INFLAMMATION

TOPICS DISCUSSED
 DEFINITION OF INFLAMMATION
 AGENTS-INFLAMMATION
 SIGNS-INFLAMMATION
 TYPES-INFLAMMATION
 PHAGOCYTOSIS
 CHEMICAL DERIVED MEDIATORS
 TOPICS DISCUSSED
 REGULATION OF INFLAMMATION
 INFLAMMATORY CELLS
 EG-CHRONIC INFLAMMATION
 INFLAMMATION TO THROMBOSIS
 ALCOHOLICS MORE PRONE TO THROMBOSIS
 DEFINITION OF INFLAMMATION
 INFLAMMATION – LOCAL RESPONSE
 RESPONSE GIVEN BY- LIVING
MAMMALIAN TISSUE
 RESPONSE IS GIVEN TO- ANY INJURY
BY ANY AGENT
 INFLAMMATION- BODY DEFENCE
REACTION TO ELIMINATE OR LIMIT
THE SPREAD OF INJURIOUS AGENT
 AGENTS OF INFLAMMATION
 PHYSICAL AGENTS –
HEAT,COLD,RADIATION,MECHANICAL
TRAUMA
 CHEMICAL AGENTS- ORGANIC AND
INORGANIC POISONS
 INFECTIVE AGENTS- BACTERIA, VIRUSES
AND THEIR TOXINS
 IMMUNOLOGICAL AGENTS- CELL MEDIATED
AND ANTIGEN-ANTIBODY REACTIONS
 SIGNS OF INFLAMMATION
 ACC TO ROMAN WRITER CELSUS THE 4
CARDINAL SIGNS OF INFLAMMATION ARE
 REDNESS
 SWELLING
 PAIN
 RISE IN LOCAL TEMPERATURE (HEAT)
 SIGNS OF INFLAMMATION
 LATERON VIRCHOW INCLUDED
LOSS OF FUNCTION AS THE
5THCARDINAL SIGN OF
INFLAMMATION
 CLASSIFICATION OF
INFLAMMATION
 DEPENDING UPON
1) DEFENSIVE CAPACITY OF HOST
2) DURATION OF RESPONSE
INFLAMMATION IS CLASSIFIED AS,
1) ACUTE INFLAMMATION
2) CHRONIC INFLAMMATION
 ACUTE INFLAMMATION
 SHORT DURATION
 REPRESENT EARLY BODY REACTION
 FOLLOWED BY REPAIR
 ACCUMULATION- FLUID AND PLASMA AT
AFFECTED SITE
 INTRAVASCULAR ACTIVATION OF
PLATELETS
 POLYMORPHONUCLEAR NEUTROPHILS AS
INFLAMMATORY CELL
 CHRONIC INFLAMMATION
 LONGER DURATION
 OCCURS EITHER AFTER CAUSATIVE AGENT
OF ACUTE INFLAMMATION PERSIST FOR A
VERY LONG TIME
 STIMULUS IS SUCH THAT IT INDUCES A.INF
FROM BEGINNING
 CHARACTERESTIC FEATURE-PRESENCE OF
INF CELLS LYMPHOCYTES,PLASMA CELLS,
AND MACROPHAGES
 EVENTS OF INF
 VASCULAR EVENTS
 CELLULAR EVENTS

1) EXUDATION OF LEUCOCYTES
2) PHAGOCYTOSIS
 PHAGOCYTOSIS
 PROCESS- ENGULFEMENT
 ENGULFMENT- SOLID PARTICULATE
MATERIAL
 ENGF BY- CELLS
 PROCESS- CELL EATING
 CELLS- PHAGOCYTES
 PHAGOCYTOSIS
 PHAGOCYTIC CELLS- MICROPHAGES
AND MACROPHAGES
 DEF MICROPHAGES:-
1) PMNs
2) APPEARANCE- EARLY INF RESPONSE
 PHAGOCYTOSIS
 MACROPHAGES:-

