Inflammation (-itis) Physiogical response to tissue injury

Beneficial effects Dilution of toxins Entry of antibodies Transport of drugs Fibrin formation Delivery of nutrients and oxygen Stimulation of immune response

Harmful effects Alteration = damage - digestion of normal tissue Swelling Inappropriate inflammatory response

Causation: mechanical, irradioation, chemical, toxic, infectious, immune Manifestation: local (Celsus signs) rubor (redness) calor (heat) dolor (pain) tumor (swelling) functio laese (loss of function) Systemic changes fever, leukocytosis, Ig, fatigue, loss of appetite, loss of weight, lymphadenitis, anemia Pyrogens bacterias IL1, 6, TNF

Cell type Main function Type of inflammation PMN eosinophils Phagocytosis, bacterial damage,fibrinolysis, (plasmin, trypsi, cathepsin) Phagocytosis of some immunocomplexes suppurative Allergic, parasitic, chronic a sign of recovery T- lymphocytes Inf. mediators, cytokines Viral, immune B- lymphocytes immunoglobulins Chronic, immune Plasma cells immunoglobulins Chronic, Histiocytes Mast cells Trombocytes Phagocytosis of larges particles, Mediators (heparin, histamin, serotonin, PAF) Serotonon, hepatrin, Ca++, fibrinogen, PDGF, hydrolases Granulomatous allergic most Fibroblasts FGF, VEGF, PDGF, proliferative

Margination, pavementing, rolling

Tissue changes Alteration Exsudation Proliferation

Classification A) According duration: acute (up to 2 weeks) subacute (2-6 weeks) chronic (more that 6 weks) B) According tissue changes alterative exudative proliferative C) According immune responce non-specific specific

1) Alterative inflammation predominates tissue damage, necrosis diphteric myocarditis fulminant hepatitis

2) Exsudative inflammation An exudate is any fluid that filters from the circulatory system into lesions or areas of inflammation. Its composition varies but generally includes water and the dissolved solutes of the main circulatory fluid such as sap or blood. In the case of blood: it will contain some or all plasma protein white blod cells, platelets and (in the case of local vascular damage) red blod cells. According type of exudate we recognise: serous lymphoplasmocytic purulent fibrinous gangrenous

Serous inflammations Serous exudate (sometimes classified as serous transudate) is usually seen in mild inflammation, with little protein content. Serous inflammations aa) Superficial seroses (pleuraitis, peritonitis) musoces (catarrhal triad edema, hyperemia, hypersecterion): Catarrhal exudate is seen in the nose and throat and is characterized by a high content of mucus skin (vesicular i.) bb) intersticial (urtica)

Lymfoplasmocytic (= non-purulent) Mostly immune or viral etiology aa) Superficial flu, meningitis, chronic inflam.) bb) Intersticial myocarditis, parotitis, viral pneumonias

Purulent inflammation Purulent or suppurative exudate consists of plasma with both active and dead neutrophils, fibrinogen, and necrotic parenchymal cells. This kind of exudate is consistent with more severe infections, and is commonly referred to as pus. aa) superficial (empyema, purulently- catarral bronchopenumonia, impetigo, foliculitis) bb) intersticial 1) Phlegmona (non- limited) fibrinolysins, hyaluronidase 2) Abscessus (acute, chronic-pyogenic membrane)

Spreading od purulent i.: Bacteriemia Sepsis (systemic symptoms) Pyemia (central peripheral portal umbilical

Fibrinous inflammation Fibrinous exudate is composed mainly of fibrinogen and fibrin. aa) Superficial (- pericarditis (uremia) pseudomembranous crupous diphteric escharotic (burn, injury,lye, acid) bb) Intersticial fibrinoid necrosis rheumatic fever

Fibrinous pericarditis kopie

Pseudomembranous inflammation

3) Proliferative inflammations A) Reparations early phase: non-specific granulation tissue (formed by proliferating fibroblasts, neoangiogenesis, macrophages) late phase: scarring B) Primarily proliferative i. fibromatoses polyserositis (Curshman disease)

Dupuytren's contracture

Acute inflammation

Chronic inflammation (Exceeding 6 weeks)

Characteristic Relatively insidious onset Prolonged course Slow resolution Cells: lymphocytes, plasma cells, macrophages x Acute i.(rapid onset and resolution, PMN)

Causes Progression from acute inflammation (persistent causal agents) delayed or inadequate drainage (abscess osteomyelitis) indigestible material (keratin, bone secvester, foreign body material /surgical suture/) Reccutent episodes of acute i. (chronic cholecystitis gallstones)

Causes Primary chronic inflammation (no initial phase of acute inflammation 1. resistence of infective agents to killing systems (TBC, leprosy viral i.) 2. Endogenous, exogenous material (necrosis, crystals, silica implantes prostheses) 3. Some autoimmune diseases (Hashimoto t., ch. gastritis, pernicious anemia, RA 4. Specific diseases of unknown etiology (chronic bowel disease) 5. Primary granulomatous i. (Crohn s disease, sarcoidosis)

Macroscopic features Fibrosis Wall thickening Adhesions (pleural, peritoneal cavity) Chronic abscessus cavity Surphace mucosa /skin changes atrophy, hypertrophy hypertrophic polyps

chronic abscessus

Microscopic features Chronic type of cell infiltrate (passsive x active, chronic active i.) Diffuse x granulomatous Granulation tissue Fibrosis (hyalinization) Epithelial metaplasia ( squamous cell cervix, bronchi, bladder leukoplakia intestinal (stomach, Barret esophagus ) glandular (bladder)

Progressive changes Regeneration restitutio ad integrum (identical tissue) labile cells (skin, blood cells, enterocytes 1-5 days stabile cells ( renal tubule cells 150 days) Postmitotic cells x stem cells Conditions: Preserved cambial layer basement membrane

Progressive changes Repair (not fully-valuable tissue) a wound is replaced by scar Primary intention x Secondary intention Local factors (type, size, location (well approximated wound x separeted edges), vascular supply, infection, movenent Systemic factors (age, circulation, malnutrition. hormones, drugs )