DOCSLIB.ORG

Ovarian Vein Syndrome: a Review

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Ovarian Vein Syndrome: a Review View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector International Journal of Surgery 7 (2009) 516–520 Contents lists available at ScienceDirect International Journal of Surgery journal homepage: www.theijs.com Review Ovarian vein syndrome: A review Hina Y Bhutta a,*, Stewart R Walsh a, Tjun Y Tang a, Colin A Walsh b, James M Clarke a a Department of Surgery, Norfolk & Norwich University Hospital NHS Trust, Colney Lane, Norwich, NR4 7UY, UK b Department of Obstetrics and Gynaecology, St George Hospital, Kogarah, New South Wales, Australia article info abstract Article history: The Ovarian Vein Syndrome was first reported in 1964, yet its existence as a true pathophysiological Received 28 June 2009 entity remains controversial. It may present as an acute or chronic disease, typically affecting young, Received in revised form multiparous women. This review discusses the literature to date on this poorly recognised cause of 23 September 2009 ureteric obstruction and pelvic pain, including developments in the diagnosis and management of this Accepted 25 September 2009 eminently treatable condition. Available online 8 October 2009 Ó 2009 Surgical Associates Ltd. Published by Elsevier Ltd. All rights reserved. Keywords: Ovarian Vein Syndrome Chronic Pelvic Pain Congestion Ureteric Obstruction 1. Review criteria chronic variants occur most commonly in multiparous women. Several pathophysiological mechanisms have been suggested. Clark Using Embase and Medline, a literature search was undertaken. postulated that an aberrant ovarian vein, which might arise from English and foreign language articles on the ovarian vein syndrome persistent embryological posterior subcardinal branches, exerts were appraised. Chronic pelvic pain, pelvic congestion syndrome occlusive pressure on the ipsilateral ureter.1 By crossing the ureter and ureteric obstruction were key terms, which were also searched. at the level of the pelvic brim, where its position is relatively fixed, In 1964, Clark published a series of 129 cases of right-sided ovarian rather than at the usual more cephalad level of L3/L4, Clark felt the vein syndrome in which he purported that an aberrant ovarian vein aberrant vessel is more likely to cause ureteric compression. He also was the cause of an obstructive uropathy, occurring at the level of the described aberrant ovarian veins as being much larger than normal, pelvic brim.1 Since then, several others have published case reports of more likely to branch into a number of distal tributaries, and more the ovarian vein syndrome (OVS),2–7 but the largest contemporary likely to drain into the right renal vein, all of which he felt could series includes only eight cases.7 That the syndrome truly exists as explain the phenomenon of right-sided OVS (Fig. 1). a distinct pathophysiological entity remains controversial. It is often Dykhuizen described a sheath of connective tissue at the pelvic encompassed within a larger collection of disorders, which share the brim, which appeared to be a retroperitoneal continuation of the unifying feature of chronic pelvic pain. suspensory ovarian ligament, encasing both ovarian vessels and ureter. This, he surmised, contributed to ureteric fixity secondary to 5 2. Pathophysiology periureteral fibrosis. Radiographically he observed that, in sus- pected right-sided OVS, the ovarian vein fixed the right ureter as OVS may present as an acute affliction during or soon after they crossed, whilst the right kidney moved with respiration. pregnancy, or as a chronic, recurring disease. Both acute and Others believe that the ureter becomes trapped within a fibrovas- cular mesh of tortuous dilated veins.3 Alternatively, pressure from the gravid uterus may cause ovarian * Corresponding author. Tel.: þ44 07773 420 717. vein dilatation and valvular incompetence. The dilated ovarian E-mail address: [email protected] (H.Y. Bhutta). veins then compress the ureter against the external iliac artery or 1743-9191/$ – see front matter Ó 2009 Surgical Associates Ltd. