DOCSLIB.ORG

Eg Phd, Mphil, Dclinpsychol

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Eg Phd, Mphil, Dclinpsychol This thesis has been submitted in fulfilment of the requirements for a postgraduate degree (e.g. PhD, MPhil, DClinPsychol) at the University of Edinburgh. Please note the following terms and conditions of use: This work is protected by copyright and other intellectual property rights, which are retained by the thesis author, unless otherwise stated. A copy can be downloaded for personal non-commercial research or study, without prior permission or charge. This thesis cannot be reproduced or quoted extensively from without first obtaining permission in writing from the author. The content must not be changed in any way or sold commercially in any format or medium without the formal permission of the author. When referring to this work, full bibliographic details including the author, title, awarding institution and date of the thesis must be given. Investigating miR‐214 as a pro‐fibrotic mediator in renal fibrosis and its potential as a therapeutic target via effective in vivo modelling of chronic kidney disease James O’Sullivan BSc. (Hons) Submitted in fulfilment of the requirements of the degree of Doctor of Philosophy in the College of Medicine and Veterinary Medicine, University of Edinburgh Centre for Cardiovascular Sciences, The Queen’s Medical Research Institute, College of Medicine and Veterinary Medicine, University of Edinburgh September 2019 Author’s Declaration I declare that this thesis was wrote entirely by myself and is composed of work carried out by myself, with the following exceptions. The work presented in this thesis has not been submitted for any other degree or professional qualification. For the purposes of my training, the majority of STNx surgeries for the chapter 4 study were carried out by Dr. Laura Denby. Sarah Finnie, Andrew Boyd, and Dr. Laura Denby assisted with the cull of animals in studies presented in chapters 3 and 4. Echocardiography imaging (chapter 4) was carried out by preclinical imaging technician Adrian Thompson (analysis of echocardiograph was carried out by myself). Biochemical analysis of serum and urine for albumin, creatinine, urea, and phosphate was carried out by Howie Forbes in the QMRI specialist biochemical analysis service. rUUO (chapter 5) surgeries were carried out by Gary Borthwick and Dr. Laura Denby, with Dr. Laura Denby carrying out sham and UUO group surgeries, while Gary Borthwick carried out the rUUO group surgeries. In the bulk rUUO RNA sequencing, RNA was extracted from whole kidney cortex, yield quantified via NanoDrop and quality assessed via Aglient Bioanalyser by Dr. Laura Denby and Carolynn Cairns. In relation to the RNA sequencing of FACS‐isolated renal cell populations (chapter 5), the protocol for preparing renal tissue for FACS, the use of the flow cytometer, RNA extraction, RNA quality and yield assessment via Aglient Bioanalyser, and amplified cDNA synthesis was carried out by Dr. Laura Denby and Carolynn Cairns. For RNA sequencing (chapter 5), library preparation, sequencing of libraries and quality control was carried out by Genewiz. IRI (chapter 5) and FACS process was carried out by Dr. Victoria Banwell, with RNA extraction carried out by myself and Dr. Victoria Banwell. James O’Sullivan September 2019 II Acknowledgements To my supervisor, Dr. Laura Denby, thank you for giving me the opportunity to learn and grow as a scientist over these four years. The advice and guidance you gave, as well as the space to explore my own ideas and interests, has allowed me to get to where I am today. Thank you to Prof. Andy Baker and Dr. Bryan Conway for the invaluable contributions and collaborations. For providing the funding that allowed me to do a PhD in the first place, I owe a debt of gratitude to Medical Research Scotland. I thank Regulus Therapeutics for generously co‐sponsoring my PhD and for inviting me to a three‐month placement in their lab, which was a great experience. Thank you to the other PhD students and staff who made the QMRI a bit more fun. Particularly to Rachel for the long coffee‐breaks, to Andrew for the random chats in the lab, and to Francesca for sharing my office‐related woes! Many members of my large family have, in some way, helped me get to the point where I’m finishing writing a PhD thesis, but a few in particular stand out. Thank you to my parents, who supported the earlier stages of this lengthy education of mine. During a recession was a pretty inconvenient time to go to college in Dublin, but we made it work. Thanks to Chloe and Conor, for always being there. Thank you to my Nanny O’Sullivan, for always, always, being there. To my Ada Wickham, thank you for telling me all the stories, teaching me so much about the world from a young age, and, of course, for bringing me to check the buoys. I owe a lot of the curiosity that drove me towards science to you. III Non scholæ, sed vitæ discimus. IV Table of Contents Author’s Declaration ............................................................................................. II Acknowledgements .............................................................................................. III Table of Contents .................................................................................................. V List of Figures ..................................................................................................... VIII List of Tables ......................................................................................................... XI Abstract ............................................................................................................... XII Lay Summary ....................................................................................................... XV List of Abbreviations ......................................................................................... XVIII Chapter One: General Introduction ..................................................................... 