Chapter 10: Acid-Base Physiology 299
Chapter 11 Part 1: Regulation of Acid Base Balance 325
Chapter 11 Part 2: Regulation of Acid Base Balance 325
Chapter 17: Introduction to Simple and Mixed Acid Base Disorders 535
Chapter 18 Part 1: Metabolic Alkalosis 551
Chapter 18 Part 2: Metabolic Alkalosis 551
Chapter 19 Part 1: Metabolic Acidosis 578
Chapter 19 Part 2: Metabolic Acidosis 578
Chapter 19 Part 3: Metabolic Acidosis 578
Chapter 20: Respiratory Acidosis 647
Chapter 21: Respiratory Alkalosis 673
Check your knowledge – 10 randomized questions on Acid-Base.
Complete as many times as you want to go through the question bank.
Results
A 71-year-old woman who has had nocturia for several years is admitted to the hospital secondary to increasing weakness and frequency of urination. She has been well until 2 days ago, when she felt weak and could not climb the stairs to her apartment. She has a history of duodenal ulcer many years ago that responded to intensive antacid therapy. She currently takes calcium carbonate for treatment of osteoarthritis, and she takes bicarbonate of soda for heartburn. She has a 40 pack-year history of smoking.
On physical examination, she is frail and oriented only to person. Pulse is 106/min, and BP is 110/80 supine and 90/70 mmHg sitting. The remainder of the examination is normal.
Laboratory studies reveal the following: Hematocrit 41, Na 152 mmol/L, K 3.0 mmol/L, Cl 100 mmol/L, HCO3 39 mEq/L, BUN 98 mg/dl, creatinine 7.1 mg/dl, Ca 14.4 mg/dl, phosphate 6.3 mg/dl, serum 1,25-dihydroxyvitamin D 30 pg/ml (35 to 85 pg/ml), parathyroid hormone 16 pg/ml (30 to 50 pg/ml). Urinalysis shows specific gravity of 1.007, trace protein, Na of 49 mmol/L, creatinine of 70 mg/dl, and urine osmolality of 260 mOsm/kgH2O. Renal ultrasound shows normal-sized kidneys and no hydronephrosis.
#1. The clinical and laboratory findings are MOST consistent with which ONE of the following?
The patient presents with metabolic alkalosis, acute renal failure, and hypercalcemia.
The history describes a patient who likely is taking large quantities of antacids for treatment of dyspepsia. ‘
These features strongly suggest a diagnosis of milk-alkali syndrome. The increased frequency of urination may be the result of a renal concentrating defect caused by hypercalcemia.
Vitamin D intoxication can be a cause of hypercalcemia but is excluded by the low levels of active vitamin D. A patient with chronic kidney disease as a result of hypertension would be expected to present with small kidneys. A serum calcium concentration of 14.4 would not be expected in such a patient.
Multiple myeloma is a consideration but is not the best answer given the clinical features in this case.
Anemia and a low anion gap are often present in patients with myeloma. Primary hyperparathyroidism is excluded by the suppressed parathyroid hormone levels, making hyperparathyroid incorrect.
A 59-year-old woman with history of Type 2 diabetes and epilepsy (last known seizure 2 years prior. Medical history well controlled with Metformin and levetiracetam. She was found by her spouse in the garage in ICU for management of status epilepticus. After failing treatment with propofol, the sedative regimen was changed to continuous infusion of pentobarbital.
Admission labs: (mEq/L) Na+ 142, K+ 4.3, Cl- 105, HCO3- 22, creatinine 1.4, BUN 25, glucose 100, Hematocrit 36, pH 7.35, pCO2 45, pO2 75. Serum osmolality 302mOsm/l.
After 24 hours of seizure control repeat labs show: (mEq/l) Na+ 138, K+ 4.8, Cl- 100, HCO3- 10, creatinine 1.8, BUN 28, glucose 120, Serum osmolality 330 mOsm/l
#2. Which is the most likely cause of the electrolyte disturbances in this patient?
A 68-year-old man with a history of well-controlled hypertension and benign prostatic hypertrophy presents to the emergency department (ED) with 3 days of fever, dysuria, and weakness and 1 day of rigors. His vital signs are temperature 38.6 C; blood pressure, 90/70 mm Hg; and pulse, 110/min and regular. The physical examination is notable for dry mucous membranes and lethargy. His laboratory values are [Na+], 138 mEq/L; potassium ([K+]), 3.1 mEq/L; [Cl−], 111 mEq/L; [HCO3−], 17 mEq/L; serum urea nitrogen (SUN), 26 mg/dL; creatinine, 1.1 mg/dL; glucose, 126 mg/ 100 mL; albumin, 2.0 g/dL. His arterial blood gas (ABG) values are pH 7.30; pCO2, 32mm Hg; [HCO3−], 15 mEq/L; and pO2, 72mm Hg.
#3. Which of the following acid-base abnormalities exist in this patient?
