CH2

response to injury in living tissues and the body
nonspecific response to injury, protective

involves coordinated reaction of cells, tissues, and organs, or
the entire human body in which vessels, blood cells, nerves, and soluble mediators of inflammation are involved

ends by healing

in living tissues

heat, redness, swelling, pain, loss of function

relaxation of precapillary sphincter in arterioles

results in flooding of the capillary network and dilation of capillaries and postcapillary venules

inc. blood flow in capillaries
capillaries and venules cannot contract
active hyperemia in inflamed area
inc pressure-filtration of fluid into area of inflam
increased hydrostatic pressure
dilated capillaries-slowdown of circulation
hemodynamic changes

increased hydrostatic pressure

RBC rouleaux formation and margination of WBC

brings inflammatory cells in close contact with endothelium, result of adhesion molecules (selectins and integrins)

neutrophils start sticking to endothelial cells

results in release of mediators of inflammation and coagulation

fibrin strands

adhesion molecules (selectins and integrins)

mediators of inflammation (TNF and interleukins)

platelets and leukocytes, RBC

increased permeability of blood vessels

1.increased intracapillary pressure
2. relative hypoxia secondary to slow blood flow
3. adhesion of leukocytes and platelets to endothelial cells
4. action of soluble mediators of inflammation in plasma
5. mediators of inflammation released from inflammatory cells in the tissue surrounding blood vessels

vasodilation, increased permeability, loss of fluid leading to increased concentration of RBC, leukocytes rolling adhesion and migration

vasodilation

leads to exudation of protein rich fluid into extravascular space causing swelling

loss of fluid leading to increased concentration of RBC, leading to decreased velocity and stasis of blood flow

leads to the accumulation of inflammatory cells

1. plasma derived-in inactive form
2. cell derived-preformed, stored in granules (platelet, WBC)

vasodilation, vasoconstriction, vascular permeability

biogenic amine released from platelets and mast cells; preformed

stimulates retraction of endothelial cells of the venules (gaps) ; increased permeability

short action 'immediate transient reaction'

histaminase

vasodilation, increased permeability of capillaries, activation of leukocyte emigration, stimulation of phagocytosis, increases adhesive property of vessels, pain

1. damaged tissues release histamines, inc blood flow to area
2. histamines cause capillaries to leak, releasing phagocytes and clotting factors to wound
3. phagocytes engulf bacteria, dead cells, and debris
4. platelets move out of the capillary to seal wounded area

Bradykinin, Plasmin, Fibrin

kininogen through enzymatic action of kallikrein

activated by Hageman factor, which also acts on clotting, fibrolytic system of blood

similar to action of histamine but longer lasting

to induce pain

group of plasma proteins produced by liver, circulating in an inactive form

leads to the formation of biologically active fragments, intermediate complexes, and terminal membrane attack complex (MAC)

Opsonization
Anaphylaxis
Chemotaxis
Cell lysis

facilitated phagocytosis of bacteria

histamine released with increased vessel wall permeability

migration of leukocytes, attract leukocytes to site of inflammation

from phospholipids in cell membranes through action of phospholipase

1. lipoxygenase pathway
2. cyclooxygenase pathway

arachidonic acid derived from phospholipids by phospholipase. Corticosteroids can inhibit phospholipase

aspirin acts on cyclooxygenase

derives leukotrienes and lipoxins

chemotaxis, vascular permeability, bronchospasm

vasodilation, inhibition of neutrophil chemotaxis, monocyte adhesion

derives thromboxane, prostacyclin, and prostaglandins

platelet aggregation, thrombosis

opposes effects of thromboxane

smooth muscle contraction

1. adhesion
2. insertion of pseudopods (between endothelial cells)
3. ameboid movement toward chemotactic stimuli
4. phagocytosis of bacteria that were the source of chemotactic stimuli

increased permeability of vessel wall; increased hydrostatic pressure, fluid into interstitial space

emigration of leukocytes

diapedesis of leukocytes and movement; movement along gradient of chemical attractants released by bacteria or tissues destroyed

active movement of PMNs along a concentration gradient

chemotactic substances stimulate PMNs to move along chemical concentration gradient until they reach its source or the site that has the highest concentration

substances mediating the uptake of phagocytosis

it was coated with IgG and complement which binds to Fc and complement receptors on surface of leukocytes

