Clinical acid-base regulation.txt

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yuiness
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39318
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Clinical acid-base regulation.txt
Updated:
2010-10-11 14:41:29
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renal
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Clinical acid-base regulation
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  1. • Normal extracellular pH | • Corresponding [H+]
    • 7.40 | • 40 nM
  2. [H+] is vigorously maintained over ± [#] nM
    10 nM
  3. Why is pH homeostasis critical?
    pH affects… | • Protein folding | • Ligand binding to enzymes | • Phospholipid charge
  4. Effect of decreased pH on… | • Excitation-contraction coupling | • Myocyte sensitivity to catecholamines | • Arrhythmogenesis
    • Reduced (Ca2+ displaced from troponin/tropomyosin) | • Decreased → reduction in inotropy → CO, BP | • Increased
  5. Effect of increased pH on… | • Arterioles (coronary/cerebral) | • Energy production | • Respiratory drive | • O2 delivery to tissues
    • Constriction | • Increased anaerobic glycolysis, lactate production | • Decreased | • Decreased (increased affinity of O2 for Hb)
  6. 3 most common metabolically generated acids
    • H2CO3 | • H2SO4 | • H3PO4
  7. How does the body handle H2CO3 in the immediate term (seconds)?
    Chemical buffering (titrate acid with HCO3-)
  8. How does the body handle increased H2CO3 over minutes to hours?
    Respiratory buffering (reduce PCO2 via ventilation)
  9. How is the respiratory drive modulated to accommodate changes in PCO2?
    Carotid and central chemoreceptors
  10. How are changes in [bicarb] titrated over hours to days?
    Renal reclamation or regeneration of bicarb (requires upregulation of transporters)
  11. In which nephron segment do these processes occur? | • Bicarb reclamation | • Bicarb generation
    • PCT | • Collecting duct
  12. How are changes in acid-base status buffered in the long-term?
    Bone resorption (takes days)
  13. 2 organic anions recycled by the liver back to HCO3- (which can be used to titrate acids)
    Lactate | β-OH butyrate
  14. Nephron segment that contains the Na/H exchanger
    PCT
  15. In the PCT, [amino acid] is broken down into [products] → [product] is excreted into the lumen via the Na/H exchanger while [product] is reabsorbed back into the bloodstream
    Glutamine | Ammonium + bicarb | Ammonium | Bicarb
  16. In the TALH, ammonium enters the cell via the [transporter] → ammonium is broken down into [products] → [product] titrates any residual bicarb in the lumen while [product] diffuses out the basolateral membrane (diffuses into CD lumen)
    Na/K/2Cl (on the K site) | Ammonia + H+ | H+ | Ammonia
  17. In the collecting duct, [gas] diffuses into the [cell type] and reacts to form [products] → [product] is transported out the basolateral membrane and [product] is transported out the apical membrane → form lumenal [cation]
    CO2 | α intercalated cell | H+ + HCO3- | HCO3- | H+ | NH4+
  18. Ultimately, decreased intracellular pH results in [increased or decreased] ammoniagenesis and [increased or decreased] bicarb reclamation
    increased | increased
  19. How does the α intercalated cell respond to chronic acidosis?
    Exocytosis of H+ pumps to the apical membrane
  20. Why is ammonium useful in a buffering system?
    It can bind sulfate, phosphate, chloride, etc.
  21. Acidemia = blood pH < [#]
    7.36
  22. Alkalemia = blood pH > [#]
    7.44
  23. Metabolic processes primarily change [[HCO3-] or PCO2]
    [HCO3-]
  24. Respiratory processes primarily change [[HCO3-] or PCO2]
    PCO2
  25. [Metabolic or respiratory] acidosis/alkalosis is faster to develop
    Respiratory
  26. T/F: Normal pH is an indication that there is no acidosis or alkalosis
    F – there could be a combined acidosis/alkalosis, balancing out to a normal pH
  27. Serum anion gap equation
    AG = [Na+] – ([Cl-] + [HCO3-])
  28. Normal anion gap
    10 ± 2
  29. % of anion gap attributable to albumin
    75%
  30. 25% of the anion gap is attributable to [ions]
    phosphate, sulfate
  31. Why is the anion gap useful?
    It can help you trace the origin of a metabolic acidosis
  32. Primary metabolic alkalosis will have a compensatory [respiratory or metabolic] [acidosis or alkalosis]
    respiratory acidosis
  33. Characterize the effect of the compensatory process on pH
    The pH will move back towards 7.4 but will not quite achieve 7.4 (and it will never overshoot it – if it does, there is some other primary process occurring)
  34. [HCO3-] if there is a… | • Metabolic acidosis (pH < 7.4) | • Metabolic alkalosis (pH > 7.4)