This patient has signs and symptoms of a urinary infection and probable sepsis. His ABG reveals acidemia (pH 7.30), a reduced [HCO3 −] of 15 mEq/L, and a reduced pCO2 of 32 mm Hg. The Winters equation predicts that his pCO2 should be about 31 mm Hg {(1.5 Å~ [HCO3−]) + 8} = 31. The patient’s laboratory results are therefore all consistent with appropriately compensated metabolic acidosis.
Is this acidosis a HAGMA, hyperchloremic, or a mixed disorder? The initial AG calculation is (138 – [111+17]) = 10 mEq/L and this suggests a normal AG (or hyperchloremic) metabolic acidosis. However, this calculation did not consider the patient’s marked hypoalbuminemia (2.0 g/100 mL). This degree of hypoalbuminemia will reduce the [AG] by 2.5 Å~ (4.5 − 2) = 6.2. Therefore, the [AG], after correction for hypoalbuminemia, is actually increased to about 16mEq/L. Subsequently the patient’s lactate level was reported to be 6 mEq/L. These results are all consistent with an HAGMA due to L-lactic acidosis. Therefore, the correct answer to question 1 is (a), HAGMA with appropriate respiratory compensation.
Blood pressure, 95/57 mm Hg;
serum K+, 2.9 mEq/L;
serum HCO3−, 45 mEq/L;
urine Na+, <10 mEq/L;
urine Cl−, <20 mEq/L;
urine K+, 23 mEq/L
#4. Match each diagnosis with the correct clinical and laboratory presentation:
A 9-yr-old girl complains of profound weakness, dizziness, and polyuria. She is taking no medications and has no gastrointestinal complaints. Pertinent clinical finding is BP of 90/50 mmHg with orthostatic dizziness. Laboratory data reveal the following: Na 140 mEq/L, K 2.5 mEq/L, Cl 100 mEq/L, CO2 33 mEq/L, blood urea nitrogen 25 mg/dl, and creatinine 0.7 mg/dl. A 24-h urine collection reveals the following: Sodium 90 mEq, potassium 60 mEq, Cl 110 mEq, and calcium 280 mg. Plasma renin and aldosterone are elevated.
#5. These findings are MOST suggestive of which ONE of the following?
The term Bartter syndrome denotes a group of renal diseases that share a common denominator of metabolic alkalosis and renal potassium wasting without hypertension. Bartter syndrome falls into four subgroups: (1) Antenatal Bartter syndrome (hyperprostaglandin E2 syndrome), (2) the Gitelman variety of Bartter syndrome (Gitelman syndrome), (3) classical Bartter syndrome, and (4) pseudo-Bartter syndrome. This patient is an example of classical Bartter syndrome, characterized by early childhood onset. Symptoms may include polyuria, polydipsia, vomiting, constipation, salt craving, and a tendency to volume depletion. Growth retardation follows if treatment is not initiated. Affected patients have hypokalemic metabolic alkalosis and, unlike patients with Gitelman syndrome, their urinary calcium excretion is elevated. Adrenal adenoma, licorice ingestion, and hemangiopericytoma (choices A, D, and E) all are causes of hypokalemia, but these disorders are associated with hypertension.
A 26-year-old woman with no known past medical history is referred to you for persistent hypokalemia. She denies taking any medications or herbs. Vital signs: height 160 cm, weight 48 kg, blood pressure 96/61 mm Hg, pulse 72 beats/min, respiratory rate 14 breaths/min. Patient is nonorthostatic. Physical examination is benign.
Laboratory findings:
Arterial blood gas: pH 7.43, Pco2 45 mm Hg. Both plasma renin activity (PRA) and aldosterone level are slightly elevated.
Urine electrolytes: sodium 52 mmol/L, potassium 37 mmol/L, chloride 92 mmol/L, creatinine 92 mg/dL, calcium 35 mg/dL
Urinalysis: specific gravity 1.009, pH 6.0, no protein, blood, cells, or casts.
Sodium: 134 mmol/L
Potassium: 3.1 mmol/L
Chloride: 92 mmol/L
Total CO2: 30 mmol/L
Blood urea nitrogen: 5 mmol/L
Creatinine: 0.6 mg/dL
Calcium: 9.2 mg/dL
Magnesium: 1.7 mg/dL
#6. Which one of the following is the most likely diagnosis?
The current patient has metabolic alkalosis, given the elevated total CO2 level and pH > 7.4. Any of the four choices would fit. The increased PRA and aldosterone level may be seen in volume depleted state, such as acute vomiting and Bartter and Gitelman syndromes. Choice C: In Liddle syndrome, the primary defect is increased activity of the epithelial sodium channel (ENaC) at the collecting duct. The associated increase in sodium reabsorption leads to volume expansion and hypertension. PRA and aldosterone level in Liddle syndrome are normal or reduced due to the increased sodium reabsorption. Liddle syndrome is, therefore, ruled out. Choice A: Urine electrolytes reveal high sodium and chloride. Although urine sodium may be high in acute vomiting due to the filtration of the high HCO3− load, urine chloride should accurately reflect the low-volume state and remain low (e.g., < 20 mmol/L). The high urine chloride makes acute vomiting less likely. Choices B versus D: Bartter syndrome is typically likened to the equivalent of taking loop diuretics. This is associated with hypercalciuria, hence nephrocalcinosis in this condition. In contrast, Gitelman syndrome is likened to the equivalent of taking thiazide diuretics and is associated with enhanced tubular calcium reabsorption, thus hypocalciuria. Hypomagnesemia is also characteristic of Gitelman, which may manifest as severe hypomagnesemia later in life.