oxygen burst and formation of oxygen radicals that are bactericidal

fusion of vacuole with lysosomes and specific granules of the leukocyte

contents of lysosomes and specific granules are bactericidal and contribute to final inactivation and degradation of bacterium

leukocytes become devoid of granules (degranulation of leukocytes)

mobility, phagocytosis, toxic enzymes, release mediators of inflammatory

allergy, parasites

allergy, mast cells (when outside vessel)

chronic inflammation
(monocytes when INSIDE blood vessel)

sticky granules, histamine, coagulation proteins, PDGF

PMNs, eosino, baso, mq, platelets, lymphocytes, plasma cells

lymphocytes

acute or chronic (based on duration)

infectious, chemical, physical, or immune

localized or widespread (bacteremia)

serous, fibrinous, purulent, ulcerative, pseudomembranous, chronic, granulomatous

extension of acute, prolonged healing, persistence of causative agents that initiated inflammation

exudation of serum, early phase of inflammation

fibrous inflammation, exudate within fibrin

pus forming from bacteria, contains yellow fluid, dead PMN and necrotic tissue remnants

ulcer inflamed on body surfaces
or mucosa of hollow organs

fibropurulent exudation

exudate that on histologic exam is found to contain lymphocytes, mq, and plasma cells
proliferation of fibroblasts

T-lymphocytes, mq, and multinucleated giant cells

viral infection of skin vesicles in herpesvirus infection or joint swelling in rheumatoid arthritis,
exudate of serum

tend to rupture, forming a sinus or fistul

a localized, purulent inflammation
older abscess surrounded by capsule that consist of granulation tissue

sinus forms a tract connecting the abscess with the skin, allowing the drainage of pus outside the body

an inflammatory tract that connects either two hollow organs or a hollow organ with the skin

accumulation of pus in a preformed cavity

resolution, chronic , or fibrosis

looks normal and healthy, return of normal function

angiogenesis, mononuclear cell infiltrate, fibrosis (scarring)

loss of function

acute > pus formation > healing > fibrosis
acute > fibrosis
acute > chronic > fibrosis

lasts a long time, extensive tissue destruction, slower healing, more functional damage

lymphocytes, fibroblasts, plasma cells

scarring stimulated by fibroblasts, loss of parenchymal cells and replaced by collagen

pelvic inflammatory disease (fallopian tubes)

lymphocytes, epithelioid cells (mq), multinucleated giant cells, not preceded by acute inflam, TB

prolonged duration in which inflammation, tissue injury, and attempts to repair coexist in varying combinations

stimulate proliferation of fibroblasts and also perpetuate the inflammation by constantly recruiting new inflammatory cells

combination of regeneration and scar formation by the deposition of collagen

scar formation that occurs when extracellular matrix framework is damaged by severe injury

localized system
systemic symptoms (fever, leukocytosis, constitutional symptoms)

endogenous pyrogens (IL-1 and TNF) are released from leukocytes or mq during inflammation

acts on thermoregulatory centers in hypothalamus which then calls upon PG to mediate fever

fever mediated by prostaglandins (PG)

aspirin which blocs prostaglandin synthesis by inhibiting cyclooxygenase

through scarring

a. continuously dividing cells (stem cells)
b. quiescent facultative mitotic cells (liver, kidney)
c. nondividing postmitotic cells (cardiac myocytes, neurons)

may be in any of the 4 phases

in G0 phase but can enter the cycle if necessary

left mitotic cycle and cannot reenter it

cell phase of division (short phase)

growth and final preparations for division

PMN leukocytes, macrophages

produce growth factors, cytokines, and mediators

myofibroblasts, fibroblasts, angioblasts

contract, secrete matrix substances

extracellular matrix including fibronectin and collagens (III,II,I)

blood vessel precursors

formation of scab
scavenger PMN
formation of granulation tissue
scarring

contains numerous mq, myofibroblasts, and blood vessels

less vascular, contains more matrix and fibroblasts and only scattered mq

occurs in wounds that are marked by a large defect of tissue that contain foreign material or that are infected

because the epithelial cells proliferating from the wound margin take longer to cover the defect

granulation tissue is more abundant; scarring is more prominent

site of wound
size of wound
mechanical factors
infection
circulatory status-diabetes
nutritional and metabolic factors
age

deficient scar formation
excess scar formation

wound dehiscence - separation of tissue margin

keloid
contractures - burns