What is the primary biochemical disturbance in metabolic acidosis?
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Details acid-base balance, biochemical disturbances, and clinical conditions causing acid-base disorders.
Mastering this deck enables clinicians and students to accurately interpret acid-base disturbances, understand their biochemical basis, and apply this knowledge to diagnose and manage related clinical conditions effectively.
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| # | Front | Back | Hint |
|---|---|---|---|
| 1 | What is the primary biochemical disturbance in metabolic acidosis? | A primary decrease in serum bicarbonate (HCO₃⁻) leading to decreased blood pH. | Think 'B' for Bicarbonate decrease. |
| 2 | Which respiratory response compensates for metabolic acidosis? | Hyperventilation, which reduces arterial CO₂ (pCO₂) to help raise blood pH toward normal. | Remember 'blow off CO₂' to compensate. |
| 3 | Name a common clinical condition that causes metabolic acidosis with an increased anion gap. | Diabetic ketoacidosis, where accumulation of keto acids increases the anion gap. | Think 'DKA' as a classic example. |
| 4 | What is the hallmark biochemical feature of metabolic alkalosis? | An increase in serum bicarbonate (HCO₃⁻), leading to elevated blood pH. | Alkali = Bicarbonate rise. |
| 5 | Which respiratory response occurs in metabolic alkalosis? | Hypoventilation to retain CO₂ and help lower blood pH. | Opposite of acidosis compensation. |
| 6 | Name a common cause of metabolic alkalosis related to gastric loss. | Vomiting, which results in loss of hydrochloric acid (HCl) from the stomach, increasing bicarbonate levels. | Think 'vomiting leads to alkalosis.' |
| 7 | What is the main difference between high anion gap and normal anion gap metabolic acidosis? | High anion gap acidosis involves accumulation of unmeasured acids (e.g., keto acids, lactic acid), whereas normal (hyperchloremic) acidosis results from bicarbonate loss with a compensatory increase in chloride. | Remember 'gap' refers to unmeasured ions. |
| 8 | Which biochemical change is characteristic of renal tubular acidosis? | Normal anion gap metabolic acidosis with impaired acid excretion by the kidneys, often showing hyperchloremia. | Think 'kidneys fail to acidify urine.' |
| 9 | How does lactic acidosis develop at the biochemical level? | Due to increased anaerobic glycolysis leading to excess lactate production, which accumulates in blood and decreases pH. | Lactate builds up when oxygen delivery or utilization is impaired. |
| 10 | What is the biochemical basis of ketoacidosis? | Increased production of keto acids (acetoacetate and beta-hydroxybutyrate) due to enhanced lipolysis and fatty acid oxidation, decreasing blood pH. | Think 'keto' as fat breakdown and acid buildup. |
| 11 | Which biochemical marker is elevated in alcoholic ketoacidosis? | Serum ketone bodies, especially beta-hydroxybutyrate. | Alcohol metabolism increases NADH, favoring ketone formation. |
| 12 | What is the biochemical cause of salicylate (aspirin) poisoning leading to mixed acid-base disorder? | Initial respiratory alkalosis caused by stimulation of the respiratory center, followed by metabolic acidosis due to accumulation of salicylate and lactic acid. | Think 'salicylate effects' on both lungs and metabolism. |
| 13 | How does hyperventilation influence blood pH in acid-base disturbances? | Hyperventilation decreases pCO₂, leading to respiratory alkalosis by reducing carbonic acid concentration. | Breathing faster 'blows off' CO₂. |
| 14 | What role does the renal system play in correcting metabolic alkalosis? | The kidneys decrease bicarbonate reabsorption and increase hydrogen ion excretion to restore acid-base balance. | Renal compensation takes hours to days. |
| 15 | Which biochemical change is typical in diarrhea-induced metabolic acidosis? | Loss of bicarbonate-rich intestinal fluids leading to decreased serum bicarbonate levels. | Think 'diarrhea causes bicarbonate loss.' |
| 16 | In what clinical scenario would you see a normal anion gap metabolic acidosis with hyperchloremia? | In cases like renal tubular acidosis or bicarbonate loss from gastrointestinal sources. | Chloride increases to maintain electroneutrality. |
| 17 | What is the biochemical mechanism behind the increase in serum anion gap in lactic acidosis? | Accumulation of lactate, an unmeasured anion, raises the anion gap. | Lactate is an unmeasured acid in blood. |
| 18 | How does correction of acid-base disturbances typically occur in clinical practice? | By addressing the underlying cause and utilizing buffering systems, respiratory compensation, and renal adjustments over time. | Treat the cause, not just the imbalance. |
| 19 | What laboratory findings would support a diagnosis of diabetic ketoacidosis? | High serum ketones, elevated anion gap metabolic acidosis, hyperglycemia, and decreased bicarbonate. | Keto + high glucose = DKA. |
| 20 | What is the biochemical consequence of ingestion of large amounts of carbonic anhydrase inhibitors like acetazolamide? | Increased renal bicarbonate excretion leading to metabolic acidosis. | Think 'carbonic anhydrase block' causes bicarbonate loss. |
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