Inflammation 2

Local signs in acute inflammation: 1-Redness 2-Hotness 3-Swelling 4-Pain 5-Loss of function Pain; is due to: Stretching of tissue by inflammatory exudate with irritation of nerve endings. Release of mediators as prostaglandins and bradykinin

Morphology of acute inflammation severity of the inflammatory response its specific cause tissue involved Morphology of acute inflammation modify the basic, producing distinctive appearances. The vascular and cellular reactions that characterize acute inflammation are reflected in the morphologic appearance of the reaction. The severity of the inflammatory response, its specific cause, and the particular tissue involved can all modify the basic morphology of acute inflammation, producing distinctive appearances

Morphological patterns of acute inflammation I-Non suppurative inflammation II-Suppurative inflammation

Morphological patterns of acute inflammation I-Non suppurative inflammation Serous Fibrinous Catarrhal Allergic Pseudomembranous Necrotizing Hgic

vesicles in herpes pericardial effussion 1-Serous inflammation Exudate: Watery Abundunt protein poor Examples: Skin blister vesicles in herpes pericardial effussion Depending upon the site of injury, this fluid is derived either from the serum or from the secretions of mesothelial cells lining the peritoneal, pleural, and pericardial cavities e.g.

2-Fibrinous inflammation More severe injury greater vascular permeability large molecules (such as fibrinogen) to pass through endothelial barrier Serous sacs. Lung alveoli in lobar pneumonia.

Grossly: 2-Fibrinous inflammation Bread &butter appearance The fibrin is precipitated on the inner surface of the parietal layer and on the outer surface of the visceral layer. So the serous membranes appear opaque and rough giving bread and butter appearance

2-Fibrinous inflammation Microscopically: fibrin appears as an eosinophilic meshwork of threads Fate -Resolution (fibrinolysis) -Organization Fate: - degraded by fibrinolysis, and the accumulated debris may be removed by macrophages, resulting in restoration of the normal tissue structure (resolution). - ingrowth of fibroblasts and blood vessels (organization), leading ultimately to scarring that may have significant clinical consequences. suppurative inflammation and acute non-suppurative inflammation

2-Fibrinous inflammation Lung alveoli in lobar pneumonia. Microscopically: fibrin threads + Inflammatory cells

3- Catarrhal inflammation: Mild In mucous membranes Eg. common cold Gross: Mucoid discharge becomes yellow Mic: Swollen mucus cells edema neutrophils

4-Allergic inflammation Cause : Antigen antibody reaction excess exudates > edema EOSINOPHILS in tissue & blood Eg: 1.Eczema 2.Urticaria 3.Allergic rhinitis 4.Bronchial Asthma

Patchy mucosal necrosis Inflammation rich in fibrin 5-Pseudo membranous inflammation: Severe - mucous membrane Bacterial Exotoxin Patchy mucosal necrosis Inflammation rich in fibrin Pseudomembrane Diffuse to blood> severe toxemia powerful exotoxin → patchy necrosis Pathogenesis: The bacteria remain on the mucosal surface and produce powerful exotoxin resulting in patchy necrosis. The exotoxin diffuses to the submucosa leading to acute inflammation with formation of exudate rich in fibrin that mixes up with the necrotic mucosa to form the pseudomembrane. The exotoxin is absorbed in the blood causing severe acute toxaemia.

5-Pseudo membranous inflammation: Upper Resp tract :Diphtheria Large intestine:Bacillary dysentery Grossly: PSEUDOMEMBRANE Mic: Causative organism Necrotic mucosa Fibrin threads PNL RBCs grayish white loosely attached to the underlying tissue easily detached leaving bleeding ulcers Diphtheria Bacillary dysentery pseudomembrane is grayish white, dirty, loosely attached to the underlying tissue and can be easily detached leaving bleeding ulcers

6-Haemorrhagic inflammation Severe destruction of wall of bl. vs with haemorrhage acute haemorrhagic pneumonia 7-Necrotizing inflammation with extensive necrosis Vincent angina

Morphological patterns of acute inflammation I-Non suppurative inflammation II-Suppurative inflammation

II- Suppurative (purulent) inflammation: .Pyogenic org. .Marked tissue necrosis Strong PNL chemotaxis Dead PNL Proteolytic enzymes liquefy necrotic tissue mixes with inflammatory exudate Staph Strept Meningiococci E.coli Def :Acute inflammation ccc by pus formation Causative organism : Pyogenic bacteria Pathogenesis of pus formation: Pyogenic organisms marked tissue necrosis strong chemotaxis to PNL Many neutrphils are killed by bacteria resulting in release of proteolytic enzymes (from dead neutrophils) that liquefy the necrotic tissue which mixes with the inflammatory exudates forming pus. PUS

Composition of pus ?

