[PL3.1] Inflammation and Repair

Primary function of inflammation

deliver leukocytes and defense molecules to sites of infection or damage

Type of tissue involved in inflammation

vascularized tissue

Purpose of inflammation

eliminate offending agents, dilute or wall off injurious agent

First step in the inflammatory response

recognition of the noxious agent

Second step in the inflammatory response

recruitment of leukocytes and plasma proteins

Third step in the inflammatory response

removal of the stimulus

Fourth step in the inflammatory response

regulation of the response

Final step in the inflammatory response

repair or healing of damaged tissue

Vascular change during inflammation

increased permeability to allow proteins into infection site

Change in endothelial lining during inflammation

permits leukocyte migration

Role of leukocytes in inflammation

ingest and destroy microbes, dead cells, and foreign bodies

Possible harmful effect of inflammation causing fluid accumulation

edema

Inflammation-related deformity can result in

disfigurement of limbs (e.g., rheumatic arthritis)

Inflammatory reaction causing exaggerated immune response

hypersensitivity reactions (e.g., rashes)

Type of inflammation confined to the site of damage

local inflammation

Type of inflammation with widespread abnormalities

systemic inflammation

Inflammation that is rapid and often self-limited

acute inflammation

Inflammation of longer duration, associated with tissue destruction and scarring

chronic inflammation

Cardinal sign of inflammation due to increased blood flow

calor (heat)

Physiologic cause of heat in inflammation

hyperemia

Cardinal sign of inflammation caused by vasodilation

rubor (redness)

Cardinal sign of inflammation caused by vascular permeability

tumor (swelling)

Cause of pain in inflammation

pressure on sensory nerves by exudate

Cardinal sign representing loss of function in inflammation

functio laesa

Common microbial cause of inflammation

infections (bacterial, viral, fungal, parasitic)

Type of cell injury causing inflammation

tissue necrosis

Examples of physical or chemical causes of inflammation

ischemia, trauma, chemical injury

Type of foreign materials that can cause inflammation

splinters, dirt, sutures

Examples of endogenous substances that trigger inflammation

urate crystals, cholesterol crystals, lipids

Type of immune-mediated cause of inflammation

hypersensitivity reactions

First major component of acute inflammation

dilation of small vessels to increase blood flow

Second major component of acute inflammation

increased permeability of microvasculature

Third major component of acute inflammation

emigration and activation of leukocytes at site of injury

Term for fluid, proteins, and blood cells escaping vessels into tissues

exudation

Type of fluid with high protein and cellular content

exudate

Type of fluid with low protein, little or no cells, and low specific gravity

transudate

Term for excess fluid in interstitial tissue or serous cavities

edema

Pus is a purulent exudate rich in

leukocytes (mostly neutrophils), dead cells, and microbes

Initial vascular change in acute inflammation

vasodilation

Chemical mediator responsible for vasodilation in inflammation

histamine

Effect of vasodilation on vascular flow and appearance

increased flow and localized redness

Next vascular step after vasodilation

increased permeability of microvasculature

Stasis refers to what condition in small blood vessels?

engorgement with slowly moving red cells

Vascular response marked by leukocytes adhering to vessel walls

leukocyte accumulation and adhesion

Mechanism of increased vascular permeability due to endothelial gaps

endothelial cell contraction

Timing of immediate transient vascular response

15–30 minutes

Mechanism of sustained vascular leakage

endothelial necrosis and detachment

Molecules that control leukocyte recruitment

adhesion molecules and chemokines

First phase of leukocyte recruitment occurring in vessel lumen

margination

Phase of leukocyte recruitment involving transient attachment and rolling

rolling

Firm attachment of leukocytes to endothelium is called

adhesion

Process of leukocyte migration through endothelium

diapedesis

Directed migration of leukocytes toward site of injury

chemotaxis

Two major types of phagocytes involved in inflammation

neutrophils and macrophages

First step of phagocytosis

recognition and attachment

Second step of phagocytosis

engulfment

Final step of phagocytosis

killing and degradation

General term for substances that initiate and regulate inflammation

inflammatory mediators

Inflammatory mediators stored in granules or synthesized by cells

cell-derived mediators

Inflammatory mediators derived from liver and circulating as inactive precursors

plasma-derived mediators

Most important mediators of acute inflammation

vasoactive amines, prostaglandins, leukotrienes, cytokines, complement products

Common characteristic of inflammatory mediators

short-lived