DISEASES

SOEKIMIN
DEPT. OF ANATOMICAL PATOLOGY
UNIVERSITAS SUMATERA UTARA
MEDAN
INTRODUCTION

- DISEASE (OUTSIDE NORMAL RANGE)
- SCIENTIFIC STUDY PATHOLOGY
1. CAUSE ([Link])
2. MANIFESTATIONS
3. PROGRESS ([Link])
- CLINICAL PRACTICE ( DX, TH, PROG)
MEDICINE & SURGERY
GROUPS DISEASE

INFLAMATORY ([Link])
DEGENERATIVE ([Link])
NEOPLASTIC
CAUSES OF DISEASE

GENETIC [Link]
SUSCEPTIBILITY TO
SOME DISEASE
ACQUIRED
ACQUIRED DISEASE
PHYSICAL : - TRAUMA
- HEAT/COLD
- RADIATION
CHEMICAL : - SIMPLE ACID
- ORGANIC PARAQUAT
INFECTION : - BACTERIA - VIRUSES
- PARASITES - YEAST
IMMUN. : - Ag-Ab. - C. MEDIATED
[Link] : - STRESS MENTAL ILL
NESS, HYPERTENSION.
CAUSES OF CELL DAMAGE
OXYGEN << RESP./[Link], ANEMIA
PHYSICAL MECHANIC, TEMP, RAD.
TOXIN BECTERIA, PLANT, ANIMAL
VIRUSES
ABNORMAL [Link] HYPER
SENSITIVITY STATE.
CELL DAMAGE
NECROSIS : - COAGULATIVE
- CILLIQUATIVE
GANGRENE
CASEATION
NECROBIOSIS
DEGENERATION

COAGULATIVE NECROSIS
LACK OF BLOOD SUPPLY.
HEART, KIDNEY AND SPLEEN.
CYTOPLASM OPAQUE
NUCLEUS PYKNOSIS
KARYORRHEXIS
KARYOLYSIS

COLLIQUITIVE NECROSIS
GANGRENE : - THOMBOEMBOLISM
- INTUSSUSCEPTION
- STRANGULATION
- VOLVULUS
- OBSTRUCTION (DM)
GANGRENE + CLOSTRIDIA GAS
GANGRENE.
CASEATION
YELLOWISH CHEESY
TOUCH SLIGHTLY GREASY
MICROS - AMORPHOUS
- GRANULAR
- CHROMATIN FLECKS
CHRONIC TUBERCULOSIS.
NECROBIOSIS
GRADUAL CELL DAMAGE
PROGRESSIVE.
SINGLY OR SMALL GROUPS CELL
REVERSIBLE (+/-)
EXAMPL HEPAR CELL DEGENE
RATING AND DEAD CELL HEALING
FIBROSIS

DEGENERATION
CLOUDY SWELLING
FATTY CAHNGE
ATROPY
HYALINE
MUCOID
AMYLOID
CALCIFICATION.
CLOUDY SWELLING
MILDEST FORM OF CELL DAMAGE
REVERSIBLE.
CELLS SWELL & PALE
CYTOPALSM COARSE GRANULE
ELECTONE MICROSCOPE :
- MITOCH. SWOLLEN & BEADED
BROKEN DOWN + LIPID
FATTY CHANGE
DAMAGING AGENT

ENZYME DIS. ANOREXIA

INTAKE (-)
UTILISATION FAT(-) MOBILISATION
FAT DEPOT

ACCUMULATION FAT
FATTY CHANGE
LIVER LACK OXYGEN (ANAEMIA,
CARDIAC FAILURE)
POISON, TOXIN (ALKOHOL,
INFEC, ORGANIC)
HEART ENLARGE
KIDNEY TUBULES
GLOMERULI (SEVERE)
FATTY CHANGE
METABOLIC UPSET
STARVATION [Link] + MO
BILISATIO FAT OXIDATION <
ACCUMULATION FAT (PARENCHYM)
DM : INSULIN LACK (CHO METAB.<) +
NORMAL [Link] OXITION FAT <
ACCUMULATION FAT (PARENCHYM)

