1 / 22

Cardinal Manifestation of Disease: EDEMA

Cardinal Manifestation of Disease: EDEMA. Dr. Meg- angela Christi Amores. Water in the body. Total body water (TBW) Compartments: Intracellular Fluid - 75% Extracellular Fluid (ECF) – 25% Plasma 25% Interstitial Fluid 75%. What is edema ?.

vera
Download Presentation

Cardinal Manifestation of Disease: EDEMA

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Cardinal Manifestation of Disease:EDEMA Dr. Meg-angela Christi Amores

  2. Water in the body • Total body water (TBW) • Compartments: • Intracellular Fluid - 75% • Extracellular Fluid (ECF) – 25% • Plasma 25% • Interstitial Fluid 75%

  3. What is edema? • clinically apparent increase in the interstitial fluid volume • weight gain of several kilograms usually precedes overt manifestations of edema

  4. Edema • Anasarca- gross, generalized edema • Ascites and hydrothorax -accumulation of excess fluid in the peritoneal and pleural cavities, respectively, and are considered to be special forms of edema

  5. Pathogenesis • Starling Forces • regulate the disposition of fluid between these two components of the extracellular compartment • hydrostatic pressure within the vascular system and the colloid oncotic pressure in the interstitial fluid – promote movement out into interstitium

  6. Starling Forces • πi – Interstitial Oncotic pressure • πc – capillary oncotic pressure • Pi – interstitial hydrostatic pressure • Pc – capillary hydrostatic pressure

  7. Starling Forces • movement of water and diffusible solutes from the vascular space at the arteriolar end of the capillaries • Fluid is returned from the interstitial space into the vascular system at the venous end and lymphatics

  8. Pathogenesis • Capillary Damage • damage to the capillary endothelium, which increases its permeability and permits the transfer of protein into the interstitial compartment • from drugs, viral or bacterial agents, and thermal or mechanical trauma • hypersensitivity reaction and is characteristic of immune injury • Usually Inflammatory edema

  9. Pathogenesis • Reduction of Effective Arterial Volume • by a reduction of cardiac output and/or systemic vascular resistance • retention of salt and, therefore, of water, ultimately leading to edema • Renal Factors and RAA System • renal retention of Na+ is central • Diminished renal blood flow = renin release • Renin = release angiotensin I = angiotensin II • Angiotensin II - enhancing salt and water reabsorption

  10. Pathogenesis • Others: • Argininine Vasopressin • Endothelin • Natriuretic peptides

  11. Clinical Causes of Edema • Obstruction of Venous Drainage of a limb • Congestive Heart Failure • Nephrotic Syndrome and Hypoalbuminemia • Cirrhosis • Drug-induced Edema • Idiopathic Edema

  12. Obstruction of Venous Return • hydrostatic pressure in the capillary bed upstream (proximal) to the obstruction increases • Alternative route may also be blocked (lymph) • there is trapping of fluid in the extremity • displacement of fluid into a limb occur at the expense of the blood volume in the remainder of the body = dec arterial blood volume - retention of NaCl and H2O

  13. Congestive Heart Failure • accumulation of blood in the venous circulation due to: • impaired systolic emptying of the ventricle(s) • impairment of ventricular relaxation • Low cardiac output leads to: • a decrease in baroreflex-mediated inhibition of the vasomotor center activates renal vasoconstrictor nerves and the RAA system, causing Na+ and H2O retention

  14. Nephrotic Syndrome • Proteinuria • Hypoalbuminemia • diminished colloid oncotic pressure due to losses of large quantities of protein into the urine • NaCl and H2O that are retained cannot be restrained within the vascular compartment • Impaired renal function contributes further to the formation of edema

  15. Nephrotic Syndrome

  16. Cirrhosis • hepatic venous outflow blockade • expands the blood volume and increases hepatic lymph formation • as a potent stimulus for renal Na+ retention • activation of the RAA system, of renal sympathetic nerves, and of other NaCl- and H2O-retaining mechanisms

  17. Drug-Induced • Nonsteroidal anti-inflammatory drugs • Antihypertensive agents •  Direct arterial/arteriolar vasodilators • Calcium channel antagonists • A -Adrenergic antagonists • Steroid hormones • Cyclosporine • Growth hormone

  18. What caused the edema? • Ascites • jaundice, and spider angiomas • collateral venous channels • = CIRRHOSIS

  19. What caused the edema? • Gallop rhythm • Dyspnea • basilar rales • Venous distention • Hepatomegaly • Cardiomegaly • = HEART FAILURE

  20. What caused the edema? • Blood in urine • Proteinuria • Hypoalbuminemia • = NEPHROTIC SYNDROME

  21. Distribution • thrombophlebitis, chronic lymphangitis, resection of regional lymph nodes, filariasis • =LOCALIZED • Heart failure, nephrotic syndrome, cirrhosis • =GENERALIZED

  22. For the next meeting, read on Stroke Syndromes • Harrison’s Principles of Internal Medicine 17th edition

More Related