<p>10-2-08 Acid-Base Physiology Buffers + -  Extracellular - Bicarbonate Buffer: H + HCO3  H2CO3  H2O + CO2 o Effectiveness – although a pKa = 6.1 (blood pH 7.4), a good buffer b/c mobile CO2 in lungs + o Acidosis – if you don’t breathe enough, CO2 buildup  creates more H  acidosis + - o Alkalosis – if you breathe too much CO2 off, H + HCO3 consumed  alkalosis</p><p> Intracellular – use hemoglobin and proteins as pH buffer Acid-Base Equations - -  Henderson-Hasselbach Equation: pH = pK + log([A ]/[HA ]) + -  Mass Action: [H ] = 24*pCO2/HCO3 pCO2 = 40, HCO3 = 24 [40] = 24* (40) / (24) Acid in Body </p><p> Acid Production – CA in lungs makes carbonic acid H2CO3, kidneys make small amount of other acids</p><p> Acid Ingestion – carbohydrates, fats, proteins  all generate CO2 in the end, thus must have been acidic PCT/DCT Acid-Base Functions -  PCT – acid-base workhorse, allows for HCO3 reabsorption  acidifies urine, alkalizes blood + + + 1) Na-H antiporter reabsorbs Na , H into lumen + - 2) H + HCO3  carbonic anhydrase: H2CO3  H2O + CO2 3) CO2 + H2O reabsorbed passively across lumen  cell + - 4) Reverse CA: CO2 + H2O  H2CO3  H + HCO3  diffuses into blood +  Collecting Duct Intercalated Cells – allows for H excretion  fine-tuning of pH in blood 1) H+ pumped out of intercalated cell into lumen via ATPase + - 2) H in lumen can combine w/ HCO3  H2CO3  CA: H2O + CO2  diffuse into cell + - + 3) Rev. CA: CO2 + H2O  H2CO3  H + HCO3  H pumped out via ATPase (step 1), CO2 wanders</p><p> Collecting Duct Principal Cells – allows for 1) Aldosterone  activates Na-K ATPase, pumps Na+ into blood, negative charge in lumen (vs. blood) 2) H+ pumps of intercalted cells now more easily pumped into negatively-charged lumen Urine Buffers </p><p> Most Acidic Urine pH  4, or 0.1mmol/L  this would require 1000L to excrete necessary 100 mmol! + +  Urine Buffers – bind H ions in order to excrete necessary 100 mmol/day of H ions</p><p> 2 Buffer Systems – include phosphates and ammonium 2- + - + o Phosphates – HPO4 binds H  H2PO4 excreted in urine (pKa ~ 7, H binds in pH = 4) o Ammonia – generated in PCT + 1) NH4 generated in PCT by glutamine breakdown + + 2) NH4 antiported against Na into lumen of PCT + + 3) NH4 again taken up in thick ascending limb, and 1% breaks down into NH3 + H + 4) NH3 back into lumen of collecting duct, binds excess H o Ammonia buffer system sensitive to pH (acidosis  more ammonium excretion), but takes time to adjust  renal compensation for acidosis/alkalosis takes a few days K+/H+ Vicious Circle 1) Vomiting  lose stomach acid, metabolic alkalosis 2) Lowered [H+]  H+ can’t fill in for intracellular K+  increased intracellular [K+], ATPase active 3) High [K+] in principal cells  much easier to secrete K+ into lumen using Na/K antiporter 4) Secreted K+ is then lost in urine  K+ depletion 5) Lowered [K+]  H+ will then fill in for intracellular K+  increased intracellular [H+], ATPase off 6) High [H+] in intercalated cells  much easier to pump H+ into lumen using H+ ATPase pump 7) Lose H+  repeat to Step 1. Process generally started by aldosterone, volume depletion In all cells</p><p>Renal</p><p>Source Undetermined</p>