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.ijsu.2009.09.008 H.Y. Bhutta et al. / International Journal of Surgery 7 (2009) 516–520 517 Fig. 1. Normal anatomy of ovarian arteries (1), veins (2) and ureters (3) demonstrated on left. Right-hand image demonstrates an aberrant, enlarged right ovarian vein (4), compressing the right ureter (5) between itself and the external iliac vessels (6). psoas muscle. However, persistent, significantly elevated venous observation that it primarily affects pre and peri-menopausal pressures are needed for the ovarian veins to feasibly occlude women.1,6,7 However, that oophorectomy does not seem to be a thick-walled muscular ureter. Such pressures are not achieved, a successful treatment for OVS weakens the hormonal hypothesis.1 even during pregnancy.8 Dure-Smith argued that whilst the pres- More rarely, an ovarian varicocele may develop as a result of sure of the gravid uterus itself may suffice to occlude the ureters, it back-pressure from the inferior vena cava or left renal vein. An seems unlikely that ovarian vein pressure could achieve this. example of this is the ‘nutcracker syndrome’, in which the left renal Quoting studies demonstrating a 60-fold increase in blood flow vein is compressed between the aorta and the superior mesenteric through the ovarian veins during pregnancy, and a 3-fold increase artery.15 in venous diameter, but a comparatively small rise in pressure in Historically, the right ureter is involved in OVS more commonly these capacitance vessels,9 he argued that ovarian veins could only than the left.1,4 This might be explained by its proximity to the iliac reach pressures high enough to occlude the ureters during labour, vessels, and the course of the right ovarian vein. The right ovarian or with transient activities such as the valsalva manoeuvre. He vein usually forms a direct anastamosis with the inferior vena contested that post-partum, the ovarian veins collapse, so post- cava.8 Aberrant veins draining into the right renal vein might be pregnancy ureteric dilatation caused by the ovarian veins seems responsible for the development of OVS.1,7 However, post-mortem implausible. He also felt that the presence of a connective tissue examinations show that the left ovarian vein, which usually drains sheath encasing vessels and ureter was dubious, and not described into the left renal vein, is twice as likely as the right to be valve- by anyone other than Dykhuizen, although subsequently, this less,16 and the left vein usually expands to a greater degree than the observation has been corroborated.10 Canine experiments repro- right both during and after pregnancy.17 These observations suggest ducing ovarian vein dilatation by ligating other main veins have that the left ovarian vein is more susceptible to becoming varicose. failed to reproduce ureteric obstruction.11 In Dykhuizen’s series, Incidental ovarian varices are present in 10–47% of females.18,19 extirpated ovarian veins demonstrated medial wall thickening, although others have found the vessels to be histologically normal.3 Hormonal changes associated with pregnancy may also explain 3. Clinical features OVS. Altered levels of circulating oestrogen and progesterone could affect the muscular ureteric wall, causing a decrease in tone that OVS is uncommon in nulliparous women.1,7 Symptoms are facilitates its compression.12,13 In Dykhuizen’s series, oral proges- variable and non-specific, including abdominal pain, particularly in togen appeared to exacerbate symptoms, presumed to be due to the iliac fossae, flanks and hypochondrium. The pain tends to be increased ovarian vein blood flow.5 Oestrogen may account for the positional, and is worse lying down on the affected side. It is often development of pelvic varicosities in the pelvic congestion cyclical, peaking shortly before menstruation.1,7 Urinary symptoms syndrome, via nitric-oxide mediated vascular smooth muscle from ureteric obstruction include recurrent urinary tract infections, relaxation.14 Similarly, oestrogen/progesterone imbalances during hydronephrosis, pyelonephritis, renal colic and frank haematuria. pregnancy are a putative biological mechanism leading to ovarian Whilst antibiotic therapy effectively treats infection, OVS pain vein dilatation and OVS. The hormonal hypothesis is strengthened is refractory, requiring more definitive treatment.5 Despite by the trend for symptoms of OVS to be cyclical, and the ureteric obstruction, there are few data regarding effects on renal 518 H.Y. Bhutta et al. / International Journal of Surgery 7 (2009) 516–520 function, unless