OBESITY
FAT DEPOSIT NORMAL SITE
BETWEEN INTERMYOCARDIAL FIBRE
CAUSE : - INTAKE >
- ENDOCRINE STATUS
- HYPOTHALAMIC FUNCTION
EFFECT - LIVE EXPECTATION <
[Link] DISEASE.
ATROPHY
DECREASE IN CELL SIZE OR NUMBER
CAUSES - BLOOD SUPPLY <
- DISUSE
- INTERRUPTED NERVE
- ENDOCRINE DEFICIENCY
- PRESSURE

HYALINE & MUCOID DEG.
HYALINE :
- GLASSY, REFRACTILE
- DENSE COLLAGEN (FIBROMYOMA)
MUCOID :
- EPITELIAL MUCINE
MUCOPLYSACCH.(CON
NECTIVE TISSUE) MYXOMATOUS.
AMYLOID DEGERATION
DEPOSIT PROTEIN >> & [Link] <
AROUND THE FIBRES
TYPES - PRIMARY CAUSE ?
- SECONDARY CHRONIC DISE-
ASES (TBC, SYPHILIS, PYOGENIC INFEC,
RHEMATOID ARTHR, MYELOMA, HODG-
KINS DISEASE)
AMYLOID DEGENERATION
DISTRIBUTION :
- PRIMARY * TONGUE * SPLEEN
* LUNGS * SKIN
* HEART * MUSCLE
* INTESTINAL
* LIVER
* KIDNEY
AMYLOID DEGENERATION
DISTRIBUTION :
- SECONDARY : - INTESTINAL
- LIVER
- KIDNEY
- SPLEEN

AMYLOID DEGENERATION
DETCTION :
- LUGOLS IODINE :
* AMYLOID BROWN
* NORMAL YELLOW
- CONGO RED :
* AMYLOID RED
* NORMAL PALE PINK/YELLOW
- ROSANILINE DYES :
* AMYLOID PINK
* NORMAL PURPLE
[Link] DEG.
AMYLOID DEPOSIT

SWELLING OF FIBRE

PRESSURE ON NARROWING OF
CELLS VESSELS

ATROPHY OF PARENCHYMA
AMYILOID DEGENERATION
LOCATION :
* KIDNEY CAPILER & TUBULUS
* [Link] CAPILARY WALLS
* HEART CARDIAC MUSCLE
* LIVER MIDZONAL VESSELS
* SPLEEN RETICULUM
SINUSOID & ARTEROLE

CALCIFICATION
DYSTROPHIC :
- NECROTIC TISSUE ABSORBED (-)
- SLOW TISSUE DEGENERATION
MATASTATIC :
- BLOOD CALCIUM (>>)
* ABSORBSI (>>) VIT D (>>)
* BONY BREAKDOWN MOBIL (>>)
* MOBILISATION (>>) PARATHYRO
ID TUMOR, RENAL DISEASE
PIGMENTATION
ENDOGEN - MELANIN
- ADDISON DISEASE
- CHLOASMA
- HAEMOGLOBIN
- HAEMOSIDERIN
- HAEMATIN
EXOGEN - 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 [Link].
CARBOHYDRATE
* DEFECT GLYCOGEN GLUCAGON
( GLUCOSE-6-PHOSPHATASE) VON
GIERKES DISEASE
* POMPES DISEASE [Link], MEN
TAL DEFICIENCY, MUSCLE WEAKNESS
* D.M. GLYCOGEN STORAGE PROBLEM
METABOLISM [Link].
LIPID :
* TRANSPORT HYPERLIPIDEMIA
HYPERCHOLEST.
* INBORN ERRORS.
GAUCHERS DISEASES
NIEMANN-PICKS DISEA
SES.
INFLAMATION