1) CIRCULATING MONOCYTES OF FIXED

MONO NUCLEAR NEUTROPHILS
 STEPS IN PHAGOCYTOSIS
 RECOGNITION AND ATTACHMENT
 ENGULFMENT STAGE
 DEGRANULATION STAGE
 KILLING AND DEGRADATION
 RECOGNITION AND
ATTACHMENT
 PHAGOCYTIC CELLS- RECG
 PHG CELLS ATTRACTED- BACTERIA
 ATTRACTION – CHEMOTACTIC
FACTORS
 CF RELEASED BY- 1) BACTERIAL
PRODUCTS 2) TISSUE PROTIENS
 PHAGOCYTOSIS
 BOND ESTB:-BETWEEN BACTERIA
AND CELL MEMBRANE OF
PHAGOCYTIC CELL
 ACCOMPLISH BOND ESTB:-MICRO-
ORGNSMS COATED WITH OPSONINS
 OPSONINS:-NATURALLY OCCURING
FACTOR
 OPSONINS PRESENT IN SERUM
 PHAGOCYTOSIS
 OPSONINS EG:-
1) IgG OPSONIN IS Fc FRAGMENT OF
IMM G
2) C3b OPSONIN FRAG COMPLEMNT
SYSTEM
3) LECTINS – CARBOHYDRATE BINDING
PROTIEN
4) LECTINS PRESENT PLASMA
 ENG STAGE
 OPSONISED PARTICLE BOUND-
SURFACE OF PHAGOCYTE
 PHAGOCYTE – READY ENG
 ENGF ACCOMPLISH –FORMATION OF
CYTOPLASMIC PSEUDOPODS
 CYTOPLASMIC PSEUDOPODS
FORMATION AROUND PARTICLE
 FORMATION OF CYT PSEUDOPODS
ACTIVATION OF ACTIN FILAMENTS
 ACTIN FILAMENTS IS BENEATH THE
CELL WALL
 DEGRANULATION STAGE
 PREFORMED GRANULES STORED
PRODUCTS OF PMNs SECRETED INTO
PHAGOSOME OR EXTRACELLULAR
ENVIRONMENT
 RELEASE SECONDARY OR SPECIFIC
GRANULES Eg LYSOSOMES
 PHAGOSOMES FUSE- AZUROPHILIC
GRANULES
 KILLINGAND DIGESTION OF MICRO-
ORGANISMS COMPLETE ROLE OF
PHAGOCYTES AS SCAVANGER CELLS
 MICRO ORGANISMS KILLED- ANTI
BACTERIAL SUBSTANCES
 MICRO ORG DEGRADED HYDROLYTIC
ENZYMES
 KILLING AND DEG FAIL- TUBERCLE
BACILLI
 ACTION ANTI MICROBIAL AGENTS
TAKES PLACE BY 2 MECHANISMS
1) OXY-DEPENDENT
2) OXY-INDEPENDENT
3) NO-MECHANISM
 OXY-DEP:-
OXY-DEP:- IMP
IMPMECHANISM
MECHANISM
1) FORMATION
1) FORMATION – –REACTIVE
REACTIVE
OXY
OXY
METABOLITES
METABOLITES
Eg H2O2,
2) Eg
2) H2O2, HOCL, HOI, HOBR,OH
3) TYPE OF BACTERICIDAL
ACTIVITY CARRIED OUT BY
ENZYME MPO OR INDEPENDENT
OF ENZYME MPO
MPO PRESENT GRANULES OF NEUTROPHILS AND MONOCYTES
OXY INDEPENDENT:-
1) SOME AGENTS RELEASED BY GRANULES OF PHAGOCYTIC CELLS
DO NOT REQUIRE
 OXY FOR THEIR BACTERICIDAL
ACTIVITY
 BAC ACTIVITY INCLUDES LYSOSOMAL
HYDROLASES, PERMEABILITY
INCREASING FACTORS,
DAFENSINS,CATIONIC PROYIENS
 NO MECHANISM:-
1) NO PRODUCE BY ENDOTHELIAL
CELLS AND ACTIVATED
MACROPHAGES
2) NO ROLE IN INFLAMMATORY
REACTION
CHEMICAL DERIVED MEDIATORS
 CHEMICAL DERIVED MEDIATORS ALSO
KNOWN AS PERMEABILITY FACTORS
OR ENDOGENOUS MEDIATORS OF
INCREASE VASCULAR PERMEABILITY
AND VASODILATATION
 MEDIATORS ARE LARGE AND
INCREASING NO ENDOGENOUS
COMPOUNDS
 MEDIATORS ARE RELEASE BY
DAMAGE TISSUE,CELLS AND
PLASMA
 DEPENDING UPON SOURCE
CLASSIFIED AS:-
1) CELL DERIVED MEDIATORS
2) PLASMA DERIVED MEDIATORS
 CELL DERIVED MEDIATORS
 VASOACTIVE AMINES
 ARACHIDONIC ACID
 LYSOSOMAL COMPONENTS
 PLATELET ACTIVATING FACTOR(PAF)
 NITRIC OXIDE AND OXYGEN
METABOLITES
 VASOACTIVE AMINES
 EARLY INF PROCESS 2 IMP PHARMACOLOGICALLY
ACTIVE AMINES TAKES PART FIRST HOUR
1) HISTAMINE
2) SEROTONIN (5HT)
 HISTAMINE
 HISTAMINE STORED
 HISTAMINE RELEASE
 HISTAMINE MAIN ACTION
 PRODUCTS OF ARACHIDONIC ACID
METABOLISM
 SLOW REACTING SUBSTANCES OF
ANAPHYLATOXINS SRS-As
 SEROTONIN
 SEROTONIN PRESENT
 LESS POTENT MEDIATOR
 SEROTONIN SECRETING TUMOUR
 ARACHIDONIC ACID
 DEF
 SOURCES
 STIMULIACTIVATES AA
 TWO PATHWAYS OF ACTIVATION OF
AA
 CYCLO OXYGENASE PATHWAY
 METABOLITES FORMED
 PROSTAGLANDIN FOUND
 FORMATION OF 3 METABOLITES
 ACTIONS OF PGD2,PGE2,PGF2-alpha
THROMBOXANE A2, PROSTACYCLIN
 LIPO OXYGENASE PATHWAY
 METABOLITES FORMED
 FORMATION OF MEDIATORS
 LTA4
 LTA4+ENZYMES =LTB4
 LTB4 CHEMOTACTIC FOR
PHAGOCYTIC CELLS AND STIMULATE
PHAGOCYTIC CELL ADHERENCE
 ACTION OF LTC4,LTD4,LTE4
 LTC4,D4,E4 INDUCES
 LYSOSOMAL COMPONENTS
 LYS GRANULES PRESENT
 LYS GRANULES ELABORATE
1) GRANULES OF NEUTROPHILS
TYPES OF GRANULES
SPECIFIC GRANULES CONTENTS
AZUROPHIL GRANULES CONTENTS
 EgOF NEUTRAL PROTEASES
 DESTRUCTION OF BACTERIA
 EXTRACELLULAR CONSTITUENTS
 PROTEASES
 HARMFUL TISSUE DESTRUCTION
 ANTI TRYPSIN
GRANULES OF MONOCYTES AND
TISSUE MACROPHAGES
 DEGRANULATION
OF GRANULES OF
MONOCYTES AND TISSUE
MACROPHAGES
 PLATELET ACTIVATING FACTOR
 SUBSTANCES RELEASES PAF
 PAF RESPONSIBLE
 ROLE OF PAF
 CYTOKINES

