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Mizzou MPP 3202 - Study guide for acid-base

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Acid-Base BalanceLect 1. Introduction, buffers1. Physiological significance of pH regulation2. Definition of acids/bases, pH scale and relation to [H+]3. Sources of H+4. Defense of pH--three arms of the regulatory system: instantaneous chemical buffering, rapid but incomplete disposal via lungs, slow, but complete restoration by kidneys5. Buffer systems6. Henderson-Hasselbalch equation7. Extracellular & intracellular buffer systems8. Bicarbonate buffer system9. Importance of [HCO3-]/PCO2What does pH represent? What is the normal range for physiological pH in ECF? With respect to that normal level, what do measurements of elevated or depressed pH mean in terms of [H+]?What are the major endogenous sources of H+?What is the body’s overall strategy for homeostasis of pH?What is the difference between a strong acid and a weak acid? What is a buffer? Why does a weak acid make for a good buffer, whereas a strong acid doesn’t?What are the major ECF buffer systems? What about ICF buffers?What is the most important ECF buffer system? Why is it the most important, and what is the major limiting factor that must be defended for this system to work?Why is the Henderson-Hasselbalch equation useful in assessing pH? What portion of theequation is the key to this?Lect 2. Integrated regulation of acid-base balance1. Review of major variables2. Respiratory response—rapid, but limited based on availability of HCO3-3. Renal response—slower, but capable of maintaining supply of HCO3-, as well as achieving net excretion of H+4. Mechanisms for renal filtration & reabsorption of HCO3-5. Mechanisms for net excretion of H+ in proximal & distal nephron6. Role of urinary buffers—phosphate (titratable acidity) and ammonia7. How urine is acidified8. Bicarbonate buffer system links respiratory & renal resplonses9. Dysfunction: respiratory/metabolic acidosis/alkalosisWhat occurs with respect to the direction of the bicarbonate buffer equilibrium during conditions of respiratory distress? What factor could become limiting in such a situation?What is the relationship between the direction of mass action in the bicarbonate buffer system equation and the respiratory response to high levels of H+?How are conditions of acidosis sensed, what happens to respiratory function as a result, and what is the mechanism for the respiratory response?What is the general basic mechanism for renal reabsorption of HCO3-? In what part of the nephron does most of this take place? Can this mechanism achieve net excretion of acid?In the nephron, can HCO3- be reabsorbed directly? If not, why not, and how is this problem solved?In order to reabsorb HCO3-, it must first be combined with H+. The HCO3- comes into the nephron via glomerular filtration. Where does the H+ come from? What enzyme is critical for HCO3- reabsorption? Where is it located?During metabolic alkalosis, the amounts of filtered HCO3- exceed the available H+ so what happens to the excess HCO3-?How does the kidney get rid of net acid? What are the two major urinary buffers, and where does each come from? Which one of them is increased in production in response to acid in the tubular lumen?In the proximal nephron, filtered HCO3- is reabsorbed. Why does this not represent anet gain of HCO3- ? Is there a way to achieve this, and if so, where and how does this occur?What is the nature of the initial defect in metabolic acidosis? What is the main regulatory response? Consider the same question for respiratory acidosis, and for respiratory/metabolic alkalosis.What acid-base defect would you expect to see in cases of severe vomiting? How ‘bout severe diarrhea?


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