Acute and Chronic Inflammation

ACUTE AND CHRONIC INFLAMMATION
INFLAMMATION - complex reaction to injurious agents such as

microbes and damaged, usually necrotic, cells that consists of vascular
responses, migration and activation of leukocytes, and systemic
reactions
- fundamentally a reactive response, the ultimate goal of
which is to rid the organism of both the initial cause of cell
injury and the consequences of such injury
- inflammatory response has two main components
vascular reaction and cellular reaction
Acute Inflammation rapid response to an injurious agent that serves
to deliver mediators of host defense leukocytes and plasma proteins
to the site of injury
3 MAJOR COMPONENTS OF ACUTE INFLAMMATION:
1) alterations in vascular caliber that lead to an increase in blood flow
2) structural changes in the microvasculature that permit plasma
proteins and leukocytes to leave the circulation
3) emigration of the leukocytes from the microcirculation, their
accumulation in the focus of injury, and their activation to eliminate
the offending agent
FIVE CARDINAL SIGNS OF INFLAMMATION:
Rubor (redness), tumor (swelling), calor (heat), dolor (pain), functio
lasea (loss of function)
EXUDATION the escape of fluid, proteins, and blood cells from the
vascular system into the interstitial tissue or body cavities
EXUDATE inflammatory extravascular fluid that has a high protein
concentration, much cellular debris, and a specific gravity above 1.020
TRANSUDATE a fluid with low protein content and a specific gravity
less than 1.012
EDEMA excess of fluid in the interstitial tissue or serous cavities; it can
be either an exudate or a transudate
PUS a purulent exudate rich in leukocytes, debris of dead cells,

microbes
STIMULI FOR ACUTE INFLAMMATION:
Infections and microbial toxins
Trauma
Physical and chemical agents
Tissue necrosis
Foreign bodies
Immune reactions/hypersensitivity reactions
VASCULAR CHANGES:
Changes in Vascular Flow and Caliber
vasodilation
increased permeability of the microvasculature
stasis
leukocyte accumulation along the vascular endothelium
Increased Vascular permeability (Vascular Leakage)
formation of endothelial gaps in venules
direct endothelial injury, resulting in endothelial cell necrosis and
detachment
delayed prolonged leakage
leukocyte-mediated endothelial injury
increased transcytosis
leakage from new blood vessels
CELLULAR EVENTS:
Leukocyte Extravasation sequence of events in the journey of
leukocytes from the vessel lumen to the interstitial tissue
1. in the lumen: margination, rolling, and adhesion to endothelium
2. transmigration across the endothelium
3. migration in interstitial tissues toward a chemotactic stimulus
Phagocytosis
1. recognition and attachment of the particle to be ingested by the
leukocyte
2. engulfment
3. killing or degradation of the ingested material
CHEMICAL MEDIATORS OF INFLAMMATION:

vasoactive amines
plasma proteins
arachidonic acid metabolites
platelet-activating factor
cytokines and chemokines
nitric oxide
OUTCOMES OF ACUTE INFLAMMATION:
complete resolution
healing by connective tissue replacement (fibrosis)
progression of the tissue response to chronic inflammation
MORPHOLOGIC PATTERNS OF ACUTE INFLAMMATION:
Serous Inflammation marked by the outpouring of a thin fluid that,
depending on the size of injury, is derived from either the blood serum or
secretions of mesothelial cells lining the peritoneal, pleural , and
pericardial cavities (skin blisters from burn or viral infections)
Fibrinous Inflammation fibrinous exudate develops when the
vascular leaks are large enough or there is a procoagulant stimulus in
the interstitium (e.g., cancer cells). Characteristic of inflammation in the
lining of body cavities, such as the meninges, pericardium
Suppurative or Purulent Inflammation characterized by the
production large amounts of pus or purulent exudate consisting of
neutrophils, necrotic cells, and edema fluid. Certain bacteria
(e.g. staphylococci) produce this localized suppuration and are
therefore referred to as pyogenic bacteria (acute appendicitis)
Abscesses localized collections of purulent inflammatory tissue
caused by suppuration buried in a tissue, an organ, or a confined space
Ulcers local defect, or excavation of the surface of an organ or tissue
that is produced by the sloughing (shedding) of inflammatory necrotic
tissue
Chronic Inflammation inflammation of prolonged duration in which

active inflammation, tissue destruction, and attempts at repair are
proceeding simultaneously
- may follow acute inflammation
- begins insidiously, as a low-grade, smoldering, often
asymptomatic response
CAUSES OF CHRONIC INFLAMMATION:
persistent infections by certain microorganisms
prolonged exposure to potentially toxic agents, either exogenous
or endogenous
autoimmunity
MORPHOLOGIC FEATURES:
infiltration with mononuclear cells
tissue destruction
attempts at healing by connective tissue replacement of
damaged tissue
angiogenesis - proliferation of small blood vessels
fibrosis proliferation of fibroblasts
MONONUCLEAR CELL INFILTRATION:
Macrophage dominant cellular player in chronic inflammation
- one component of the mononuclear phagocyte system or
reticuloendothelial system
- tissue macrophages connective tissue
- kupffer cells liver
- sinus histiocytes spleen/lymph nodes
- alveolar macrophages lungs
OTHER CELLS IN CHRONIC INFLAMMATION:
lymphocytes
eosinophils
mast cells
plasma cells
GRANULOMATOUS INFLAMMATION:
- distinctive pattern of chronic inflammatory reaction
characterized by focal accumulation of activated
macrophages, which often develop an epithelial-like
(epithelioid) appearance
- encountered in immunologically mediated, infectious, and
some noninfectious conditions
- seen in tuberculosis, sarcoidosis, cat-scratch diseae,
lymphogranuloma inguinale, leprosy, brucellosis, syphilis,
berylliosis
granuloma 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
Types of Granulomas:
foreign body granulomas incited by relatively inert foreign bodies
immune granulomas caused by insoluble particles, typically
microbes, that are capable of inducing a cell-mediated immune
response
LYMPHATICS IN INFLAMMATION:
- lymphatic system and lymph nodes filters and polices the
extravascular fluids
- together with mononuclear phagocyte system, it represents
a secondary line of defense
- lymphangitis inflammation of lymphatics
- lymphadenitis inflammation of lymph nodes
SYSTEMIC EFFECTS OF INFLAMMATION:
fever
acute phase proteins
leukocytosis
acute phase response - pulse and BP, sweating, rigors, chills,
anorexia, somnolence, malaise
production of TNF and IL-1

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ACUTE AND CHRONIC INFLAMMATION

INFLAMMATION - complex reaction to injurious agents such as

PUS a purulent exudate rich in leukocytes, debris of dead cells,

CHEMICAL MEDIATORS OF INFLAMMATION:

Chronic Inflammation inflammation of prolonged duration in which

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