redness

swelling

heat

pain

loss of function

herpes sores

2nd degree burns

serosal surfaces affected by rheumatoid arthritis

serous pericarditis

serous pleuritis

early pneumonia

serous peritonitis

transduate is clear fluid

easy healing if causative factor is removed

serous fluid can be reabsorbed into tissue

strep throat

bacterial pericarditis

exudate rich in albumin, immunoglobins, and fibrin

Exudate may organize to form fibrous tissue, which can then cause adhesion and scarring

staph and strep infections

acne pustules

accumulation of pus

abcess can form

sinus/fistula can form

empyema can form

1. change in blood circulation

2. change in blood vessel permeability

3. WBC response

4. release of soluble mediators

1. constriction of arterioles

2. relaxation of precapillary sphinctors

3. capillary dilation

4. venule dilation

5. plasma leaks through vessel walls

6. edema

1. increased hydrostatic pressure of blood in congested blood vessels forces fluid out

2. slowing of the circulation, which reduces supply of oxygen & nutrients to endothelial cells, causing shrinkage of cells and wider spaces between cells, causing fluids and proteins to leak out

3. adhesion of leukocytes and platelets to endothelial cells with the release of soluble mediators from leukocytes, platelets, endothelial cells causing even more shrinkage of endothelial cells

4. Formation of exudate, causing increase of tissue osmotic pressure outside blood vessels, attracting fluid outside of blood vessels

In dilated capillaries, there is congestion of RBCs and rouleaux, causing margination of neutrophils and platelets.

There is adhesion of platelets to endothelial cells, platelets release mediators, mediates cause activation of endothelial cells to express sticky protein molecules. 

Stickiness facilitates pavementing of neutrophils onto endothelial cell lining of capillaries.

Neutrophils develop pseudopods to emigrate between endothelial cells, through basement membrane, and out of blood vessels.

Neutrophils migrate by chemotaxis to site of injury

active movement of of PMNs along a concentration gradient of chemicals

chemicals are derived from bacteria, dead cells and tissues, activated complement

lysosomal enzymes released when lysozymes fuse with phagocytic vacuole and degranulation occurs

these enzymes kill and digest bacteria

1. adhesion

2.insertion of pseudopods between endothelial cells

3.passage through basement membrane

4. movement towards source of chemotactic stimuli

5. phagocytosis of bacteria

Pseudopods of PMNs recognize the foreign bacteria.

Cell membrane of PMN attaches to bacterial cell wall

Opsonization: Bacteria is coated (IgG antibody, C3b complement, CRP)

Receptors of the surface of the PMNs can bind to IgG, C3b complement or CRP on surface of bacterium.

Cytoplasm of PMN surrounds the bacterium and encloses it into an invagination of the surface membrance of the PMN.

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Lysosomes fuse with this newly formed phaghocytic vacuole and other granules discharge into the vacuole.  Bacterium is killed by released of bactericidal substances from lysosomes and granules into the vacuole.

When particle is too large to be engulfed by PMN or particle is attached to a surface and cannot be engulfed.

Release of PMN products (lysosonal enzymes, O2 compounds, PGs, LTs) can cause further inflammation and tissue injury, important in chronic inflammation

more important

Formation of oxygen compounds such as hydrogen peroxide, superoxides which are toxic to microorganisms.

MPO is an enzyme in lysosomes that combines a halide with hydrogen peroxide to produce antibacterial substances

All these compounds which are toxic to microorganisms are oxgen compounds

preformed substances killed microogranisms

BPI

Lysozyme

major basic protein

defensins elastase and collagenase aid in removal of debris

1. absence of LAD1, LAD2 adhesion molecules

2. Chediak-Higashi syndrome

3. Chronic granulomatous disease

lysosomal enzymes cannot enter phagocytotic granules

Other characteristics

albinism

neuronal damage

bleeding disorders

absence of enzymes to make lysosomal free radicals

histamine

PGs

LTs

TXA2

prostacyclin

chemokines

cytokines

NO

bradykinin

complement proteins

factor XLLA/Hageman factor

The lipoxygenase pathway leads to formation of leukotrienes.

Leukotrienes are active in chemotaxis and increased vascular permeability.

Leukotrienes are also known as slow acting substance of anaphylaxis

Formation of prostaglandins in acute inflammation

COX 2 Pathway

formed from arachidonic acid by the action of COX2

• vasodilation
• pain
• fever

These are proteins produced by lymphocytes, macrophages, other cells.

Important ones:

IL-1, TNFa (macrophages) and TNFb (T cells) are important in endothelial activation (stickiness)

Effects:

• fever
• decreased appetite
• sleep
• increased corticosteroid levels

20 proteins act in a cascade leading to formation of MAC and lysis of cell being attacked

C3a and C5a: cause histamine to be released from mast cells and vasodilation

C3b: Opsonin involved in phagocytosis

C5a: chemotaxis

Factor XLLa/Hageman factor

1. initiates clotting

• thrombin formation mediates inflammation and leads to fibrin formation/clotting

2. increases bradykinin levels

• increased vascular permeability and pain

3.activates plasmin

• breaks down clots and activates compliment system

• fatigue
• weakness
• depression
• decreased appetite
• generalized pain
• exhaustion
• lymphadenitis (swelling of lymph nodes)
• lymphangitis (inflammation of lymphatic vessels)
• fever
• leukocytosis

• neutrophilia: indicate bacterial infection or ischemic damage

• lymphocytosis: indicates viral infection

• eosinophilia: allergy or parasitic infection

cold application: causes vasoconstriction and decreased formation of exudate to reduce swelling

heat application: increases phagocytosis

elevation or pressure: reduce swelling and promote drainage

drug treatments: Antihistamines, NSAIDS, corticosteroids

• complete resolution
• abscess formation
• healing by fibrosis
• chronic inflammation

a) extension of acute inflammation

b)prolonged healing of acute inflammation

c)persistence of cause of inflammation (microorganisms, prolonged exposure to toxins, autoimmune diseases, foreign bodies)

lasts from a few hours to a few days

onset is usually rapid

lasting more than 6 weeks

Macrophages are main cells involved, kill bacteria, release cytokines, long life

Eosinophils and lymphocytes (T and B cells, plasma cells)

Chronic inflammation is usually initiated by acute inflammation, but cause persists and macrophages and lymphocytes are unable to to remove the cause

Immune response is provoked...

• T and B cells become involved
• Released lymphokines
• Attract macrophages
• Increasing inflammation

a focal response leading to formation of granuloma

a type IV hypersensitivity reaction

not preceeded by acute inflammation

Inflammatory lesion that is composed of macrophages, fibroblasts, epitheloid cells, giant cells, lymphocytes, and that forms microscopic aggregates or nodules

Forms when an antigen stimulates Type 4 hypersensitivity or by antigens that persist at site of inflammation

macrophages and T cells accumulate, T cells and fibroblasts are on outside of lesion

On inside, some macrophages combine into epitheliod cells, some epitheloid cells combine to form giant cells

Center of lesion may become area of caseous necrosis

examples: TB, leprosy, syphilis, sarcoidois

Destroy tissue and tend to persist for long time

In lungs: can cause cavities, destroy lung tissue and blood vessels, bleeding

can destroy organs

incapacitate patient