1‐1 1.1: Renal physiology ................................................................................................. 1‐2 1.2: Chronic kidney disease ........................................................................................ 1‐6 1.3: Markers of CKD ................................................................................................... 1‐7 1.3.1: Creatinine ........................................................................................................................ 1‐7 1.3.2: Cystatin C ......................................................................................................................... 1‐8 1.3.3: Albuminuria ..................................................................................................................... 1‐8 1.3.4: Serum phosphate .......................................................................................................... 1‐10 1.3.5: Serum urea .................................................................................................................... 1‐11 1.4: Cardiorenal syndrome ....................................................................................... 1‐12 1.5: Renal Fibrosis .................................................................................................... 1‐14 1.5.2: Cytokines and extracellular mediators in renal fibrosis ................................................ 1‐16 1.5.2.1: TGFβ ....................................................................................................................... 1‐16 1.5.2.2: Angiotensin II ......................................................................................................... 1‐17 1.5.2.3: TNFα ....................................................................................................................... 1‐18 1.5.3: Fibroblasts in renal fibrosis ............................................................................................ 1‐18 1.5.4: Macrophages in renal fibrosis ....................................................................................... 1‐22 1.5.5: Proximal tubular epithelial cells in renal fibrosis ........................................................... 1‐25 1.5.6: Endothelial cells in renal fibrosis ................................................................................... 1‐29 1.6: Animal models of renal injury ........................................................................... 1‐33 1.6.1: Unilateral ureteral obstruction (UUO) ........................................................................... 1‐33 1.6.2: Reversal of unilateral ureteral obstruction (rUUO) ....................................................... 1‐36 1.6.3: Subtotal nephrectomy ................................................................................................... 1‐38 1.6.4: Ischemia reperfusion injury (IRI) .................................................................................... 1‐41 1.7: microRNA ......................................................................................................... 1‐42 1.7.1: miRNA biogenesis and function ..................................................................................... 1‐42 1.7.2: miRNA in development .................................................................................................. 1‐46 1.7.3: miRNA in disease and as therapeutic targets ................................................................ 1‐47 1.8: miR‐214 in development, disease and homeostasis ........................................... 1‐49 1.8.1: miR‐214 in cardiac injury
Load more

Recommended publications
  • Why Are Spider Veins of the Legs a Serious and a Dangerous Medical
    1 Anti-aging Therapeutics Volume 9–2007 Prevention or Reversal of Deep Venous Insufficiency and Treatment: Why Are Spider Veins of the Legs a Serious and A Dangerous Medical Condition? Imtiaz Ahmad M.D., F.A.C.S a, b, Waheed Ahmad M.D., F.A.C.S c, d a Cardiothoracic and Vascular Associates (Comprehensive Vein Treatment Center), Hamilton, NJ, USA b Robert Wood Johnson University Hospital, Hamilton, NJ, USA. c Comprehensive Vein Treatment Center of Kentuckiana, New Albany, IN 47150, USA. d Clinical professor of surgery, University of Louisville, Louisville, KY, USA. ABSTRACT Spider veins (also known as spider hemangiomas) unlike varicose veins (dilated pre-existing veins) are acquired lesions caused by venous hypertension leading to proliferation of blood vessels in the skin and subcutaneous tissues due to the release of endothelial growth factors causing vascular neogenesis. More than 60% of the patients with spider veins of the legs have significant symptoms including pain, itching, burning, swelling, phlebitis, cellulites, bleeding, and ulceration. Untreated spider veins may lead to serious medical complications including superficial and deep venous thrombosis, aggravation of the already established venous insufficiency, hemorrhage, postphlebitic syndrome, chronic leg ulceration, and pulmonary embolism. Untreated spider vein clusters are also responsible for persistent low-grade inflammation; many recent peer- reviewed medical studies have shown a definite association of chronic inflammation with obesity, cardiovascular disease, arthritis, Alzheimer’s disease, and cancer. Clusters of spider veins have one or more incompetent perforator veins connected to the deeper veins causing reflux overflow of blood that is responsible for their dilatation and eventual incompetence.
