injury may be caused by chem agents, physical forces, living microbes and many other endogenous and exogenous pathologic stimuli that can disturb the normal steady state of the body

A dynamic process, evolving through several phases which lasts from a few minutes to days or even months and years

inflammation which lasts a long time and produces extensive tissue destruction and has a tendency to heal less readily

Marked by an exudate which contains lymphs, macrophages, and plasma cells, all which can stimulate proliferation of fibroblasts, with loss of parenchymal cells and scarring

1. calor (heat)

2. rubor (redness)

3. tumor (swelling)

4. dolor (pain)

5. functio laesa (loss of fxn)

the mechanical stimulus stimulates nerves that transmit signals to smooth muscle cells on pre-capillary arterioles, which acts as sphincters, regulating the inflow of blood into the capillaries

The relaxation of smooth muscle cells allows the blood to rush into the capillaries, and this accounts for the redness, swelling, and warmth of the tissue

vasoconstriction, which lasts for a few seconds, and is then followed by vasodilation, with the relaxation of pre-capillary sphincters

this results in the flooding if the capillary network with arteriole blood, with redness and swelling of the tissue

the arteriole blood is warm and is pumped into the area in large quantities, so the inflamed tissue also becomes warm (hypermia)

This influx of blood also dilates the capillaries and venules, which consists of only an endothelial layer and basement membrane, and therefore cannot actively regulate the incoming blood flow.

The increased pressure in the capillaries and venules forces plasma filtration through the vessel wall, leading to edema

this causes the blood flow in the dilated capillaries and venules to be slow due to the increased hemoconcentration, and leads to congestion

Pavementing

WBCs marginate and become attached to the edge of the endothelium

These leukocytes develop elongated protrusions on their surface cytoplasm and become sticky, which allows them to adhere to endothelial cells lining the capillaries and venules

what activates surface adhesion molecules?

1. Adhesion of PMNs to the endothelium

2. Insertion of cytoplasmic pseudopods btwn the junctions of the endothelial cells

3. Passage through the basement membrane

4. Ameboid movement away formthe vessel toward the cause of the inflammation (ex bacteria)

• active movement of PMNs along a concentration gradient

• chemotactic substances stimulate PMNs to move along this gradient until they reach their source or site of inflammation

• the chemoattractant derived from bacteria or tissues destroyed by inflammation or from activated complement

• PMNs that reach the bacteria or other sources of chemotactic substances lose their mobility and begin acting as scavengers

• a PMN encounters and recognizes a bacterium as foreign by the pseudopods extending from the surface of the PMN

engulfment of the bacterium is a process by which the cytoplasm of the PMN surrounds the bacteria and encloses it into an invagination of the cell membrane (by its pseudopods) into a vacuole

Inside the phagocytic vacuole, the bacterium is killed by bacteriocidal substances released from the cytoplasm of the PMN

dead and dying PMNs, admixed with tissue debris, form

a viscous yellow fluid

Inflammations dominated by this formation are called purulent or suppurative inflammations

• considered to be the mildest form, characterized by the exudation of fluid that is clear like serum, and occurs in the very early stages of most inflammations

• In early stages of pneumonia, it can be recognized as a prteinaceous material inside the alveolar space that contains only a few inflammatory cells (transudate) that, as time goes by, proliferate in the fluid (exudate)

• typical of many viral infections, such as skin vesicles caused by herpes virus

• Autoimmune disorders, such as SLE, can affect the serosal surfaces and cause a serous pericarditis, pleurits, or peritonitis

• Second degree skin burns cause serous blisters

• The serous fluid is readily resorbed without consequences if the cause is eliminated

• characterized by an exudate that is rich in fibrin, formed from long strands of polymerized fibrinogen, which is one of the largest plasma proteins

• Fibrinous exudates are indicitive of severe inflammation, and in contrast to serous exudates, which contains predominately serum and albumin, that have leaked from intact blood vessels, extravasation of fibrin occurs through larger vascular or tissue defects

seen in many bacterial infections, such as strept throat or pneumonia

In different types of pericarditis, the surface of the heart is covered with shaggy, yellowish layers of fibrin that bridges the space btwn the two layers of the pericardial sac, obliterating the cavity (bread and butter)

• inflammation typically caused by pus-forming bacteria, such as Staph and Strept.

• A viscous, yellow fluid composed of dead and dying PMNs and necrotic tissue debris

• Pus may accumulate on the mucosa, skin, or in the internal organs.

consists of a central portion of purulent material surrounded by a wall composed of a capsule of fibrotic granulation tissue. They do not heal spontaneously and must be evacuated.

Large ones tend to rupture, forming a sinus

a form of ulcerative inflammation that is combined with fibrinopurulent exudation.

The exudate of fibrin, pus, cellular debris and mucous forms a pseudomembrane on the surface of ulcers that can be scraped away to expose ulcerative defects that bleed profusely

C. difficile causes pseudomembranous colitis, caused by a bacterial overgrowth secondary to intake of broad spectrum antibiotics

a special form of chronic inflammation that typically is not preceded by an acute, PMN-mediated inflammation

it may be caused by antigens that evoke a cell-mediated hypersensitivity rxn, or by antigens that persist at the site of inflammation (Sarcoidosis)

TBis the prototype granulomatous disease, as are certain fungal diseases

• mediated by macrophages and T-lymphocytes that accumulate at the site of injury, forming nodules in which the macrophages interconnect with one another and transform into so-called epithelioid cells

• In contrast to macrophages that are motile and phagocytic, epithelioid cells are immobile and produce secretory products that act as mediators of inflammation