BIOL 320 1st Edition Lecture 23 Outline of Last Lecture I J Urethra II Developmental Aspects of Renal System III Body Water Content IV Fluid Compartments V Composition of Body Fluids VI Water Balance ECF Osmolality VII Regulation of Water Intake VIII Regulation of Water Output IX Disorders of Water Balance X Edema XI Electrolyte Balance Outline of Current Lecture XII Sodium Balance Regulation XIII Baroreceptors XIV Blood Pressure Homeostasis XV Other Hormones with Effects on Sodium XVI Electrolyte Balance Potassium XVII Calcium Regulation XVIII Anion Regulation XIX Acid Base Balance XX Bicarbonate Buffer System XXI Phosphate Buffer System XXII Protein Buffer System XXIII Respiratory Buffer System XXIV Renal pH Regulation XXV Diagnosis of pH Anomalies XXVI Respiratory Compensation XXVII Renal Compensation XXVIII Developmental Aspects Current Lecture Sodium Balance Regulation Aldosterone Sodium reabsorption o 65 proximal tubules o 25 loop of Henle When aldosterone is high all remaining sodium actively reabsorbed When tubule permeability is increased with ADH water follow sodium Renin angiotensin mechanism JGA sympathetic nervous system can also activate this Baroreceptors Pressure diuresis 1 Baroreceptors alert brain of increased blood pressure 2 S ANS impulses to kidneys decrease 3 Afferent arterioles dilate 4 GFR increases 5 Sodium and water output increases 6 Blood pressure decreases If blood pressure drops the opposite 1 6 Blood Pressure Homeostasis Other Hormone with Effect on Sodium Estrogen enhances NaCl reabsorb in tubules water retention functions to increase fluid edema in pregnancy Progesterone decreases sodium reabsorb functions as a diuretic water sodium loss Glucocorticoids enhance sodium reabsorb edema Electrolyte Balance Potassium Usually maintained inside cells Increases in blood can depolarize cells damage nerve and muscle function Kidney filters secretes potassium Aldosterone stimulates tubule cells to secrete potassium Hyperkalemia too much blood potassium due to renal or adrenal problems cardiac muscle CNS malfunction Hypokalemia too little blood potassium due to GI and or adrenal disorders Calcium Regulation Calcium in ECF is important for 1 Neuromuscular function 2 Blood clotting 3 Membrane permeability secretions Hypocalcemia excitable tetany Hypercalcemia muscle nerve inhibition arrhythmias Calcium balance controlled by PTH calcitonin PTH promotes increased blood calcium concentration Inhibited by hi normal blood calcium concentration Targets bones increase osteoclast activity kidney reabsorb calcium GI absorb all calcium Calcitonin in response to increase blood calcium concentration antagonistic to PTH not major player in calcium regulation Anion Regulation Major anion Chlorine Reabsorbed under normal pH 99 chlorine reabsorbed During acidosis fewer chlorine reabsorbed Acid Base Balance Blood pH limits 7 0 7 8 Outside these ranges proteins damaged cease to function Normal blood pH 7 35 7 45 Intracellular fluid 7 0 carbon dioxide Acids by product of metabolism Carbonic acid from carbon dioxide Lactic acid anaerobic metabolism Phosphoric acid protein metabolism Organic acids from carbohydrate fat metabolism Stomach acid HCl Concentration of hydrogen ions is regulated sequentially by o Chemical buffer systems rapid first line of defense o Brain stem respiratory centers within 1 3 minutes o Renal mechanisms most potent but takes time hours days to effect pH changes Acidosis pH is too low less than 7 35 Alkalosis pH is too high greater than 7 45 Respiratory acidosis due to impaired breathing Respiratory alkalosis due to hyperventilation Metabolic acidosis starvation untreated diabetic body oxidized fatty acids and amino acids for fuel Metabolic alkalosis loss of stomach acid vomiting Bicarbonate Buffer System Mix of H2CO3 carbonic acid weak acid NaHCO3 sodium bicarbonate weak base The only important buffer in both ECF plasma buffers both ICF ECF pH changes only slightly Supply almost limitless from carbon dioxide respiration Phosphate Buffer System Buffer system commonly in urine intracellular fluid Protein Buffer System Amphoteric can act as both acid base COOH NH2 Proteins plentiful inside cell also in plasma Respiratory Buffer System CO2 H20 H2CO3 H HCO3 Hypercapnia elevated carbon dioxide in blood acidotic blow off Alkalosis respiratory activity decreases shallower breathing Respiratory system impairment emphysema Renal pH Regulation Chemical buffers tie up excess acid base but cannot remove from body Elimination of carbonic acid via lungs Elimination of metabolic acids via kidneys lactic phosphoric keto uric acid Mechanisms 1 Reabsorb or generate new bicarb ion 2 Excrete bicarb ion Losing a bicarb ion gaining H Diagnosis of pH Anomalies P CO2 35 mm Hg respiratory alkalosis P CO2 45 mm Hg respiratory acidosis Metabolic any pH imbalance not caused by abnormal blood concentration of carbon dioxide checked by bicarbonate ion levels in blood Compensation respiratory system compensates for metabolic disturbances problems kidneys attempt to balance correct respiratory imbalances Respiratory Compensation For metabolic alkalosis slow shallow breathing accumulates CO2 For metabolic acidosis increase respiration lower CO2 levels Renal Compensation For respiratory alkalosis low CO2 levels high pH levels renal compensation indicated by decreased bicarb levels For respiratory acidosis renal compensation indicated by increased bicarb levels Developmental Aspects At birth water content highest In youth buffer problems are typical due to 1 Low lung volume 2 High fluid exchange rate 3 High metabolic rate 4 High insensible water loss 5 Kidneys inefficient in infants At puberty gender differences muscle vs fat differences water differences With age homeostatic mechanisms slow The elderly often unresponsive to thirst cues Most frequent victims of buffer imbalances very young old