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BIOE 2010 Week 4 Notes

by: Sara Littlejohn

BIOE 2010 Week 4 Notes BIOE 2010

Marketplace > Clemson University > Bioengineering > BIOE 2010 > BIOE 2010 Week 4 Notes
Sara Littlejohn
GPA 3.0

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About this Document

These notes cover what was discussed in class on 9/13/2016 and 9/15/2016.
Intro to Biomedical Engineering
Dr. Alexis and Dr. Webb
Class Notes
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This 6 page Class Notes was uploaded by Sara Littlejohn on Friday September 16, 2016. The Class Notes belongs to BIOE 2010 at Clemson University taught by Dr. Alexis and Dr. Webb in Fall 2016. Since its upload, it has received 6 views. For similar materials see Intro to Biomedical Engineering in Bioengineering at Clemson University.


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Date Created: 09/16/16
Wound Healing Wound healing is a reparative process not a regenerative process. The process includes: 1. The injury 2. Wound healing response a. No implant i. Resolution b. Implant i. Synthetic 1. Never reaches a resolution ii. Degradable 1. Reaches resolution Regeneration: complete restoration of native tissue structure and function  Bone has a tremendous regenerative capacity because it contains stem cells that have the capability to form new bone.  Liver also has a very high regenerative capacity  Places to see regeneration in nature: o Lizards can lose a tail and grow it back o Deer antlers  Fastest rate of bone growth in the animal kingdom o Pregnancy Wound Healing: most common response to tissue damage; repair process resulting in scar tissue  Does not produce complete restoration Absence/ Failure of Healing  The spinal cord does not regenerate  A defect can become a critical-sized defect and healing/regeneration does not occur after this point  Underlying pathologies can inhibit the ability to regenerate and heal correctly Characteristics of Scar Tissue  An organ contains 2 different cells and an extracellular matrix (ECM/Everything besides the cells) o Parenchymal cell: cell that provides specialized function o Fibroblasts: “stromal cell”; maintains the ECM  Every organ has: o Parenchymal component composed of cells that have a specialized function  Ex: brain cells o Stromal component composed of fibroblasts and ECM that provides mechanical structure and integrity  Ex: tendon, ligament  During wound healing the parenchymal has a very low capacity for cell division and fibroblasts have very high capacity for cell division. Scar tissue enrichment of the stromal component relative to the parenchymal component Phases of Wound Healing  Inflammatory o Coagulation: stop bleeding o Prevent infection o Takes about 48 hours  Proliferative o Granulation tissue formation: replacement of cell and extracellular matrix o Angiogenesis: blood vessel formation  Cancer is very good at angiogenesis so most modern cancer treatments are anti-angiogenesis (stop cell growth)  Proangiogenic compounds can be put in the heart to relieve blockages (they make more blood vessels to alleviate the clot) o Re-epithelialization o Needs energy o Takes 2-3 weeks  Remodeling o Restoration of function/ Development of mechanical strength o Lasts up to 12 months o Strength gradually increases o Cross-linking makes it stronger Components of Wound Healing  Cells  Extracellular matrix  Growth Factors o Growth factors are small soluble proteins that diffuse and bind to receptors on neighboring cells and change gene expression Coagulation  Within all our blood vessels there is a monolayer of cells and they are called endothelial cells, they line the entire cardiovascular system, it does not activate the proteins that are in our blood and disruption of this layer starts coagulation  Circulating proteins in blood o Enzymes: proteins that catalyze a chemical reaction o Zymogen: enzyme that is inactive o Activated by contact with a non-endothelial surface  Fibrinogen polymerization (fibrin) o Provisional matrix-scaffold for repair (clot)  Hemostasis: stable blood volume  Platelets- circulating cells bind to fibrin  Platelets add microscopic material to the clot and they have granules filled with growth factors and when they get damaged they release the growth factors. Coagulation Cascade  2 ways to initiate coagulation o Intrinsic pathway  Blood contact with non-endothelial surface o Extrinsic pathway  Benefits of cascade: o Amplification  At each step you can amplify the process o Each step is open to regulation  The more steps you have in a process the more you can control the outcome X (inactive)  Xa (active) Control of Coagulation  Damaged cells at the site of injury (mast cells) release heparin (glycosaminoglycan)  Heparin binds to anti-thrombin III (thrombin inhibitor) and increases its potency 1000-fold  Thrombin also activates Protein C-which deactivates earlier factors in the cascade (negative feedback)  When you give blood the bag contains heparin, this keeps it from clogging. Inflammation  Neutrophils and monocytes (macrophages)  Monocyte: cell in the blood  Macrophage: same cell in the tissue  Recruited to injury site by chemotaxis- directed cell migration in response to a concentration gradient of a soluble molecule  Phagocytes-engulf and destroy foreign particles (bacteria and debris)- phagocytosis  Neutrophils and macrophages are short-lived (days)- limits time span of inflammation  Persistent presence of bacteria (infection) or other stimuli (implanted biomaterial) result in continued recruitment of additional neutrophils and monocytes from the circulation (Chronic inflammation) Re-epithelialization  Proliferation and migration of epithelial cells to restore dermal integrity  Top layer of skin is composed of epithelial cells Granulation Tissue Formation  Macrophage-derived growth factors (transforming growth factor beta- 1) activate fibroblast proliferation, migration, and extracellular matrix synthesis (fibroplasia) o TGFB stimulates fibroblasts to migrate, divide, and synthesize collagen to replace the fibrin patch with a more durable material.  Macrophages and fibroblasts also produce proteases that degrade the fibrin provisional matrix  Proteases- enzymes that cleave and degrade other proteins- plasmin degrades fibrin Fibrinolysis  Fibrinolysis: enzymatic degradation of fibrin o Highly regulated process  Plasminogen-inactive Angiogenesis  Cellular hypoxia (lack of oxygen) induces the expression of vascular endothelial growth factor (VEGF)  VEGF stimulates endothelial cell division and the formation of new blood vessels Wound Contraction  Some fibroblasts become highly contractile (myofibroblasts)  Contract the collagen matrix to close the wound Long-term Remodeling  Crosslinking of the collagen matrix results in gradually increasing mechanical strength Role of Medical Devices  Medical devices become necessary in coagulation when there is o Pathological tissue damage o Traumatic wounds that overwhelm the native healing capacity


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