INFLAMATION

DISEASES SOEKIMIN DEPT. OF ANATOMICAL PATOLOGY UNIVERSITAS SUMATERA UTARA MEDAN

INTRODUCTION

- DISEASE (OUTSIDE NORMAL RANGE)- SCIENTIFIC STUDY PATHOLOGY 1. CAUSE (INCL.MECHANISMS) 2. MANIFESTATIONS 3. PROGRESS (INCL.SEQUELE) - CLINICAL PRACTICE ( DX, TH, PROG) MEDICINE & SURGERY

GROUPS DISEASE

INFLAMATORY (INCL.INFECTION)DEGENERATIVE (EXCL.AGEING)NEOPLASTIC

CAUSES OF DISEASE

GENETIC ABN.CHROMOSOME SUSCEPTIBILITY TO SOME DISEASEACQUIRED

ACQUIRED DISEASEPHYSICAL : - TRAUMA - HEAT/COLD - RADIATIONCHEMICAL : - SIMPLE ACID- ORGANIC PARAQUATINFECTION : - BACTERIA - VIRUSES - PARASITES - YEASTIMMUN. : - Ag-Ab. - C. MEDIATEDPSYCHO.FC : - STRESS MENTAL ILL NESS, HYPERTENSION.

CELL DAMAGENECROSIS: - COAGULATIVE - CILLIQUATIVE GANGRENE CASEATION NECROBIOSISDEGENERATION

COAGULATIVE NECROSISLACK OF BLOOD SUPPLY.HEART, KIDNEY AND SPLEEN.CYTOPLASM OPAQUENUCLEUS PYKNOSIS KARYORRHEXIS KARYOLYSIS

COLLIQUITIVE NECROSISGANGRENE :- THOMBOEMBOLISM- INTUSSUSCEPTION- STRANGULATION- VOLVULUS- OBSTRUCTION (DM) GANGRENE + CLOSTRIDIA GAS GANGRENE.

CASEATIONYELLOWISH CHEESYTOUCH SLIGHTLY GREASYMICROS- AMORPHOUS- GRANULAR- CHROMATIN FLECKSCHRONIC TUBERCULOSIS.

NECROBIOSISGRADUAL CELL DAMAGEPROGRESSIVE.SINGLY OR SMALL GROUPS CELLREVERSIBLE (+/-) EXAMPL HEPAR CELL DEGENERATING AND DEAD CELL HEALING FIBROSIS

DEGENERATIONCLOUDY SWELLINGFATTY CAHNGEATROPYHYALINEMUCOIDAMYLOIDCALCIFICATION.

CLOUDY SWELLINGMILDEST FORM OF CELL DAMAGEREVERSIBLE.CELLS SWELL & PALECYTOPALSM COARSE GRANULEELECTONE MICROSCOPE :- MITOCH. SWOLLEN & BEADED BROKEN DOWN + LIPID

FATTY CHANGE DAMAGING AGENT

ENZYME DIS. ANOREXIA INTAKE (-)UTILISATION FAT(-) MOBILISATION FAT DEPOT

ACCUMULATION FAT

FATTY CHANGELIVER LACK OXYGEN (ANAEMIA, CARDIAC FAILURE) POISON, TOXIN (ALKOHOL, INFEC, ORGANIC)HEART ENLARGEKIDNEY TUBULES GLOMERULI (SEVERE)

OBESITYFAT DEPOSIT NORMAL SITE BETWEEN INTERMYOCARDIAL FIBRECAUSE : - INTAKE > - ENDOCRINE STATUS - HYPOTHALAMIC FUNCTIONEFFECT- LIVE EXPECTATION < C.VASCULAR DISEASE.

ATROPHYDECREASE IN CELL SIZE OR NUMBERCAUSES- BLOOD SUPPLY > & M.P.SACCH >)* ABSORBSI (>>) VIT D (>>)* BONY BREAKDOWN MOBIL (>>)* MOBILISATION (>>) PARATHYRO ID TUMOR, RENAL DISEASE

PIGMENTATIONENDOGEN- MELANIN- ADDISON DISEASE- CHLOASMA- HAEMOGLOBIN- HAEMOSIDERIN- HAEMATINEXOGEN- INHALATION- INGESTION- INJECTION

MELANIN.SKIN, CHOROID, EYE, +/- MENINGES & ADRENAL (NORMAL).LOCAL TUMOR (SKIN, CHOROID)GENERAL U.V.(SKIN) ADDISON DISEASE CHLOASMA

HAEMOGLOBINE DERIVATE.HAEMOGLOBINE BROKEN (NORMAL)- SPLEEN- LIVER- BONE MORROW- BILE DUCT- INTESTINE.

