Costanzo-Acid-Base Physiology
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| 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
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| 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)
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| carbonic anhydrase | catalyzes conversion of CO2 + H2O => H2CO3
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| 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
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| fixed acids from pathological states | diabetes=>beta-hydroxybutyric acid and acetic acid
strenuous exercise/hypoxic tissues=>lactic acid
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| fixed acids from ingestion | salicylic acid=>aspirin overdose
formic acid=>methanol ingestion
glycolic and oxalic acids=>ethylene glycol ingestion
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| 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
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| 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
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| 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
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| 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
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| phosphate buffer | major buffer of ECF
pK=6.8
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| plasma protein | buffers H+
can either bind H+ or Ca2+=>relationship between plasma proteins, H+, and Ca2+
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| organic phosphates | ATP, AMP, glucose-1-phosphate, 2,3-diphosphoglycerate (2,3-DPG)
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| hemoglobin | most significant intracellular buffer=>deoxyhemoglobin more effective buffer
present in high concentration inside RBCs
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| respiratory compensation | stimulated by acidemia and carotid chemoreceptors in the carotid bodies=>produces immediate hyperventilation
excess CO2 is expired
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| EFC volume expansion | inhibits isosmotic reabsorption in the proximal tubule
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| ECF volume contraction | stimulates isosmotic reabsorption in the proximal tubule
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| angiotensin II | activated by ↓ in ECF volume
stimulates Na+-H+ exchange in proximal tubule
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| 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
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| respiratory acidosis | Pco2 is ↑ => ↑ generation of H+ for secretion by Na+-H+ exchanger=> ↑ reabsorption of HCO3- => ↑ arterial pH (compensation)
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| respiratory alkalosis | Pco2 ↓ => ↓ generation of H+ for secretion by Na+-H+ exchanger =>less HCO3- reabsorbed=> ↓ arterial pH (compensation)
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| 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
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| H+-ATPase | mechanism for H+ secretion=>located in alpha-intercalated cell luminal membrane
stimulated by aldosterone
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| H+-K+ ATPase | mechanism for H+ secretion=>located in alpha-intercalated cell luminal membrane
also responsible for K+ reabsorption
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| minimum urine pH | 4.4
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| 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
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| 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
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| diffusion trapping of NH4+ | NH4+ not lipid soluble=>trapped in collecting duct lumen and excreted
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| 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+
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| chronic acidosis | adaptive ↑ in NH3 synthesis in proximal tubule
↓ in intracellular pH induces synthesis of enzymes involved in glutamine metabolism
what happens in DKA
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| hyperkalemia effect on NH3 synthesis | inhibits NH3 synthesis
reduces ability to excrete H+ as NH4+=>causes type 4 renal tubular acidosis
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| hypokalemia effect on NH3 synthesis | stimulates NH3 synthesis
↑ ability to excrete H+ as NH4+
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| diabetic ketoacidosis | cause of metabolic acidosis=> ↑ fixed acid production
induces NH4+ synthesis
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| chronic renal failure | cause of metabolic acidosis
progressive loss of nephrons=>renal mechanisms for excreting fixed acid severely impaired
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| acidemia | caused by acidosis=> ↑ in H+ concentration in blood=> ↓ in pH
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| alkalemia | caused by alkalosis=> ↓ in H+ concentration in blood=> ↑ pH
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| 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
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| metabolic alkalosis | caused by ↑ in HCO3- concentration=> ↑ in pH
caused by loss of fixed H+ from body or gain of HCO3-
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| respiratory acidosis | caused by hypoventiliation=>CO2 retention=> ↑ Pco2=> ↓ pH
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| respiratory alkalosis | caused by hyperventilation=>CO2 loss=> ↓ Pco2=> ↑ pH
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| 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
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| 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
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| 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
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| osmolar gap | normally little difference between measured and estimated plasma osmolarity
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| 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
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| 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
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| 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
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| 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-
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| 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-
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| acute respiratory acidosis | renal compensation hasn't started=>pH low
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| chronic respiratory acidosis | renal compensation started=>pH somewhat normalized from ↑ HCO3- concentration
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| 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-
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| acute respiratory alkalosis | renal compensation hasn't started=>pH high
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| chronic respiratory alkalosis | renal compensation started=>pH somewhat normalized from ↓ HCO3- concentration
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