Pathology Lecture 4: Inflammation PDF

prof.Marwa Mosaad Head of Pathology dep.BUC Professor of pathology ASU Resources  USMLE step 1 lecture notes in pathology page 15-24 MM shakweer ILOs Define inflammation Differentiate between acute and chronic inflammation Explain mechanism of acute inflammation List type...

prof.Marwa Mosaad Head of Pathology dep.BUC Professor of pathology ASU Resources  USMLE step 1 lecture notes in pathology page 15-24 MM shakweer ILOs Define inflammation Differentiate between acute and chronic inflammation Explain mechanism of acute inflammation List types of acute inflammation and give examples Recognize signs of acute inflammation Explain pathogenesis of suppurative inflammation Identify fates of acute inflammation Compare between acute and chronic inflammation MM shakweer It is a vital process by which living tissues react to injury as a protective response to localize and eliminate MM shakweer  Types of Inflammation Acute Chronic ▪ Rapid onset ▪ Gradual ▪ Short duration (minutes- ▪ Longer (days-years) days) ▪  productive (granulation ▪  exudative tissue) ▪ fibrosis MM shakweer  Acute inflammation MM shakweer  Causes Physical : Chemicals: Infective: Trauma acids & alkalies bacteria, heat viruses, cold parasites irradiation fungi Tissue injury Inflammation MM shakweer  A. Acute inflammation Reactive changes in the first few minutes after tissue injury 1. Vascular changes including: Vasoconstriction followed by vasodilatation Increased permeability 2. Leucocyte emigration: from the microcirculation & accumulation in the focus of injury MM shakweer  Vascular changes A]Changes in vascular caliber & blood flow (local vascular phenomenon) 1- Constriction of arterioles direct vascular smooth muscle response to injurious stimulus resolves within seconds to minutes 2-Dilatation of arterioles → redness & hotness 3- Stasis B] Increased vascular permeability d.t the effect of chemical mediators on the arterioles, capillaries, post capillary venules → Inflammatory exudate →swelling of MM shakweer the affected site  Leucocyte emigration 1-Leucocyte margination 2-Rolling 3- adhesion (selectin) (integrin) 4- transmigration 5- chemotaxis 6- phagocytosis MM shakweer N.B: Some RBCs come out through inter endothelial gaps (Diapedesis) Chemotaxis Certain bacterial products & inflammatory substances (chemotaxins) are able to attract leucocytes towards them Phagocytosis PNL & macrophages ingest bacteria & foreign particles →digested by their lysosomal enzymes Opsonization: -Recognition of and attachment of organisms to leucocytes -Coat bacteria and facilitate their phagocytosis -Most important opsonins are IgG and C3b Agglutinins: Fix pathogens to facilitate phagocytosis MM shakweer MM shakweer  Inflammatory exudate Pathogenesis Vascular permeability Arteriolar V.D Osm.pr. of IFd.t splitting of pr. mol. into ones Fluid Cells Plasma fluid rich in fibrinogen Neutrophils Macrophages (subjected to clotting, Ptn.4gm%, Sp.gr.1018) 1.Dilute bacterial toxins 1- Phagocytosis 2.Bring abs. to area of inflammation 2- Killed PNLs (pus cells) -Bacteriolysins -Agglutinins Proteolytic enzymes -Opsonins 3. Fibrinogen fibrin Liquefy necrotic debris -Facilitate leukocyte movement -Localize infection MM shakweer Prepare area for repair Chemical mediators of inflammation  Types: vasodilatation Histamine, PG, NO a) Cell derived mediators Increased vascular Histamine, permeability serotonin, b) Plasma derived substance P, mediators bradykinin Leukocyte C3a, C5a recruitment fever IL1, TNF, PG pain PG, bradykinin MM shakweer Signs of acute inflammation Red Hot Local Pain Swelling Loss of function fever leukocytosis systemic MM shakweer  Local signs in acute inflammation: Redness Hotness Swelling Pain d.t stretching of tissues by inflammatory exudates with irritation of nerve endings Loss of function MM shakweer Types of acute inflammation Non suppurative suppurative Allergic Localized (allergic (abscess) nasal polyp) Diffuse Serofibrinous (cellulitis (acute lobar &empyema) pneumonia) Membranous (diphtheria) MM shakweer A-Non suppurative inflammation 1-Serous inflammation: cc by :excessive clear watery fluid exudates with: ↓protein content ↓cellular content e.g.:- Blister following skin burns - Vesicles of herpes simplex - Inflammation of serous cavities e.g. pleurisy MM shakweer 2-Serofibrinous inflammation: Exaudate: Rich in serous fluid & fibrin Ex. -Serous sacs -Lung alveoli in acute lobar pneumonia -gross : bread and butter appearance - fate: resolution or organization 3-Catarrhal inflammation: Exaudate: Excess mucous secretion Ex. Common cold MM shakweer 4-Membranous inflammation: Examples 1-Diphtheria 2-Bacillary dysentery Pathogenesis Bacteria remains on the mucosal surface → powerful exotoxin → patchy necrosis Exotoxin→ diffuse to s.m → acute inflammation → exudates rich in fibrin → mixes with necrotic parts of mucosa membrane Grossly: Greyish white dirty and loosely attached and can be easily removed. Microscopically: membrane is formed of: necrotic mucosa, fibrin, polymorphs, red blood cells, causative organism MM shakweer 5-Allergic inflammation: Cause Exudates: excess Tissue & blood eosinophilia Ex. -Eczema -Urtecaria -Allergic rhinitis -Nasal polyps -Bronchial asthma 6-Haemorrhagic inflammation 7-Necrotizing inflammation MM shakweer B- Suppurative inflammation: Pathogenesis of pus formation: -Pyogenic organisms→ marked tissue destruction -Many PNL are killed by bacteria → pus cells → proteolytic enzymes→ liquefaction of necrotic tissue → fluid material mixes up with elements of inflammatory exudate→ pus Composition of pus 1. Living and dead microorganisms 2. Liquefied necrotic tissue. 3. PNL and, many pus cells, as well as 4. MCs and RBCs. 5. Inflammatory fluid exudates MM shakweer Localized suppurative inflammation ABCESS -Definition: Localized suppurative inflammation →cavity containing pus -Cause Pyognic bacteria as staph. aureus strept. pyogenes -Site Sct (most common) MM shakweer -The abscess enlarges by further necrosis & liquefaction of the surrounding inflamed zone until staph produce coagulase enzyme which helps localization -The tension inside the abscess cavity gradually ↑d.t increase in the amount of fluid →increased tension →pain -The abscess always tries to open & discharge its contents outside Abscess in sct → narrow tract which connects abscess cavity with surface outside (sinus) (blind end deeply & open end on the surface ) MM shakweer Furuncle (boil) Small abscess Related to hair follicle or sebaceous gland Caused by Staph. Site: Face, back of neck ,axilla Carbuncle Multiple loculi of pus separated by fibrous tissue strands Open on the surface by multiple openings Site: Back of neck & scalp Common P.F → D.M Causative organism → Staph. aureus MM shakweer  Abscess “Complications” -Chronic abscess: if acute abscess is not drained -Blood spread: toxaemia, septicaemia, pyaemia -Lymphatic spread: lymphangitis, lymphadenitis -Complications of healing: ulcer, keloid, sinus fistula Skin Ulcer MM shakweer Definition: Fistula Abnormal tract lined by septic granulation tissue connecting 2 cavities or between hollow viscera & the surface Differs from sinus Types: Congenital→thyroglossal fistula Inflammatory→appendicular Neoplastic →vesicovaginal MM shakweer Definition: Cellulitis Diffuse type of suppurative inflammation Sites: sct→ cellulitis Mm → Phlegmonous inflammation Cause Streptococci secrete →fibrinolysins, streptokinase, hyaluronidase →spread of infection Ccc Pus is less common & contains blood Inflamed area………….. MM shakweer  Fate of Acute Inflammation Healing/Repair Tissue destruction and scarring Acute Chronicity Inflammatio Resolution n Injurious agent persists (TB) Interference with healing Restoration of normalcy Progression - Local -Lymphatic (lymphangitis and lymphadenitis) -Blood (bacteraemia, septicaemia, pyaemia) MM shakweer - Natural passages (ureter)  B. Chronic inflammation: If persists for weeks or months after initial injury Cause: -Progression from acute inflammation -Recurrent episodes of acute inflammation -Chronic inflammation de novo Types: 1-Chronic non specific inflammation 2-Chronic specific inflammation (granulomas) MM shakweer  Differences between acute & chronic inflammation Acute inflammation Chronic inflammation Onset Sudden Gradual Duration Short Long Vascular phenomenon Prominent Less prominent Local (cardinal)signs Prominent Less prominent Toxaemia Acute Chronic Microscopy: a) Cells PNLs.MCs Lymphocytes, plasma cs, ,fbl b) B.Vs Thin-walled, dilated EAO c) Inflam.reaction Exudative Productive Parenchymal organs Cloudy swelling Amyloidosis Fate: Healing Fibrosis Progression MM shakweer Chronic Assignment 4  Attach a link from youtube illustrating the process of leukocyte emigration  Copy and paste the URL in the assignment box MM shakweer Thank you