IRON FREE PIGMEN (JAUNDICE)OBSTRUCTION BILE DUCT.

INCREASED DESWTRUCTION OF RED CEELS

HEPATITIS

METABOLISM INHER.DISTR.CARBOHYDRATE* DEFECT GLYCOGEN GLUCAGON ( GLUCOSE-6-PHOSPHATASE) VON GIERKES DISEASE* POMPES DISEASE C.FAILURE, MEN TAL DEFICIENCY, MUSCLE WEAKNESS* D.M. GLYCOGEN STORAGE PROBLEM

METABOLISM INHER.DISTR.LIPID :* TRANSPORT HYPERLIPIDEMIA HYPERCHOLEST.* INBORN ERRORS. GAUCHERS DISEASES NIEMANN-PICKS DISEA SES.

INFLAMATION

DYNAMIC PROSSES LIVING TISSUEREACT INJURY (VASC & CON.TIS)

ACUTE INFLAMATIONGROSS :- REDNESS ( RUBOR )- HEAT ( CALOR )- SWELLING ( TUMOR )- PAIN ( DOLOR )- LOSS OF FUNCT. (FUNCTIO LAESA)

ACUTE INFLAMATION

MICROS :- HYPERAEMIA- EXUDATION- EMIGRATION OF LEUCOCYTES

HYPERAEMIAMICRO-VASCULAR CHANGES LEWISS TRIPLE RESPONSE :- FLUSH, - FLARE, - WEALSTROKE WHITE LINE (VS.CONTR)FLUSH DULL RED LINE (CAP.DIL)FLARE BRIGHT RED (ART.DIL)

EXUDATIONPROTEIN FLUID INTTIAL(WEAL)FLUID INCR. DILUTION OF TOXINPROTEIN INCR :- GLOBULIN ANTIBODIES- FIBRIN TO LIMIT SPREAD (BACT) WOUND HEALING

EXUDION (MECHANISM)PROTEIN PASSAGE :

- CHEM.MED. ENDLIAL DAMAGE

INC.PERMEABILITAS

EXUDION (MECHANISM)FLUIT MOVEMENT :- HYPERAEMIA CAP. B.P. INCR. INCR.FILTR.PRESSURE.-LOSS OF PROTEIN (CAP) DECR.PLM.OSMOTIC PRSS INCR.FILTR.PRSS.-TISSUE PROTEIN INCR. INCR.TISS.OSM.PRSS. INCR.FILTR.PRSS.-INCR.FILTR.PRSS. OEDEMAINCR. LYMPH FLOW FROM AREA.

EMIGRATION OF LEUCO.PMN & MN PASS (AMOEBOID)NORMAL AXIAL STREAM(VENULE)ACUTE INFL: EXUD.FLD INCR.VISC.SLOWING FLW AXIAL STR (-) MARGINATION (PMN) EMIGR/PMN& DIAPEDESIS OF RED CELLS.

CHEMICAL FACTOR.1. MEDIATORS :- VASO-ACTIVE AMINES.INJURY : - MAST CELLS HIST INCR.PERM & DILATION. - PLATELETS SERETONIN (5HT) DILATATION.

CHEMICAL FACTOR- VASO-ACTIVE POLYPEPTIDE.INJURY ACTIV.PROTEASE (KALLIKREIN) @-2GLOB BRADYKINININJURY ACT.PROTEASE POLYPEPTIDES BRADYKININ.BRADYKININ VASODIL. & ENDO-THELIAL DAMAGE (EARLY STAGES)

CHEMICAL FACTOR- ETC VASC.DIL AND INCR.PERMEA BILITY. (TOXIN, COMPLEMENT, EN ZYMES (LYSOSOMAL), PROSTAGLAN DINE, GLOB.PERM.FCT, L.ND PERM FCT, DEG.DNA/RNA, Ag-Ab COMPL.

CHEMICAL FACTOR2. CHEMOTACTIC AGENT : - COMPLEMENT - BACTERIA - LYMPHOKINES MOVEMENT OF LEUCOCYTES AND AGREGATION INLAMATION.

