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23 Cards in this Set
- Front
- Back
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Transudate
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Low molecular weight fluid
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Mild Injury Exudate
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Water/serous exudate (similar to transudate)
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Moderately Sever Injury Exudate
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Fibrinous Exudate (sticky exudate because of leakage of serum proteins and clotting factors)
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Severe Injury Exudate
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Hemorrhage Exudate (white/red blood cells coming out)
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Leukocyte Migration
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Macrophages release Cytokines (IL-1, TNF) > attract leukocytes > leukocytes bind to E-SELECTIN & P-SELECTIN (early on) > bind to integrin ligand (ICAM-1) > pulled between interepithelial space by PECAM-1 (CD31). Chemokines also attract leukocytes. DIAPODESIS (TRANS-MIGRATION) movement of leukocytes into tissue
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Reasons for Exudate
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Dilute injury. Watery medium for leukocyte movement.
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Opsonization
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precipitation of native material on the native material.
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Opsonins
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1. Complement 3 breakdown
2. Non-immune immunoglobulin (IgG) 3. Plasma carbohydrate-binding lectins |
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Opsonin Receptors
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C3b: complement receptor
Fc: Immunoglobulin receptor |
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Lysosomal Enzymes
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1. Myloperoxidase (promotes formation of bactericidal peroxide/ROS)
2. Nitrous Oxide |
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Acute Inflammation - Cell Phase
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Granulocytes:
1. Neutrophils (PMNs) 2. Eosinphils (for hypersensitivity reactions) 3. Basophils 4. Macrophages (monocytes that become macrophages in tissue) |
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-ITIS
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"Inflammation"
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Mediators of Acute Inflammation (Cellular derived)
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In granules: 1. Histamine 2. Serotonin 3. Lysosomal enzymes
Newly Synthesized: Prostoglandins, Leukotriens, ROS, NO, Cytokines |
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Mediators of Acute Inflammation (Liver Derived)
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Factor XII [Hageman Factors: (bradykinin, coagulation/fibrinolysis system)
COMPLEMENT ACTIVATION C3a/C5a (anaphylotoxins) |
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Arachidonic Acid Derrivatives
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Derived from fatty acid of plasma membrane.
Cellular Derived Mediator e.g. PG, TX: cyclooxygenases LT, LX: Lipoxygenases |
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Arachidonic Acid System (Vasodilation)
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Cell Membrane Phospholipid > Phospholipase > Arachidonic Acid> Cyclooxygenase > Prostaglandin> Prostacyclin (vasodilation/inhibition of platelet aggregation)
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Abscesse
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Focal areas of suppuration (pus exudate)
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Phlegmons
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(Cellulitis) Spreading Abscess
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Systemic Effects of Acute Inflammation
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Fever: ENDOGENOUS PYROGENS > IL-1, IL-6, TNF, Prostaglandins, NO
Leukocytosis: IL-1, TNF, CSF, GSF Acute Phase reactants: CRP, complement, Serum Amyloid A |
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Role of Macrophage
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1.Antimicrobial activity (nitric acid, ROS)
2. Chemotaxis and proliferation of fibroblasts and keratinocytes (growth factors) 3. Angiogenesis (VEGF) 4. Deposition and remodeling of ECM (TGF |
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Mediators of Chronic Inflammation
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1.Cytokines (Interferon Gamma)
2. Lymphokines, monokines 3. C5a 4. Angiogenesis factors VEGF |
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Types of Granulomas
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(Morphology)
1. Non-necrotizing (FB, sarcoid, fungi) 2. Necrotizing (Tb, fungi, RA) 3. Supperative (chalazion, CSD, LGV) |
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Repair Process (Wound Healing)
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1. Granulation Tissue formation (VEGF, PDGF, TGF-b)
2. Growth factors (EGF, PDGF, TGF-aj, TGF-b, FGF, IL-1/TNF) 3. Scarring (collagen deposition) |