DYNAMIC PROSSES LIVING TISSUE
REACT INJURY (VASC & [Link])


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

MICROS :
- HYPERAEMIA
- EXUDATION
- EMIGRATION OF LEUCOCYTES

HYPERAEMIA
MICRO-VASCULAR CHANGES
LEWISS TRIPLE RESPONSE :
- FLUSH, - FLARE, - WEAL
STROKE WHITE LINE ([Link])
FLUSH DULL RED LINE ([Link])
FLARE BRIGHT RED ([Link])

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

EXUDION (MECHANISM)
PROTEIN PASSAGE :

- [Link]. ENDLIAL DAMAGE

[Link]

EXUDION (MECHANISM)
FLUIT MOVEMENT :
- HYPERAEMIA CAP. B.P. INCR.
[Link].
-LOSS OF PROTEIN (CAP) [Link].
OSMOTIC PRSS [Link].
-TISSUE PROTEIN INCR. [Link].
[Link]. [Link].
-[Link]. OEDEMAINCR.
LYMPH FLOW FROM AREA.
EMIGRATION OF LEUCO.
PMN & MN PASS (AMOEBOID)
NORMAL AXIAL STREAM(VENULE)
ACUTE INFL: [Link] [Link].
SLOWING FLW AXIAL STR (-)
MARGINATION (PMN) EMIGR/PMN
& DIAPEDESIS OF RED CELLS.

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

CHEMICAL FACTOR
- VASO-ACTIVE POLYPEPTIDE.
INJURY [Link] (KALLI
KREIN) @-2GLOB BRADYKININ
INJURY [Link] POLYPEP
TIDES BRADYKININ.
BRADYKININ VASODIL. & ENDO-
THELIAL DAMAGE (EARLY STAGES)
CHEMICAL FACTOR

- ETC [Link] AND [Link]
BILITY. (TOXIN, COMPLEMENT, EN
ZYMES (LYSOSOMAL), PROSTAGLAN
DINE, [Link], [Link] PERM
FCT, [Link]/RNA, Ag-Ab COMPL.
CHEMICAL FACTOR
2. CHEMOTACTIC AGENT :
- COMPLEMENT
- BACTERIA
- LYMPHOKINES
MOVEMENT OF LEUCOCYTES AND
AGREGATION INLAMATION.
ACUTE INFLAMATION
PHAGOCYTOSIS :
- PMN/MACROPHAGE INGEST (DEB
BRIS AND FORIGN PARTICLE).
INFLUENCE FCT :
- OPSONIN
- COMPLEMENT
- PHYSIC OF [Link].
POLYMORPH
LIFE-SPAN (1 - 3 DAYS)
LYSOZOMAL ENZYMES
TO KILL SUCCESSFUL/FAILURE
TO INGEST BACTERIA
MACROPHAGE
LIFE-SPAN ( MTH - YRS)
TO KILL SUCCESSFUL/FAILURE
TO INGEST DEBRIS

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

RESOLUTION
TO NORMAL CONDITION.
POTENTIALE CONDITION :
* MINIMAL LESION
* RAPID ELIMINATION
* LOCAL CONDITION
EXAMPLE RESOLUTION OF LOBAR
PNEOMONIA.
SUPPURATION
FORMATION PUS ABSCESS
PYOGENIC INFECTION : COCCI
COMPOSITION :
- SUPERNATANT PROTEIN FLUIT
- DEPOSIT PMN, BACTERIA, FRAG
MENTS CELL

EVOLUTION ABSCESS
TISSUE DEMAGE (BACTERIA)
INFLAMATION (EDEMA, HYPEREMIA)
BACT. MULTIPLY, PMN (CENTRAL)
PUS (+) EPID. (THIN) RUPTURE
[Link] ORG & FIBROSIS
FINAL SMALL SCAR.

