Acid-Base Balance PDF Lecture Notes

Acid-base balance Lecture Number 5.3 Status Done Type Lecture 5.3 Renal Control of Acid-Base Balance Overview The kidneys regulate acid-base balance by excreting either acidic or basic urine. This process manages the body’s extracellular pH through hydrogen io...

Acid-base balance Lecture Number 5.3 Status Done Type Lecture 5.3 Renal Control of Acid-Base Balance Overview The kidneys regulate acid-base balance by excreting either acidic or basic urine. This process manages the body’s extracellular pH through hydrogen ion secretion, bicarbonate reabsorption, and the generation of new bicarbonate. Acidic urine reduces acid in extracellular fluid, while basic urine removes base. The lecture details the mechanisms of renal secretion of hydrogen ions, reabsorption and production of bicarbonate, and buffering systems (phosphate and ammonia) that correct acidosis and alkalosis. Learning Objectives Objective 1: Describe the process of renal secretion of hydrogen ions. Objective 2: Explain renal reabsorption of filtered bicarbonate. Objective 3: Understand renal production of new bicarbonate. Objective 4: Explain phosphate and ammonia buffer systems. Objective 5: Differentiate how kidneys correct alkalosis and acidosis. Key Concepts and Definitions Acidic and Basic Urine: Kidneys excrete acidic urine to decrease extracellular acid by secreting hydrogen ions; excreting basic urine removes bicarbonate to reduce extracellular base. Hydrogen Ion Secretion : Occurs in renal tubules through counter-transport with sodium, with CO₂ and H₂O forming carbonic acid, which dissociates into H⁺ and HCO₃⁻. Bicarbonate Reabsorption : Filtered HCO₃⁻ combines with secreted H⁺ to form H₂CO₃, which dissociates into CO₂ and H₂O to allow reabsorption. Phosphate Buffer System : Buffers H⁺ through HPO₄²⁻, especially effective in tubular fluid due to its concentration. Ammonia Buffer System : Uses NH₃ and NH₄⁺ derived from glutamine to buffer H⁺, critical in acidosis. Clinical Applications Case Study Example: A patient with metabolic acidosis due to diarrhoea may exhibit low bicarbonate levels due to gastrointestinal bicarbonate loss, highlighting renal compensation by increased hydrogen excretion. Diagnostic Approach: Assess ABG values (pH, pCO₂, bicarbonate, anion gap) to differentiate between metabolic and respiratory acid-base disturbances. Treatment Options: Metabolic acidosis is managed by bicarbonate reabsorption, while respiratory acidosis involves compensatory increases in plasma bicarbonate. Complications/Management: Uncontrolled acidosis can impair cellular functions, and alkalosis can lead to hypokalaemia; managing through renal bicarbonate handling and ventilation adjustments is essential. Pathophysiology Hydrogen Secretion Mechanism : In early tubular segments (proximal tubule, thick ascending limb, early distal tubule), CO₂ diffuses into cells and forms H₂CO₃ under carbonic anhydrase influence, dissociating into H⁺ and HCO₃⁻. Diagram : Cellular mechanism illustration—CO₂ diffuses, forms H₂CO₃, dissociates, and H⁺ is secreted via Na⁺-H⁺ counter-transport.  Late Distal and Collecting Tubules: Active H⁺ secretion occurs through H⁺-ATPase and H⁺-K⁺ ATPase in intercalated cells, which allows a lower tubular pH (to 4.5). New Bicarbonate Production : Excess H⁺ combines with phosphate or ammonia buffer to generate new HCO₃⁻, especially important during acidosis. Pharmacology Diuretics: Influence acid-base balance by altering Na⁺ and K⁺ levels, indirectly affecting H⁺ secretion and bicarbonate reabsorption. ACE Inhibitors and ARBs: Lower angiotensin II, which reduces Na⁺ reabsorption and indirectly modulates H⁺ and bicarbonate handling, beneficial in acidosis or alkalosis management. Differential Diagnosis Metabolic Acidosis: High anion gap (e.g., lactic acidosis, ketoacidosis) vs. normal anion gap (e.g., GI loss of bicarbonate). Respiratory Acidosis: Caused by hypoventilation, elevated pCO₂. Metabolic Alkalosis: Primary increase in HCO₃⁻ (e.g., vomiting, diuretic use). Respiratory Alkalosis: Result of hyperventilation, decreased pCO₂. Investigations Arterial Blood Gas (ABG): Measures pH, pCO₂, HCO₃⁻, pO₂, and anion gap. Purpose: Identifies acid-base disturbances; aids in distinguishing metabolic from respiratory origin. Expected Outcome: pH changes, bicarbonate/pCO₂ ratio alterations indicate compensatory responses. Anion Gap Calculation : [Na⁺] - ([Cl⁻] + [HCO₃⁻]); normal range is 6-12, higher in lactic or ketoacidosis. Key Diagrams and Visuals Summary and Key Takeaways Takeaway 1: Kidneys maintain pH by balancing H⁺ secretion and bicarbonate reabsorption. Takeaway 2: Phosphate and ammonia buffer systems are critical for handling excess H⁺, especially in acidosis. Takeaway 3: Differentiating metabolic vs. respiratory causes of acidosis or alkalosis is essential for diagnosis and management. Further Reading/References Guyton and Hall’s Medical Physiology: Comprehensive chapter on renal physiology and acid-base balance. Clinical Acid-Base Balance: Textbook by Astrup, focused on practical ABG interpretation. Questions/Clarifications Question 1: How do ammonia and phosphate buffers compare in their effectiveness across different pH levels? Question 2: What are the implications of prolonged metabolic alkalosis on renal bicarbonate handling?