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41 Cards in this Set

  • Front
  • Back

?- white cell assume a peripheral position along the endothelial surface

Margination

- leukocytes tumble slowly along the endothelium and adhere transiently


Rolling

- the endothelium is lined firmly by white cells ( resembling pebbles over which a stream runs without disturbing them )

Pavementing

in most forms of acute inflammation, neutrophils predominatein the inflammatory infiltrate during the first 6-24 hours, then are replaced by monocytes in 24-28 hours


Leukocyte Adhesion & Transmigration-

- in most forms of acute inflammation, neutrophils predominatein the inflammatory infiltrate during the first 6-24 hours, then are replaced by monocytes in 24-28 hours


Leukocyte Adhesion & Transmigration-

Why ? first?


→ they are more numerous in the blood


→ they respond more rapidly to chemokines


→ they attach more firmly to the adhesion molecules

neutrophils

certain infxns have different pattern of cellular exudation

Leukocyte Adhesion & Transmigration-

- neutrophils predominate over 2-4 days

Pseudomonas infxn

- lymphocytes first

Viral infxns

some hypersensitivity reaction - ? are the main cell type

eosinophils

- after extravasation, leukocytes emigrate in tissues toward thesite of injury by a process called

CHEMOTAXIS

defined as locomotion oriented along a chemical gradient

CHEMOTAXIS

- the chemoattractants could be exogenous or endogenous

CHEMOTAXIS

• Exogenous chemoattractants


• Endogenous chemoattractants

CHEMOTAXIS

- bacterial products


 most common

Exogenous chemoattractants

1. components of the complement system, particularly C5a


2. products of the lipooxygenase pathway, mainly leukotriene B4 (LTB4)


3. cytokines

Endogenous chemoattractants

- the efficiency of phagocytosis is greatly enhanced when microbesare opsonized by specific proteins (opsonins) for w/c thephagocytes express high-affinity receptors

Phagocytosis

the major opsonins are :


 IgG antibodies


 the C3b breakdown products


 plasma lectins

Phagocytosis

the 2 most important are:


 Mast cells


 Tissue macrophages

Phagocytosis

- complement proteins- kinins

Plasma-derived mediators

 are normally sequestered in intracellular granulesthat need to be secreted (e.g. histamine in mast cells)

Cell-derived mediators

or are synthesized de novo (e.g. prostaglandins, cytokines) in response to a stimulus

Cell-derived mediators

- is marked by the outpouring of a thin fluid

SEROUS INFLAMMATION

- is derived from either the plasma or the secretions of mesothelial cells lining the peritoneal, pleural, and pericardial cavities (called effusion)

SEROUS INFLAMMATION

- the skin blister resulting from a burn or viral infection represents a large accumulation of serous fluid

SEROUS INFLAMMATION

- w/ more severe injuries & the resulting greater vascular permeability  larger molecules such as fibrinogen pass the vascular barrier

FIBRINOUS INFLAMMATION

- & fibrin is formed & deposited in the extracellular space

FIBRINOUS INFLAMMATION

-is charac. of inflammation in the lining of body cavities, such as the meninges, pericardium & pleura

FIBRINOUS INFLAMMATION

- charac. by the production of large amounts of pus or purulent exudate consisting ofcertain bacteria (e.g. staphylococci) produce this localized suppuration


SUPPURATIVE OR PURULENT INFLAMMATION

- are localized collections of purulent inflammatory tissue caused by suppuration buried in a tissue / organ

ACUTE AND CHRONIC INFLAMMATIONABSCESS

- is a local defect, or excavation, of the surface of an organ or tissue that is produced by sloughing (shedding) of inflammatory necrotic tissue

ULCERS

- occur only when tissue necrosis exist on or near a surface

ULCERS

- commonly encountered in:


 mucosa of the mouth, GIT & genitourinary tract


 subcutaneous tissue

ULCERS

- is an inflammation of prolonged duration (weeks or months) in w/c


 active inflammation


 tissue destruction


 attempts at repair


are proceeding simultaneosly

CHRONIC INFLAMMATION

- arise in the following settings (causes):


• Persistent infections


• Prolonged exposure to potentially toxic agents (exogenous or endogenous)


• Autoimmunity

CHRONIC INFLAMMATION

- Morphologic features are:


 infiltration with mononuclear cells

CHRONIC INFLAMMATION

- Morphologic features are:


 tissue destruction, induced by persistent offending agentor by the inflammatory cells

CHRONIC INFLAMMATION

- Morphologic features are:


 attempts at healing by connective tissue replacement of damaged tissue, accomplished by proliferation of small bld vessels (angiogenesis) &, in particular, fibrosis

CHRONIC INFLAMMATION

- the dominant cellular player in chronic inflammation

Macrophage

- derived from blood monocyte

Macrophage

- secrete a variety of biologically active products

Macrophage