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BIOE 2010 Exam 2 Study Guide

by: Sara Littlejohn

BIOE 2010 Exam 2 Study Guide BIOE 2010

Marketplace > Clemson University > Bioengineering > BIOE 2010 > BIOE 2010 Exam 2 Study Guide
Sara Littlejohn
GPA 3.0

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About this Document

This study guide covers all the material that will be on exam 2 (9/29/2016).
Intro to Biomedical Engineering
Dr. Alexis and Dr. Webb
Study Guide
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This 9 page Study Guide was uploaded by Sara Littlejohn on Friday September 23, 2016. The Study Guide belongs to BIOE 2010 at Clemson University taught by Dr. Alexis and Dr. Webb in Fall 2016. Since its upload, it has received 63 views. For similar materials see Intro to Biomedical Engineering in Bioengineering at Clemson University.


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Date Created: 09/23/16
BIOE 2010 Exam 2 Study Guide Highlighted or Red text- important concepts 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 Biocompatibility Host Response Definitions  Host response: changes in cellular and systematic physiology resulting from the implantation of a medical device  Biocompatibility: the ability of a material to perform with an appropriate host response in a specific application  All devices are approved for a specific application and that application only. Types of Biocompatibility  Bioinert: the material has no interaction with physiological tissue o We have never been able to achieve a material that the body just ignores (that is totally bioinert)  Bioactive: the material incorporates mechanisms capable of eliciting specific cellular responses and tissue integration  Hemocompatability: the ability of a material to perform appropriately in the presence of blood Biocompatibility  Dynamic and continual process governed by effects of that material on the surrounding tissue as well as effects of the physiological environment on the material  Biocompatibility changes over time. Factors governing Biocompatibility  Chemical/ Physical properties of the material  Wear  Corrosion  Mechanical integration/ micro-motion  Leachables  Implant geometry  Surface properties o Chemistry o Topography/roughness Implant Response  Extrusion: pocket formed around an implant adjacent to epithelial tissue o Uncommon but can happen o Example:  splinter  Resorption (degradation): implant site resolves into a collapsed scar (soft tissue) or may completely disappear (bone) (Desired-degradable)  Integration: close, possibly adhesive, approximation of nearly normal host tissue to implant without intervening fibrous capsule (Desired-permanent) o Most desired  Encapsulation: implant blocked off from surrounding tissue by fibrous capsule Wound Response vs. Implant response  The response of host tissue to an implant is similar to normal wound response at first o Inflammation, cellular invasion and proliferation  Process then enters chronic phase in response to continued presence of implant  Chronic phase is characterized by chronic inflammation and classic foreign body response o Macrophages o Macrophage fusion (foreign body giant cells) o Fibrous encapsulation Capsule Formation  Maintained by continuous presence of implant  The thickness of the capsule is related to several factors: o Chemical activity of material o Motion between tissue and implant o Shape of implant o Presence of electrical current Surface Modification  Prevent protein adsorption (make bioinert) o Chemical modification with polyethylene oxide (PEO)  PEO is one of the more inert materials in nature  PEO repels blood proteins  Immobilize anti-coagulation molecules (heparin) o Activates anti-thrombin III, blocks thrombin cleavage of fibrinogen  Surface modification allows us to select our material for its mechanical properties and we can change the surface to target the biological response Biocompatibility of Biological Materials  Sources of biological materials (grafts) o Autologous: the patient’s own tissue  No immunological response  Example:  ACL repair  Skin graphs o Allogenic: another humans tissue  Example: Organ transplant o Xenogeneic: animal tissue Synthetic vs. Natural Materials  Synthetic materials: non-specific response involving primarily macrophages o Synthetic materials are non-specific because there is no protein  Naturally derived materials: specific immune response mediated by lymphocytes and antibodies which recognize foreign proteins (rejection)  The proteins that mediate rejection are very specific cell surface proteins that are bound to the plasma membrane and exposed to the extracellular environment and hence the immune system  In general, out immune systems recognize proteins Autologous Materials  No immune rejection complications  All proteins in autologous graft material are derived from the patient’s own body  The immune system does not recognize “self” proteins Allogenic Grafts  Generally rejected over 1-2 weeks  Exceptions: some minimally vascularized tissues such as tendons/cartilage are tolerated  Mechanism: immune recognition of blood group proteins (A, B, O) and major histocompatibility (MHC) cell surface proteins o MHC is special because it is composed of 6 genes. For each gene there are approximately 100 copies within the human population  Can be controlled for organ transplantation through chronic administration of immune suppressive drugs Xenogeneic Grafts  Always rejected within 1-2 days  Mechanism: differences in blood group protein and MHC How to use Allogenic/Xenogeneic Materials  Immunosuppression: allogenic transplantation  De-cellularization: a variety of techniques that are used for extracting all cells and cell associated proteins from tissue, it leaves intact extracellular matrix which is often a useful biomaterial itself  Removal of cellular proteins results in removal of basis for immune rejection


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