
thighs, oral cavity
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
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