Renal Physiology (GFR, Tubular Function, Acid-Base, Concentration) MCQs

Physiology · 125 free questions with answers & explanations.

1. A substance is freely filtered at the glomerulus. Its plasma concentration is 1 mg/mL, its urine concentration is 60 mg/mL, and the urine flow rate is 1 mL/min. If GFR is 120 mL/min, this substance is best characterized as:
2. A patient has arterial blood gas results showing pH 7.28, PaCO2 50 mmHg, and HCO3− 22 mEq/L. What is the primary acid-base disorder?
3. The concentration of urine to 1200 mOsm/kg in the collecting duct requires which of the following prerequisites?
4. Aldosterone acts primarily on which segment of the nephron to regulate sodium and potassium balance?
5. A 30-year-old woman presents with muscle weakness and a serum potassium of 2.8 mEq/L. Her urine K+ is 45 mEq/day (elevated). ABG shows metabolic alkalosis. Which mechanism most likely explains her hypokalemia?
6. A 45-year-old man has plasma creatinine of 2 mg/dL and urine creatinine of 160 mg/dL with a urine flow rate of 1 mL/min. His plasma urea is 60 mg/dL and urine urea is 1800 mg/dL. What is his GFR, and what does comparison with urea clearance indicate?
7. A patient's arterial blood gas shows: pH 7.30, PaCO₂ 24 mmHg, HCO₃⁻ 11 mEq/L. Serum electrolytes: Na⁺ 140, Cl⁻ 116, K⁺ 4 mEq/L. What is the anion gap and what is the most likely acid-base disorder?
8. ADH (vasopressin) acts on V2 receptors in the collecting duct. At maximum ADH secretion, the kidney can concentrate urine to 1200 mOsm/kg. This requires which prerequisite medullary condition to be intact?
9. Tubuloglomerular feedback (TGF) is a key autoregulatory mechanism. Which cell type and which ion are central to TGF, and what is the net effect when tubular flow increases?
10. Aquaporin-2 (AQP2) water channels are inserted into the apical membrane of collecting duct principal cells in response to ADH. The second messenger that drives AQP2 vesicle exocytosis is:
11. In type 1 (distal) renal tubular acidosis, the patient cannot acidify urine below pH 5.5. The fundamental defect involves failure of which membrane protein in alpha-intercalated cells of the collecting duct?
12. A patient with SIADH has serum Na⁺ of 118 mEq/L, plasma osmolality 245 mOsm/kg, and urine osmolality 620 mOsm/kg. The appropriate physiological response to hypo-osmolality — suppression of ADH and production of maximally dilute urine — is absent because:
13. The countercurrent multiplier in the loop of Henle depends on active NaCl reabsorption without water in the thick ascending limb (TAL). Which transporter on the apical membrane of TAL cells performs this function and is the target of loop diuretics?
14. In chronic metabolic alkalosis secondary to prolonged vomiting, the kidney retains HCO₃⁻ rather than excreting it. The 'contraction alkalosis' is perpetuated by which renal mechanism?
15. A patient with chronic respiratory alkalosis from prolonged mechanical hyperventilation develops a serum HCO3- of 16 mEq/L. This represents which renal compensatory mechanism at the molecular level?
16. In the thin descending limb of the loop of Henle, water is reabsorbed passively via which aquaporin isoform, and what drives this movement?
17. A patient with type 4 renal tubular acidosis (hyperkalemic, hyperchloremic metabolic acidosis) most likely has dysfunction of which transporter or hormone pathway?
18. Which protein is primarily responsible for generating the medullary urea gradient essential for maximum urinary concentration, and where is it located?
19. A patient on a thiazide diuretic develops hyponatremia. The mechanism involves impaired diluting capacity due to inhibition of which transporter in which nephron segment?
20. In the thick ascending limb (TAL) of Henle's loop, the Na-K-2Cl cotransporter (NKCC2) is electrogenic. What maintains the driving force for NKCC2 and what unique property of the TAL is explained?
21. A patient with chronic kidney disease has serum bicarbonate 14 mEq/L, pH 7.30, and pCO₂ 30 mmHg. Which buffering mechanism is most important for excreting the daily fixed acid load in CKD?
22. Tubuloglomerular feedback (TGF) is mediated by the macula densa sensing increased NaCl delivery. What is the final effector mechanism that reduces GFR?
23. In renal tubular acidosis type 4 (hyperkalemic distal RTA), the primary defect involves which mechanism?
24. Aquaporin-2 (AQP2) trafficking to the apical membrane of collecting duct principal cells is regulated by ADH. What is the intracellular signaling pathway?