EVOLUTION ABSCESS
DEEP ABSCESS :
SINUS ([Link])
LOCALISED PUS :
- SMALL ABSORB. SCAR
- LARGE COLLECTED
SUROUND (FIBROUS) CALCIUM SALT.

CHRONIC INFLAMATION

- PMN < LYMPHOCYT * PLASMA (+)
- [Link] (+) NEW CAPILARE
- FIBROBLASTS + COLLAGEN FIBRO
SIS.
ORGANISATION
CONDITION FACTOR :
- EXUDATE OR NECROSIS >>>
- LOCAL CONDITION ( BAD)
EXAMPLE : - PLEURA.(PAR-VES)
ACUTE INFL (FIBRINE EXUDATE)
CAPILLARIES (+) FIBRINE FI
BROSIS ADHETION PLEURAL.
NOMENCLATURE
ORGAN + IT IS
EXAMP :
- GASTER GASTRITIS
- COLON COLITIS
- HEPAR HEPATISIS
- VESICA VELEA CHOLITIS
- LUNG PNEUMONIA
- PLEURA -- PLEURISY
COMPONENT TYPE OF INFL.
CATARRHAL
PSEUDO-MEMBRANE
EXUDATIVE : - SEROUS
- FIBINOUS
- SUPPURATIVE
- HAEMORRHAGIC
CHRONIC INFLAMATION
*GRANULOMA : - TBC
- SARCOIDOSIS
- TALC
GRANULOMA
- CROHNS
*ENDARTERITIS/ENDOPHLEBITIS
[Link] FIBROSIS NECROSIS
ULCER
ULCER
COMPLICATION PROCESSES.
LOST OF COVERING TISSUE (NECRO
SIS) & REPLACED BY [Link].
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 & ACQUIRED
EMPYEMA (PUS CAVITY)
CELLULITIS [Link] (PLANE)

INFECTION
INVATION (M.O) TISSUE
DISEASE SUBSEQUENT MULTIPLI
CATION OF INVATION [Link]
BACTERIA AND VIRUSES >>
FUNGI AND OTHER GROUPS <<

SITE OF CONTAMINATION
SKIN : - NOSE - ANUS
- MOUTH - U.R.T
- HANDS - G.I.T
COMMENSAL BACTERIA
- SKIN, R.T, G.I.T. NON PATHOGEN
BENEFICIAL : - [Link]-
MICALS (B12)
- COMPETING PA-
THOGEN
ROUTES OF INFECTION
SKIN/MUCOUS MEMBRANE
- DIRECT CONTACT VENERAL DSS
- CONTAMINATION ABRATION AND
WOUND WOUND INF, RABIES.
- INOCULATION INSECT BITE ([Link])
SYRINGE ([Link])

ROUTES OF INFECTION

INGESTION :
- CONT. FOOD/WATER [Link], [Link]
TIS (A), POLIT IS, CHOLERA
INHALATION :
- DUST AND DROPLETS INFLUENZA

PREVENTIVE FACTOR
HOST :
- 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 FACTOR
MICRO ORGANISM :
- CAPACITY OF INVASIVE :
* DOSES
* VIRULENT
COURSE OF INFECTION
* INFLAMATION * PHAGOSIIS
* IMM. RESPONSE * INTERFERON
PROTECTIVE FAILURE
SKIN.
[Link].
GASTER.
SECRETIONS
COMMENSAL GROWTH
[Link]
[Link]
DEBILITATING DISEASES
INFECTION MECHANISM
TOXIN PRODUCTION : (EXO/ENDO)
HYPERSENSITIVITY REACTION
BLOD STREAM : - BACTERAEMIA
- SEPTICAEMIA
- PYEMIA

LOCAL INFL NON LCL INFL

BLOOD STREAM

BACTEAE SEPTICAE PYAEMIA
MIA MIA
BACTERIAL INFECTION
BACTERAEMIA
COMMONLY
NO SERIOUS
INTEGRAL PART OF SOME INFECTION
TYPHOID FEVER
DENTAL EXTRACTION BACTERAEMIA
[Link] / SEPTICAEMIA