ACUTE INFLAMATIONPHAGOCYTOSIS :- PMN/MACROPHAGE INGEST (DEB BRIS AND FORIGN PARTICLE).INFLUENCE FCT :- OPSONIN- COMPLEMENT- PHYSIC OF CELL.ENVIRONMENT.

POLYMORPHLIFE-SPAN (1 - 3 DAYS)LYSOZOMAL ENZYMESTO KILL SUCCESSFUL/FAILURETO INGEST BACTERIA MACROPHAGELIFE-SPAN ( MTH - YRS)TO KILL SUCCESSFUL/FAILURETO INGEST DEBRIS

SQ OF ACUTE INFLAMATION RESOLUTION SUPURATION DISCAHARGE OF PUS ACUTE INFL. REPAIR & ORG. FIBOSIS CHRONIC INFL.

RESOLUTIONTO NORMAL CONDITION.POTENTIALE CONDITION :* MINIMAL LESION* RAPID ELIMINATION* LOCAL CONDITIONEXAMPLE RESOLUTION OF LOBARPNEOMONIA.

SUPPURATION FORMATION PUS ABSCESS PYOGENIC INFECTION : COCCICOMPOSITION :- SUPERNATANT PROTEIN FLUIT- DEPOSIT PMN, BACTERIA, FRAG MENTS CELL

EVOLUTION ABSCESSTISSUE DEMAGE (BACTERIA)INFLAMATION (EDEMA, HYPEREMIA)BACT. MULTIPLY, PMN (CENTRAL) PUS (+) EPID. (THIN) RUPTURECAV.COLLAP ORG & FIBROSIS FINAL SMALL SCAR.

EVOLUTION ABSCESSDEEP ABSCESS : SINUS (CHR.INFC) LOCALISED PUS :- SMALL ABSORB. SCAR- LARGE COLLECTED SUROUND (FIBROUS) CALCIUM SALT.

CHRONIC INFLAMATION

- PMN < LYMPHOCYT * PLASMA (+)CAP.BAD (+) NEW CAPILAREFIBROBLASTS + COLLAGEN FIBROSIS.

ORGANISATIONCONDITION FACTOR :- EXUDATE OR NECROSIS >>>- LOCAL CONDITION ( BAD)EXAMPLE : - PLEURA.(PAR-VES) ACUTE INFL (FIBRINE EXUDATE) CAPILLARIES (+) FIBRINE FIBROSIS ADHETION PLEURAL.

NOMENCLATUREORGAN + IT ISEXAMP : - GASTER GASTRITIS- COLON COLITIS - HEPAR HEPATISIS- VESICA VELEA CHOLITIS- LUNG PNEUMONIA- PLEURA -- PLEURISY

COMPONENT TYPE OF INFL.CATARRHAL PSEUDO-MEMBRANEEXUDATIVE : - SEROUS - FIBINOUS - SUPPURATIVE - HAEMORRHAGIC

CHRONIC INFLAMATION*GRANULOMA : - TBC - SARCOIDOSIS - TALC GRANULOMA - CROHNS *ENDARTERITIS/ENDOPHLEBITIS T.INTIMA FIBROSIS NECROSIS ULCER

ULCERCOMPLICATION PROCESSES.LOST OF COVERING TISSUE (NECROSIS) & REPLACED BY INFL.TISSUE.TYPE : - SIMPLE (INFLAM) - CHRONIC (CONTINOUS) - MALIGNANT (CANCEROUS)

ANATOMICAL FORM OF INF.SINUS (CAVITY SUFACE)EXAMP :- OSTEOMYELITIS (SINUS)- PILOIDAL SINUS (NEST OF HAIR) MID-LINE OF THE SACRUM.FISTULA (SURFACE SURFACE):- CONGENITAL & ACQUIREDEMPYEMA (PUS CAVITY)CELLULITIS CONN.TISSUE (PLANE)

SITE OF CONTAMINATIONSKIN: - NOSE- ANUS - MOUTH- U.R.T - HANDS- G.I.TCOMMENSAL BACTERIA- SKIN, R.T, G.I.T. NON PATHOGEN BENEFICIAL: - PROD.NUTR.CHE- MICALS (B12) - COMPETING PA- THOGEN

ROUTES OF INFECTIONSKIN/MUCOUS MEMBRANE- DIRECT CONTACT VENERAL DSS- CONTAMINATION ABRATION AND WOUND WOUND INF, RABIES.- INOCULATION INSECT BITE (Y.FFR) SYRINGE (S.HEPIS)

