2. CHRONIC INFLAMMATION-DEFENSE AT
A PRICE
PROLONGED DURATION
WKS TO MONTHS
ACTIVE INFLAMMATION,
TISSUE DESTRUCTION AND
REPAIR
ALL occurs SIMULTANEOUSLY
3. CAUSES
PERSISTENT INFECTION
Eg:TB,SYPHILIS
LOW TOXICITY
EVOKE DELAYED HYPERSENSITIVITY REACTION
PROLONGED EXPOSURE TO TOXIC AGENTS
ENDO-TOXIC LIPIDS IN ATHEROMA
EXO-SILICOSIS,
AUTOIMMUNE:caused by excessive and
inappropriate activation of the immune system
Eg. RA,MS,IBD, Br. Asthma
4. FEATURES
MONONUCLEAR INFILTRATIION-
MACROPHAGES,LYMPHOS,PLASMA CELLS
TISSUE DESTRUCTION
ATTEMPTS AT HEALING:
angiogenesis+ fibrosis
5. Chronic infl. Acute infl.
collection of chronic inflammatory cells (*) alveolar spaces filled with neutrophils
destruction of parenchyma Congested blood vessels
fibrosis, (arrows)
6. CELLS-MACROPHAGES
KEY ROLE
PART OF MONOCYTE PHAGOCYTE SYSTEM
ORIGIN IN BM BLOOD MONOCYTES
TISSUE MACROPHAGES
TISSUE MACROPHAGES-MICROGLIA,KUPFFER
CELLS,ALVEOLAR MACROPHAGES,OSTEOCLASTS
7.
8. CELLS-MACROPHAGES
AFTER 48 HRS EMIGRATE INTO SITE OF
INFLAMMATION
ACTIVATION
BY CYTOKINES(IFN GAMMA), ENDOTOXINS
INCREASE IN SIZE, MORE LYSOSOMAL ENZYMES,
INCREASED METABOLIC ACTIVITY
WIDE VARIETY OF BIOLOGICALLY ACTIVE SUB
12. CELLS-MACROPHAGES
PRODUCTS OF MACROPHAGES
ELIMINATION OF MICROBES
TISSUE INJURY-PROTEASES,NO,AA METABOLITES
FIBROSIS
13. CELLS-OTHERS
LYMPHOCYTES
BOTH IN IMMUNE AND NON IMMUNE
TWO WAY INTERACTION WITH MACRO
PLASMA CELLS
FROM ACTIVATED B-LYMPHOS
tertiary lymphoid organs: long standing R.A.
EOSINOPHILS
IMMUNE,PARASITIC d/t MBP
EOTAXIN
14.
15. GRANULOMATOUS INFLAMMATION
It is a cellular attempt to contain an offending agent
that is difficult to eradicate.
A granuloma is a focus of chronic inflammation consisting
of a microscopic aggregation of macrophages that are
transformed into epithelium-like cells, surrounded by a
collar of mononuclear leukocytes, principally
lymphocytes and occasionally plasma cells.
17. GRANULOMA
EPITHELIOID CELLS
ACTIVATED/MODIFIED MACROPHAGES
INDISTINCT CELL BORDERS
PALE PINK CYTOPLASM
VESICULAR NUCLEUS-SLIPPER SOLE SHAPED
LYMPHOCYTES
USUALLY FORM A CUFF AROUND EP CELLS
MAY BE ADMIXED WITH PLASMA CELLS
18. GRANULOMA
GIANT CELLS
FUSION OF EPITHELIOID CELLS
LANGHANS G.C-NUCLEUS IN PERIPHERY-HORSE SHOE MANNER
FOREIGN BODY-HAPHAZARD ARRANGEMENT
NO SP SIGNIFICANCE ABOUT UNDERLYING CAUSE
FIBROSIS
SURROUNDING LYMPHOS
BURNT OUT-SCARRING
19. GRANULOMA
TWO MAIN TYPES BASED ON PATHOGENESIS- FB
(SUTURE,TALC) AND IMMUNE (TB)
IMMUNE
POORLY DEGRADABLE AGENT
CELL MEDIATED IMMUNITY
20. GRANULOMA
CENTRAL NECROSIS IS SEEN IN SOME
GRANULOMAS
PROTOTYPE-TB
CASEOUS NECROSIS
GROSSLY-CHEESE LIKE
MICRO-EOSINOPHILIC,AMORPHOUS GRANULAR DEBRIS
25. SYSTEMIC EFFECTS OF INFLAMMATION
ACUTE PHASE RESPONSE OR SYSTEMIC
INFLAMMATORY RESPONSE(SIRS)
DUE TO CYTOKINES-TNF,IL-1
26. SYSTEMIC EFFECTS OF INFLAMMATION
FEVER
IL-1 AND TNF ACT ON HYPOTHALAMUS
PRODUCE PGs
RESET TEMP AT HIGHER LEVEL
HOW USEFUL??????
27. OSLER
“HUMANITY HAS BUT 3 GREAT
ENEMIES-FEVER ,FAMINE AND
WAR,OF THESE BY FAR THE
GREATEST ,THE MOST TERRIBLE IS
FEVER”
28. SYSTEMIC EFFECTS OF INFLAMMATION
ACUTE PHASE PROTEINS
SYN IN LIVER,CIRCULATE IN PLASMA
MANY FOLD INCREASE IN INFLAMMATION
CRP,FIBRINOGEN,SAA
POSSIBLE ROLE AS OPSONINS
INCREASED ESR-DUE TO FIBRINOGEN
29. SYSTEMIC EFFECTS OF INFLAMMATION
LEUCOCYTOSIS
INCREASED RELEASE FROM BM
INCREASED PROLIFERATION FROM PRECUSORS
NEUTROPHILIA-MOST BACTERIA
LYMPHOCYTOSIS-VIRAL
EOS-PARASITIC,ALLERGIC
30. SYSTEMIC EFFECTS OF INFLAMMATION
ANOREXIA,SOMNOLENCE,DECREASED APPETITE
SEV BACTERIAL INFECTION-SEPTIC SHOCK
31. IMPT TOPICS
ESSAY
CHEMICAL MEDIATORS OF INFLAMMATION
CELLULAR EVENTS OF INFLAMMATION
SHORT TOPICS
ADHESION MOLECULES
PHAGOCYTOSIS
GRANULOMAS
SYSTEMIC EFFECTS OF INFLAMMATION
CELLULAR EVENTS OF INFLAMMATION
VASCULAR EVENTS OF INFLAMMATION
KILLING AND DEGRADATION