SEPTICAEMIA
VERY SERIOUS CONDITION TOXAE
MIA AND SHOCK
FORM : - PRIMARY
- COMPLICATE
- IMMUNE DECREASED

PYAEMIA
SEVERE CONDITION (+ TOXAEMIA)
SMALL AGGREGATE [Link]
FORM : - PYAEMIC ABSCESSES
- SEPTIC INFARCTION

PYAEMIC ABSCESS
SEPTIC FOCUS ( STAPH ) THROMBO-SIS
OF VENULES MICROEMBOLI
MULTIPLE ABSCESS (VARIOUS ORGANS)
- CEREBRAL CORTEX, MYOCARDIUM,
LUNGS, RENAL CORTEX.
SEPTIC INFARCTION
LARGE
SEPTIC THROMBOSIS
- [Link] THROMBOPHLEBITIS
EMBOLISM INFARCTTION + SUP
PURATION LUNG & LIVER.
- ACUTE [Link] 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 [Link] !!
- BLOOD STREAM PYAEMIA


PYOGENIC BACTERIA
[Link] PHARYNX
HYALURONIDASE, STREPTOKINASE,
LEUCOCIDIN.
- SKIN IMPETIGO, ERISIPELAS, CEL
LULITIS, LYMPHANGITIS.
- WOUND TONSILITIS, PHARYNGITIS
- BLOOD STREAM SEPTICAEMIA
PYOGENIC BACTERIA
MENINGOCOCCUS NASOPHARYNX
PURULENT MENINGITIS (CHILD)
FATAL SEPTICAEMIA. SKIN RASH &
MASSIVE ADRENAL HAEMORRHAGE
(WATERHOUSE FRODERICHSEN SYN
DROME)
PYOGENIC BACTERIA
GONOCOCCUS ( GENITAL [Link])
PURULENT (URETHRA & CERVIX)
[Link], PROSTATITIS,
EPIDIDYMITIS (MALE)
CERVICITIS, ACUTE SALPINGITIS
( FEMALE) STERIL
COMMENSAL BACILLI
GIT (COLIFORM, PROTEUS, PSEUDOMO
NAS.
LOW GRADE VIRULENT.
WOUND INFC, PYELONEPH, CYSTITIS,
DIVERTICULITUIS, APPENDIT IS.
GIT, U.T INFECTION
ENDOTOXIN SHOCK

