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ACUTE INFLAMMATION
Inflammation
• Injurious stimuli cause a protective vascular
connective tissue reaction called “inflammation.”
– Dilute
– Destroy
– Isolate
– Initiate repair
Blood vessel
! !
c h
u
O
Invading organisms
or trauma
injury
Vasoactive Chemotactic
factors factors
Increased
Blood Phagocytes
vascular Neutrophils
vessel permeability macrophages
migration
Antibodies
Edema
and Opsonization
Swelling complement Phagocytosis
Destruction
Pain
pathogen-associated
molecular patterns
pain
heat
redness
Serous exudate/subcutaneous edema, photosensitization, skin of the nose and ears, ewe. The nonhaired skin of the nose is covered
by a crust resulting from dehydration of the serous exudate released from injured blood vessels following a short exposure to the
sun. The ears are edematous and droopy.
Catarrhal inflammation. Abomasum, cow. The mucosal epithelium is moderately thickened, covered by a
glistening layer of clear mucus, and has a subtle nodular appearance caused by accumulation of mucinous
secretory products (catarrhal exudate) in the gastric pits.
The principal cellular and vascular responses during the inflammatory response. The majority of leukocyte
transmigration and hemorrhage occurs in the capillaries and postcapillary venules.
Blood pressure and plasma colloid osmotic forces in normal and inflamed microcirculation. Acute inflammation.
Arteriole pressure is increased to 50 mm Hg; the mean capillary pressure is increased because of arteriolar dilation,
and the venous pressure increases to approximately 30 mm Hg. At the same time, osmotic pressure is reduced
(averaging 20 mm Hg) because of protein leakage across the venule. The net result is an excess of extravasated
fluid.
The major local manifestations of
acute inflammation compared with
normal. (1) Vascular dilation (causing
erythema and warmth), (2)
extravasation of plasma fluid and
proteins (edema), and (3) leukocyte
emigration and accumulation in the
site of injury.
How Invaders are Recognized?
5. The sentinel cells are macrophages, dendritic cells and mast cells.
nucleus
Metachromatic
granules
scrolls
Mast Cells
Mast Cells
Some of the stimuli that make mast cell degranulate.
Normal mast cell Degranulating mast cell
Vascular leakage
Four mechanisms known to cause vascular leakiness
HISTAMINE
SEROTONINE
VASOACTIVE POLYPEPTIDES
KININS
EICOSANOIDS
PROSTAGLANDIN
LEUCOTRIENS VASOACTIVE LIPIDS
(B4, C4, D4, E4)
PLATELET-
ACTIVATING
NEUTROPHIL-DERIVED MOLECULES
FACTOR
(PAF)
FIBRINOGEN
COAGULATION SYSTEM
BREAKDOWN
PRODUCTS
COMPLEMENT
C3a, C5a
Vascular leakage
necrosis
thrombus
lymphocyte Mφ plasma cell
PMN
Mφ
Vascular leakage
phospolipases
Arachidonic
acid
Lipooxigenase Ciclooxigenase
Leucotrienes Prostaglandins
Thromboxans
Protacyclins
Proinflammatory
Proagglutination
Thrombotic