ROUTES OF INFECTION

INGESTION :- CONT. FOOD/WATER E.FFR, INF.HEP TIS (A), POLIT IS, CHOLERAINHALATION :- DUST AND DROPLETS INFLUENZA

PREVENTIVE FACTORHOST: - GENERAL: - GOOD STATE- SPECIAL: - PHYSICAL BARRIERS :* SKIN* FILTRATION - SECRETION :* TEARS* URINE* MUCINE

PREVENTIVE FACTOR- CHEMICAL ACTION :* ACID SECRETION (GASTER/URINE)* LYSOZYMES ENZYMES (TEARS/ SALIVA)* IgA (TEARS/INTESTINAL SECRT)* NON SPECIFIC INHIBITORY SUBST. (URINE/SWEAT/SEBUM)

PREVENTIVE FACTORMICRO ORGANISM :- CAPACITY OF INVASIVE :* DOSES* VIRULENTCOURSE OF INFECTION* INFLAMATION* PHAGOSIIS* IMM. RESPONSE* INTERFERON

PROTECTIVE FAILURESKIN.REP.TRACT.GASTER.SECRETIONSCOMMENSAL GROWTHDEF.IMMUNDEF.PHAGOCYTOSISDEBILITATING DISEASES

INFECTION MECHANISMTOXIN PRODUCTION : (EXO/ENDO)HYPERSENSITIVITY REACTIONBLOD STREAM: - BACTERAEMIA - SEPTICAEMIA - PYEMIA

BACTERIAL INFECTIONLOCAL INFL NON LCL INFL

BLOOD STREAM

BACTEAE SEPTICAE PYAEMIA MIA MIA

BACTERAEMIACOMMONLYNO SERIOUSINTEGRAL PART OF SOME INFECTION TYPHOID FEVERDENTAL EXTRACTION BACTERAEMIA B.ENDOCARDITIS / SEPTICAEMIA

SEPTICAEMIAVERY SERIOUS CONDITION TOXAEMIA AND SHOCKFORM: - PRIMARY - COMPLICATE - IMMUNE DECREASED

PYAEMIASEVERE CONDITION (+ TOXAEMIA)SMALL AGGREGATE MICR.EMBLMFORM: - PYAEMIC ABSCESSES - SEPTIC INFARCTION

PYAEMIC ABSCESSSEPTIC FOCUS ( STAPH ) THROMBO-SIS OF VENULES MICROEMBOLI MULTIPLE ABSCESS (VARIOUS ORGANS)- CEREBRAL CORTEX, MYOCARDIUM, LUNGS, RENAL CORTEX.

SEPTIC INFARCTIONLARGE SEPTIC THROMBOSIS- SUPP.VEIN THROMBOPHLEBITIS EMBOLISM INFARCTTION + SUP PURATION LUNG & LIVER.- ACUTE BACT.ENDOCARDITIS VE GETATION MITRAL VALVE VIA AR TERIAL BRAIN, KIDNEYS & SPLEEN

PYOGENIC BACTERIA STAPH.A.(PHARYNX, NOSE, PERINEAL) COAGULASE + FIBRINE ABSCESS- SKIN PUS, BOILS, CARBUNCLE- WOUND STAPH.PNEUMONIA !!- BLOOD STREAM PYAEMIA

PYOGENIC BACTERIASTREPT.PYOGENES PHARYNX HYALURONIDASE, STREPTOKINASE,LEUCOCIDIN.- SKIN IMPETIGO, ERISIPELAS, CEL LULITIS, LYMPHANGITIS.- WOUND TONSILITIS, PHARYNGITIS- BLOOD STREAM SEPTICAEMIA

PYOGENIC BACTERIAMENINGOCOCCUS NASOPHARYNX PURULENT MENINGITIS (CHILD) FATAL SEPTICAEMIA. SKIN RASH &MASSIVE ADRENAL HAEMORRHAGE(WATERHOUSE FRODERICHSEN SYNDROME)

PYOGENIC BACTERIAGONOCOCCUS ( GENITAL M.MEMBR) PURULENT (URETHRA & CERVIX) ANT.URETHRITIS, PROSTATITIS, EPIDIDYMITIS (MALE) CERVICITIS, ACUTE SALPINGITIS ( FEMALE) STERIL

