Introduction The kidneys play an important role in regulating the body's acid-base status via HCO3− reabsorption this is the major extracellular buffer and is thus why it is important to conserve HCO3− ~99.9% of filtered HCO3− is reabsorbed the proximal convoluted tubule is the site where most of the filtered HCO3− is reabsorbed Na+H+ exchanger secretes H+ into the tubular lumen and combines with filtered HCO3− to form H2CO3 H2CO3 is converted into CO2 and H2O with the aid of brush border carbonic anhydrase CO2 and H2O enters the proximal tubular cell to be converted into H2CO3 via intracellular carbonic anhydrase H2CO3 becomed HCO3− and H+ H+ gets secreted by the Na+-H+ exchanger to reabsorb more HCO3− there is no net secretion of H+ since it is being recycled angiotensin II stimulates the Na+-H+ exchanger which subsequently increases HCO3− reabsorption this explains contraction alkalosis HCO3− gets transported into the blood via Na+-HCO3− cotransport Cl−-HCO3− exchanger excess of HCO3− exceeds HCO3− reabsorption capacity and results in HCO3− excretion arterial CO2 and renal compensation not completely understood respiratory acidosis increased CO2 exposed to renal cells generates more H+ to be secreted by the Na+-H+ exchanger this increases HCO3− reabsorption respiratory alkalosis decreased CO2 exposed to renal cells decrease H+ secretion by the the Na+-H+ exchanger this decreases HCO3− reabsorption H+ excretion H+ excretion is accompanied by new HCO3− synthesis and reabsorption there are two mechanisms involved excretion of titratable acid (e.g., urinary buffers such as inorganic phosphate) this is accomplished by H+ATPase (which can be stimulated by aldosterone) and H+-K+ ATPase on α-intercalated cells of the late distal convoluted tubule and collecting ducts H+ binds to HPO4-2 to form H2PO4− (the titratable acid) every titratable acid that excreted results in the synthesis of HCO3− excretion of NH4+ proximal convoluted tubule NH4+ is secreted via the Na+-H+ exchanger glutamine is metabolized into glutamate and NH4+ by the enzyme glutaminase in the proximal convoluted tubular cells NH3 is lipid soluble and diffuses from the tubular cell into the lumen because it is lipid soluble Na+-H+ exchanger secretes H+ which will bind to NH3 to form NH4+ this is diffusion trapping collecting duct H+-ATPase and H+-K+ ATPase on α-intercalated cells secrete H+ to bind with NH3 and form NH4+ this is diffusion trapping Acid-Base Disorders Acidosis results in acidemia due to an increased serum H+ (decreased pH) Alkalosis results in alkalemia due to a decreased serum H+ (increased pH) These acid base disorders may be due to primary disturbances in HCO3− (metabolic) or arterial CO2 (PCO2) (respiratory) the Hendersen-Hasselbalch equation shows that changes in HCO3− or PCO2 changes pH pH = pKa + log ([HCO3-]/(0.03 * PCO2) Metabolic acidosis due to a decrease in HCO3− either because of increased H+ or loss of HCO3− Metabolic alkalosis due to an increase in HCO3− Respiratory acidosis due to an increase in CO2 secondary to hypoventilation (which retains CO2) Respiratory alkalosis due to a decrease in CO2 secondary to hyperventilation Winter's formula determines expected respiratory compensation in response to metabolic acidosis PCO2 = 1.5 (HCO3-) + 8 +/- 2 if actual PCO2 is greater than expected PCO2 → also has a primary respiratory acidosis if actual PCO2 is less than expected PCO2 → also has a primary respiratory alkalosis Acid-Base Disorders Acid-Base Disorder pH PCO2 [HCO3-] Compensatory Response Metabolic acidosis ↓ ↓ ↓ (primary disturbance) Hyperventilation Metabolic alkalosis ↑ ↑ ↑ (primary disturbance) Hypoventilation Respiratory acidosis ↓ ↑ (primary disturbance) ↑ ↑ renal HCO3- reabsorption Respiratory alkalosis ↑ ↓ (primary disturbance) ↓ ↓ renal HCO3- reabsorption
QUESTIONS 1 of 5 1 2 3 4 5 Previous Next Sorry, this question is for PEAK Premium Subscribers only Upgrade to PEAK Sorry, this question is for PEAK Premium Subscribers only Upgrade to PEAK (M1.RL.15.11) A 52-year-old man with a history of type I diabetes mellitus presents to the emergency room with increasing fatigue. Two days ago, he ran out of insulin and has not had time to obtain a new prescription. He denies fevers or chills. His temperature is 37.2 degrees Celsius, blood pressure 84/56 mmHg, heart rate 100/min, respiratory rate 20/min, and SpO2 97% on room air. His physical exam is otherwise within normal limits. An arterial blood gas analysis shows the following:pH 7.25, PCO2 29, PO2 95, HCO3- 15.Which of the following acid-base disorders is present? QID: 104285 Type & Select Correct Answer 1 Metabolic acidosis with appropriate respiratory compensation 81% (124/154) 2 Respiratory acidosis with appropriate metabolic compensation 2% (3/154) 3 Mixed metabolic and respiratory acidosis 15% (23/154) 4 Metabolic alkalosis with appropriate respiratory compensation 0% (0/154) 5 Respiratory alkalosis with appropriate metabolic compensation 1% (2/154) M 2 Question Complexity D Question Importance Select Answer to see Preferred Response SUBMIT RESPONSE 1 Review Tested Concept Review Full Topic Sorry, this question is for PEAK Premium Subscribers only Upgrade to PEAK Sorry, this question is for PEAK Premium Subscribers only Upgrade to PEAK
All Videos (3) Login to View Community Videos Login to View Community Videos MEDCRAM Acid Base Series Gio Sabal Renal - Acid-Base Disorders D 10/11/2015 128 views 4.8 (4) Login to View Community Videos Login to View Community Videos Acid Base Physiology Determination Chris Robinson Renal - Acid-Base Disorders D 2/14/2015 84 views 5.0 (2) Login to View Community Videos Login to View Community Videos Acid Base Physiology Renal - Acid-Base Disorders D 2/14/2015 219 views 5.0 (5) Renal | Acid-Base Disorders Renal - Acid-Base Disorders Listen Now 14:4 min 10/29/2022 40 plays 0.0 (0)