 CYTOKINES PRODUCE
 CYT SUBSTANCES
 CYT ACTING AS MEDIATORS
 CHEMOKINES INCLUDE
 PRODUCTION OF IL1,TNF-ALPHA,TNF-
BETA,IF-GAMMA,IL-8,PF-4
 POTENT CHEMOATTRACTANT FOR
INF CELLS
 CYTOKINES INDUCES
 ACTIVATION OF MACROPHAGES AND
NEUTROPHILS
 IL-GAMMA ASSOCIATED WITH
 IL-8 ,PF-4, MCP-1 AND EIOTAXIN
ACTS AS CHEMOTACTIC AGENT FOR
NO AND OXYGEN METABOLITES
 ORIGINALLYDESCRIBE AS
 NO & O2 METABOLITES ARE
RELEASED BY
 MEDIATOR OF INF
 ACT MACROPHAGES
 ARGININE
 NO SYNTHASE
 ROLE IN INF
 ACT MACROPHAGES AND
NEUTROPHILS RELEASE
 ACTION OF FREE RADICALS
 O2 DERIVE MEDIATORS ACTIVATES
AND INACTIVATES
 EFFECT IS COUNTERACTED BY
 ALCOHOL TO
THROMBOSIS
 ALCOHOL METABOLISM IN LIVER ALCOHOL
IN THE PRESENCE OF ADH (ALCOHOL
DEHYDROGENASE) AND COENZYME
NICOTINAMIDE DINUCLEOTIDE) CONVERTS
INTO ACETALDEHYDE TO ACETATE AND
ACETYL CoA
 ACETATE IS RESPONSIBLE FOR
FORMATION OF FATS
 IN
CHRONIC CASE IT MAY CAUSE
HYPERCHOLESTRAEMIA-ONE OF THE
ENDOGENOUS AGENT IN CAUSING
THROMBOSIS
 COMMON SITE OF THROMBOSIS IS
LEFT VENTRICLE
 THROMBOSIS CAUSES DISTURBENCE
IN NORMAL FLOW OF BLOOD
 THE END
A STRONG POSITIVE SELF-
IMAGE IS THE BEST POSSIBLE
PREPARATION FOR SUCCESS