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24 Cards in this Set
- Front
- Back
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How does the body regulate pH?
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1. Buffering of acid-base equivalents in the body fluids-buffers combine with acids or base to prevent excessive changes in pH (immediate)
2. respiratory system-Regulates removal of volatile CO2 from the plasma (responds in minutes) 3. kidneys-Excrete either acid or alkaline urine, thereby adjusting the pH of the blood (response takes place over hours or days, but represents a more powerful regulatory system) |
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explain the carbonic acid-bicarbonate buffer system
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H2O + CO2 <--> H2CO3 (carbonic acid)-catalyzed by carbonic anhydrase <--> H + HCO3 (bicarbonate)
Carbonic acid can catalyze both the forward and reverse reaction, depending on the relative concentrations of CO2 and HCO3- |
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Explain the Henderson-Hasselbach equation
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pH=pKa + log (HCO3)/alpha PCO2
=6.1 + log (HCO3)/.03 * PCO2 normal ratio of (HCO3)/alpha PCO2=20:1; if ratio decreases, so will pH, and vice versa (increased ratio=increased pH) HCO3 is regulated by kidneys PCO2 regulated by lungs pH=kidneys/lungs |
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Explain the mass balance of acids/alkali in the body
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A. Intake (typical american diet is overall acidic)
1. acids-meat, grains, dairy (20mmol/day) 2. alkali-fruits and veggies B. Metabolic production 1. acids-CO2 (15,000mmol/day), fixed acids (40mmol/day) 2. alkali-basic amino acids, organic anions C. Excretion 1. Acids-loss of CO2 in lungs; loss of H+ in urine or vomit; use of H+ in metabolism 2. alkali-loss of HCO3 in urine or diarrhea (10mmol/day) D. Net balance: Acid/alkali intake + acid/alkali production = acid/alkali excretion |
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What is the daily acid load?
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Volatile acid: 15,000 mmol/day-oxidative metabolism of carbohydrates, fats and proteins to CO2
Fixed acid: 70 mmol/day-40 mmol/day from net metabolic non-volatile acid production; 30 mmol/day dietary acid absorption and GI alkali secretion (Alkali secreted into GI tract is equivalent to acid absorption) All of daily acid load must be excreted to maintain acid-base homeostasis |
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Explain renal acid excreation
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The kidneys:
1. Filter ~4300 mmol HCO3-/day (Must reabsorb all of that) 2. Must excrete 70 mmol H+/day (fixed acid)-30 mmol as “titratable acid”; 40 mmol as NH4+ (ammonium) Must produce and reabsorb 70 mmol “new” HCO3- to offset H+ excretion |
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Describe how the body handles non-volatle acid
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1. Immediate neutralization of the acid load as it is produced, using ECF buffers (HCO3- primary ECF buffer -->CO2 production
2. For acids buffered by HCO3, excrete the resulting CO2 in the lungs 3. Regenerate buffer in the kidneys-Create “new” HCO3- to replace that lost as CO2 |
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Explain what happens to H+ when it's secreted into the lumen of the nephron
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Immediately buffered in 3 ways:
1. HCO3- + H+ --> CO2 + H2O The majority of the H+ secreted into the lumen reacts with HCO3- 2. Titratable acid: non-bicarbonate buffers (B-) + H+ -->HB (B- includes HPO42-, creatinine-, urate) 3. NH3 + H+ --> NH4+ NH3 = ammonia; NH4+ = ammonium ion NH3 is primarily synthesized in the epithelium of the nephron and secreted into the lumen |
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Describe net (urinary) acid secretion (NAE)
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NAE=H+ secreted as titratable acid (Uta * V) + urinary ammonia nitrogen (Unh4 * V) - excretion of filtered HCO3 (Uhco3 * V)
To maintain acid-base homeostasis, NAE must equal non-volatile acid production (70mmol) TA: 30-50 mmol/day NH4+: 30-50 mmol/day HCO3-: negligible Free H+: negligible |
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explain HCO3 reabsorption by H+ secretion and "new" HCO3 production
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Filtered load of HCO3- is ~4300 mmol/day; Virtually all reabsorbed (Majority in proximal tubule)
1. Apical H+ secretion 2. H+ reacts with HCO3- via a lumenal carbonic anhydrase (CA), forming CO2 3. CO2 diffuses into cell and is rehydrated by cytoplasmic CA 4. H+ secreted, HCO3- transported across basal membrane (reabsorbed) "New" HCO3 is produced in the same manner, with diffused CO2 and CA --> HCO3, and HCO3 then transported across basal membrane (in this case produced, not reabsorbed) |
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explain pKa and buffer effectiveness
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For a given pKa, the lower the pH, the greater the proportion of protonated forms of the buffer
For a given pH, the higher the pKa, the more likely the buffer will be protonated Buffer pKa's: A. Ammonia-9.2 (95% NH4 at pH 7.4) B. Phosphate-6.8 (20% protonated at pH 7.4) C. Urate-5.8 (2.5%) D. Creatinine-5.0 (.4%) |
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Explain acid-base handling in the proximal tubule
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A. HCO3
1. reabsorbed (80%)-transported across basolateral membrane by NBCe1 (Na-HCO3 cotransporter) 2. produced (55mmol-15mmol buffered by TA; 40 by NH3) B. H+: secreted across apical membrane by NHE3 (Na/H exchanger) C. Ammonium synthesis: Glutamine transported into proximal tubule across both apical and basolateral membranes-->2 NH4-->NH3 (2)-->NH3 diffuses across apical membrane; NHE transports NH4-->becomes mostly NH4 in lumen (pKa 9.2) |
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Explain acid-base handling in the thick ascending loop of Henle (TALH)
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A. HCO3-reabsorbed (10%)
B. H+ secretion-through both apical membrane (NHE3-Na/H exchanger) and basolateral membrane (AE2-anion exchange HCO3/Cl) C. Ammonium-reabsorbed (80%); secreted into thin descending loop of henle (tDLH), medullary collecting duct (MCD) where its excreted, or systemic circulation |
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Explain acid-base handling in the distal tubule and collecting system
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A. HCO3
1. reabsorbed (10%) 2. produced (15mmol-5 in DCT, 10 in MCD) B. Ammonium-secreted into meduallary collecting duct (MCD) and then excreted (trapped in MCD lumen by the low pH) |
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What are the collecting duct HCO3 transporters?