    [Show full text]
  • Cardiovascular System 9
    Chapter Cardiovascular System 9 Learning Outcomes On completion of this chapter, you will be able to: 1. State the description and primary functions of the organs/structures of the car- diovascular system. 2. Explain the circulation of blood through the chambers of the heart. 3. Identify and locate the commonly used sites for taking a pulse. 4. Explain blood pressure. 5. Recognize terminology included in the ICD-10-CM. 6. Analyze, build, spell, and pronounce medical words. 7. Comprehend the drugs highlighted in this chapter. 8. Describe diagnostic and laboratory tests related to the cardiovascular system. 9. Identify and define selected abbreviations. 10. Apply your acquired knowledge of medical terms by successfully completing the Practical Application exercise. 255 Anatomy and Physiology The cardiovascular (CV) system, also called the circulatory system, circulates blood to all parts of the body by the action of the heart. This process provides the body’s cells with oxygen and nutritive ele- ments and removes waste materials and carbon dioxide. The heart, a muscular pump, is the central organ of the system. It beats approximately 100,000 times each day, pumping roughly 8,000 liters of blood, enough to fill about 8,500 quart-sized milk cartons. Arteries, veins, and capillaries comprise the network of vessels that transport blood (fluid consisting of blood cells and plasma) throughout the body. Blood flows through the heart, to the lungs, back to the heart, and on to the various body parts. Table 9.1 provides an at-a-glance look at the cardiovascular system. Figure 9.1 shows a schematic overview of the cardiovascular system.
    [Show full text]
  • Microlymphatic Surgery for the Treatment of Iatrogenic Lymphedema
    Microlymphatic Surgery for the Treatment of Iatrogenic Lymphedema Corinne Becker, MDa, Julie V. Vasile, MDb,*, Joshua L. Levine, MDb, Bernardo N. Batista, MDa, Rebecca M. Studinger, MDb, Constance M. Chen, MDb, Marc Riquet, MDc KEYWORDS Lymphedema Treatment Autologous lymph node transplantation (ALNT) Microsurgical vascularized lymph node transfer Iatrogenic Secondary Brachial plexus neuropathy Infection KEY POINTS Autologous lymph node transplant or microsurgical vascularized lymph node transfer (ALNT) is a surgical treatment option for lymphedema, which brings vascularized, VEGF-C producing tissue into the previously operated field to promote lymphangiogenesis and bridge the distal obstructed lymphatic system with the proximal lymphatic system. Additionally, lymph nodes with important immunologic function are brought into the fibrotic and damaged tissue. ALNT can cure lymphedema, reduce the risk of infection and cellulitis, and improve brachial plexus neuropathies. ALNT can also be combined with breast reconstruction flaps to be an elegant treatment for a breast cancer patient. OVERVIEW: NATURE OF THE PROBLEM Clinically, patients develop firm subcutaneous tissue, progressing to overgrowth and fibrosis. Lymphedema is a result of disruption to the Lymphedema is a common chronic and progres- lymphatic transport system, leading to accumula- sive condition that can occur after cancer treat- tion of protein-rich lymph fluid in the interstitial ment. The reported incidence of lymphedema space. The accumulation of edematous fluid mani- varies because of varying methods of assess- fests as soft and pitting edema seen in early ment,1–3 the long follow-up required for diagnosing lymphedema. Progression to nonpitting and irre- lymphedema, and the lack of patient education versible enlargement of the extremity is thought regarding lymphedema.4 In one 20-year follow-up to be the result of 2 mechanisms: of patients with breast cancer treated with mastec- 1.
