Pathology 3245B Lecture Notes - Lecture 11: Osteodystrophy, Bladder Stone, Acute Kidney Injury
Document Summary
Has -tive charges proteins (albumin is -tive too and we don"t want it leaking out, so barrier (glomerular-based membrane) repels albumin to prevent it from leaving) Endothelium first, then gbm, then podocyte slits to get out the whole filter. After getting through filter, must go into tubules. Cells in tubules leak/absorb fluid/ions/etc (requires energy) Proximal convoluted tubule has microvilli to increase surface area. Kidney failure can be chronic or acute. Pre-renal/systemic: shock, dehydration, blood loss, etc not enough blood going through kidney = renal shock. Acute: potential reversible, acute onset of symptoms. Chronic: often asymptomatic at first, slow and progressive and irreversible damage, loss of glomeruli, scarring, inflammation, etc. Consequences of kidney failure pressure goes down) Specialized kidney cells detect low 02 levels, kidney releases erythropoietin (epo stimulates. Electrolyte disturbances (heart failure due to ion imbalance, etc) Waste products accumulate (azotemia: nitrogenous waste accumulation) Anemia (hormonal function of kidney, less rbc prod)