25. In a patient with proximal renal tubular acidosis (type 2 RTA), the primary defect is reduced bicarbonate reabsorption in the proximal tubule. The molecular mechanism most directly responsible involves dysfunction of which transporter?
26. A patient receiving furosemide for heart failure develops hypokalemic metabolic alkalosis. The direct mechanism by which furosemide causes metabolic alkalosis is best explained by:
27. Tubuloglomerular feedback (TGF) regulates GFR through the macula densa. When NaCl delivery to the macula densa increases, adenosine released from the macula densa acts on:
28. A 30-year-old woman with polyuria and polydipsia has a serum sodium of 148 mEq/L. After water deprivation for 8 hours, urine osmolality is 200 mOsm/kg. After desmopressin administration, urine osmolality rises to 650 mOsm/kg. The diagnosis and mechanism are:
29. During hemorrhagic shock, activation of the renin-angiotensin-aldosterone system helps restore blood pressure. Angiotensin II preferentially constricts the efferent arteriole over the afferent arteriole, helping to maintain GFR. This selectivity exists because:
30. The ROMK channel (Kir1.1, encoded by KCNJ1) in the thick ascending limb and cortical collecting duct is critical for K⁺ recycling in TAL and K⁺ secretion in CCD. Genetic loss of ROMK results in which condition and what is the paradoxical electrolyte finding?
31. A patient on long-term topiramate (carbonic anhydrase inhibitor) develops a metabolic acidosis with a urine pH of 6.2 (alkaline relative to the acidemic state). What is the precise tubular defect and what type of renal tubular acidosis does this mimic?
32. The vasopressin (ADH) V2 receptor on principal cells of the collecting duct signals via Gs → adenylyl cyclase → cAMP → PKA. PKA phosphorylates AQP2 at Ser256 to promote vesicle insertion. Which additional action of phosphorylated AQP2 also reduces its degradation and contributes to sustained antidiuresis?
33. In the countercurrent multiplication system, the single effect in the thin descending limb of Henle differs from that in the thick ascending limb. Which statement correctly distinguishes their individual contributions to generating the corticomedullary osmotic gradient?
34. A patient with type 4 RTA secondary to diabetic nephropathy has a serum K⁺ of 6.1 mEq/L, serum HCO₃⁻ of 18 mEq/L, and urine pH of 5.1. The primary pathophysiological mechanism is reduced aldosterone effect leading to impaired collecting duct acidification. What is the key buffer in the urine that fails to be adequately generated in this condition?
35. The tubuloglomerular feedback (TGF) mechanism senses NaCl concentration at the macula densa and adjusts GFR. Which mediator is released by macula densa cells to constrict the afferent arteriole when NaCl delivery is high?
36. In the thick ascending limb (TAL) of the loop of Henle, the Na⁺-K⁺-2Cl⁻ (NKCC2) cotransporter is energized indirectly by the Na⁺/K⁺-ATPase. Which ion's recycling via the ROMK channel on the apical membrane is essential to maintain NKCC2 activity, and why?
37. A patient has an arterial pH 7.28, PaCO₂ 20 mmHg, HCO₃⁻ 9 mEq/L. Expected compensation is PaCO₂ = 1.5 × HCO₃⁻ + 8 (± 2), giving expected PaCO₂ ≈ 21.5 mmHg. What is the acid-base diagnosis?
38. Aquaporin-2 (AQP2) channels are inserted into the principal cell apical membrane in response to ADH. The intracellular signaling cascade involves: ADH → V2 receptor → Gs → adenylyl cyclase → cAMP → PKA → phosphorylation of AQP2 → vesicle fusion. Which specific amino acid residue on AQP2 is phosphorylated by PKA to trigger exocytosis?
39. In distal renal tubular acidosis (Type 1 RTA), the alpha-intercalated cells of the collecting duct fail to secrete H⁺. This failure is most often due to a defect in which transporter/channel?
40. In the thick ascending limb of the loop of Henle, the NKCC2 cotransporter moves ions with a fixed stoichiometry. The exact stoichiometry and the driving force for this transporter are:
41. A patient with chronic respiratory acidosis (pH 7.31, PaCO₂ 68 mmHg, HCO₃⁻ 34 mEq/L) has been stable for 3 weeks. The primary renal compensatory mechanism involves increased activity of which tubular protein?