    [Show full text]
  • Lower Limb Venous Drainage
    Vascular Anatomy of Lower Limb Dr. Gitanjali Khorwal Arteries of Lower Limb Medial and Lateral malleolar arteries Lower Limb Venous Drainage Superficial veins : Great Saphenous Vein and Short Saphenous Vein Deep veins: Tibial, Peroneal, Popliteal, Femoral veins Perforators: Blood flow deep veins in the sole superficial veins in the dorsum But In leg and thigh from superficial to deep veins. Factors helping venous return • Negative intra-thoracic pressure. • Transmitted pulsations from adjacent arteries. • Valves maintain uni-directional flow. • Valves in perforating veins prevent reflux into low pressure superficial veins. • Calf Pump—Peripheral Heart. • Vis-a –tergo produced by contraction of heart. • Suction action of diaphragm during inspiration. Dorsal venous arch of Foot • It lies in the subcutaneous tissue over the heads of metatarsals with convexity directed distally. • It is formed by union of 4 dorsal metatarsal veins. Each dorsal metatarsal vein recieves blood in the clefts from • dorsal digital veins. • and proximal and distal perforating veins conveying blood from plantar surface of sole. Great saphenous Vein Begins from the medial side of dorsal venous arch. Supplemented by medial marginal vein Ascends 2.5 cm anterior to medial malleolus. Passes posterior to medial border of patella. Ascends along medial thigh. Penetrates deep fascia of femoral triangle: Pierces the Cribriform fascia. Saphenous opening. Drains into femoral vein. superficial epigastric v. superficial circumflex iliac v. superficial ext. pudendal v. posteromedial vein anterolateral vein GREAT SAPHENOUS VEIN anterior leg vein posterior arch vein dorsal venous arch medial marginal vein Thoraco-epigastric vein Deep external pudendal v. Tributaries of Great Saphenous vein Tributaries of Great Saphenous vein saphenous opening superficial epigastric superficial circumflex iliac superficial external pudendal posteromedial vein anterolateral vein adductor c.
    [Show full text]
  • Comprehensive Review of the Superficial Veins of the Forearm from a Historical, Anatomical and Clinical Point of View
    IJAE Vol. 124, n. 2: 142-152, 2019 ITALIAN JOURNAL OF ANATOMY AND EMBRYOLOGY Circulatory system Comprehensive review of the superficial veins of the forearm from a historical, anatomical and clinical point of view Lucas Alves Sarmento Pires1,2,*, Albino Fonseca Junior1,2, Jorge Henrique Martins Manaia1,2, Tulio Fabiano Oliveira Leite3, Marcio Antonio Babinski1,2, Carlos Alberto Araujo Chagas2 1 Medical Sciences Post Graduation Program, Fluminense Federal University, Niterói, Rio de Janeiro, Brazil 2 Morphology Department, Fluminense Federal University, Niterói, Rio de Janeiro, Brazil 3 Interventional Radiology Unit, Radiology Institute, University of São Paulo Medical School, São Paulo, Brazil Abstract The superficial veins of the forearm are prone to possess different patterns of anastomosis. This is highly significant, as venipunctures in the upper limb are among the most performed procedures in the world and they often rely on the veins of the cubital fossa. In addition, the relationship of these veins to the cutaneous nerves are also prone to vary and are often uncer- tain. These veins are also manipulated in the creation of arteriovenous fistula for dialisis, which remains as the best choice of treatment for renal failure patients. Such fistulas are often per- formed on the wrist or the cubital fossa, with the cephalic vein or basilic vein. It is known that anatomical variations of the vessels and nerves on the cubital fossa may induce the profession- als to error, and one of the most common complications of venipuncture are accidental nerve puncture, which can lead to paresthesia and pain. We aim to perform a comprehensive review of the venous arrangements of the cubital fossa and their clinical aspects, as well as of veni- puncture from a historical perspective and of the complications of venipuncture and arterio- venous fistula from an anatomical point of view, with the purpose of compiling available data and help healthcare professionals to reduce puncture errors or arteriovenous fistula complica- tions and improve patient care.
    [Show full text]
  • The Venous System
    The Venous System Discussion paper prepared for The Workplace Safety and Insurance Appeals Tribunal October 2004 Prepared by: Robert Maggisano MD, FRCS(C), FACS, GKHS Assistant Professor, University of Toronto Chief of Vascular Surgery and Director of Non-invasive Vascular Laboratory, Sunnybrook and Women’s Health Sciences Centre A.W. Harrison MD, FRCS(C) Professor of Surgery, University of Toronto Former Chief of Surgery and VP Medical Affairs, Sunnybrook and Women’s Health Sciences Centre Dr. Robert Maggisano obtained his Medical degree from the University of Toronto in 1974. He did post-graduate training in surgery at the University of Toronto from 1975 to 1980, including in cardiovascular surgery at Toronto General Hospital as well as in vascular surgery at Wellesley Hospital and at Toronto General Hospital. He subsequently did a fellowship in vascular surgery with Dr. E. Wylie at the University of California in San Francisco, in 1980, and with Dr. S. Crawford at the Baylor College of Medicine in Houston, Texas, in 1981. He was granted his Canadian Fellowship in general surgery (FRCS (C)) in 1979, and he was Board certified in general surgery by the American College of Surgery in 1981. He obtained his Certificate of Competence in vascular surgery from the Royal College of Physicians and Surgeons of Canada in 1983, and he was admitted to the American College of Surgery (FACS) in 1985. He joined the University of Toronto faculty in 1981 and holds the rank of Associate Professor at the Division of Vascular Surgery of the Department of Surgery. His clinical and research interests are in vascular surgery.