GANGGRENE
SPECIAL TYPE OF NECROSIS
PRIMARY GAS GANGGRENE
DEEP WOUND + CLOSTRIDIA (ANAE-
ROBIC SPORULATING) GAS (SACHA
ROLYTIC & PROTEOLYTIC)
RAPIDLY SPREAD SEVERE TOXAEMIA
GANGGRENE
SECONDARY :
- WET : - OEDEMA
- VENOUS CONGETION
(STRANGULATION & OCCLUTION)
- DRY : - GRADUAL OCCLUTION ( TOES
AND FEET
PURIFICATION PROSSES (SLOW)
TETANUS
CLOSTRODIUM TETANI
ANAEROB
GRAM + DRUM STICK (FAECES)
INFC : PENETRATING WOUND
EFFECT : INFC EXOTOXIN
EXOTOXIN LOCAL NERVE SPASM
MOTOR NERVE
TRISMUS,RISUS SARDONICUS, CONVULSION,
RESP SPASM EXHAUSTION & DEATH.
IMM : TOXOID (PROP) , ANTI TOXIN (THE/)
GRANULOMA
CHRONIC INFECTION
TUBERCULOSIS.
SYPHILIS
ACTINOMYCOSIS
LEPROSY
TUBERCULOSIS
MYCOBACTERIUM TUBERCULOSIS
DISEASE DECLINED :
* NUTRITION & HYGIENE
* CHEMOTHERAPY
* BCG IMMUNISATION.
TUBERCLE : 1 2 DAYS PMN
1 WEEK MACROPHAGE
2 WEEK GIANT CELL,
LYMPOSITE, EPOID.
3 WEEK + CASEATION.
TUBERCULOSIS
PRIMARY INFECTION.
- FIRST CONTAC (CHILDREN)
- PERIPHERAL LUNG (GHON)
- WITH LYMPH NODE ( GHON COMP)
HEALING CALCIFICATION
SPREAD BLOOD STREAM MILIARY
(GENERALLY)
LOCAL (ORGAN) MENING, JOINT, BONE
TUBERCULOSIS
REINFECTION APEX PROGRES.
VARIATION FORM :
* EXUDATIVE PLEURAL EFFUSION
ASCITES (ABDOMEN)
COLD ABSCESS SINUS (ABSCESS)
FIBROTIC BODY REPARATIVE.
ACUTE CASEATING IMPAIRED IMM.
SYPHILIS
VENERAL INFECT.
TREPONEMA PALLIDUM
FORM : * PRIMARY
* SECONDARY
* TERTIARY (LATE)
- GUMMA
- [Link]
- NEUROLOGICAL SYPH.
PRIMARY SIPHYLIS
3 WEEKS SIRCULATION HARD C.
LIPMPHOCYTE & PALMA, PERI & END
ARTERITIS.
SWELLING LYMPH NODES HARD AND
PAINLESS.
HARD CHANCRE RAISED BUTTON
NODULE.

SECONDARY SYPHILIS
2 OR 3 MONTH
SKIN RASH (+), ULCER MUCOUS MEMBRA
NE, GENERALLY LYPHADENOPHATY
FEVER AND ANAEMIA (+)
SPIROCHAETA (>>) + FOCAL INFILTRATION
LYMPHOCYTE, PLASMA CELL AND
MACROPHAGE, MILD ARTERITIS.
TISSUE DESTRUCTION MINIMAL
HEALING WITHOUT SCARING.
TERTIARY SYPHILIS
GUMMA : - LOCAL NECROTIC.
- BONE, TESTIS, LIVER.
[Link] : - ARCH & THORACIC
- [Link] DESTR. FOCAL
DESTRUCTION ( WINDOWING)
- PERIARTERITIS
- ANEURISMA PRESSURE
EFFECT OR RUPTURE

TERTIARY SYPHILIS
NEUROLOGICAL
* MENINGOVASCULAR MENINGEAL
BLOOD VESSELS NEUROLOGICAL
EFFECT
* PARENCHYMATOUS :
- GENERAL PARALISIS (SEVERE DESTRUC-
TION OF CEREBRAL TISSUE).
- TABES [Link]

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

IMMUNITY
ANTIBODY PRODUCTION :
- ANTIBODY ACTIVE (COMPLEMENT)
WASSERMANN REACTION.
- SPECIFIC ANTI-TREPONEMAL [Link]
USED SPESIFIC COMPLEMENT FIXING,
IMMOBTION AND FLUORESCENCE TEST

IMMUNITY
CELL MEDIATED DELAYED HYPERSENSI
TIVITY ALSO DEVELOPS. SENSITIVITY
REACTION ARE IMPORTANT IN THE ME-
CHANISM OF SYPHILITIC DAMAGE TO
TISSUE.

ACTINOMYCOSIS
LOCALISED SPREADING (CHRONIC
SUPPURATION)
SITE OF INFECTION : - LOWER JAW
- ILEO-CAECAL
- LUNG
LOBULATED ABSCES PUS (SULPUR
GRANULE), PMN, FOAMY MACROFAGE
AND SUROUNDED BY FIBROUS TISSUE.
LEPROSY
SLOW PROGRESIVE DISEASE.
DAMAGE PERIPHERAL NERVE.
ACQUIRED (CLOSE PROLONG CONTACT)
FORM : * LEPROMATOUS
* TUBERCULOID.

