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84 Cards in this Set
- Front
- Back
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First step in wound healing
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Clot formation
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First cell type in healing wound
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Platelet
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Growth factors released by platelets
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TGF-beta and PDGF
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Phases of wound healing (in order)
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Inflammatory, proliferative, remodeling
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Most essential cell type for wound healing
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Macrophage
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Overproduction of this growth factor can result in fibrosis
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TGF-beta
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Growth factor proven to accelerate wound healing
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PDGF
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Growth factor involved in tumor metastasis
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VEGF
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Factors released by endothelium in response to tissue injury
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PAF and TF
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Primary effector cells in parasitic infections
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Eosinophils
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Released by mast cells
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Histamine
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Main source of histamine in the blood
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Basophils
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Histamine effects
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Vasodilation, edema, and capillary leak
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Increases cGMP resulting in vascular smooth muscle dilation
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NO
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Primary cytokines of inflammatory repsonse
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TNF-alpha and IL-1
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Largest producers of TNF-alpha and IL-1
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Macrophages
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Cytokine causing cachexia in cancer patients
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TNF-alpha
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Cytokine predominant in circulatory collapse and MSOF
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TNF-alpha
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Cytokine most responsible for fevers
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IL-1
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Cytokine which increases hepatic acute phase proteins
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IL-6
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Released by lymphocytes in response to viral infections
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IFN
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Mechanism of action of interferons
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Inhibit viral replication
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Two major proteins decreased during inflammation
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Albumin and transferrin
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Cytokine which has been used to treat cancer patients
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IL-2
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Cytokine which stimulates NK cells to release IFN-gamma and TNF-alpha
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IL-12
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Cytokine which stimulates IgA production
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IL-5
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Cytokine which stimulates neutrophil chemotaxis
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IL-8
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Receptors involved in rolling adhesion of leukocytes
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Selectins (L - leukocyte; E - endothelial; P - platelets)
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Receptors on leukocytes and platelets involved in tight adhesions and migration
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Integrins
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Ligands on endothelial cells involved in tight adhesions and migration
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CAMs
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The classic complement pathway is activated by . . .
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Antigen-antibody complexes (IgG/IgM)
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The alternative complement pathway is activated by . . .
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Endotoxin or bacteria
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The convergence point for both complement pathways . . .
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C3
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Essential element for the complement pathways . . .
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Mg
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Anaphylatoxins . . .
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C3a, C4a, C5a
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Membrane attack complex . . .
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C5b-9b
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Opsonization . . .
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C3b
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Chemotactic complement factors . . .
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C3a and C5a
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PGs which cause bronchodilation . . .
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PGI2 and PGE2
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PG which causes bronchoconstriction . . .
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PGD2
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Mechanism of anticoagulation by aspirin . . .
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Decreases TXA2 inhibiting platelet adhesion (irreversible COX inhibition)
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Mechanism by which steroids decrease inflammation . . .
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Inhibition of phospholipase
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Effect of leukotrienes on bronchioles and blood vessels . . .
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Bronchoconstriction, vasoconstriction and increased permeability (wheal and flare)
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Timing of peak catecholamines after injury . . .
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24-48 hours
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Primary cellular mediator of reperfusion injury . . .
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PMNs
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Chemokine receptor type . . .
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G-protein-linked
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Rate of epithelialization of a wound . . .
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1-2 mm/day
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Timing of proliferative phase . . .
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5 days to 3 weeks
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Rate of peripheral nerve regeneration . . .
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1 mm/day
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Primary type of collagen in early wound healing . . .
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Type III
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Primary collagen type in the healed wound . . .
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Type I
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Role of type IV collagen . . .
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Basement membrane
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Collagen type in cartilage . . .
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Type II
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Time at which wound reaches 80% of its final strength . . .
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6 weeks
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Time at which wound reached 80% of its original strength . . .
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8 weeks (maximum tensile strength)
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Time at which maximum collagen accumulation occurs . . .
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2-3 weeks
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Mechanism by which a healing wound regains its strength . . .
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Collagen crosslinking (remodeling phase)
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Medication which inhibits collagen crosslinking . . .
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Penicillamine
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Last cell type in a healing wound . . .
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Fibroblasts
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Two main components of the platelet plug . . .
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Platelets and fibrin
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Three main components of the provisional matrix (before collagen deposition) . . .
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1. Platelets
2. Fibrin 3. Fibronectin |
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Four components of platelet alpha granules . . .
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1. Platelet factor 4
2. Beta-thrombomodulin 3. PDGF 4. TGF-beta |
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Three components of platelet dense granules . . .
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1. Adenosine
2. Serotonin 3. Calcium |
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Three platelet aggregation factors . . .
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1. TXA2
2. Thrombin 3. Platelet factor 4 |
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Prostaglandin which induces vasoconstriction . . .
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PGF2
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Most important factors in healing by primary and secondary intention respectively . . .
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Tensile strength and epithelial integrity
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Tensile strength is determined by . . .
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Collagen deposition and crosslinking
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Epithelial cells migrate from these three locations in a healing wound . . .
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1. Wound edges
2. Hair follicles 3. Sweat glands |
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Strength layer of the bowel . . .
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Submucosa
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Most likely timing of an anastomotic leak . . .
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Day 3-5
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Cell type involved in wound contraction . . .
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Myofibroblasts
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Four elements required for hydroxylation and crosslinking of proline . . .
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1. Vitamin C
2. Alpha-ketoglutarate 3. Fe 4. Oxygen |
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Two amino acids abundant in collagen . . .
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Proline and lysine
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Bacterial count which impedes wound healing . . .
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>100,000/cm2
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Medication administered to counteract steroidal effects on wound healing . . .
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Vitamin A (25,000 IU daily)
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Defect in osteogenesis imperfecta . . .
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Type I collagen
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Defect in Marfan's syndrome . . .
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Fibrillin defect
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Cause and typical location of Charcot's joint . . .
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Diabetes/ 2nd MTP joint
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Predominant cause and treatment of leg ulcers . . .
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Venous insufficiency/ Unna boot (zinc oxide)
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Effect of denervation on wound healing . . .
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None
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Time after which chemotherapy no longer affects wound healing . . .
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14 days
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Four treatments for keloids . . .
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1. XRT
2. Steroids 3. Silicone 4. Pressure garments |
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Typical location of hypertrophic scar tissue . . .
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Flexor surfaces of upper torso
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Characteristic of collagen in keloids . . .
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Extends beyond the original scar
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