    [Show full text]
  • VENOUS HEMODYNAMICS WHAT HAPPENS WHEN FLOW IS WRONG…… Liz Lawrence, RDMS,RDCS, RVT KNOW YOUR ANATOMY the START of VENOUS ANATOMY the Capillary Bed
    OBJECTIVES OF THIS LECTURE: UNDERSTAND VENOUS ANATOMY AND HEMODYNAMICS BE ABLE TO IDENTIFY NORMAL AND ABNORMAL VENOUS ANATOMY AND HEMODYNAMICS BY DUPLEX ULTRASOUND RECOGNIZE THE CLINICAL SIGNS AND SYMPTOMS OF VENOUS HYPERTENSION BECOME FAMILIAR WITH SUPERFICIAL VENOUS ANATOMY AND HEMODYNAMIC ABNORMALITIES KNOWLEDGE OF THE SCANNING PROTOCOL, PATIENT POSITIONS, AND MANEUVERS TO DEMONSTRATE VENOUS INSUFFICIENCY Liz Lawrence, RDMS,RDCS, RVT VENOUS HEMODYNAMICS WHAT HAPPENS WHEN FLOW IS WRONG…… Liz Lawrence, RDMS,RDCS, RVT KNOW YOUR ANATOMY THE START OF VENOUS ANATOMY The Capillary Bed Arterioles Venules Size is 20-30µm Micrometer On millionth of a meter SUPERFICIAL VENOUS ANATOMY Superficial veins flow to the major superficial veins - Saphenous Veins: Greater Lessor / Small Perforators: Hunterian Dodd Boyd Cockett LOWER EXTREMITY DEEP VENOUS ANATOMY Superficial veins flow into the Deep Veins Common Femoral Profunda/Deep Femoral Femoral Vein Popliteal Vein Gastrocnemius Veins Posterior Tibial Veins Anterior Tibial Veins Peroneal Veins LOWER VEINS FLOW TO THE HEART Carried to the heart by the Inferior Vena Cava VENOUS FLOW IS EFFECTED BY ABDOMINAL AND THORACIC PRESSURE This is important to remember when looking at venous flow patterns VENOUS VALVES Valves are responsible for keeping flow going in the right direction – TOWARD THE HEART When the valves fail it results in Venous Hypertension NORMAL VALVES WHEN VEIN VALVES ARE ABNORMAL VALVE SEEN BY ULTRASOUND INCOMPETENT VALVE BY COLOR DOPPLER The flow color of this popliteal vein is red at a valve– the same color as the artery (which is in the direction of the foot) this is indicative of an incompetent vein valve 2D VENOUS ULTRASOUND IMAGING NORMAL VEINS VEINS WITH COMPRESS WITH THROMBUS PRESSURE DON’T! VARIATIONS OF VEIN THROMBUS CHRONIC VENOUS DISEASE Veins that have residual matter left after an acute thrombus resolves.
