The document discusses the anatomy, physiology, and pathology of the glomerulus. It describes the structural components of the glomerulus including the glomerular capillaries lined by fenestrated endothelium, the basement membrane, and the podocytes with slit diaphragms. It explains how glomerular filtration occurs based on starling forces and the factors that influence glomerular filtration rate. It also provides an overview of various primary and secondary glomerular diseases characterized by changes to the glomerular structures.

1. Anannya ghosh Ritasman Baisya Shinjan Patra Chirantan Mandal

2. Medical College &Hospital Bengal 88 college street, Kolkata West Bengal India Anannya ghosh Ritasman Baisya Shinjan Patra Chirantan Mandal

4. A nannya ghosh

6. glomerulus the great

29. Slit diaphragm

43. Glomerular Physiology RITASMAN BAISYA

49. Fenestration (70 to 90 nm) Slit pore 25 nm

50. Effect of Size and Electric charge on GFR

55. Effect of Net Filtration Pressure - The Starling Forces

59. P B NFP P B - NFP

62. K f can be altered by the Messengial Cells . With contraction of these cells producing decreasing K f , i.e., largely due to reduction of surface area of filtration.

64. FILTRATION FRACTION The fraction of renal plasma flow that is filtered. FF = GFR/ Renal Plasma Flow. The value of FF averages about 0.2.

65. Increase P B , decrease GFR. Precipitation of Calcium or Uric acid (stones) in urinary tract leads to increased P B .

69. Constriction of efferent arteriole. PGC increase If within normal limit. FF increase If severe. RPF decrease GFR decrease. π GC increase GFR slightly increase.

72. Angiotensin II constricts Efferent arteriole leading to increase P GC which maintains GFR. Due to Efferent arteriole constriction by Angiotensin II, renal blood flow is decreased, so flow through peritubular capillaries is decreased leading to sodium and water reabsorption. NO causes renal vasodilatation, GFR is increased. Postaglandins, Bradykinin cause increase GFR.

75. Glomerulonephritis shinjan patra

99. Chirantan Mandal

100. Focal Segmental Glomerulosclerosis

103. diffuse thickening of the glomerular capillary wall due to the accumulation of Ig deposits along the subepithelial side of the GBM thickened GBM producing “duplication”, as if formation of a new basement Membrame above the existing 1 Membranous Nephropathy

114. immune complex deposition in the glomeruli, peritubular capillary basement membranes due to antibodies Lupus Nephritis

115. Class Features Class I Normal looking glomeruli Class II Mesangial expansion Class III Focal proliferative <50% Class IV Diffuse Prolif. >50% Class V Membranous Class VI Adv. sclerosing lesions

121. 1)subepithelial humps, as in acute glomerulonephritis 2) epimembranous deposits, as in MGN 3) subendothelial deposits, as in SLE nephritis & MPGN 4) mesangial deposits, as in IgA nephropathy 5) basement membrane. EN = endothelium EP = epithelium LD = lamina densa LRE = lamina rara externa LRI = lamina rara interna MC = mesangial cell MM = mesangial matrix