LEPROMATOUS
NODULE SKIN LEONINE FACIES
AFFECTED NERVE (LATE)
LESION : - LYMPHOCYTE
- PLASMA
- MACROFAGE + ORG.
- ORG +++ (TISSUE)
CELL MEDIATED IMMUNITY (-)
TUBERCULOID
SKIN PALLOR AND ANAESTHESIA
INVOLVED NERVE (EARLY)
FOLLICULAR GRANULOMA (TUBERCLE)
ORGANISM (SCANTY)
CELL MEDIATED IMMUNITY (WELL)
VIRAL INFECTIONS
ACUTE VIRAL :
- POLIO, HEPATITIS, SMALLPOX
LATENT VIRAL :
- HERVES SIMPLEX/ZOSTER, CHICKEN
POX (VARICELLA)
SLOW VIRAL :
- SCARPIE, KURU
ONCOGENIC VIRAL.
- VERUCAE VULGARIS, EPSTEIN BARR
HOST/VIRUS INTERACTION
CHANGES CELL
INTERFERON PRODUCTION
IMMUN RESPONSE
INFLAMATORY RESPONSE
CHANGES CELL
CELL DEGENERATION : LOSS OF
FUNCTION DEATH
VACUOLATION LYSIS (RAPID)
[Link]
CONDENSATION SLOW LYSIS
FUSION OF CELLS GIANT CELL ( WAR
THIN-FINKELDY CELL OF MEASLES)
CHANGES CELLS
CELL PROLOFERATION WARTY +
CELL DEATH.
INCLUTION BODIES FORMATION
IN CYTOPLASM.
NO APPARENT LATEN OR SLOW IN
FECTION.
NO APPARENT BUT MALIGNANT
(LATER) OR SLOW INFECTION
INTERFERON PRODUCTION
INTERFERON PRODUCT REPLICATION
VIRAL INHIBITION.
INTERFERON (PROTEIN) NOT ANTIBODY
THE FIRST DEFENCE.
IMMUNE RESPONSE
ANTIBODIES TO VIRUS
CELL MEDIATED IMMUNITY
+/- VIRAL/ANTIBODY COMPLEXES
ARTERITIS, KIDNEY DAMAGE
INFLAMATORY RESPONS VASCULAR
AND EXUDATIVE ELEMENT.

OPPORTUNISTIC INFECT.
NON PATHOGEN ORGANISM
LOW GRADE VIRULENCE
IMMUNITY IMPAIRED :
- CONGENITAL [Link].
- ACQUIRED URAEMIA, LIVER DISE
ASES, MALIGNANT TUMORS ETC
THERAPY, ANTIBIOTIC,
TRANSPLANT SURGERY ETC

GENERAL EFFECTS
FEVER (PYREXIA) :
[Link] HEAT
COLD, [Link] RATE AND DEHY
DRATION.
PYREXIA : INFARCT, TUMORS, CERE
BRAL DISEASE, HEAT STROKE
HYPERPYREXIA > 41 C
GENERAL EFFECTS
MATABOLISM CHANGES :
FEVER [Link] UTILISATION
CHO RESERVE ([Link])BREAK
DOWN TISSUE PROTEIN INCR. NITRO
GEN URINE (KETOACIDOSIS) INCR.
CONSENTRATION AND SMALL VOLUME

GENERAL EFFECTS
CHONIC INFECTION :
HYPERGAMMAGLOBULINEMIA
INCREASED BLOOD PROTEIN
INCREASED ESR.