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A. alpha intercalated cell
1. Apical-H+ATPase; H/K + ATPase (gHKA) 2. Basolateral-Cl/HCO3 exchange (AE1); Cl- channel B. Beta intercalated cell 1. Apical-Cl/HCO3 exchange (Pendrin) 2. Basolateral-H+ATPase: Cl channel |
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What's the difference b/t an -osis and an -emia
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-emia is the state of the blood pH
-osis is the process that causes the -emia |
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Explain respiratory acid-base disorders
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change in arterial pH due to a change in PCO2 is termed respiratory (change in pulmonary CO2 excretion rates)
Respiratory acidosis-increase in PCO2 (decreased ratio) Respiratory alkalosis-decrease in PCO2 (increased ratio) |
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Describe how the body compensates for respiratory acidosis
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Compensatory responses involve increasing ECF [HCO3-] by renal mechanisms:
1. Adjust amount of filtered HCO3- reabsorbed 2. Change rate of H+ secretion acute increase in PCO2-directly stimulates the proximal tubule to increase H+ secretion chronic increase in PCO2-upregulates expression of acid-base transporters (NHE3, NBCe1, Na-citrate cotransporter) |
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Describe metabolic acid-base disorders
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change in arterial pH due to a change in [HCO3-] is termed metabolic:
due to: 1. Increased acid load (ingestion, metabolic production) 2. Decreased renal production of HCO3-, decreasing renal H+ secretion 3. Direct loss of HCO3- from body (diarrhea) Metabolic acidosis-decrease in HCO3- (decreased ratio) Metabolic alkalosis-increase in HCO3- (increased ratio) |
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What is the body's compensation to metabolic acidosis?
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A. Initial compensatory response is respiratory, decreasing arterial PCO2
1. ECF H+ acid load buffered by HCO3-, increasing PCO2 2. Hyperventilation decreases PCO2, increasing HCO3-/aPCO2 ratio B. Renal response is used to increase new HCO3- production 1. HCO3- buffering of initial acid load decreases plasma [HCO3-] --> reduces filtered load 2. More H+ secretion secreted as TA/NH4+ (Chronic metabolic acidosis stimulates glutamine metabolism, so even more NH3/NH4+ is excreted) |
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What are the primary factors that regulate H+ secretion?
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A. increase secretion-decrease in renal plasma HCO3; increase in arterial PCO2
B. decrease secretion-increase in plasma HCO3; decrease in arterial PCO2 |
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Explain the interrelationship between potassium and extracellular H+
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A. Changes in ECF [H+] lead to exchanges of H+ with cellular K+
acidosis--> hyperkalemia alkalosis--> Hypokalemia B. Changes in ECF [K+] lead to exchanges of H+ with cellular K+ Hypokalemia-->induce H+ influx--> alkalosis Hyperkalemia--> induce H+ efflux--> acidosis |
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Explain the effects of acute and chronic metabolic acidosis on potasssium
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A. Acute metabolic acidosis
leads to hyperkalemia Low ECF pH stimulates influx of H+, lowering intracellular pH--> inhibits basolateral Na+/K+ ATPase; inhibits apical K+ channel Thus K+ secretion from collecting duct principal cells is inhibited, adding to the systemic hyperkalemia B. Chronic metabolic acidosis leads to eventual K secretion Initial development of hyperkalemia, as with acute metabolic acidosis-->directly stimulates aldosterone secretion from adrenal gland-->Aldosterone stimulates K+ secretion from collecting duct principal cells |
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How does a decreased circulating volume cause alkalosis?
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Decreased volume--> Stimulates the RAAS
Angiotensin II stimulates proximal tubule NHE--> H+ excretion Aldosterone stimulates H+ secretion three ways: 1. H+ secretion by alpha intercalated cells 2. Indirectly via stimulation of Na+ reabsorption (lumen negative voltage) 3. Indirectly via hypokalemia induced H+ secretion |