there is a pre-existing anatomical renal tract historically been regarded as the gold standard investigation in abnormality.20,21 OVS, clearly identifying varicose veins and demonstrating retro- Given the non-specific features of OVS, the differential diagnosis grade blood flow.It is especially useful if considering ovarian vein is broad. Gynaecological conditions such as endometriosis, pelvic embolization. Ovarian veins>10 mm in diameter are accepted as inflammatory disease and salpingitis must be considered. Ovarian being varicose on venography.27 vein thrombophlebitis, a condition which typically presents in the Ovarian varicosities may also be apparent on contrast-enhanced first few days post-partum with iliac fossa pain, fevers, and often computed tomography (CT) or magnetic resonance imaging (MRI). a pelvic or abdominal mass should be excluded if
Load more

Recommended publications
  • Hydronephrosis
    Hydronephrosis Natasha Brownrigg RN(EC), MN, NP-Pediatrics Assistant Clinical Professor, McMaster School of Nursing Nurse Practitioner, Pediatric Urology, McMaster Children’s Hospital, Hamilton, ON, Canada Dr. Jorge DeMaria Pediatric Urologist, McMaster Children’s Hospital Professor Department of Surgery/Urology, McMaster University, Hamilton, ON, Canada Dr. Luis H.P. Braga Pediatric Urologist, McMaster Children’s Hospital. Associate professor Department of Surgery/Urology, McMaster University, Hamilton, ON, Canada What is hydronephrosis? Hydro Nephrosis Hydronephrosis += Refers to water Refers to the kidney A build up of fluid or fluid (urine) in the kidney Hydronephrosis is the medical term for a build-up of urine in the kidney. As the urine builds up, it stretches or dilates the inside of the kidney, known as the collecting system. If an unborn baby has hydronephrosis, an ultrasound scan will show a build-up of urine in the kidney. This is called “antenatal hydronephrosis.” Hydronephrosis is found in as many as five out of 100 pregnancies. Hydronephrosis may also be found after birth. For example, if a baby has a urinary tract infection, an ultrasound of the baby’s kidneys and bladder may detect hydronephrosis. Key points to remember if your baby has hydronephrosis • Your baby can grow and develop normally with hydronephrosis. • Hydronephrosis may affect one kidney or both. • Hydronephrosis is a finding, not a disease. • Further tests are needed to find the cause of hydronephrosis. • If the cause is known, a pediatric urologist will discuss the possible treatment. Surgery is sometimes required to correct the cause of the hydronephrosis. Hydronephrosis is often transient and improves without any intervention.
    [Show full text]
  • Heart Vein Artery
    1 PRE-LAB EXERCISES Open the Atlas app. From the Views menu, go to System Views and scroll down to Circulatory System Views. You are responsible for the identification of all bold terms. A. Circulatory System Overview In the Circulatory System Views section, select View 1. Circulatory System. The skeletal system is included in this view. Note that blood vessels travel throughout the entire body. Heart Artery Vein 2 Brachiocephalic trunk Pulmonary circulation Pericardium 1. Where would you find the blood vessels with the largest diameter? 2. Select a few vessels in the leg and read their names. The large blue-colored vessels are _______________________________ and the large red-colored vessels are_______________________________. 3. In the system tray on the left side of the screen, deselect the skeletal system icon to remove the skeletal system structures from the view. The largest arteries and veins are all connected to the _______________________________. 4. Select the heart to highlight the pericardium. Use the Hide button in the content box to hide the pericardium from the view and observe the heart muscle and the vasculature of the heart. 3 a. What is the largest artery that supplies the heart? b. What are the two large, blue-colored veins that enter the right side of the heart? c. What is the large, red-colored artery that exits from the top of the heart? 5. Select any of the purple-colored branching vessels inside the rib cage and use the arrow in the content box to find and choose Pulmonary circulation from the hierarchy list. This will highlight the circulatory route that takes deoxygenated blood to the lungs and returns oxygenated blood back to the heart.
