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Odema types
- 1. IMPORTANT TYPES OFOEDEMA
- 2. EXAMPLES OF ODEMA: 1-Renal Oedema 2- Cardiac Oedema 3- Pulmonary Oedema 4- Cerebral Oedema 5- Myxoedema 6- Nutritional Oedema 7- Hepatic Oedema
- 3. RENAL OEDEMA • Generalizedoedema occurs in certain diseases of renal origin Eg: Oedema in Nephrotic Syndrome, Oedema in Nephritic Syndrome, and Oedema in Acute Tubular Injury.
- 4. 1. Oedema inNephrotic Syndrome DAMAGE TO THE RENAL GLOMERULUS (IN CHRONIC GLOMERULAR DISEASES) LEAKAGE OF PROTEINS (ALBUMINS) THROUGH GLOMERULAR BASEMENT MEMBRANE HEAVY PROTEINURIA (>1g/dl) DECREASED PLASMA PROTEINS (Hypoalbuminaemia) DECREASED PLASMA ONCOTIC PRESSURE (PRIMARY REASON FOR ODEMA) DECREASED PLASMA VOLUME ACTIVATION OF RENIN-ANGIOTENSIN- ALDOSTERONE MECHANISM SODIUM, WATER RETENSIONNEPHROTIC OEDEMA
- 5. • The nephroticoedema is classically more severe, generalized and marked and is present in the subcutaneous tissues as well as in the visceral organs.
- 6. 2. Oedema inNephritic Syndrome GLOMERULONEPHRITIS (ACUTE, RAPIDLY PROGRESSIVE) HEMATURIA (Hypovolaemia) ACTIVATION OF RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM (PRIMARY REASON FOR OEDEMA) EXCESSIVE REABSORPTION OF SODIUM AND WATER IN THE RENAL TUBULES NEPHRITIC OEDEMA
- 7. • NOTE: inNephritic syndrome the primary reason behind the oedema is due to activation of RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM. • However proteinuria (<0.5g/dl) which is moderate in nephritic syndrome leads to mild hypoproteinaemia and initiates oedema formation secondarily.
- 8. •The degree ofoedema is mild in nephritic oedema •Usually observed in the loose connective tissues of the body like face, genitalia, eyes.
- 10. 3. Oedema inAcute Tubular Injury ACUTE TUBULAR INJURY
- 11. ACUTE TUBULAR INJURY byshock or toxic chemicals DAMAGED TUBULES LOSE THEIR CAPACITY FOR SELECTIVE REABSORPTION AND CONCENTRATION OF THE GLOMERULAR FILTRATE EXCESSIVE RETENTION OF WATER AND ELECTROLYTES GENERALISED ODEMA
- 12. CARDIAC OEDEMA • Generalisedoedema develops in right-sided and congestive cardiac failure. • Pathogenesis of cardiac oedema is explained on the basis of the following mechanisms: 1- Due to Heart Failure 2- Due to Chronic hypoxia 3- Due to reduced Cardiac output.
- 13. 1- Due toHeart Failure Heart Failure Increased Central Venous Pressure Increased Capillary Hydrostatic Pressure Oedema
- 14. 2- Due toChronic hypoxia Chronic Hypoxia Injury to the Capillary endothelium Increased Capillary Permeability Oedema
- 15. 3- Due toReduced Cardiac output. Reduced Cardiac Output Hypovoleamia Activation of Intrinsic-renal and Extra-renal Hormonal Mechanisms & ADH Secretion Sodium and Water Retention Oedema
- 16. Pulmonary Oedema • Acutepulmonary oedema is the most important form of local oedema as it causes serious functional impairment. • However, it has special features and differs from oedema elsewhere in that the fluid accumulation is not only in the tissue space but also in the pulmonary alveoli.
- 17. ETIOPATHOGENESIS : • Thehydrostatic pressure in the pulmonary capillaries is much lower (average 10 mmHg). • A normal plasma oncotic pressure prevents the escape of fluid into the interstitial space and lungs are normally free of oedema. • However can Pulmonary oedema can result from either: - ELEVATION OF PULMONARY HYDROSTATIC PRESSURE OR - THE INCREASED CAPILLARY PERMEABILITY. - HIGH ATITUDES
- 18. 1. Elevation inpulmonary hydrostatic pressure (Haemodynamic oedema) INCREASED PRESSURE IN PULMONARY VEINS WHICH IS TRANSMITTED TO PULMONARY CAPILLARIES LEFT HEART FAILURE (eg: due to Mitral Stenosis) INCREASED PULMONARY CAPILLARY HYDROSTATIC PRESSURE EXCESS FLUID GETS ACCUMULATED IN THE INTERSTITIUM (INTERSTITIAL OEDEMA) i.e., IN THE LOOSE TISSUES AROUND BRONCHIOLES, ARTERIES AND IN THE LOBULAR SEPTA.
- 19. THICKENING OF THEALVEOLAR MEMBRANE (NO DISTURBANCE IN GASEOUS EXCHANGE UPTO THIS STAGE) PROLONGED ELEVATION OF HYDROSTATIC PRESSURE AND INTERSTITIAL ODEMA PRESSURE ALVEOLAR MEMBRANE CELL DAMAGE RUSH OF INTERSTITIAL FLUID INTO ALVEOLAR AIR SPACES (ALVEOLAR ODEMA) (SERIOUS DISTURBANCE TO THE LUNG FUNCTION)
- 20. INTERSTITIAL SPACE INTERSTITIAL OEDEMA ALVEOLARMEMBRANE THICKENED ALVEOLAR MEMBRANE
- 21.
- 22. PULMONARY INFECTIONS/ INHALATIONOF TOXIC SUBSTANCES/ASPIRATION/HYPERSENSITIVITY TO DRUGS ALVEOLO-CAPILLARY MEMBRANE DAMAGE INCREASED VASCULAR PERMEABILITY PLASMA PROTEINS LEAK OUT INITIALLY INTO THE INTERSTITIUM 2. Increased vascular permeability (Irritant oedema) ALVEOLAR OEDEMA INTERSTITIAL OEDEMA PLASMA PROTEINS LEAK OUT LATER INTO THE ALVEOLI
- 23. 3. Acute highaltitude oedema: CLIMBING TO HIGH ALTITUDE SUDDENLY WITHOUT HALTS > 2500 METRES HYPOXIA & SYMPATHETIC ACTIVATION DUE TO COLD AND PHYSICAL WORK CAUSES VASOCONSTRICTION VASOCONSTRICTION INCREASES PULMONARY CAPILLARY HYDROSTATIC PRESSURE PULMONARY OEDEMA