A 25-year-old man with a 10-year history of type 1 diabetes mellitus becomes anorexic after developing gastroenteritis and reducing his insulin dose. He then develops nausea, vomiting, polyuria, and dyspnea and presents to the ED. The patient also has a long history of depression and is taking fluoxetine. He has orthostatic hypotension. His breath has a fruity odor. The initial laboratory studies reveal SUN, 40 mg/dL; creatinine, 1.5 mg/dL; glucose, 800 mg/100 mL; [Na+], 120 mEq/L; [Cl−], 75 mEq/L; [HCO3−], 12mEq/L; K+, 3.0 mEq/L; ([AG], 32 mEq/L); and albumin, 4.0 g/100 mL. The measured osmolality is 330 mOsm/L; serum β-hydroxybutyrate, >8 mEq/L; and urine ketones, 3+ by dipstick. Blood ethanol level is nondetectable. ABG values are pH 7.16; PO2, 90 mm Hg; pCO2, 35 mm Hg; and [HCO3−], 12 mEq/L.
#7. What is the most likely cause of this patient’s 25 mOsm/L osmolal gap?
When a HAGMA develops, the increase in acid anions is generally matched by the reduction in [HCO3−]. Therefore, multiplying the [Na+] by 2 accounts for the chloride, bicarbonate, and any additional strong acid anions. Consequently, a HAGMA should not directly generate an osmolal gap. However, the addition to the blood of alcohols, acetone, glycerol, and so on will raise the measured osmolality and create an “osmolal gap.”
This osmolal gap disappears if the alcohol/glycol/etc. is metabolized to an acid. Patients with ketoacidosis often develop an osmolal gap because of increased levels of acetone (and to a smaller extent glycerol). This phenomenon also occurs commonly in patients with alcoholic ketoacidosis, so be cautious about diagnosing a toxic alcohol or glycol poisoning in that situation on the basis of a high osmolal gap. Also, note that acetone is not an acid and does not reduce the [HCO3 −] or raise the [AG]. Thus the correct answer to question 3 is (c), this patient’s osmolal gap is most likely due to acetone.
A 38-year-old woman with a history of short-bowl surgery for complication of trauma and kidney stones. She presents with slured speech, confusion, weakness, multiple loose stools, impaired motor coordination, and irritability. She likes ice cream and developed these symptoms after eating a large container of ice cream. She is not on any medications or special diet. ABG: pH 7.27, pCO2 24 mmHg, and calculated HCO3- 16. Urine ketones are negative. Serum lactate levels are 1.5 mmol/L. Serum Cr is normal. The anion gap is 20 and osmolar gap is 10. A urinalysis with microscopy as performed with crystals shown.
#8. Which of the following is the MOST likely cause of this acid-base disturbance in this patient?
A 32-year-old woman presents to the hospital with generalized fatigue. She has no known diarrhea and denies taking any medications. Physical examination reveals a thin woman, otherwise unremarkable. Blood pressure 95/57 mm Hg, heart rate 55 beats/min, respiratory rate 12 breaths/min.
Laboratory findings:
Arterial blood gas: pH 7.49, Pco2 50 mm Hg, HCO3− 38 mmol/L
Urine sodium 12 mmol/L, chloride 16 mmol/L, potassium 37 mmol/L
Sodium 132 mmol/L
Potassium: 3.3 mmol/L
Chloride: 80 mmol/L
Total CO2: 39 mmol/L
Blood urea nitrogen: 5 mg/dL
Creatinine: 0.5 mg/dL
Calcium: 7.8 mg/dL
Magnesium: 1.6 mg/dL
Albumin: 3.8 g/dL
#9. Which one of the following is the most likely diagnosis?
A 55 year old man with chronic alcoholism presents to the ED with agitation, blurred vision, and eye pain. Blood pressure and pulse rate are normal. He is afebrile. Lab findings are as follows.
Sodium: 144 mmol/L
Potassium: 3.1 mmol/L
Chloride: 101 mmol/L
Total CO2: 12 mmol/L
Blood urea nitrogen: 9 mg/dL
Creatinine: 1.5 mg/dL
Glucose: 103 mg/100mL
Calcium: 7.8 mg/dL
Magnesium: 1.5 mg/dL
Phosphorus: 2.1 mg/dL
Lactate: 2.1 mmol/L
Osmolality: 335 mOsm/L
Arterial blood gas: pH 7.10, pCO2 28 mm Hg
#10. What enzyme does initial treat for this underlying processes competitively inhibit?
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