    [Show full text]
  • Prep for Practical II
    Images for Practical II BSC 2086L "Endocrine" A A B C A. Hypothalamus B. Pineal Gland (Body) C. Pituitary Gland "Endocrine" 1.Thyroid 2.Adrenal Gland 3.Pancreas "The Pancreas" "The Adrenal Glands" "The Ovary" "The Testes" Erythrocyte Neutrophil Eosinophil Basophil Lymphocyte Monocyte Platelet Figure 29-3 Photomicrograph of a human blood smear stained with Wright’s stain (765). Eosinophil Lymphocyte Monocyte Platelets Neutrophils Erythrocytes "Blood Typing" "Heart Coronal" 1.Right Atrium 3 4 2.Superior Vena Cava 5 2 3.Aortic Arch 6 4.Pulmonary Trunk 1 5.Left Atrium 12 9 6.Bicuspid Valve 10 7.Interventricular Septum 11 8.Apex of The Heart 9. Chordae tendineae 10.Papillary Muscle 7 11.Tricuspid Valve 12. Fossa Ovalis "Heart Coronal Section" Coronal Section of the Heart to show valves 1. Bicuspid 2. Pulmonary Semilunar 3. Tricuspid 4. Aortic Semilunar 5. Left Ventricle 6. Right Ventricle "Heart Coronal" 1.Pulmonary trunk 2.Right Atrium 3.Tricuspid Valve 4.Pulmonary Semilunar Valve 5.Myocardium 6.Interventricular Septum 7.Trabeculae Carneae 8.Papillary Muscle 9.Chordae Tendineae 10.Bicuspid Valve "Heart Anterior" 1. Brachiocephalic Artery 2. Left Common Carotid Artery 3. Ligamentum Arteriosum 4. Left Coronary Artery 5. Circumflex Artery 6. Great Cardiac Vein 7. Myocardium 8. Apex of The Heart 9. Pericardium (Visceral) 10. Right Coronary Artery 11. Auricle of Right Atrium 12. Pulmonary Trunk 13. Superior Vena Cava 14. Aortic Arch 15. Brachiocephalic vein "Heart Posterolateral" 1. Left Brachiocephalic vein 2. Right Brachiocephalic vein 3. Brachiocephalic Artery 4. Left Common Carotid Artery 5. Left Subclavian Artery 6. Aortic Arch 7.
    [Show full text]
  • Pelvic Anatomyanatomy
    PelvicPelvic AnatomyAnatomy RobertRobert E.E. Gutman,Gutman, MDMD ObjectivesObjectives UnderstandUnderstand pelvicpelvic anatomyanatomy Organs and structures of the female pelvis Vascular Supply Neurologic supply Pelvic and retroperitoneal contents and spaces Bony structures Connective tissue (fascia, ligaments) Pelvic floor and abdominal musculature DescribeDescribe functionalfunctional anatomyanatomy andand relevantrelevant pathophysiologypathophysiology Pelvic support Urinary continence Fecal continence AbdominalAbdominal WallWall RectusRectus FasciaFascia LayersLayers WhatWhat areare thethe layerslayers ofof thethe rectusrectus fasciafascia AboveAbove thethe arcuatearcuate line?line? BelowBelow thethe arcuatearcuate line?line? MedianMedial umbilicalumbilical fold Lateralligaments umbilical & folds folds BonyBony AnatomyAnatomy andand LigamentsLigaments BonyBony PelvisPelvis TheThe bonybony pelvispelvis isis comprisedcomprised ofof 22 innominateinnominate bones,bones, thethe sacrum,sacrum, andand thethe coccyx.coccyx. WhatWhat 33 piecespieces fusefuse toto makemake thethe InnominateInnominate bone?bone? PubisPubis IschiumIschium IliumIlium ClinicalClinical PelvimetryPelvimetry WhichWhich measurementsmeasurements thatthat cancan bebe mademade onon exam?exam? InletInlet DiagonalDiagonal ConjugateConjugate MidplaneMidplane InterspinousInterspinous diameterdiameter OutletOutlet TransverseTransverse diameterdiameter ((intertuberousintertuberous)) andand APAP diameterdiameter ((symphysissymphysis toto coccyx)coccyx)
    [Show full text]
  • Corona Mortis: the Abnormal Obturator Vessels in Filipino Cadavers
    ORIGINAL ARTICLE Corona Mortis: the Abnormal Obturator Vessels in Filipino Cadavers Imelda A. Luna Department of Anatomy, College of Medicine, University of the Philippines Manila ABSTRACT Objectives. This is a descriptive study to determine the origin of abnormal obturator arteries, the drainage of abnormal obturator veins, and if any anastomoses exist between these abnormal vessels in Filipino cadavers. Methods. A total of 54 cadaver halves, 50 dissected by UP medical students and 4 by UP Dentistry students were included in this survey. Results. Results showed the abnormal obturator arteries arising from the inferior epigastric arteries in 7 halves (12.96%) and the abnormal communicating veins draining into the inferior epigastric or external iliac veins in 16 (29.62%). There were also arterial anastomoses in 5 (9.25%) with the inferior epigastric artery, and venous anastomoses in 16 (29.62%) with the inferior epigastric or external iliac veins. Bilateral abnormalities were noted in a total 6 cadavers, 3 with both arterial and venous, and the remaining 3 with only venous anastomoses. Conclusion. It is important to be aware of the presence of these abnormalities that if found during surgery, must first be ligated to avoid intraoperative bleeding complications. Key Words: obturator vessels, abnormal, corona mortis INtroDUCTION The main artery to the pelvic region is the internal iliac artery (IIA) with two exceptions: the ovarian/testicular artery arises directly from the aorta and the superior rectal artery from the inferior mesenteric artery (IMA). The internal iliac or hypogastric artery is one of the most variable arterial systems of the human body, its parietal branches, particularly the obturator artery (OBA) accounts for most of its variability.