INFLAMATION CELLS
NEUTROPHIL POLYMORPHONUCLEAR
LEUCOCYTE (PMN)
LYMPHOCYTE
EOSINOPHILS
MONOCYTE
MAST CELLS (BASOPHILS)
POLYMORPHONUCLEAR
FROM BONE MORRO
LIFE SPAN 2 3 DAYS
FUNCTION : - PHAGOCYTOSIS
- KILLING [Link]
NORMAL COUNT : 3.000 7.500/MM3
INFECTION > 10.000/MM3
LYMPHOCYTES
FROM LYMPHOID NODE
PROD. ANTIBODIES & CELLULAR
COMPONENT IMMUN RESPONSE
COUNT : 1,500 3.500 / MM3
VIRAL INFECT. & CHRONIC [Link]
LYMPHOSITOSIS
B. LYMPHOCYTE PLASMA CELLS &
Ig
EOSINIPHILS
DERIVED FROM BONE MORROW
NORMAL 1 4 %
EOSINOPHILIA : - HELMIN INFECT.
- PARASITES
- ALLERGIC ASTHMA

MONOCYTES
TOTAL WHITE CELLS : 4 7 %
AS MACROPHAGE, LOCAL INFLAMA-TION
REACTION
INCREASED :- [Link].(TB)
- PROTOZOAL (MALARIA)
EPITHELOID CELLS MACROPHAGES
FUSION GIANT CELLS

MAST CELLS
BASOPHILS < 1 %
SCATTERED [Link]
DERIVED FROM BONE MORROW
CONTAIN : - HIATAMINE
- HEPARINE
- ENZYMES
REALEASED BY CHEMICAL FACTOR
(INFLAMATORY REACTION)
HEALING
WOUND HEALING
COMPLICATIONS : - CONTRACTURE
- GRANULATION
- KELOID
- FIBROSIS
REGENERATION
SPECIAL SITUATION.
WOUND HEALING
PRIMARY HEALING :
- CLEAN EXISED WOUND
- GOOD POSITION (PALNED [Link])
IMMEDIATELY: - BLOOD CLOT
2-3 HOURS : - INFLAMATION (+)
- MILD HYPERAEMIA
- FEW POLYMORPHS
WOUND HEALING
2-3 DAYS : - MACROPHAGE REMO-
VING CLOT
- FIBROBLASTIC
10-14 DAYS : - SCAB LOOSE
- EPITHELIAL COVERING.
- FIROUS UNION

WOUND HEALING
WEEKS : - SCAR TISSUE SLIGHLY
HYPERAEMIA
- GOOD FIBROUS UNION
MONTHS YEAR:
- DEVASCULARISATION
- COLLAGEN(-) ENZYME
- SCAR MINIMAL.



SECONDARY HEALING
LOSS OF TISSUE >>
NECROSIS (+)
INFECTION (+)
EARLY : BLOOD & FIBRIN CLOT (+)
ACUTE INFL. CELLS (+)
FEW DAYS : - [Link]
- NEW CAPILARY
- MACROPHAGE
- PMN, FIBROBLAST

SECONDARY HEALING
1 WEEK : - SURFACE DEBRIS (-)
- FIBROBLASTS >>
- [Link]
- CAPILARY >>
- GRANULATION

SECONDARY HEALING
2 WEEKS : - [Link] COMPL
- TRANSVERS COLLAGEN
- DECREASED CAPILARY
- FEW CELLS
MONTH : - FULL [Link]
- SURFACE DEPRETION (< )
- THICK COLLAGEN SCAR
- VASCULAR ( < )
REGENERATION
CELL TYPE :
* LABILE CELLS : - EPITHELIUM
- BONE MORROW
- LYMPHOID
* STABLE CELLS: - LIVER
- ENDOCRINE CELLS
* PERMANENT CELLS : - NERVE CELLS
SPECIAL HEALING
INTERNAL SURFACE G.I.T.
SOLID EPITHELIAL ORGANS :
- KIDNEY
- LIVER
- MUSCLE
NERVOUS TISSUE : - CNS
- PERIPHERAL N
SPECIAL HEALING
BONE : - IMMEDIATE EFFECT
- EARLY REACTION ( 4-5 DAYS)
- AFTER 1
ST
WEEK
- > 3 WEEK
- WEEK MONTH
- MONTH LATER