Inflammation

Inflammation

1. L.P response to T.j but usual a manifestation of disease

   • acute: initial,transient series
     • causes:' pctmh بكتمه -p:physical agents(t,i,h,c) -c:chemical (a.a.corrosive ) -t:tissue n(ii) -m:microbial infection e.g pyogenic bacteria V -H : hypersensitivity e.g tubercle bracilli
     • gross :- redness,heat, swelling, pain lof
     • A-local changes
       • 1-local T.D وrelease c mediators:- (Epcb) 1-early:histamine and thromin(viice) 2-plasma factors :C.Kinins.C.fs 3-cytokines:IL-1 وTNFalpha 4-bacterial products
         • IL=interleukin IL-1*tumer necrosis factor alpha produce by T macrophages
       • vascularphase: 1-transient V.C: irritation of V.W 2-V.D و⬆BF:due action of ChemicL M on V W➡ to open of pre capillary sphincter➡causing b to f through all C (R.H ) 3-⬆vascular Permeability and formation fluid exudates 4-vascular slowing :-⬆B.Viscosity due f exudation ➡slow of bF later leukocytes exudation
         • fluid exudates:- p-rich fluid that escape intravascular compartment into the interstitial t mechanism :- a-V.D ⬆Capillar y hydrostatic p b-⬆V.permeability c-reduce intravascular osmotic p increase interstitial p
           • features:- -high protein to 50g/L -high specific gravity
           • FEDts. matrix absorb by lymphatics if viable bacteria within it lead to spread information to lymph v lymph nodes (lymphadenitis which can be more complicated spread to blood stream with resultant bacteremia toxemia,septicemia
             • Functions of fluid exudates: • Dilution of toxins; be carried away in lymphatics. • Entry of antibodies, due to increased vascular permeability • Transport of drugs such as antibiotics to the site of bacteria . • Fibrin formation; 1-Impede the movement of microorganisms, trapping them and so facilitating phagocytosis. 2- It serves as a matrix for the formation of granulation tissue; helps movement of fibroblast during process of repair. • Delivery of nutrients and oxygen, essential for cells. • Stimulation of immune response by drainage of this fluid exudate into the lymphatics allows soluble antigens to reach the local lymph nodes, where they may stimulate the immune response.
     • b-cellular phase of acute inflammation aim emigration to neutrophil polymorphs into extra vascular
       • P.C med: *p=pavementin:- adhesion of leuco to v endothelium at site of a i *C=chemotaxis:- movement of emigrating L to cc substance in solution *m=margination:- (s.bf at site of a i that allow N و M to PP zone) * Emigration *D=diapedesis:- Rc passively can escape from vessels due to hydrostatic p
     • the main cells of acute inflammation
       • neutrophils:- intra-map:- M=movement = chemotaxis A=adhesion P=phagocytosis -intracellular killing like H2o2 dependent او independent as lysozymal lactoferri
         • fate:- most die locally but leave the site via the lymphatics some actively by apoptosis
       • macrophages:- clearing away tissue debris and damaged cells
         • Sequelae of acute inflammation: It depends on: 1- The type of tissue involved. 2- The amount of tissue destruction. The nature of the injurious agent.
         • 1- Resolution Definition: complete restoration of the tissues to normal after an episode of acute inflammation. e.g. acute lobar pneumonia
         • 2- Suppuration Definition: It is the formation of pus; a mixture of living, dying and dead neutrophils and bacteria, cellular debris and sometimes globules of lipid. The causative stimulus: usually pyogenic bacteria
           • It may be diffuse or localized (an abscess), and bacteria within the abscess cavity are relatively inaccessible to antibodies and to antibiotic.
             • 1- ‘pointing then bursts; followed by organization and fibrosis.
             • 2- Empyema: If pus accumulates inside a hollow viscus (e.g. the gall bladder).
             • 3- A sinus tract: Deep-seated abscesses sometimes discharge their pus along (an abnormal connection, lined by granulation tissue, between the abscess and the skin or a mucosal surface).
             • 4- A fistula formation: An abnormal passage connecting two mucosal surfaces or one mucosal surface to the skin surface.
             • 5- Long-standing: may become complicated by dystrophic calcification
         • III-Organisation: It is replacement of the dead tissue by granulation tissue then by fibrosis; (Repair) e.g. the pleural space following acute lobar pneumonia leading to, fibrous adhesion occurs between the parietal and visceral pleura
         • IV- Progression and spread: With lowered immunity the bacterial infection may spread: direct, lymphatic and blood.
         • V- Progression to chronic inflammation If the agent causing acute inflammation is not removed, the acute inflammation may progress to the chronic stage.
     • harmFul effect :' release of lysosomal enzymes by inflammatory cells may also have harmful effects. 1-Digestion of normal tissues e.g. vascular damage. 2- Swelling: e.g. cerebral abscess may raise intracranial tension. 3- Inappropriate inflammatory response: e.g. Type I hypersensitivity reactions (e.g. hay fever)
     • systemic effect;-Fever, Constitutional symptoms, Weight loss, Reactive hyperplasia of the reticuloendothelial system, Haematological changes; • Increased erythrocyte sedimentation rate • Anemia • Leucocytosis: o Neutrophilia occurs in pyogenic infections and tissue destruction o Eosinophilia in allergic disorders and parasitic infection; o Lymphocytosis: chronic infection (e.g.tuberculosis), viral infections. o monocytosis occurs in infectious mononucleosis and certain bacterial infections (e.g. tuberculosis, typhoid).
   • chronic :-subsequent and prolong T R
     • It is an inflammatory process in which lymphocytes, plasma cells and macrophages predominate. Characterized by fibrosis. It is extended over a long period of time.
     • first cause 1- Primary chronic inflammation: a-Resistance of infective agent to phagocytosis .g. TB b- Endogenous abnormal materials: Necrotic adipose tissue, bone, uric acid crystals c-Exogenous abnormal materials: Suture materials, implanted prostheses d-Some autoimmune diseases e.g. Crohn’s disease,
     • *second case 2- Progression from acute inflammation: Not common Mostly deep-seated abscess, and drainage is delayed or inadequate, e.g. (osteomyelitis),