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Acid-Base Physiology
Costanzo-Acid-Base Physiology
| Question | Answer |
|---|---|
| normal range of arterial pH | 7.37 to 7.42 pH<7.37 called acidemia pH>7.42 alkalemia pH range compatible with life 6.8 to 8 |
| CO2 (acid production) | volatile acid=>expired in the lungs end product of aerobic respiration with help of carbonic anhydrase reacts with water and converted into carbonic acid within RBCs (weak acid) |
| carbonic anhydrase | catalyzes conversion of CO2 + H2O => H2CO3 |
| fixed acid | produced from metabolism of proteins (sulfuric acid) and phospholipids (phosphoric acid) produced in excess in pathophysiological states may be ingested not volatile=>must be buffered in body fluid until kidney excretion causes metabolic aci |
| fixed acids from pathological states | diabetes=>beta-hydroxybutyric acid and acetic acid strenuous exercise/hypoxic tissues=>lactic acid |
| fixed acids from ingestion | salicylic acid=>aspirin overdose formic acid=>methanol ingestion glycolic and oxalic acids=>ethylene glycol ingestion |
| buffer | mixture of weak acid and its conjugate base OR weak base and its conjugate acid resists change in pH=>important 1st defense against changes in pH |
| pK | characteristic of value of buffer pair strong acids=>low pK weak acid=>high pK pH=pK=>equal concentrations of HA and A- small pH changes occur in linear portion of pK titration curves |
| bicarbonate buffer | most important extracellular buffer first line of defense when H+ gained/lost from body because 1)concentration of HCO3- high (24 mEq/L) 2)pK=6.1=>close to pH of ECF 3)CO2 is volatile and can be expired by lungs |
| acid-base map | represents Henderson-Hasselbach equation=>shows relationships between Pco2 and HCO3- isohydric lines have same pH and gives all combos of Pco2 and HCO3- that yield same value of pH *abnormal combinations can yield normal values of pH |
| phosphate buffer | major buffer of ECF pK=6.8 |
| plasma protein | buffers H+ can either bind H+ or Ca2+=>relationship between plasma proteins, H+, and Ca2+ |
| organic phosphates | ATP, AMP, glucose-1-phosphate, 2,3-diphosphoglycerate (2,3-DPG) |
| hemoglobin | most significant intracellular buffer=>deoxyhemoglobin more effective buffer present in high concentration inside RBCs |
| respiratory compensation | stimulated by acidemia and carotid chemoreceptors in the carotid bodies=>produces immediate hyperventilation excess CO2 is expired |
| EFC volume expansion | inhibits isosmotic reabsorption in the proximal tubule |
| ECF volume contraction | stimulates isosmotic reabsorption in the proximal tubule |
| angiotensin II | activated by ↓ in ECF volume stimulates Na+-H+ exchange in proximal tubule |
| contraction alkalosis | metabolic alkalosis secondary to ECF volume contraction occurs during loop diuretics/thiazide diuretics treatment can be caused by vomiting treatment: infusing isotonic NaCl |
| respiratory acidosis | Pco2 is ↑ => ↑ generation of H+ for secretion by Na+-H+ exchanger=> ↑ reabsorption of HCO3- => ↑ arterial pH (compensation) |
| respiratory alkalosis | Pco2 ↓ => ↓ generation of H+ for secretion by Na+-H+ exchanger =>less HCO3- reabsorbed=> ↓ arterial pH (compensation) |
| titratable acid | H+ excreted with urinary buffers=>phosphate buffer the most important bc high concentration in urine and ideal pK primarily excreted in alpha-intercalated cells of distal tubule and collecting ducts |
| H+-ATPase | mechanism for H+ secretion=>located in alpha-intercalated cell luminal membrane stimulated by aldosterone |
| H+-K+ ATPase | mechanism for H+ secretion=>located in alpha-intercalated cell luminal membrane also responsible for K+ reabsorption |
| minimum urine pH | 4.4 |
| nephron segments that participate in excreting H+ as NH4+ | proximal tubule=>secreted by Na+-H+ exchanger (after glutamine metabolism) thick ascending limb of Henle's loop=>exchanged for K+ in Na+-K+-2Cl- cotransporter (participates in countercurrent multiplication) alpha-intercalated cells of collecting d |
| NH3 diffusion | NH3 lipid soluble diffuses from high concentration in medullary interstitial fluid into the lumen of the collecting duct=>combines with H+ to form NH4+=>stuck in lumen bc of diffusion trapping |
| diffusion trapping of NH4+ | NH4+ not lipid soluble=>trapped in collecting duct lumen and excreted |
