INFLAMMATION

INFLAMMATION


LOCAL PHYSIOLOGICAL RESPONSE TO TISSUE INJURY.

FUNDAMENTALLY PROTECTIVE. DISEASE MANIFESTATION

INFLAMMATION
BENEFICIAL EFFECT
      

DESTRUCTION OF MICRO ORGANISM ENTRY OF ANTIBODIES TRANSPORT OF DRUGS FIBRIN FORMATION DELIVERY OF NUTRIENTS AND OXYGEN STIMULATION OF IMMUNE RESPONSE WALLINGWALLING-OFF OF ABSCESS CAVITY.

PATHOLOGICAL EFFECTS
     

DISEASE: DISEASE: BRAIN ABSCESS, APPENDICITIS S.O.L. SWELLING COMPRESSION, DIGESTION OF NORMAL TISSUE BY COLLAGENASES ,PROTEASES, ,PROTEASES, FIBROSIS. SCAR FORMATION INAPPROPRIATE RESPONSE POLLEN / HAY FEVER PROCESS DESCRIBED BY SUFFIX ITIS.

INFLAMMATION


   

INFLAMMATION IS THE REACTION OF A TISSUE AND ITS MICROCIRCULATION TO A PATHOGENIC INSULT DEFENSIVE PROCESS THAT A LIVING BODY INITIATES AGAINST LOCAL TISSUE DAMAGE INFLAMMATIO LATIN PHLOGOSIS GREEK IMBALANCE OF VARIOUS HUMORS MUCUS / BLOOD / BILE

DEFINITION
 INFLAMMATION IS A COMPLEX REACTION TO INJURIOUS AGENTS SUCH AS MICROBES AND DAMAGED USUALLY NECROTIC CELLS THAT CONSISTS OF VASCULAR RESPONSE, RESPONSE, MIGRATION AND ACTIVATION OF LEUCOCYTES AND SYSTEMIC REACTIONS.

INFLAMMATION


UNIQUE FEATURES OF INFLAMMATORY PROCESS

REACTION OF BLOOD VESSEL LEADING TO ACCUMULATION OF FLUID AND LEUCOCYTES IN EXTRAVASCULAR TISSUE

 

INFLAMMATORY RESPONSE INTERTWINED WITH THE PROCESS OF REPAIR INJURED TISSUE REPLACED THROUGH
REGENERATION OF NATIVE PARENCHYMAL CELLS FILLING OF DEFECT WITH FIBROUS TISSUE

INFLAMMATION
   

EGYPTIAN PAPYRUS 3000BC CELSUS ROMAN WRITER 1ST CENTURY AD

4 CARDINAL SIGNS OF INFLAMMATION

VASCULAR BASIS 18TH CENTURY JOHN HUNTER

DILATION OF BLOOD VESSELS PUS REPRESENTED MATERIAL DERIVED FROM BLOOD NOT A DISEASE

RODOLF VIRCHOW 1793

REACTION TO PRIOR TISSUE INJURY FIFTH SIGN FUNCTIO LASEA

INFLAMMATION
 JULIUS

COHNHEIM 1839-1884 1839-

EMIGRATION OF LEUCOCYTES THROUGH THE WALL OF MICROVASCULATURE

 METCHNIKOFF  THOMAS

1880

ROLE OF PHAGOCYTOSIS

LEWIS 1927

CHEMICAL MEDIATORS

SIGNS OF INFLAMMATION


ROMAN ENCYCLOPEDIST AULUS CELSUS 1st Century. 4 CARDINAL SIGNS RUBOR REDNESS TUMOR SWELLING CALOR HEAT DOLOR PAIN VIRCHOW FUNCTIO LASEA LOSS OF FUNCTION

CELLULITIS EDEMA REDNESS

ACUTE APPENDICITIS

EMPYEMA GALL BLADDER

SUPPURATIVE AND FIBRINOUS

CELLS OF INFLAMMATION POLYMORPHS EOSINOPHILS PLASMA CELLS

LUNG ABSCESS ACUTE INFLAMMATORY CELLS

FALLOPIAN TUBE NORMAL

FALLOPIAN TUBE NORMAL

FALLOPIAN TUBE INFLAMMATION

INFLAMMED TUBO-OVARIAN MASS TUBO-

FALLOPIAN TUBE ACUTE INFLAMMATORY CELLS

FALLOPIAN TUBE PELVIC INFLAMMATORY DISEASE

CLASSIFICATION
 ACCORDING

TO ITS TIME COURSE  DIFFERENCES IN THE CELL TYPES ACUTE INFLAMMATION



INITIAL AND OFTEN TRANSIENT SERIES OF TISSUE REACTION TO INJURY.

