front 1 A 65-year-old man with COPD has chronic CO2 retention. His kidneys
gradually increase H+ secretion and HCO3- reabsorption. Which
mechanism best explains this response? | back 1 D. ↑Proximal Na+-H+ countertransport |
front 2 A patient with severe diarrhea develops metabolic acidosis. Which
parameter is most likely decreased? | back 2 A. Plasma HCO3- level |
front 3 An emphysematous patient is somnolent. ABG: pH 7.28, PCO2 60, HCO3-
27. Best diagnosis? | back 3 B. Respiratory acidosis |
front 4 In metabolic acidosis, Kussmaul breathing occurs primarily
to: | back 4 D. Lower PCO2, reduce H+ |
front 5 Hyperventilation during high-altitude exposure most directly
causes: | back 5 A. Respiratory alkalosis |
front 6 A patient with Conn syndrome develops metabolic alkalosis. Which
finding supports the diagnosis? | back 6 C. ↑H+ secretion, intercalated |
front 7 In diabetic ketoacidosis, the elevated anion gap is primarily due
to: | back 7 B. Unmeasured anions, ketoacids |
front 8 Which buffering system plays the major role inside red blood
cells? | back 8 B. Hemoglobin buffer |
front 9 In chronic renal failure, metabolic acidosis develops mainly
because: | back 9 C. Nonvolatile acids accumulate |
front 10 A patient with prolonged vomiting develops hypochloremic metabolic
alkalosis. Primary mechanism? | back 10 A. Loss of gastric acid |
front 11 Which is a primary cause of respiratory acidosis? | back 11 B. CNS depression |
front 12 What is the renal response to sustained respiratory acidosis? | back 12 C. ↑Titratable acid excretion |
front 13 Which buffer system is especially important for acid excretion in the
distal nephron? | back 13 C. Phosphate buffer |
front 14 In metabolic alkalosis due to diuretic therapy, which secondary
change is expected? | back 14 D. Hypoventilation |
front 15 The phosphate buffer pK (6.8) makes it ideal for buffering: | back 15 A. Intracellular, tubular fluid |
front 16 Which renal process produces a “new” bicarbonate ion? | back 16 A. H+ binds phosphate/ammonia |
front 17 Which hormone stimulates H+ secretion in cortical collecting
ducts? | back 17 B. Aldosterone |
front 18 Chronic metabolic acidosis increases excretion of: | back 18 C. NH4+ |
front 19 Salicylate overdose presents early with respiratory alkalosis
primarily due to: | back 19 C. CNS respiratory stimulation |
front 20 Which would decrease renal H+ secretion? | back 20 C. Hyperkalemia |
front 21 A patient develops severe diarrhea. Which acid–base abnormality is
most likely? | back 21 B. Metabolic acidosis |
front 22 Which enzyme catalyzes carbonic acid formation in renal tubular
cells? | back 22 A. Carbonic anhydrase |
front 23 In metabolic acidosis, renal compensatory responses include: | back 23 A. ↑H+ secretion, new HCO3- |
front 24 ABG: pH 7.49, PCO2 50, HCO3- 36. Best diagnosis? | back 24 B. Metabolic alkalosis |
front 25 Fanconi syndrome primarily causes: | back 25 A. ↓HCO3- reabsorption |
front 26 Lactic acidosis with an anion gap of 24 suggests: | back 26 A. Unmeasured anion accumulation |
front 27 How are ammonium ions “trapped” in urine? | back 27 B. NH3 + H+ → NH4+ |
front 28 "Hyperchloremic metabolic acidosis” is best defined as: | back 28 B. Cl- rises as HCO3- falls |
front 29 Renal tubular acidosis is best described as: | back 29 C. Tubular H+ or HCO3- defect |
front 30 IV ammonium chloride is given to treat alkalosis. Physiologic
effect? | back 30 C. Liver urea cycle releases HCl |
front 31 A diabetic patient has pH 7.29, HCO3- 12, PCO2 24. Best
description? | back 31 D. Metabolic acidosis |
front 32 In metabolic acidosis, which change helps restore pH? | back 32 C. ↑Alveolar ventilation |
front 33 Vomiting of intestinal contents causes metabolic acidosis because
of: | back 33 A. Loss of intestinal bicarbonate |