COMMENSAL BACILLIGIT (COLIFORM, PROTEUS, PSEUDOMONAS.LOW GRADE VIRULENT. WOUND INFC, PYELONEPH, CYSTITIS, DIVERTICULITUIS, APPENDIT IS. GIT, U.T INFECTION ENDOTOXIN SHOCK

GANGGRENESPECIAL TYPE OF NECROSISPRIMARY GAS GANGGRENEDEEP WOUND + CLOSTRIDIA (ANAE-ROBIC SPORULATING) GAS (SACHAROLYTIC & PROTEOLYTIC)RAPIDLY SPREAD SEVERE TOXAEMIA

GANGGRENESECONDARY :- WET: - OEDEMA - VENOUS CONGETION(STRANGULATION & OCCLUTION)- DRY: - GRADUAL OCCLUTION ( TOES AND FEET PURIFICATION PROSSES (SLOW)

TETANUSCLOSTRODIUM TETANIANAEROBGRAM + DRUM STICK (FAECES)INFC : PENETRATING WOUNDEFFECT : INFC EXOTOXINEXOTOXIN LOCAL NERVE SPASM MOTOR NERVE TRISMUS,RISUS SARDONICUS, CONVULSION, RESP SPASM EXHAUSTION & DEATH.IMM : TOXOID (PROP) , ANTI TOXIN (THE/)

GRANULOMACHRONIC INFECTIONTUBERCULOSIS.SYPHILISACTINOMYCOSISLEPROSY

TUBERCULOSISMYCOBACTERIUM TUBERCULOSISDISEASE DECLINED :* NUTRITION & HYGIENE* CHEMOTHERAPY* BCG IMMUNISATION. TUBERCLE : 1 2 DAYS PMN 1 WEEK MACROPHAGE2 WEEK GIANT CELL, LYMPOSITE, EPOID.3 WEEK + CASEATION.

TUBERCULOSISPRIMARY INFECTION.- FIRST CONTAC (CHILDREN)- PERIPHERAL LUNG (GHON)- WITH LYMPH NODE ( GHON COMP)HEALING CALCIFICATIONSPREAD BLOOD STREAM MILIARY(GENERALLY)LOCAL (ORGAN) MENING, JOINT, BONE

TUBERCULOSISREINFECTION APEX PROGRES.VARIATION FORM :* EXUDATIVE PLEURAL EFFUSION ASCITES (ABDOMEN)COLD ABSCESS SINUS (ABSCESS)FIBROTIC BODY REPARATIVE.ACUTE CASEATING IMPAIRED IMM.

SYPHILISVENERAL INFECT.TREPONEMA PALLIDUMFORM :* PRIMARY* SECONDARY* TERTIARY (LATE)- GUMMA- SYPH.AORTITIS- NEUROLOGICAL SYPH.

PRIMARY SIPHYLIS3 WEEKS SIRCULATION HARD C. LIPMPHOCYTE & PALMA, PERI & ENDARTERITIS.SWELLING LYMPH NODES HARD ANDPAINLESS.HARD CHANCRE RAISED BUTTON NODULE.

SECONDARY SYPHILIS2 OR 3 MONTHSKIN RASH (+), ULCER MUCOUS MEMBRANE, GENERALLY LYPHADENOPHATYFEVER AND ANAEMIA (+)SPIROCHAETA (>>) + FOCAL INFILTRATIONLYMPHOCYTE, PLASMA CELL AND MACROPHAGE, MILD ARTERITIS.TISSUE DESTRUCTION MINIMALHEALING WITHOUT SCARING.

TERTIARY SYPHILISGUMMA : - LOCAL NECROTIC. - BONE, TESTIS, LIVER.S.AORTITIS: - ARCH & THORACIC - T.MEDIA DESTR. FOCALDESTRUCTION ( WINDOWING) - PERIARTERITIS - ANEURISMA PRESSUREEFFECT OR RUPTURE

TERTIARY SYPHILISNEUROLOGICAL* MENINGOVASCULAR MENINGEAL BLOOD VESSELS NEUROLOGICAL EFFECT* PARENCHYMATOUS :- GENERAL PARALISIS (SEVERE DESTRUC- TION OF CEREBRAL TISSUE). - TABES DORSALISCOL.VERT.POST

CONGENITAL SYPHILISTRANSPLACENTAL * ABORTION/STILLBIRTH MANY OR- GAN DAMAGE.* MARASMIC INFANT ORGAN AND TISSUE DAMAGE (BIRTH AND LATER CHILDHOOD)

IMMUNITYANTIBODY PRODUCTION :- ANTIBODY ACTIVE (COMPLEMENT) WASSERMANN REACTION.- SPECIFIC ANTI-TREPONEMAL A.BODY USED SPESIFIC COMPLEMENT FIXING,IMMOBTION AND FLUORESCENCE TEST

IMMUNITYCELL MEDIATED DELAYED HYPERSENSITIVITY ALSO DEVELOPS. SENSITIVITYREACTION ARE IMPORTANT IN THE ME-CHANISM OF SYPHILITIC DAMAGE TOTISSUE.