II- Suppurative (purulent) inflammation: strept Localized a.Abscess b.variants Diffuse a.cellulitis b.Phlegmnous Staph

Empyema: Localized suppurative inflammation Staph aureus a.Abscess Localized suppurative inflammation > cavity filled with pus Staph aureus Coagulase enzyme Fibrinogen to fibrin localize infection Empyema: Pus in hollow organ

Pathogenesis of abscess 1 Organism Marked tissue necrosis Strong chemotaxis Central necrotic 2 Vascular phenomena >pyogenic membrane = dilated congested capillaries, many neutrophils & organisms 3 Neutrophils die >Proteolytic enzymes >Liquefy periphery of necrotic area >Pus pyogenic membrane which is composed of many dilated congested capillaries, many neutrophils and the organisms.

How many zones in the abscess? Central necrotic zone Mid zone containing pus Peripheral zone (pyogenic membrane) 3 1 2

Pathogenesis of abscess(cont.) 5 abscess enlarges by further necrosis & liquefaction 6 coagulase enzyme→ transforming fibrinogen into fibrin localize the suppuration 7 Pain Open & discharge pus The tension inside the abscess cavity gradually ↑→pain

Where abscess opens? Deep > Sinus Subcutaneous tissue kidney : covering epidermis undergo necrosis and pus escapes Deep > Sinus kidney : into the calyces & contents discharged with urine narrow tract which connects abscess cavity with surface outside (sinus) ↓ blind end deeply & open end on the surface

II- Suppurative (purulent) inflammation: Localized Abscess variants Diffuse cellulitis Phlegmnous Localized Abscess variants Diffuse cellulitis Phlegmnous

Furuncle b.Variants of abscess (boil) Related to hair follicle or sebaceous glands Staph. aureus. Face, back of neck & axilla

More in Back of neck & scalp carbuncle Pus is found in multiple loculi separated by f.t strands Loculi open on the surface by multiple openings More in Back of neck & scalp PDF:DM Each suppurative loculus develops in the same way as an abscess.

Complications of abscess Chronic abscess Blood spread >Toxemia –pyemia –bacteremia Lymphatic spread>lymphangitis - lymphadenitis Complications of healing: -ulcer- keloid- sinus- fistula

Ulcer Ulcer:  Sinus Local defect of skin or mucosal surface d.t necrosis and sloughing of cells of the skin, mucosa of the mouth, stomach, intestines, or genitourinary tract. abnormal tract lined by septic granulation tissue connecting a cavity to the outside-has a blind end. Abnormal tract lined by septic granulation tissue connecting 2 cavities or between hollow viscera & the surface Sinus Differs from sinus as it is opened from both ends Fistula

Sinus fistula

Fistula : Abnormal tract lined by septic granulation tissue connecting 2 cavities or between hollow viscera & the surface Types of fistula Congenital: thyroglossal Inflammatory Neoplastic vesicovaginal fistula in case of carcinoma of the urinary bladder.  Congenital; thyroglossal fistula.  Inflammatory; appendicular fistula complicating acute suppurative appendicitis

Fistula Vagina & rectum

a.Abscess b.variants a.cellulitis b.Phlegmnous II- Suppurative (purulent) inflammation: Localized a.Abscess b.variants Diffuse a.cellulitis b.Phlegmnous Localized Abscess variants Diffuse cellulitis Phlegmnous

Diffuse Suppurative inflammation Cellulitis CT of orbit –pelvis-scrotum Subcutaneous tissue Phlegmonous Mucous membrane

Cellulitis Streptococci Streptokinase Hyaluronidase Fibrinolysin dissolve the mucopolysaccharide matrix spread of infection Stap aureus