42. Tubuloglomerular feedback (TGF) involves macula densa sensing of luminal NaCl concentration. The signaling pathway linking high luminal NaCl to afferent arteriolar vasoconstriction is:
43. Aquaporin-2 (AQP2) water channels are regulated by ADH (vasopressin) in the collecting duct. The intracellular signaling cascade linking V2 receptor activation to AQP2 membrane insertion is:
44. Type 4 renal tubular acidosis (hyperkalemic distal RTA) is caused by aldosterone deficiency or resistance. The resulting hyperkalemia itself worsens the acidosis through which additional mechanism?
45. A patient with SIADH has serum Na+ 118 mEq/L and urine osmolality 580 mOsm/kg. The mechanism by which ADH excess causes hyponatremia in SIADH despite the kidney's ability to excrete free water normally is:
46. The tubuloglomerular feedback (TGF) mechanism regulates GFR locally. When GFR increases, tubular flow rises at the macula densa; the resulting vasomotor response and mediator are:
47. In the loop of Henle, the thick ascending limb (TAL) is impermeable to water. Furosemide, a loop diuretic, blocks NKCC2 in the TAL. The consequence on the renal medullary interstitial gradient is:
48. A patient on lithium therapy develops nephrogenic diabetes insipidus. The mechanism is impaired aquaporin-2 (AQP2) insertion in collecting duct principal cells because lithium:
49. The clearance of para-aminohippuric acid (PAH) at low plasma concentrations measures effective renal plasma flow (ERPF) because:
50. Counter-current multiplication in the loop of Henle generates the medullary osmotic gradient. Which segment is impermeable to water but actively transports NaCl, making this mechanism possible?
51. A patient with syndrome of inappropriate antidiuretic hormone secretion (SIADH) has: serum Na+ 118 mEq/L, serum osmolality 245 mOsm/kg, urine osmolality 620 mOsm/kg, urine Na+ 55 mEq/L. The mechanism by which excess ADH causes hyponatremia despite relatively high urine sodium excretion is:
52. The countercurrent multiplication system in the renal medulla generates a hyperosmotic medullary interstitium. The key active transport process that powers countercurrent multiplication in the ascending thick limb of Henle's loop is:
53. Type 4 renal tubular acidosis (RTA) is most commonly caused by hypoaldosteronism. The mechanism by which aldosterone deficiency causes hyperkalemic metabolic acidosis is:
54. A patient with long-standing type 1 diabetes develops overt nephropathy with GFR 28 mL/min. Serum K+ is 5.8 mEq/L. Urine pH is 5.2. Which renal tubular defect PRIMARILY explains the hyperkalemia?
55. A patient is given furosemide. After achieving diuresis, which change in the tubular fluid reaching the macula densa ACTIVATES the tubuloglomerular feedback to reduce GFR?
56. A patient with nephrotic syndrome has a GFR of 80 mL/min, serum creatinine 1.2 mg/dL, and 24-hour urine creatinine excretion of 1200 mg in 1500 mL urine. Using the urine:plasma creatinine ratio, which segment of the nephron is responsible for the observation that creatinine clearance consistently OVERESTIMATES GFR by approximately 10–20%?
57. A 65-year-old man with CKD stage 4 (GFR 22 mL/min) develops peripheral neuropathy and recurrent nephrolithiasis. Serum oxalic acid is elevated. Which transport abnormality at the proximal tubule BEST explains primary oxaluria type 1, the inherited form that mimics this presentation?
58. The countercurrent multiplier system in the loop of Henle generates the renal medullary osmotic gradient. Which of the following mechanisms is MOST important for maintaining the papillary tip interstitial osmolality of approximately 1200 mOsm/kg?
59. A patient has urine osmolality 900 mOsm/kg, urine flow 0.5 mL/min, and plasma osmolality 290 mOsm/kg. What is the free water clearance (CH2O)?
60. In the thick ascending limb (TAL) of Henle's loop, the apical NKCC2 cotransporter reabsorbs Na⁺, K⁺, and Cl⁻ in a 1:1:2 ratio. Loop diuretics block this transporter. Beyond diuresis, why do loop diuretics also impair urinary concentrating ability?
61. A 35-year-old woman with recurrent kidney stones is found to have normal anion gap metabolic acidosis, hypokalemia, urine pH 6.2 despite systemic acidosis, and urinary Ca²⁺ >250 mg/day. Which type of renal tubular acidosis (RTA) is most consistent?