ACTINOMYCOSISLOCALISED SPREADING (CHRONICSUPPURATION) SITE OF INFECTION : - LOWER JAW - ILEO-CAECAL - LUNGLOBULATED ABSCES PUS (SULPUR GRANULE), PMN, FOAMY MACROFAGEAND SUROUNDED BY FIBROUS TISSUE.

LEPROSYSLOW PROGRESIVE DISEASE.DAMAGE PERIPHERAL NERVE.ACQUIRED (CLOSE PROLONG CONTACT)FORM : * LEPROMATOUS* TUBERCULOID.

LEPROMATOUSNODULE SKIN LEONINE FACIESAFFECTED NERVE (LATE)LESION : - LYMPHOCYTE - PLASMA - MACROFAGE + ORG. - ORG +++ (TISSUE) CELL MEDIATED IMMUNITY (-)

TUBERCULOIDSKIN PALLOR AND ANAESTHESIAINVOLVED NERVE (EARLY)FOLLICULAR GRANULOMA (TUBERCLE)ORGANISM (SCANTY)CELL MEDIATED IMMUNITY (WELL)

VIRAL INFECTIONSACUTE VIRAL :- POLIO, HEPATITIS, SMALLPOXLATENT VIRAL :- HERVES SIMPLEX/ZOSTER, CHICKEN POX (VARICELLA)SLOW VIRAL :- SCARPIE, KURU ONCOGENIC VIRAL.- VERUCAE VULGARIS, EPSTEIN BARR

HOST/VIRUS INTERACTIONCHANGES CELLINTERFERON PRODUCTIONIMMUN RESPONSEINFLAMATORY RESPONSE

CHANGES CELLCELL DEGENERATION : LOSS OFFUNCTION DEATH VACUOLATION LYSIS (RAPID)N.CELLS CONDENSATION SLOW LYSISFUSION OF CELLS GIANT CELL ( WAR THIN-FINKELDY CELL OF MEASLES)

CHANGES CELLSCELL PROLOFERATION WARTY +CELL DEATH.INCLUTION BODIES FORMATION IN CYTOPLASM.NO APPARENT LATEN OR SLOW INFECTION.NO APPARENT BUT MALIGNANT (LATER) OR SLOW INFECTION

INTERFERON PRODUCTIONINTERFERON PRODUCT REPLICATIONVIRAL INHIBITION.INTERFERON (PROTEIN) NOT ANTIBODYTHE FIRST DEFENCE.

IMMUNE RESPONSEANTIBODIES TO VIRUSCELL MEDIATED IMMUNITY+/- VIRAL/ANTIBODY COMPLEXES ARTERITIS, KIDNEY DAMAGEINFLAMATORY RESPONS VASCULARAND EXUDATIVE ELEMENT.

OPPORTUNISTIC INFECT.NON PATHOGEN ORGANISMLOW GRADE VIRULENCEIMMUNITY IMPAIRED :- CONGENITAL IMM.DEFICIENCIES.- ACQUIRED URAEMIA, LIVER DISE ASES, MALIGNANT TUMORS ETC THERAPY, ANTIBIOTIC, TRANSPLANT SURGERY ETC

GENERAL EFFECTSFEVER (PYREXIA) : INCR.METABOLISM HEAT COLD, INCR.PULSE RATE AND DEHYDRATION.PYREXIA : INFARCT, TUMORS, CERE BRAL DISEASE, HEAT STROKEHYPERPYREXIA > 41 C

GENERAL EFFECTSMATABOLISM CHANGES :FEVER INCR.ENERGY UTILISATIONCHO RESERVE (DECR.INTAKE)BREAK DOWN TISSUE PROTEIN INCR. NITRO GEN URINE (KETOACIDOSIS) INCR. CONSENTRATION AND SMALL VOLUME

GENERAL EFFECTSCHONIC INFECTION : HYPERGAMMAGLOBULINEMIAINCREASED BLOOD PROTEIN INCREASED ESR.

INFLAMATION CELLSNEUTROPHIL POLYMORPHONUCLEAR LEUCOCYTE (PMN)LYMPHOCYTEEOSINOPHILSMONOCYTEMAST CELLS (BASOPHILS)

POLYMORPHONUCLEARFROM BONE MORROLIFE SPAN 2 3 DAYSFUNCTION : - PHAGOCYTOSIS- KILLING M.ORGANISMNORMAL COUNT : 3.000 7.500/MM3INFECTION > 10.000/MM3

LYMPHOCYTESFROM LYMPHOID NODE PROD. ANTIBODIES & CELLULAR COMPONENT IMMUN RESPONSECOUNT : 1,500 3.500 / MM3VIRAL INFECT. & CHRONIC BACT.INF LYMPHOSITOSISB. LYMPHOCYTE PLASMA CELLS & Ig

EOSINIPHILSDERIVED FROM BONE MORROWNORMAL 1 4 %EOSINOPHILIA : - HELMIN INFECT. - PARASITES - ALLERGIC ASTHMA

MONOCYTESTOTAL WHITE CELLS : 4 7 %AS MACROPHAGE, LOCAL INFLAMA-TION REACTIONINCREASED :- CHR.BACT.INFECT.(TB)- PROTOZOAL (MALARIA) EPITHELOID CELLS MACROPHAGES FUSION GIANT CELLS

MAST CELLSBASOPHILS < 1 %SCATTERED CONN.TISSUEDERIVED FROM BONE MORROWCONTAIN : - HIATAMINE - HEPARINE - ENZYMES REALEASED BY CHEMICAL FACTOR (INFLAMATORY REACTION)

HEALINGWOUND HEALINGCOMPLICATIONS: - CONTRACTURE - GRANULATION - KELOID - FIBROSISREGENERATIONSPECIAL SITUATION.

WOUND HEALINGPRIMARY HEALING :- CLEAN EXISED WOUND- GOOD POSITION (PALNED SURG.INCIS)IMMEDIATELY: - BLOOD CLOT2-3 HOURS : - INFLAMATION (+) - MILD HYPERAEMIA - FEW POLYMORPHS

WOUND HEALING2-3 DAYS : - MACROPHAGE REMO- VING CLOT - FIBROBLASTIC10-14 DAYS : - SCAB LOOSE - EPITHELIAL COVERING. - FIROUS UNION

WOUND HEALINGWEEKS: - SCAR TISSUE SLIGHLY HYPERAEMIA - GOOD FIBROUS UNIONMONTHS YEAR: - DEVASCULARISATION - COLLAGEN(-) ENZYME - SCAR MINIMAL.

SECONDARY HEALINGLOSS OF TISSUE >>NECROSIS (+)INFECTION (+)EARLY: BLOOD & FIBRIN CLOT (+) ACUTE INFL. CELLS (+)FEW DAYS : - EPITH.PROLIFERATION - NEW CAPILARY - MACROPHAGE - PMN, FIBROBLAST

SECONDARY HEALING1 WEEK: - SURFACE DEBRIS (-) - FIBROBLASTS >> - EPITH.PROLIFTION - CAPILARY >> - GRANULATION

SECONDARY HEALING2 WEEKS : - EPITH.COVERING COMPL - TRANSVERS COLLAGEN - DECREASED CAPILARY - FEW CELLSMONTH : - FULL EPITH.COVERING - SURFACE DEPRETION (< ) - THICK COLLAGEN SCAR - VASCULAR ( < )

REGENERATIONCELL TYPE :* LABILE CELLS : - EPITHELIUM- BONE MORROW- LYMPHOID* STABLE CELLS: - LIVER - ENDOCRINE CELLS* PERMANENT CELLS : - NERVE CELLS

SPECIAL HEALINGINTERNAL SURFACE G.I.T.SOLID EPITHELIAL ORGANS :- KIDNEY- LIVER- MUSCLENERVOUS TISSUE : - CNS - PERIPHERAL N

SPECIAL HEALINGBONE : - IMMEDIATE EFFECT - EARLY REACTION ( 4-5 DAYS) - AFTER 1ST WEEK - > 3 WEEK - WEEK MONTH - MONTH LATER