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60 Cards in this Set

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Antigen
Foreign proteins capable of eliciting an immune response
Non-protein Antigens
Polysaccharides and polypeptides
Auto-Immunity
Host molecules incite antibody response
Inflammation Definition
Process specific to vascularized tissues where fluids from blood vessels and WBC accumulate at site of injury to defend body
Innate Immune protection
Most of innate immune system are developed in utero
Inflammation Function
Response to pathogenic environmental insult & begins wound/ tissue healing
Mistakes of Inflammation
Inadequate response, misdirected response, exaggerated response.
Acute Inflammatory Response
Immediate

Gets Intravascular leukocytes delivered in time to extravascular locations.
Phlegmone
Egyptians- 4500 years ago

Greeks- 2500 years ago

'The burning thing.’
Cardinal Signs of Inflammation
2000 years ago

Roman- Cornelius Celsus

Rubor, Tumor, Calor, Dolor
John Hunter
1973- Scottish surgeon

Inflammation not a problem but a curative response
Julius Cohnheim
1867

Observed diapedesis under microscopic in a live frog.

Student of Rudolph Virchow.
Elie Metchinkoff
1880’s

Discovered process of phagocytosis.

Demonstrated that both serum factors (antibodies) & cellular factors (phagocytes) are involved in immune response.
Sir Thomas Lewis
Demonstrated that chemical substances made at inflammation site also mediate the response.
Characteristics of Acute Inflammation
1. Recent onset; short duration (few minutes to 2 days)

2. Movement of WBC neutrophils

3. Blood proteins & blood serum to extracellular space
Key Events in Acute Inflammation
1. Change in diameter of small blood vessels

2. Change in vascular permeability

3. Stage of Exudation

4. Change in vascular flow
Exudation Definition
Escape of fluid, proteins, & leukocytes from blood vessels into the extravascular environment resulting in edema (and pus if there are cells & cellular debris)
Features of Changes in Vascular Flow
1. Vasoconstriction (not important and brief)

2. Vasodilation- increases blood flow (redness and heat)

3. Increase in pressure drives out non-protein fluid and concentrates protein in vascular system.

4. Increase of viscocity, decreases blood flow and causes increased leakage.

5. Margination and Emmigration of Leukocytes
Features of Changes in Permeability
Endothelium membrane becomes 'leaky. (Due to contraction of individual endothelial cells)
Transudation
Increased hydrostatic pressure drives protein-poor liquid out
Exudation
Increased permeability allows protein- rich fluid to escape
3 responses to increased Permeability
Immediate Transient

Immediate-sustained

Delayed-prolonged leakage
Immediate Transient Response
5-10 minutes after injury, lasting 15-30 minutes.

Mediated by histamine and proceeds via endothelium contraction
Immediate Sustained Response
Immediately upon injury. Lasts a few hours or days.

Severe injury

Related to leakage from torn vessels
Delayed-Prolonged Leakage
Doesn't start for several hours. Lasts for days.

NOT involving epithelial contraction but still is leaky capillaries and venules.

(i.e. sunburn response)
Stage of Leukocytic Exudation
1. Stasis initiates margination, pavementing and emigrating.
Margination of Leukocytes
White cells travel near the periphery
Pavementing
A mechanism causes adhesion between Leukocytes and the walls of the capillaries and venules.

*** chemicals or genetic defects can increase or decrease pavementing and thus the inflammatory response.
Emigration
Leukocytes emigrate to extravascular space to find whatever has caused the inflammation.

6-24 hours: Neutrophils
24-48 hours: Monocytes
Opsonins
Serum factor antibodies

Tag foreign proteins for distruction
Lysosomal Enzymes
Kill invaders in an oxygen-dependent reaction. (hydrogen peroxide)

Oxygen -independent kills with other stubstances that alter permeability of bacteria membrane.
Leukopenia
Decreased circulation of leukocytes.
Potential Defects related to Leuckocytic Exudation
Leukopenia

Impaired Adhesion: alcohol poisening

Impaired Chemotaxis & migration: Diabetes

Defective Phagocytosis: Diabetes

Impaired degradative ability (diminished hydrogen peroxide formation- chronic granulomatous disease)
Arthus Reaction
Swarm of neutrophils digest the walls of venule.

(negative impact of inflammatory focus)
Lymphangitis
Exudate and debris of tissue move through lymph. Surviving bacteria is spread as well.
Chemical Mediators of Inflammation
Triple response

Sir Thomas Lewis

1920's
Triple response
1. Red Line: Blood vessel dilation

2. Red Flare: General Arteriolar Vasodilation (within 30 seconds)

3. White Wheal: Localized Edima caused by histamine. (within 1-3 minutes)
Net Result of chemical mediators
1. Vasodilation

2. Increased Vascular Permeability

3. Chemotaxis of Leukocytes

4. Pain
Vasoactive Amines
Histamines & Seratonin (5-hydroxytryptamine)

Increase permeability & Transudation
Agents which promote the release of Vasoactive Amines
1. Physical Agents (heat, cold)

2. Immunological Reactions

3. Anaphylatoxins (fragments of complement proteins)

4. Allergens (cause IgE to bind to mast cells and secrete histamine)
Plasma Proteases
Complements

Kinins

Clotting Systems
Complements
20 proteins involved in antibody-antigen immune response.

Antigen-Antibody complex binds to complement which releases histmine and neutrophilic infiltration


C3a, C5a
C3a
Increase vascular permeability
C5a
Increase vascular permeability

Enhances Chemotactic Behavior
Kinins
Endogenous peptides produced by cascade caused by Factor 12 (Hageman Factor)

Bradykinin
Bradykinin
Vasoactive nonapeptide

Increases permeability

Pain perception
Clotting System Constituents
Activated by Factor 12 (Hageman Factor)

Converts Fibronogen to fibrin

Fibrinopeptides increase permeability and chemotaxis
Arachidonic Acid Metabolites
20-carbon polyunsaturated fatty acid

Ingested through diet or from linoleic acid
NSAIDS inhibit this enzyme
Cylooxygenase

This transforms arachidonic acid into protaglandin PGG2
Cylooxygenase
type 1: secretes mucous that protects tummy

Type 2: makes protglandin which is involved in inflammation and should be the REAL target of NSAIDS
5-Lipxygenase (5-LO)
Converts Arachidonic acid into Leukotrienes
Leukotrienes
More potent inflammatory agent than Prostaglandins
Mast Cells version of lysosomes
Eosiniphil Chemotactic Factor of Anaphylaxis

(ECF-A)
Lymphokinines
From lymphocyte when attacking an antigen.

Impact adhesion, histamine release, etc.
Exogenous Factors initiating chemical mediators
Direct injury to blood vessels

Bacterial by-products
Primary Chemical Mediators related to Increased Vascular Permeability
Vasoactive Amines (especially histamines)

Kinins (especially bradykinin)

Prostaglandins
Primary Chemical Mediators related to Emigration of Leukocytes
C5a

Neutrophil Lysosomal Proteins

Eosinophil Chemotactic Factor of Anaphylaxis (ECF-A)
Opsonizing Agent
C3b
Tissue Damage ensues from this agent
Neutrophil Lysosomal Products
Endogenous Pyrogens
Cytokinins produced by leukocytes travel to brain to raise the thermostat

Sympathetic vasoconstricion