62. A patient with syndrome of inappropriate ADH secretion (SIADH) has serum Na⁺ 118 mEq/L, serum osmolality 245 mOsm/kg, urine Na⁺ 65 mEq/L, and urine osmolality 520 mOsm/kg. Which statement correctly identifies the key physiological defect?
63. Which segment of the nephron is responsible for the generation of 'free water' (electrolyte-free water) for urinary dilution, and what is the transport mechanism?
64. A patient is given inulin intravenously and reaches a steady plasma concentration of 1.5 mg/mL. Urine inulin concentration is 150 mg/mL, and urine flow rate is 1 mL/min. The calculated GFR is:
65. In the loop of Henle, the countercurrent multiplier creates a hypertonic medullary interstitium. The single effect achieved at each level of the thick ascending limb is:
66. A patient with nephrotic syndrome has reduced plasma oncotic pressure. This affects the Starling forces at the glomerulus. What is the NET effect on GFR?
67. Which renal tubular acidosis (RTA) type is characterised by inability to lower urine pH below 5.5 despite systemic acidosis, and what is the primary defect?
68. A patient with SIADH has serum Na+ of 118 mEq/L, serum osmolality 248 mOsm/kg, urine osmolality 620 mOsm/kg, urine Na+ 55 mEq/L. Which feature confirms SIADH rather than hypovolaemic hyponatraemia?
69. Tubuloglomerular feedback (TGF) is a mechanism by which increased NaCl delivery to the macula densa DECREASES GFR. The mediator released by macula densa cells that constricts the afferent arteriole is:
70. A patient with Fanconi syndrome has glycosuria at normal plasma glucose levels, phosphaturia, aminoaciduria, and RTA. The defect in Fanconi syndrome primarily involves:
71. A patient with diabetes insipidus (central) has serum osmolality of 305 mOsm/kg and urine osmolality of 80 mOsm/kg. After administration of desmopressin (DDAVP), urine osmolality rises to 650 mOsm/kg. Which conclusion is correct?
72. Fanconi syndrome is a generalized proximal tubular dysfunction. Which combination of urinary findings is pathognomonic?
73. The tubuloglomerular feedback (TGF) mechanism is mediated by the juxtaglomerular apparatus. Which sequence correctly describes TGF when NaCl delivery to the macula densa is high?
74. A 55-year-old man is found to have renal tubular acidosis (RTA). His urine pH is persistently above 5.5 despite systemic acidosis (serum pH 7.28). Urine anion gap is positive (+8 mEq/L). Which type of RTA does this represent, and where is the defect?
75. The maximum urinary concentrating ability of the human kidney is approximately 1200 mOsm/kg. This depends on the cortico-medullary osmotic gradient. Which segment of the nephron is the critical 'pump' generating this gradient?
76. Inulin clearance is the gold standard for GFR measurement. A patient has a plasma inulin concentration of 1 mg/mL and is excreting inulin in urine at 120 mg/min. What is his GFR?
77. The alveolar-arterial (A-a) gradient for O2 is useful in determining the cause of hypoxaemia. In a patient breathing room air at sea level (FiO2 0.21, PB 760 mmHg, PaCO2 40 mmHg) with PaO2 60 mmHg, calculate the A-a gradient:
78. A 60 kg man with serum Na 115 mEq/L (severe hyponatraemia from psychogenic polydipsia) requires correction. Calculating Na deficit: Target Na = 125 mEq/L. Using the Na deficit formula:
79. Fanconi syndrome involves a global proximal tubular dysfunction. Which combination of urinary losses is pathognomonic?
80. The counter-current multiplier system in the loop of Henle creates the medullary osmotic gradient. Which segment of the loop is water-permeable but NaCl-impermeable, allowing concentration of tubular fluid?
81. A 58-year-old with chronic COPD (PaCO2 = 58 mmHg, pH = 7.36, HCO3- = 33 mEq/L) is admitted. His acid-base status and compensation should be characterized as:
82. A 19-year-old mountaineer at 4500m altitude has ABG: pH 7.48, PaCO2 28 mmHg, HCO3- 20 mEq/L, PaO2 52 mmHg. Which best characterizes his acid-base state?
83. Renal tubular acidosis type I (distal RTA) is characterized by inability to lower urine pH below 5.5 despite systemic acidosis. The primary defect is in:
84. A patient with severe vomiting develops ABG: pH 7.52, HCO3- 40 mEq/L, PaCO2 48 mmHg. The expected respiratory compensation for this degree of metabolic alkalosis is:
85. A mechanically ventilated ICU patient has ABG: pH 7.52, PaCO2 28 mmHg, HCO3- 22 mEq/L. What is the primary disorder and is compensation appropriate?
