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DISEASES SOEKIMIN DEPT. OF ANATOMICAL PATOLOGY UNIVERSITAS SUMATERA UTARA MEDAN

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  • 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.

  • CAUSES OF CELL DAMAGEOXYGEN
  • 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)

  • FATTY CHANGEMETABOLIC UPSET STARVATION METAB.DIST + MO BILISATIO FAT OXIDATION < ACCUMULATION FAT (PARENCHYM) DM : INSULIN LACK (CHO METAB.
  • 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)

  • INFECTIONINVATION (M.O) TISSUEDISEASE SUBSEQUENT MULTIPLI CATION OF INVATION M.ORGANISMBACTERIA AND VIRUSES >>FUNGI AND OTHER GROUPS
  • 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