| effect of urinary pH on excretion of NH4+ | as urinary pH ↓ =>excretion of H+ as NH4+ ↑ underlying mechanism based on diffusion trapping of NH3/NH4+ |
| chronic acidosis | adaptive ↑ in NH3 synthesis in proximal tubule ↓ in intracellular pH induces synthesis of enzymes involved in glutamine metabolism what happens in DKA |
| hyperkalemia effect on NH3 synthesis | inhibits NH3 synthesis reduces ability to excrete H+ as NH4+=>causes type 4 renal tubular acidosis |
| hypokalemia effect on NH3 synthesis | stimulates NH3 synthesis ↑ ability to excrete H+ as NH4+ |
| diabetic ketoacidosis | cause of metabolic acidosis=> ↑ fixed acid production induces NH4+ synthesis |
| chronic renal failure | cause of metabolic acidosis progressive loss of nephrons=>renal mechanisms for excreting fixed acid severely impaired |
| acidemia | caused by acidosis=> ↑ in H+ concentration in blood=> ↓ in pH |
| alkalemia | caused by alkalosis=> ↓ in H+ concentration in blood=> ↑ pH |
| metabolic acidosis | caused by ↓ in HCO3- concentration=> ↓ pH=>respiratory compensation leads to ↓ Pco2 caused by gain of fixed H+ in the body or loss of HCO3- ex)diarrhea, type 2 renal tubular acidosis |
| metabolic alkalosis | caused by ↑ in HCO3- concentration=> ↑ in pH caused by loss of fixed H+ from body or gain of HCO3- |
| respiratory acidosis | caused by hypoventiliation=>CO2 retention=> ↑ Pco2=> ↓ pH |
| respiratory alkalosis | caused by hyperventilation=>CO2 loss=> ↓ Pco2=> ↑ pH |
| respiratory/renal compensation rule of thumb | if acid-base disturbance metabolic=>compensatory response respiratory=>adjust Pco2 if disturbance respiratory=>compensatory response renal=>adjust HCO3- concentration compensatory response always in same direction as original disturbance |
| anion gap of plasma | based on principle of electroneutrality in all body fluid compartments useful measurement in diagnosis of acid-base disorders=>primarily metabolic acidosis PAG=[Na+]-([HCO3-]+[Cl]) =>normal range 8-16 mEq/L |
| increased ion gap | often seen in several forms of metabolic acidosis=>accumulation of organic anion ex. of metabolic acidosis with ↑ anion gap: DKA, lactic acidosis, salicylate poisoning, methanol poisoning, ethylene glycol poisoning, chronic renal failure |
| osmolar gap | normally little difference between measured and estimated plasma osmolarity |
| hyperchloremic metabolic acidosis with a normal anion gap | seen in few forms of metabolic acidosis=>diarrhea, renal tubular acidosis no organic anion accumulation=> ↓ in HCO3- offset by ↑ in Cl- concentration |
| metabolic acidosis sequence of events | 1)gain of fixed H+ 2)buffering=> ↓ HCO3- concentration=> ↓ pH=>hyperkalemia can occur 3)respiratory compensation=>hyperventilation=> ↓ Pco2 4)renal correction=>excess H+ excreted and new HCO3- synthesized and reabsorbed |
| metabolic alkalosis sequence of events | 1)loss of fixed acid (ex. vomiting)=> ↑ in HCO3- concentration=> ↑ in pH 2)buffering=>hypokalemia can occur 3)respiratory compensation=>hypoventilation=> ↑ Pco2 4)renal correction=>complicated by ECF volume contraction |
| ECF volume contraction/contraction alkalosis | effects maintain metabolic alkalosis 1) ↑ HCO3-reabsorption in proximal tubule 2)stimulates RAA system=>ATII stimulates Na+-H+=>promotes reabsorption of HCO3- 3) ↑ levels of aldosterone stimulate secretion of H+ and reabsorption of HCO3- |
| respiratory acidosis sequence of events | 1) retention of CO2=> ↑ in Pco2=> ↓ pH 2)buffering=>occurs exclusively in ICF (esp. RBC) 3)no respiratory compensation 4)renal compensation=> ↑ H+ secretion and reabsorption of new HCO3- |
| acute respiratory acidosis | renal compensation hasn't started=>pH low |
| chronic respiratory acidosis | renal compensation started=>pH somewhat normalized from ↑ HCO3- concentration |
| respiratory alkalosis sequence of events | 1)loss of CO2=> ↓ in Pco2=> ↑ in pH 2)buffering=>exclusively in ICF (esp. RBCs) 3)no respiratory compensation 4)renal compensation=> ↓ H+ excretion with ↓ synthesis and reabsorption of new HCO3- |
| acute respiratory alkalosis | renal compensation hasn't started=>pH high |
| chronic respiratory alkalosis | renal compensation started=>pH somewhat normalized from ↓ HCO3- concentration |
Created by:
kphom001
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