    • [HCO3-] < 24 mEq/L | • [HCO3-] > 24 mEq/L
  35. PCO2 if there is a… | • Respiratory acidosis (pH < 7.4) | •Respiratory alkalosis (pH > 7.4)
    • PCO2 > 40 mm Hg | • PCO2 < 40 mm Hg
  36. Chemical reaction that results in metabolic acidosis
    HA + HCO3- → A- + H2O + CO2 | <size .5>HA = organic acid</size>
  37. What happens if [HCO3-] moves out of the range of 20-30?
    Reduce ability to titrate acid/base changes → tiny change in [PCO2] or [bicarb] will result in large pH change
  38. Metabolic acidosis: | How does increased organic acid production affect the anion gap?
    Increases AG
  39. Causes of increased organic acid production
    • Lactic acidosis | • Ketoacidosis → β-OH butyrate | • Toxic ingestions | • Aspirin → lactate, salicylate | • Ethylene glycol → glycolate, oxylate | • Methanol → formate | • Acetaminophen → lactate
  40. Metabolic acidosis: | How does loss of bicarb from the stool/urine affect the anion gap?
    Normal AG
  41. Patients losing bicarb in the stool/urine will have elevated blood levels of which anion?
    Chloride
  42. Causes of bicarb loss in stool or urine
    • Diarrhea | • Decreased bicarb reabsorption by PCT
  43. Metabolic acidosis: | How does decreased urinary H+ secretion affect the anion gap?
    Normal AG
  44. Patients with decreased urinary H+ secretion will have elevated blood levels of which anion?
    Chloride
  45. Causes of decreased urinary H+ secretion
    • Renal failure | • Decreased bicarb generation by collecting duct | • Decreased ammoniagenesis
  46. Causes of increased serum [HCO3-] in metabolic alkalosis
    • Increased HCO3- reclamation or generation by the nephron | • Increased HCO3- secretion by the gastric parietal cell
  47. Gastric parietal cells secrete [ion] into the stomach lumen and [ion] into the bloodstream
    H+ | HCO3-
  48. How is production of bicarb by the parietal cells normally balanced out?
    In the small intestine, cells secrete bicarb into the intestinal lumen and H+ into the bloodstream
  49. “Saline (or Cl-) responsive” alkalosis: | • Is also known as… | • Initiating process | • Volume depleted?
    • Contraction alkalosis | • Loss of acid- or K+-rich fluid | • Yes
  50. “Saline unresponsive” alkalosis: | • Initiating process | • Volume depleted?
    • Primary increase in mineralcorticoids | • No
  51. Treatment of contraction alkalosis
    • Replacement of ECF volume | • Repletion of K+ (if hypokalemic)
  52. Treatment of saline unresponsive alkalosis
    • Repletion of K+ | • Minercorticoid receptor blocker | • Fluid infusion will not help!
  53. What are the ketoacids (ketone bodies)?
    • β-hydroxybutyrate | • Acetoacetate | • Acetone
  54. Ketoacids: | • Where produced? | • Where used as a preferred metabolite? | • Hormones controlling their production
    • Liver | • Muscle | • Insulin/glucagon ratio
  55. [Insulin or glucagon] favors the formation of ketone bodies (over free fatty acids)
    Glucagon
  56. 3 types of ketoacidosis
    • Diabetic (DKA) | • Starvation (SKA) | • Alcoholic (AKA)
  57. A high [?/?] ratio favors formation of β-hydroxybutyrate (alcoholics)
    NADH/NAD+
  58. Respiratory compensation for metabolic acidosis: | Equation for expected PCO2
    PCO2 = 1.5 x [HCO3-] + 8 (± 2)
  59. Specific initiating processes of metabolic alkalosis
    • Loss of stomach acid (vomiting) | • Massive antacid ingestion | • Loop diuretics | • Mineralcorticoid excess | • IV bicarb administration
  60. Maintenance processes for metabolic alkalosis
    • Volume depletion (through vomiting, diuretics)
    • Renal insufficiency
    • Mineralcorticoid excess
  61. Most common cause of metabolic alkalosis in an otherwise healthy person
    Vomiting
  62. How does volume depletion result in maintenance of metabolic alkalosis?
    Decreased ECF → activate rennin-angiotensin-aldosterone axis → increase renal bicarb absorption and generation → increase plasma threshold for bicarb → maintain metabolic alkalosis
  63. What organ is ultimately responsible for the maintenance of a metabolic alkalosis?
    Kidney
  64. How can obesity result in a respiratory acidosis?
    • Abdomen pushes on chest cavity → decreased volume for expansion
    • Sleep apnea
  65. Severe liver disease and salicylate poisoning could result in respiratory [acidosis or alkalosis]
    alkalosis
  66. Causes of combined respiratory and metabolic acidosis
    Sepsis (lactic acidosis + pulmonary edema) | Diabetic ketoacidosis/toxic ingestion + COPD
  67. Diabetic ketoacidosis with vomiting will result in which acid-base imbalance?
    Metabolic acidosis + alkalosis
  68. Sepsis and diabetic ketoacidosis result in an [increased, decreased, or normal] anion gap
    increased
  69. T/F: Diabetic ketoacidosis is often accompanied by nausea and vomiting
    T
  70. How can you tell there is a metabolic acidosis + alkalosis, if the pH is normal?
    Significant anion gap | Bicarb might be slightly increased (or it might be normal)
  71. Salicylate intoxication can result in a metabolic [?] and respiratory [?]
    acidosis | alkalosis
  72. How does salicylate intoxication result in metabolic acidosis?
    Mitochondrial uncoupling → peripheral production of lactic acid plus hepatic inability to reconvert lactic acid
  73. How does salicylate intoxication result in respiratory alkalosis?
    Mitochondrial uncoupling → histotoxic hypoxia of chemoreceptors → increased respiratory drive

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