CHRONIC INFLAMMATION

CHRONIC INFLAMMATION-DEFENSE AT

A PRICE

PROLONGED DURATION

WKS TO MONTHS

ACTIVE INFLAMMATION,

TISSUE DESTRUCTION AND

REPAIR

ALL occurs SIMULTANEOUSLY

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

FEATURES

MONONUCLEAR INFILTRATIION-MACROPHAGES,LYMPHOS,PLASMA CELLS

TISSUE DESTRUCTION

ATTEMPTS AT HEALING:

angiogenesis+ fibrosis

Chronic infl. Acute infl.

collection of chronic inflammatory cells (*) alveolar spaces filled with neutrophils

destruction of parenchyma Congested blood vessels

fibrosis, (arrows)

CELLS-MACROPHAGES

KEY ROLE

PART OF MONOCYTE PHAGOCYTE SYSTEM

ORIGIN IN BM BLOOD MONOCYTES TISSUE MACROPHAGES

TISSUE MACROPHAGES-MICROGLIA,KUPFFER CELLS,ALVEOLAR MACROPHAGES,OSTEOCLASTS

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

CELLS-MACROPHAGES

IF IRRITANT PERSISTS MACROS ACCUMULATE

RECRUITMENT LOCAL PROLIF IMMOBILIZATION

CELLS-MACROPHAGES

PRODUCTS OF MACROPHAGES

ELIMINATION OF MICROBES

TISSUE INJURY-PROTEASES,NO,AA METABOLITES

FIBROSIS

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

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.

GRANULOMATOUS INFLAMMATION-

EXAMPLES

TB

SARCOID

SYPHILIS(GUMMA)

CAT SCRATCH DISEASE

LEPROSY

BERYLLIOSIS

HISTOPLASMA

FOREIGN BODY

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

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

GRANULOMA

TWO MAIN TYPES BASED ON PATHOGENESIS- FB

(SUTURE,TALC) AND IMMUNE (TB)

IMMUNE

POORLY DEGRADABLE AGENT

CELL MEDIATED IMMUNITY

GRANULOMA

CENTRAL NECROSIS IS SEEN IN SOME

GRANULOMAS

PROTOTYPE-TB

CASEOUS NECROSIS

GROSSLY-CHEESE LIKE

MICRO-EOSINOPHILIC,AMORPHOUS GRANULAR DEBRIS

Granuloma

A granuloma: a collection of

epithelioid histiocytes

SYSTEMIC EFFECTS OF INFLAMMATION

ACUTE PHASE RESPONSE OR SYSTEMIC

INFLAMMATORY RESPONSE(SIRS)

DUE TO CYTOKINES-TNF,IL-1

SYSTEMIC EFFECTS OF INFLAMMATION

FEVER

IL-1 AND TNF ACT ON HYPOTHALAMUS

PRODUCE PGs

RESET TEMP AT HIGHER LEVEL

HOW USEFUL??????

OSLER

“HUMANITY HAS BUT 3 GREAT

ENEMIES-FEVER ,FAMINE AND

WAR,OF THESE BY FAR THE

GREATEST ,THE MOST TERRIBLE IS

FEVER”

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

SYSTEMIC EFFECTS OF INFLAMMATION

LEUCOCYTOSIS

INCREASED RELEASE FROM BM

INCREASED PROLIFERATION FROM PRECUSORS

NEUTROPHILIA-MOST BACTERIA

LYMPHOCYTOSIS-VIRAL

EOS-PARASITIC,ALLERGIC

SYSTEMIC EFFECTS OF INFLAMMATION

ANOREXIA,SOMNOLENCE,DECREASED APPETITE

SEV BACTERIAL INFECTION-SEPTIC SHOCK

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