86. A patient with pyloric stenosis from peptic ulcer disease presents with vomiting of 3 weeks' duration. ABG shows pH 7.55, PaCO2 50 mmHg, HCO3- 42 mEq/L. The paradoxical aciduria in this setting results from:
87. In type 4 (hyperkalaemic) renal tubular acidosis, the pathophysiology centres on:
88. A 68-year-old COPD patient has: pH 7.32, PaCO2 68 mmHg, HCO3- 34 mEq/L. Using the 'expected compensation' formula, this blood gas most likely represents:
89. In metabolic acidosis, the immediate respiratory compensation (hyperventilation) is triggered by chemoreceptors. The sequence of events in this compensatory ventilatory response is:
90. A patient has serum electrolytes: Na+ 140, Cl- 95, HCO3- 15 mEq/L, with pH 7.35 and PaCO2 28 mmHg. The anion gap is 30 mEq/L. The most likely additional disturbance superimposed on the high-anion-gap metabolic acidosis is:
91. The Henderson-Hasselbalch equation predicts that for every 1 mEq/L rise in HCO3-, the pH change in the blood is:
92. A 55-year-old patient with COPD has ABG: pH 7.34, PaCO2 58 mmHg, HCO3 30 mEq/L, Na 140, Cl 96 mEq/L. What is the CORRECT interpretation?
93. A marathon runner collapses after a race. ABG shows: pH 7.20, PaCO2 20 mmHg, HCO3 7.5 mEq/L. Serum Na 140, Cl 102 mEq/L. What is the primary disorder and is respiratory compensation adequate?
94. A patient with chronic metabolic alkalosis (from villous adenoma causing K+ and Cl- loss) shows persistent alkalemia despite volume repletion. Which renal mechanism perpetuates metabolic alkalosis in this scenario?
95. In a patient with type 4 renal tubular acidosis (hyperkalemic hyperchloremic metabolic acidosis), which specific mechanism is PRIMARILY responsible for the hyperkalemia?
96. A 22-year-old woman presents with vomiting for 3 days. ABG: pH 7.52, PaCO2 52 mmHg, HCO3⁻ 42 mEq/L. Serum electrolytes: Na⁺ 138, K⁺ 2.8, Cl⁻ 88 mEq/L. What is the acid-base disorder and is the respiratory compensation appropriate?
97. A 45-year-old man with salicylate poisoning has the following ABG: pH 7.46, PaCO2 22 mmHg, HCO3⁻ 15 mEq/L. Serum anion gap is 20 mEq/L (normal 8–12). What is the CORRECT characterization of this acid-base picture?
98. In type 4 renal tubular acidosis (RTA), what is the PRIMARY mechanism causing the hyperchloremic non-anion-gap metabolic acidosis?
99. A 60-year-old man with COPD (PaCO2 55 mmHg chronically) presents with an acute exacerbation. ABG: pH 7.28, PaCO2 78 mmHg, HCO3⁻ 35 mEq/L. Serum Na+ 140, Cl⁻ 98 mEq/L. What is the CORRECT interpretation?
100. A 22-year-old woman with Type 1 diabetes presents in DKA: pH 7.10, PaCO2 18 mmHg, HCO3⁻ 5 mEq/L, Na+ 135, Cl⁻ 100 mEq/L. What is the expected compensatory PaCO2 using Winter's formula, and does this patient have a concomitant respiratory acid-base disorder?
101. A patient with severe vomiting has pH 7.55, PaCO2 48 mmHg, HCO3⁻ 40 mEq/L, Na+ 138, K+ 2.8 mEq/L, Cl⁻ 88 mEq/L. The anion gap is ___. What acid-base diagnosis is MOST accurate?
102. Regarding renal compensation in respiratory acidosis, which tubular mechanism is MOST important for the delayed (2–5 day) rise in plasma HCO3⁻?
103. A 55-year-old woman with COPD and chronic CO2 retention has ABG: pH 7.37, PaCO2 58 mmHg, HCO3⁻ 33 mEq/L. Her serum Cl⁻ is 92 mEq/L and Na⁺ is 140 mEq/L. Which statement best characterises her acid-base status and the renal mechanism responsible?
104. A patient with prolonged nasogastric suction develops metabolic alkalosis. The urine chloride is 8 mEq/L. Which mechanism best explains why this alkalosis is chloride-responsive (saline-responsive)?