    [Show full text]
  • Acute Phosphate Nephropathy Alexander K
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector http://www.kidney-international.org the renal consult & 2009 International Society of Nephrology Acute phosphate nephropathy Alexander K. Rocuts1, Sushrut S. Waikar1, Mariam P. Alexander1,2, Helmut G. Rennke2 and Ajay K. Singh1 1Renal Division, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA and 2Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA minute. The rest of the examination was unremarkable. CASE PRESENTATION HerlaboratorydataissummarizedinTable1. A 60-year-old white Latino female with a clinical diagnosis A postoperative kidney ultrasound showed no of diabetes mellitus (diagnosed in 1993) and hypertension hydronephrosis. was referred to the chronic kidney disease clinic at The etiology of the acute kidney injury was unclear. Brigham and Women’s Hospital for the evaluation of acute Progressive diabetic nephropathy exacerbated by other kidney injury; serum creatinine had increased from a contributory factors, such as exposure to lisinopril, baseline of 0.9 to 1.5 mg/dl in a 11-week period. She was acetylsalicylic acid, or naproxen, was regarded as the most asymptomatic at the time of presentation. Her past plausible explanation. Despite discontinuation of these medical history included a total abdominal hysterectomy medications, kidney function did not improve; it worsened with bilateral salpingo oophorectomy and upper in a 4-week period after presentation. Hence, a kidney vaginectomy for high-grade squamous intraepithelial biopsy was performed. lesion of the cervix, 11 weeks prior to presentation. Three weeks prior to presentation (8 weeks after surgery) and within a week of each other, she was evaluated for two consecutive episodes of acute onset of chest pain with pulmonary edema in the setting of severe hypertension.
    [Show full text]
  • Vascular Density and Distribution in Neocortex
    Zurich Open Repository and Archive University of Zurich Main Library Strickhofstrasse 39 CH-8057 Zurich www.zora.uzh.ch Year: 2019 Vascular density and distribution in neocortex Schmid, Franca ; Barrett, Matthew J P ; Jenny, Patrick ; Weber, Bruno Abstract: An amazingly wide range of complex behavior emerges from the cerebral cortex. Much of the information processing that leads to these behaviors is performed in neocortical circuits that span throughout the six layers of the cortex. Maintaining this circuit activity requires substantial quantities of oxygen and energy substrates, which are delivered by the complex yet well-organized and tightly-regulated vascular system. In this review, we provide a detailed characterization of the most relevant anatomical and functional features of the cortical vasculature. This includes a compilation of the available data on laminar variation of vascular density and the topological aspects of the microvascular system. We also review the spatio-temporal dynamics of cortical blood flow regulation and oxygenation, many aspects of which remain poorly understood. Finally, we discuss some of the important implications of vascular density, distribution, oxygenation and blood flow regulation for (laminar) fMRI. DOI: https://doi.org/10.1016/j.neuroimage.2017.06.046 Posted at the Zurich Open Repository and Archive, University of Zurich ZORA URL: https://doi.org/10.5167/uzh-146003 Journal Article Accepted Version The following work is licensed under a Creative Commons: Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) License. Originally published at: Schmid, Franca; Barrett, Matthew J P; Jenny, Patrick; Weber, Bruno (2019). Vascular density and distribution in neocortex.
    [Show full text]
  • Impact of Urolithiasis and Hydronephrosis on Acute Kidney Injury in Patients with Urinary Tract Infection
    bioRxiv preprint doi: https://doi.org/10.1101/2020.07.13.200337; this version posted July 13, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. Impact of urolithiasis and hydronephrosis on acute kidney injury in patients with urinary tract infection Short title: Impact of urolithiasis and hydronephrosis on AKI in UTI Chih-Yen Hsiao1,2, Tsung-Hsien Chen1, Yi-Chien Lee3,4, Ming-Cheng Wang5,* 1Division of Nephrology, Department of Internal Medicine, Ditmanson Medical Foundation Chia-Yi Christian Hospital, Chia-Yi, Taiwan 2Department of Hospital and Health Care Administration, Chia Nan University of Pharmacy and Science, Tainan, Taiwan 3Department of Internal Medicine, Fu Jen Catholic University Hospital, Fu Jen Catholic University, New Taipei, Taiwan 4School of Medicine, College of Medicine, Fu Jen Catholic University, New Taipei, Taiwan 5Division of Nephrology, Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan *[email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.07.13.200337; this version posted July 13, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. Abstract Background: Urolithiasis is a common cause of urinary tract obstruction and urinary tract infection (UTI). This study aimed to identify whether urolithiasis with or without hydronephrosis has an impact on acute kidney injury (AKI) in patients with UTI.
    [Show full text]
  • Vessels and Circulation
    CARDIOVASCULAR SYSTEM OUTLINE 23.1 Anatomy of Blood Vessels 684 23.1a Blood Vessel Tunics 684 23.1b Arteries 685 23.1c Capillaries 688 23 23.1d Veins 689 23.2 Blood Pressure 691 23.3 Systemic Circulation 692 Vessels and 23.3a General Arterial Flow Out of the Heart 693 23.3b General Venous Return to the Heart 693 23.3c Blood Flow Through the Head and Neck 693 23.3d Blood Flow Through the Thoracic and Abdominal Walls 697 23.3e Blood Flow Through the Thoracic Organs 700 Circulation 23.3f Blood Flow Through the Gastrointestinal Tract 701 23.3g Blood Flow Through the Posterior Abdominal Organs, Pelvis, and Perineum 705 23.3h Blood Flow Through the Upper Limb 705 23.3i Blood Flow Through the Lower Limb 709 23.4 Pulmonary Circulation 712 23.5 Review of Heart, Systemic, and Pulmonary Circulation 714 23.6 Aging and the Cardiovascular System 715 23.7 Blood Vessel Development 716 23.7a Artery Development 716 23.7b Vein Development 717 23.7c Comparison of Fetal and Postnatal Circulation 718 MODULE 9: CARDIOVASCULAR SYSTEM mck78097_ch23_683-723.indd 683 2/14/11 4:31 PM 684 Chapter Twenty-Three Vessels and Circulation lood vessels are analogous to highways—they are an efficient larger as they merge and come closer to the heart. The site where B mode of transport for oxygen, carbon dioxide, nutrients, hor- two or more arteries (or two or more veins) converge to supply the mones, and waste products to and from body tissues. The heart is same body region is called an anastomosis (ă-nas ′tō -mō′ sis; pl., the mechanical pump that propels the blood through the vessels.
    [Show full text]
  • Cardiovascular System Summary Notes the Cardiovascular System
    Cardiovascular System Summary Notes The cardiovascular system includes: The heart, a muscular pump The blood, a fluid connective tissue The blood vessels, arteries, veins and capillaries Blood flows away from the heart in arteries, to the capillaries and back to the heart in the veins There is a decrease in blood pressure as the blood travels away from the heart Arterial branches of the aorta supply oxygenated blood to all parts of the body Deoxygenated blood leaves the organs in veins Veins unite to form the vena cava which returns the blood to the heart Pulmonary System This is the route by which blood is circulated from the heart to the lungs and back to the heart again The pulmonary system is exceptional in that the pulmonary artery carries deoxygenated blood and the pulmonary vein carries oxygenated blood Hepatic Portal Vein There is another exception in the circulatory system – the hepatic portal vein Veins normally carry blood from an organ back to the heart The hepatic portal vein carries blood from the capillary bed of the intestine to the capillary bed of the liver As a result, the liver has three blood vessels associated with it Arteries and Veins The central cavity of a blood vessel is called the lumen The lumen is lined with a thin layer of cells called the endothelium The composition of the vessel wall surrounding the endothelium is different in arteries, veins and capillaries Arteries carry blood away from the heart Arteries have a thick middle layer of smooth muscle They have an inner and outer layer of elastic fibres Elastic
    [Show full text]
  • Cat Dissection
    Cat Dissection Muscular Labs Tibialis anterior External oblique Pectroalis minor Sartorius Gastrocnemius Pectoralis major Levator scapula External oblique Trapezius Gastrocnemius Semitendinosis Trapezius Latissimus dorsi Sartorius Gluteal muscles Biceps femoris Deltoid Trapezius Deltoid Lumbodorsal fascia Sternohyoid Sternomastoid Pectoralis minor Pectoralis major Rectus abdominis Transverse abdominis External oblique External oblique (reflected) Internal oblique Lumbodorsal Deltoid fascia Latissimus dorsi Trapezius Trapezius Trapezius Deltoid Levator scapula Deltoid Trapezius Trapezius Trapezius Latissimus dorsi Flexor carpi radialis Brachioradialis Extensor carpi radialis Flexor carpi ulnaris Biceps brachii Triceps brachii Biceps brachii Flexor carpi radialis Flexor carpi ulnaris Extensor carpi ulnaris Triceps brachii Extensor carpi radialis longus Triceps brachii Deltoid Deltoid Deltoid Trapezius Sartorius Adductor longus Adductor femoris Semimembranosus Vastus Tensor fasciae latae medialis Rectus femoris Vastus lateralis Tibialis anterior Gastrocnemius Flexor digitorum longus Biceps femoris Tensor fasciae latae Semimembranosus Semitendinosus Gluteus medius Gluteus maximus Extensor digitorum longus Gastrocnemius Soleus Fibularis muscles Brachioradiallis Triceps (lateral and long heads) Brachioradialis Biceps brachii Triceps (medial head) Trapezius Deltoid Deltoid Levator scapula Trapezius Deltoid Trapezius Latissimus dorsi External oblique (right side cut and reflected) Rectus abdominis Transversus abdominis Internal oblique Pectoralis
    [Show full text]
  • Renal Tubular Acidosis in Children: State of the Art, Diagnosis and Treatment
    www.medigraphic.org.mx Bol Med Hosp Infant Mex 2013;70(3):178-193 REVIEW ARTICLE Renal tubular acidosis in children: state of the art, diagnosis and treatment Ricardo Muñoz-Arizpe,1 Laura Escobar,2 Mara Medeiros3 ABSTRACT Overdiagnosis of renal tubular acidosis (RTA) has been recently detected in Mexican children, perhaps due to diagnostic errors as well as due to a lack of knowledge regarding the pathophysiology and molecular biochemistry involved in this illness. The objective of the present study is to facilitate the knowledge and diagnosis of RTA, a clinical condition infrequently seen worldwide. RTA is an alteration of the acid-base equilibrium due to a bicarbonate wasting in the proximal renal tubules [proximal RTA, (pRTA) or type 2 RTA] or due to a distal nephron hy- drogen ion excretion defect [distal RTA (dRTA) or type 1 RTA]. Hyperkalemic, or type 4 RTA, is due to alterations in aldosterone metabolism. RTA may be primary, secondary, acquired or hereditary and frequently presents secondary to an array of systemic diseases, usually accom- panied by multiple renal tubular defects. The main defect occurs in the transmembrane transporters such as carbonic anhydrase (CA I and + - - + - II), H -ATPase, HCO3 /Cl (AE1) exchanger and Na /HCO3 (NBCe1) cotransporter. Diagnosis should include the presence of hyperchloremic metabolic acidosis with normal serum anion gap (done in an arterial or arterialized blood sample), lack of appetite, polyuria, thirst, growth failure, and rickets; nephrocalcinosis and renal stones (in dRTA); abnormal urine anion gap and abnormal urine/serum pCO2 gradient. Diagnosis of a primary systemic disease must be made in cases of secondary RTA.
    [Show full text]