front 34 Which compensatory mechanism occurs in respiratory alkalosis? | back 34 A. ↓Renal H⁺ secretion and ↓HCO₃⁻ reabsorption |
front 35 In chronic metabolic acidosis, renal ammonium excretion increases up
to: | back 35 A. 500 mEq/day |
front 36 The renal response to metabolic alkalosis is to: | back 36 C. ↓H+ secretion, excrete HCO3- |
front 37 Which abnormality is most likely with hyperaldosteronism? | back 37 B. Hypokalemic alkalosis |
front 38 In COPD-related respiratory acidosis, which values are
expected? | back 38 D. ↑PCO2, ↓pH |
front 39 Which statement best describes how kidneys respond to respiratory
acidosis? | back 39 A. ↑H+ secretion, new HCO3- |
front 40 What is the effect of carbonic anhydrase inhibition on acid–base
balance? | back 40 D. ↓HCO3- reabs, acidosis |
front 41 A patient with severe lactic acidosis would most likely show: | back 41 C. Increased anion gap |
front 42 Which condition most commonly causes normal anion gap metabolic
acidosis? | back 42 A. Diarrhea |
front 43 Which is the most powerful acid–base regulatory system? | back 43 C. Kidneys |
front 44 ABG: pH 7.55, PCO2 30, HCO3- 22. Which value is primarily driving
alkalemia? | back 44 D. Decreased PCO2 |
front 45 “New” bicarbonate is added to plasma when: | back 45 C. H+ binds phosphate/ammonia |
front 46 Which would produce respiratory acidosis? | back 46 D. Airway obstruction |
front 47 Why is the bicarbonate buffer effective despite pK 6.1? | back 47 B. CO2 and HCO3- regulated |
front 48 In metabolic acidosis, respiratory compensation begins in: | back 48 A. Minutes |
front 49 Which finding differentiates metabolic alkalosis from respiratory
alkalosis? | back 49 C. Increased plasma HCO3- |
front 50 During chronic acidosis, urinary ammonium excretion: | back 50 B. Increases dramatically |
front 51 Which of the following is a cause of metabolic alkalosis? | back 51 A. Loop diuretics |
front 52 ABG: pH 7.31, PCO2 45, HCO3- 22. Primary disturbance is: | back 52 B. Respiratory acidosis |
front 53 Which lab finding suggests compensation in respiratory
acidosis? | back 53 B. Increased plasma bicarbonate |
front 54 Major nonvolatile acids requiring renal excretion are: | back 54 B. Sulfuric and phosphoric acids |
front 55 A “mixed” acid–base disorder means: | back 55 D. Two primary disorders coexist |
front 56 In Addison disease (low aldosterone), expected acid–base
disturbance: | back 56 B. Metabolic acidosis |
front 57 After rapid ascent to high altitude, the earliest arterial change
is: | back 57 D. Decreased PCO2 |
front 58 Immediate buffer response to sudden extracellular H+
increase: | back 58 D. ↑H+ binding to buffers |
front 59 COPD patient receives high-flow O2 and retains CO2. Acid–base
change? | back 59 D. Respiratory acidosis |
front 60 Most appropriate immediate therapy for severe metabolic
acidosis: | back 60 C. IV sodium bicarbonate |
front 61 Which renal process prevents bicarbonate loss without creating “new”
bicarbonate? | back 61 A. Reabsorb filtered HCO3- |
front 62 After days of respiratory alkalosis, kidneys primarily: | back 62 D. Decrease HCO3- reabs |
front 63 The pK of the bicarbonate buffer system is: | back 63 B. 6.1 |
front 64 In hypochloremic metabolic alkalosis from vomiting, which plasma
change is expected? | back 64 A. Decreased chloride |
front 65 Hyperchloremic metabolic acidosis typically features a: | back 65 D. Normal anion gap |
front 66 Diabetic ketoacidosis classically produces: | back 66 D. High gap acidosis |
front 67 For ammonium trapping, which species diffuses most readily into
tubular lumen? | back 67 B. NH3 |
front 68 Salicylate toxicity classically presents as: | back 68 D. Metabolic acidosis + resp alkalosis |
front 69 Respiratory compensation for metabolic alkalosis tends to: | back 69 D. Increase PCO2 |
front 70 In hyperchloremic metabolic acidosis, plasma chloride is
usually: | back 70 C. Increased |