    [Show full text]
  • Venous Insufficiency
    The Multi-Billion Dollar Vascular Disease No One Teaches, But Should!!! Venous Insufficiency Thomas E. Eidson, DO Certified Venous Disease Specialist Board Certified Family Medicine Disclosure of Conflict of Interest I do not have relevant financial relationships with any commercial interests 1 Bio • Certified Phlegologist (Vein Disease Specialist) – American Board of Venous and Lymphatic Medicine • Board Certified Family Medicine • Successfully performed over 6000 vein procedures since 2011 • Published in Vein Therapy News • Founder of Atlas Vein Care in Arlington, TX Questions for Thought 1. Which of these vascular diseases is most common in the United States? A – Peripheral Arterial Disease (PAD) B – Venous Insufficiency/Reflux Disease C – Coronary Artery Disease D – Stroke 2 Questions for Thought 2. Which of the following is a correct statement? A – Venous disease affects men more than women B – Venous disease affects women more than men C – Venous disease affects women and men the same D – I don’t know but I think I am going to find out very soon Questions for Thought 3. Which of these statements is FALSE? A – Venous reflux is a disease of old people B – Venous insufficiency is purely cosmetic and not a big deal C – Insurance does not cover treatment of venous reflux D – Varicose veins should be treated with vein stripping E – All of the above 3 Questions for Thought 4. According to most recent estimates, how many people in the US are afflicted with venous reflux disease? A – between 5 and 10 Million people B – between 10 and 20 million people C – between 40 to 50 million people D – 50+ million people E – I don’t know but I bet it’s a lot or you would not be up here talking about it Questions for Thought 5.Which of these symptoms CANNOT be associated with chronic venous insufficiency? A – leg pain, aching, and heaviness B – Night cramps and Restless Legs C – Lower extremity and ankle edema D – Skin darkening and texture changes E – All of the above can be caused by venous reflux 4 Questions for Thought 6.
    [Show full text]
  • Treatment of Superficial Vein Thrombosis: Role of Anticoagulation
    4/14/2016 Suman Rathbun MD, MS No relevant disclosures Professor of Medicine Director, Vascular Medicine University of Oklahoma Health Sciences Center Epidemiology More common than DVT 1:1000 Clinical Presentation Estimated 3 to 8% of the general population Diagnosis Risk factors: varicose veins, immobilization, trauma, surgery, Treatment pregnancy and post-partum, hormonal contraception or -Medical replacement therapy, increasing age, obesity, history of VTE, -Surgical malignancy, autoimmune disease, thrombophilia, IV catheter -Topical Females>Males -Clinical trials Varicose vein SVT • Most common risk factor for SVT • Lower risk of progression to DVT Varicose veins • May be precipitated by trauma • Tender nodules Traumatic • Localized induration Septic and Suppurative • More common after foam sclera vs. thermal ablation Migratory Mondor’s Disease Small saphenous Upper extremity Post endovascular vein treatment 1 4/14/2016 Septic thrombophlebitis • Infusion therapy • IV lines with septicemia • Direct endothelial injury of irritating solutions • Leukocytosis • Pain, tenderness and erythema at catheter insertion • Intense pain • Vein may contract rather than recanalize • Staph aureus, Pseudomonas, Klebsiella, Candida • Removal of catheter; IV antibiotics • Excision of vein in rare cases Great/Small Saphenous Vein SVT Mondor’s disease • Can progress to common femoral or popliteal DVT • Similar morbidity with GSV or SSV SVT • Thoracoepigastric vein of the breast/chest wall • Breast carcinoma or hypercoagulable states • Benign
    [Show full text]
  • Venous Disease Venous Disease People Take Better Care of Their Health When They Know What’S Going on in Their Bodies
    Venous Disease Venous Disease People take better care of their health when they know what’s going on in their bodies. For those with venous disease, this means understanding how the veins work and what happens when disease affects or damages them. This booklet has been written so that you may better understand one of the most common types of circulation prob- lems. How the Venous System Works The veins return blood to the heart. There are two main sets of veins in the legs; the deep veins, which lie well within the tissue and the superficial veins, which are close to the skin. A third set, per- forater veins, connect the superficial and deep veins. The veins of the leg are easily collapsible; blood flows under low pressure and against gravity. Muscle contracts, propelling blood Two mechanisms allow upward with open valve for the efficient return of blood in the legs; the calf muscle pump and venous valves. As you walk, calf muscle movement propels blood upward while the one way valves prevent blood from Valves close flowing backward. preventing backward flow of blood Testing for venous reflux and incompetent valves which cause varicose veins Varicose Veins The superficial veins of the leg are poorly sup- ported beneath the skin. Normally, the venous valves serve to protect the veins from the increased pressure caused by the upright posi- tion. When the valves break down, or are absent, blood can flow backward. This causes the veins to stretch and enlarge. They are seen bulging and twisted beneath the skin. The more common symptoms of varicose veins are: aching and pain, particularly after standing swelling alteration in physical appearance Treatment of varicose veins will depend upon the nature and extent of the problem.