105. A patient with diabetic ketoacidosis has pH 7.15, PaCO2 18 mmHg, HCO3⁻ 6 mEq/L, Na⁺ 135 mEq/L, Cl⁻ 98 mEq/L. What is the calculated anion gap and the expected respiratory compensation (PaCO2)?
106. A patient has pH 7.30, PaCO2 28 mmHg, HCO3− 13 mEq/L, Na+ 140, Cl− 112. The calculated anion gap (AG) is: (pick calculation from options). Using a normal AG of 12, is there a concurrent metabolic alkalosis?
107. A patient with chronic COPD and stable hypercapnia has pH 7.38, PaCO2 60 mmHg, HCO3− 35 mEq/L. This is consistent with:
108. A 30-year-old woman is hyperventilating acutely due to anxiety. pH 7.52, PaCO2 24 mmHg, HCO3− 19 mEq/L. Which buffering response accounts for the fall in HCO3−?
109. A 55-year-old man with COPD and compensated chronic respiratory acidosis has: pH 7.36, PaCO2 68 mmHg, HCO3− 38 mEq/L, Na+ 140, Cl− 90. The expected renal compensation for chronic respiratory acidosis is a rise in HCO3− of approximately:
110. A patient with diabetic ketoacidosis (pH 7.18, HCO3− 8 mEq/L, PaCO2 20 mmHg, anion gap 28) is intubated and ventilated at a rate that raises PaCO2 to 40 mmHg. What will happen to the pH immediately?
111. A patient with pyloric stenosis from chronic vomiting presents with pH 7.58, HCO3− 44 mEq/L, PaCO2 50 mmHg. The expected respiratory compensation for metabolic alkalosis is:
112. The anion gap (AG) in a patient with normal albumin is calculated as Na+ − (Cl− + HCO3−). Which condition causes an elevated AG metabolic acidosis without an elevated lactate or ketones?
113. A 55-year-old diabetic patient has the following arterial blood gas: pH 7.22, PaCO2 28 mmHg, HCO3− 11 mEq/L. Na+ 138, Cl− 100, K+ 4.2. What is the anion gap, and is the respiratory compensation adequate?
114. A patient with chronic obstructive pulmonary disease on home oxygen presents with ABG: pH 7.38, PaCO2 58 mmHg, HCO3− 33 mEq/L. How should this be interpreted?
115. A patient with pyloric stenosis secondary to peptic ulcer disease has protracted vomiting. ABG shows pH 7.52, PaCO2 48 mmHg, HCO3− 38 mEq/L. Urine pH is 5.0 (paradoxical aciduria). What explains the paradoxical aciduria?
116. A mountaineer at 4500 m altitude has been acclimatized for 1 week. Which acid-base pattern best describes the steady-state acclimatization?
117. Which buffer system provides the FASTEST response to an acute acid load in the blood, and why?
118. A 65-year-old man with severe COPD has the following arterial blood gas: pH 7.34, PaCO2 68 mmHg, HCO3 35 mEq/L, Na 140, Cl 98, albumin 4 g/dL. What is the expected compensatory HCO3 for this degree of chronic respiratory acidosis, and is additional metabolic alkalosis present?
119. A patient has the following ABG: pH 7.46, PaCO2 30 mmHg, HCO3 21 mEq/L. Na 138, Cl 105. What is the primary acid-base disorder and calculated anion gap?
120. A 22-year-old woman with type 1 diabetes presents with DKA: pH 7.10, PaCO2 18 mmHg, HCO3 5 mEq/L, Na 132, Cl 94. Using Winter's formula, is the respiratory compensation appropriate?
121. In metabolic alkalosis, the renal threshold for bicarbonate reabsorption is normally exceeded. Which factor is most important in 'maintaining' metabolic alkalosis rather than allowing urinary bicarbonate excretion to correct it?
122. A 70 kg patient with COPD has ABG: pH 7.35, PaCO2 60 mmHg, HCO3 32 mEq/L. This ABG is consistent with:
123. A patient with chronic diarrhoea has: pH 7.32, PaCO2 28 mmHg, HCO3 14 mEq/L, Na 140, Cl 112, K 3.1. Calculate the anion gap and classify the acid-base disorder:
124. The renal mechanism of HCO3 reabsorption in the proximal tubule involves carbonic anhydrase. Which of the following correctly describes the process?
125. A patient on mechanical ventilation has ABG: pH 7.55, PaCO2 28 mmHg, HCO3 24 mEq/L. This is: