#NephroticSyndrome #NephriticSyndrome #Nephrology

Nephrotic and Nephritic Syndrome | Causes Symptoms & Treatment

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▬▬▬▬▬▬▬▬▬▬ Contents of this video ▬▬▬▬▬▬▬▬▬▬
00:00:00 Glomerulopathies
00:00:56 Basic Structure Of Glomerulus
00:10:00 Grade I Injury
00:11:40 Grade Ii Injury
00:12:49 Grade Iii Injury
00:15:36 Liver Role
00:18:30 Clinical Manifestations Of Glomerular Injury
00:24:45 Anasarca
00:26:29 Why Edema Is More In Preorbital Area
00:28:00 Concept About Pitting And Non Pitting Edema
00:39:01 Activation Of Renin Angiotensin Aldosterone System
00:41:50 Adh Effect
00:42:53 Triangle Of Clinical Features
00:43:43 Hyperlipidemia
00:48:30 Nephrotic Syndrome
00:54:13 Thrombus Formation
00:56:26 More Chances Of Infections
00:58:02 Nephritic Syndrome And Mechanism
01:13:25 Recap
01:14:14 Differences In All The Glomerular Injuries
01:27:13 Chronic Renal Failure



Nephrotic & Nephritic SyndromeCauses, Symptoms & TreatmentNephrology Basic anatomy of a Glomeruli; Fenestrated Endothelial cells, Filtrations slits; Significance of these structures as size barriers, charge barriers; Albumin. Injury to Glomeruli; Albuminuria, Explanation of terms: Selective Proteinuria & Nonselective Proteinuria. Proteinuria less than 3.5gm/day; Catabolism of large number of proteins in PCT before they end up as Proteinuria; Hypoalbuminemia. Consequence of Hypoproteinemia (mainly hypoalbuminemia); Reduced Osmotic Pressure, Severe Generalized Edema [Anasarca], Periorbital edema. Pitting and Nonpitting edema; Oncotic and Osmotic Pressures; Clinical Implications; Breast Cancer; lymphatics involved or not. Heavy Proteinuria (Hypoproteinemia); Significance of decreased blood volume & resulting low renal perfusion; activation of RAAA; saltwater retention; Hyperosmolar blood, Release of ADH; causing further retention: Triangle of Heavy Proteinuria, Hypoproteinemia and Generalized Edema. Liver: Increased Lipoprotein synthesis resulting in Hyperlipidemia/Dyslipidemia; Lipidurea; Defining Nephrotic Syndrome; Nephrotic & Subnephrotic Range Proteinuria. Additional protein losses through urine: Transferrin loss in long term/chronic proteinuria; Iron Deficiency Anemia. Antithrombin3 loss; Procoagulant blood (Increased Thrombotic tendency). Complement loss in proteins; weakened immune system; increased susceptibility to pneumococcal infections. Nephritic Syndrome: Advanced injury to Glomeruli; Leakage of all types of proteins, even RBCs; Hematuria (of glomerular origin) Dysmorphic star shaped RBCs, Cylindrical RBC casts Nephritic Syndrome continued: Inflamed, clogged glomeruli; Decreased Renal Blood Flow, Reduced GFR; Oliguria. Proteinuria paradoxically decreased; clinical; need to differentiate from an improving Nephrotic Syndrome. Nephritic Syndrome continued: Urea, Creatinine levels rise; Azotemia. Powerful stimulation of RAAA axis; Hypertension. Triangle of Hematuria, Oliguria and Hypertension. Recap. Rapidly Progressive Glomerulonephritis/Crescent Glomerulonephritis: Very intense injury to Glomerular Membrane: Fibrin leaks; Macrophages arrive, Growth Factors released, proliferating epithelial cells & macrophages; Cellular Crescents. Clinical features of (Acute) Renal Failure develop; High K; Arrhythmia, Uremic pericarditis & encephalopathies.

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