    [Show full text]
  • Testing the Venous Circulation 79
    58097_ch04.qxd 11/18/09 5:49 PM Page 77 CHAPTER4 PART TWO: UPPER EXTREMITIES Testing the Venous CHAPTER Circulation 4 Chapter Outline General Concepts in Upper Extremity Venous General Concepts in Examining Evaluation 79 Hemodialysis Access 94 Tips/Rationale 80 Tips/Rationale 95 Protocol Algorithm 81 Protocol Algorithm 97 Duplex Exam of Upper Extremity Duplex Exam for Examining Venous Circulation 82 Hemodialysis Access 98 Test Preparation 82 Test Preparation and Test Sequence 98 Testing Sequence 82 Results and Interpretation 99 Results and Interpretation 86 Concluding Tips 103 Concluding Tips 93 77 58097_ch04.qxd 11/18/09 5:49 PM Page 78 78 PART II ● Upper Extremities IJ Brachiocephalic EJ trunk or innominate Cephalic vein Superficial temporal Supraorbital artery artery and vein Deep temporal artery Frontal branch Supratrochlear artery Parietal branch Dorsal nasal artery Middle temporal artery and vein Infraorbital artery Middle meningeal artery Angular vein Superficial temporal artery and vein Buccal artery SVC Maxillary artery and vein Masseteric artery Superior labial artery and vein Occipital artery and vein Inferior labial artery and vein Retromandibular vein Facial artery and vein Submental artery and vein External jugular vein Lingual artery and vein Internal jugular vein Superior laryngeal artery and vein 4 Basilic vein Superior thyroid arteries and veins External carotid artery Internal jugular vein Internal carotid artery External jugular vein Transverse cervical artery Brachial vein Middle thyroid vein Inferior thyroid artery Transverse Vertebral artery cervical vein CHAPTER 1st rib Ulnar vein Radial vein A B FIGURE 4.1. Diagram of the upper extremity venous system. Brachial vein (cut) and artery C5 Brachial plexus C6 Scalenus medius Scalenus posterior C7 Scalenus anterior Median nerve Subclavian vein (cut) Lateral Axillary cord artery Medial cord Pectoralis minor FIGURE 4.2.
    [Show full text]
  • Treatment of Lower Extremity Superficial Venous Insufficiency with Endovenous Thermal Ablation
    Multi-society Consensus Quality Improvement Guidelines for the Treatment of Lower- extremity Superficial Venous Insufficiency with Endovenous Thermal Ablation from the Society of Interventional Radiology, Cardiovascular Interventional Radiological Society of Europe, American College of Phlebology, and Canadian Interventional Radiology Association Neil M. Khilnani, MD, Clement J. Grassi, MD, Sanjoy Kundu, MD, FRCPC, Horacio R. D’Agostino, MD, Arshad Ahmed Khan, MD, J. Kevin McGraw, MD, Donald L. Miller, MD, Steven F. Millward, MD, Robert B. Osnis, MD, Darren Postoak, MD, Cindy Kaiser Saiter, NP, Marc S. Schwartzberg, MD, Timothy L. Swan, MD, Suresh Vedantham, MD, Bret N. Wiechmann, MD, Laura Crocetti, MD, John F. Cardella, MD, and Robert J. Min, MD, for the Cardiovascular Interventional Radiological Society of Europe, American College of Phlebology, and Society of Interventional Radiology Standards of Practice Committees J Vasc Interv Radiol 2010; 21:14–31 Abbreviations: CEAP ϭ clinical status, etiology, anatomy, and pathophysiology [classification], CVD ϭ chronic venous disorder, DVT ϭ deep vein thrombosis, EVTA ϭ endovenous thermal ablation, GSV ϭ great saphenous vein, HL/S ϭ high ligation and stripping, RF ϭ radiofrequency, SSV ϭ small saphenous vein, SF-36 ϭ Short Form–36, SFJ ϭ saphenofemoral junction, SPJ ϭ saphenopopliteal junction, SVI ϭ superficial venous insufficiency, VCSS ϭ venous clinical sever- ity score, VSS ϭ venous severity score PREAMBLE and subsequent major disability. Ve- for incompetence in these veins was to nous hypertension caused by incom- remove them. Endovenous thermal LOWER-extremity chronic venous dis- petent valves in the superficial veins is ablation (EVTA) of the saphenous order (CVD) is a heterogeneous medical by far the most common cause of this veins has been used by physicians condition whose spectrum ranges from condition.
    [Show full text]