CHRONIC INFLAMMATION


SUBSEQUENT AND OFTEN PROLONGED TISSUE REACTION

CHRONIC GRANULOMATOUS INFLAMMATION

CAUSES OF ACUTE INFLAMMATION



INFECTION
BACTERIAL EXOTOXIN AND ENDOTOXINS , VIRUS INTRACELLULAR, PARASITE- HYPERSENSITIVITY PARASITE-

 

TRAUMA
BLUNT AND PENETRATING

PHYSICAL AND CHEMICAL AGENTS

THERMAL / FROSTBITE, ULTRAVIOLET / IONISING RADIATION,CORROSIVE CHEMICALS ACID / ALKALI

  

TISSUE NECROSIS
ANY CAUSE

FOREIGN BODIES
SPLINTER, SUTURES

IMMUNE REACTION
HYPERSENSITIVITY REACTIONS

MAIN FEATURES OF ACUTE INFLAMMATION

 ACCUMULATION

OF FLUID AND PLASMA AT AFFECTED SITE

 INTRAVASCULAR

ACTIVATION

OF PLATELETS AND POLYMORPHONUCLEAR NEUTROPHILS AS INFLAMMATORY CELLS

HAEMODYNAMIC CHANGES
 

TRANSIENT VASOCONSTRICTION
OF ARTERIOLE 3-5 SEC

PERSISTENT PROGRESSIVE VASODILATATION

OF ARTERIOLE HR INCREASED BLOOD FLOW WARMTH REDNESS

INCREASED PERMEABILITY OF MICROVASCULATURE

LOCAL HYDROSTATIC PRESSURE TRANSUDATION OF FLUID SWELLING

SLOWING STASIS
MIGRATION OF NEUTROPHILS

TRIPLE RESPONSE


RED LINE
APPEARS WITHIN FEW SEC LOCAL VASODILATATION OF CAPILLARIES VENULES

FLARE
RED FLUSH SURROUNDING THE RED LINE VASODILATATION OF ADJACENT ARTERIOLE

WHEAL
SWELLING OR EDEMA DUE TO TRANSUDATION OF FLUID

CHANGES IN ACUTE INFLAMMATION

 VASCULAR

EVENTS  CELLULAR EVENTS

NEUTROPHIL

NEUTROPHIL

LYMPHOCYTE

MONOCYTE

PLASMA CELL

EOSINOPHIL

BASOPHILS

ACUTE INFLAMMATION POLYMORPHS

ACUTE SALPINGITIS

EARLY STAGES OF ACUTE INFLAMMATION



EDEMA FLUID , FIBRIN, NEUTROPHIL POLYS

ACCUMULATE IN EXTRACELLULAR SPACE OF DAMAGED TISSUE

INVOLVES THREE PROCESSES CHANGES IN VESSEL CALIBRE AND FLOW INCREASED VASCULAR PERMEABILITY
 AND FORMATION OF FLUID EXUDATE

FORMATION OF CELLULAR EXUDATE

 EMIGRATION OF NEUTROPHIL POLYS INTO EXTRAVASCULAR SPACE

VASCULAR CHANGES
VASODILATION EARLIEST MANIFESTATION TRANSIENT CONSTRICTION FIRST INVOLVES ARTERIOLE NEW CAPILLARY BEDS OPEN SEVERAL MEDIATORS HISTAMINE ,NITRIC OXIDE ACT ON VASCULAR SMOOTH MUSCLE PREPRE-CAPILLARY SPHINCTERS OPEN

FIRST PHASE

SECOND PHASE

THIRD PHASE

ENDOTHELIAL DAMAGE AND VASCULAR PERMEABILITY

TYPE OF PERMEABILITY CHANGES

MEDIATORS OF PERMEABILITY CHANGES

INCREASED VASCULAR PERMEABILITY

ESCAPE OF PROTEIN RICH FLUID
SMALL BLOOD VESSELS SINGLE LAYER OF ENDOTHELIAL CELLS

LOSS OF PROTEIN
REDUCES INTRAVASCULAR OSMOTIC PRESSURE INCREASES OSMOTIC PRESSURE OF INTERSTITIAL FLUID INCREASED CAPILLARY HYDROSTATIC PRESSURE OUTFLOW OF FLUID AND ITS ACCUMULATION EDEMA

HEMODYNAMIC FORCES NORMAL

ACUTE INFLAMMATION

NORMAL BLOOD FLOW

BLOOD FLOW CHANGES IN INFLAMMATION

INCREASED VASCULAR PERMEABILITY

PROTEINS IMMUNOGLOBULINS DESTRUCTION OF INVADING MICROMICROORGANISM COAGULATION FACTORS INCLUDING FIBRINOGEN FIBRIN DEPOSITION

INCREASED VASCULAR PERMEABILITY

FORMATION OF ENDOTHELIAL GAPS IN VENULES, CONTRACTION OF ENDOTHELIAL CELLS FAST AND SHORT LIVED HISTAMINE / BRADYKININ /LEUKOTRIENE MEDIATE DIRECT INJURY SEVERE BURNS LYTIC INFECTIONS IMMEDIATE SUSTAINED DELAYED PROLONGED LEAKAGE DELAY OF 2-12 HRS LASTS HRS TO DAYS 2VENULES / CAPILLARIES THERMAL INJURY / RADIATION / TOXINS

INCREASED VASCULAR PERMEABILITY

LEUCOCYTE MEDIATED ENDOTHELIAL INJURY RELEASE PROTEOLYTIC ENZYME TOXIC RADICALS INCREASED TRANSCYTOSIS ACROSS ENDOTHELIAL CYTOPLASM VESICULOVACUOLAR ORGANELLE LEAKAGE FROM NEW BLOOD VESSEL ANGIOGENESIS LEAKY UNTIL ENDOTHELIAL CELLS MATURE

MECHANISMS OF INCREASED VASCULAR PAERMEABILITY IN INFLAMMATION