Lytesr

Front 1

A 45-year-old male has asthma, which is well controlled with inhaled steroids. He comes to you for a regular follow-up and on examination he has a BP of 153/92 mm Hg. After confirming the rise in blood pressure on consequent visits, you start the patient on a salt restricted diet and a thiazide diuretic. However, he is admitted in the ER after 4 months for multiple complaints. His laboratory panel was sent to you for evaluation:

Blood pH: 7.50
PaO2: 100 mmHg
PaCO2: 50 mm Hg
HCO3-: 32 meq/L
BUN: 19 mg/dl
S. Creatinine: 1.3 mg/dl

Which of the following is the most likely cause of acid base disorder in this patient?


A. Diabetic nephropathy
B. Hypertensive nephropathy
C. Thiazide induced
D. Steroid toxicity
E. Exacerbation of asthma

Back 1

This patient is having an alkaline pH with increase bicarbonate concentration suggestive of metabolic alkalosis. Diuretic use is one of the most common causes of metabolic alkalosis. Diuretic induced metabolic alkalosis is due to following reasons:

1.The persistent high distal tubular delivery of sodium and chloride in kidney due to natriuretic and chloruretic action of diuretics.
2.The ECF contraction and activation of aldosterone secretion.

The treatment of the alkalosis is achieved by providing isotonic saline to correct the ECF volume deficit.

Choice A: Diabetic nephropathy can cause RTA or renal failure and result into acidosis and not alkalosis.

Choice B: Hypertensive nephropathy would lead to acidosis and not alkalosis.

Choice D: Steroid toxicity can lead to alkalosis; however, this patient is taking inhalation steroids, which usually do not cause systemic toxicity.

Choice E: Exacerbation of asthma would cause a respiratory acid base disorder and not a metabolic one.

Educational Objective:
Diuretic use is one of the most common causes of metabolic alkalosis.

Front 2

A 32-year-old pregnant female comes to the clinic at 32 weeks of gestation, for her regular follow-up. Her physical examination and ultrasonogram (USG) are normal for the gestational age. Her lab profile shows:

Blood pH: 7.44
PaO2 : 100 mmHg
PaCO2: 30 mm Hg
HCO3- : 20 meq/L
WBC count: 9,000/cmm
Hb: 11 mg/dl.

Na+ : 134 meq/L
K+ : 3.6 meq/l
Cl- : 98 meq/L
BUN : 5 mg/dl
Creatinine: 0.6 mg/dl

Which of the following best explain her acid base status?


A. Anemia
B. Deep vein thrombosis (DVT)
C. Perfectly normal acid base status
D. Normal phenomenon of pregnancy
E. Hyperemesis gravidarum

Back 2

This patient has a pH of 7.44, with a decrease in PaCO2, suggestive of respiratory alkalosis. (Choice C is thus incorrect)

There are a number of physiological conditions, which lead to some imbalances in the acid base state of the body. Pregnancy is one of these. There is a high concentration of progesterone in pregnancy, which has a direct stimulatory effect on the respiratory center leading to tachypnea and thus chronic respiratory alkalosis. Progesterone concentration increases with the increasing gestational age and thus chronic respiratory alkalosis with metabolic compensation, as in this patient, is very common in later pregnancy.

The patient does not have anemia, as blood Hb of 11 is normal for pregnancy considering the dilutional state of pregnancy. (Choice A)

A complication of DVT is pulmonary embolism, which leads to tachypnea and respiratory alkalosis, but this patient has a normal physical examination and normal PaO2. Therefore, a DVT with PE is highly unlikely. (Choice B)

Hyperemesis gravidarum (Choice E) is a complication of early pregnancy and not late pregnancy and its consequence is metabolic alkalosis.

Educational Objective:
Pregnancy leads to a physiological chronic respiratory alkalosis.

Front 3

A 48-year-old diabetic male is admitted to the hospital for severe gastroenteritis. He was diagnosed with proteinuria 4 years ago and was started on enalapril. His lab profile shows pH of 7.31, HCO3- of 18 meq/L, and PaCO2 of 37 mmHg. Anionic gap is calculated and it is found to be 10. Which of the following information would best explain the acid base profile of this patient?

A. Calculation of bicarbonate gap.
B. Calculation of osmolar gap.
C. Calculation of urine anion gap.
D. Renal biopsy.
E. Urine pH.

Back 3

The patient has a low pH with a low bicarbonate and an AG of 10 suggestive of normal anion gap metabolic acidosis. The cause of this normal anionic gap metabolic acidosis could be either the gastrointestinal loss of bicarbonate secondary to diarrhea or defective renal NH4+ synthesis secondary to diabetic nephropathy. The next step in diagnosing the underlying cause is to calculate the urine anionic gap (Choice C).

Urine anionic gap is the measure of urinary unmeasured cations. These are mainly represented by NH4+. It is calculated as:

[Urinary (Na + K) – Urinary Cl]

Normal UAG is 0 to –50 because ammonium’s accompanying ion is Cl. A positive UAG is suggestive of a defective urinary acidification (relatively lower urinary Cl- and thus lower ammonium excretion due to a renal tubular defect) like in type 1 (distal) renal tubular acidosis (RTA), or hypoaldosteronism (type 4 RTA). A negative UAG is suggestive of relatively higher urinary Cl- and thus adequate NH4+ production suggestive of gastrointestinal causes of metabolic acidosis.

Calculation of bicarbonate gap (Choice A) is useful to find out if there is a mixed acid base disorder.

Calculation of osmolar gap (Choice B) is useful in case of increased anionic gap metabolic acidosis.

Renal biopsy (Choice D) would not be a proper step until there is indication of some renal dysfunction.

Urine pH (Choice E) can help to differentiate various types of RTA, but it would not be the initial best step, as a renal cause of acidosis is not yet defined in this patient.

Educational Objective:
Know how to approach the diagnosis of a non-anion gap metabolic acidosis in a diabetic patient with gastroenteritis.

Front 4

A 28-year-old primigravida is admitted to the hospital at 10 weeks of gestation for hyperemesis gravidarum. Her vitals are, Temperature: 36.7C(98.2F); RR: 10/min; PR: 96/min. She is confused and her ABG shows pH of 7.49, PaCO2 of 60 mm Hg, HCO3- of 44 meq/L. Which of the following is the most likely cause of her hypercapnia?

A. Normal phenomenon of pregnancy.
B. Respiratory compensation of metabolic acidosis.
C. Hypoxia.
D. Aspiration pneumonitis.
E. Compensatory phenomenon for her metabolic alkalosis.

Back 4

This patient is having a high pH with high bicarbonate, which is suggestive of metabolic alkalosis. Metabolic alkalosis in this patient is secondary to vomiting, due to hyperemesis gravidarum, which lead to loss of gastric HCL.

Increase in body bicarbonate, secondary to metabolic alkalosis, would lead to a decrease in CO2 concentration in the cerebral circulation, depressing the respiratory center in an effort to compensate for metabolic alkalosis thereby leading to hypercapnia (Choice E).

Respiratory compensation for metabolic acidosis would lead to hypocapnia and not hypercapnia (Choice B).

Hypoxia (Choice C) can coexist with hyper or hypocapnia but there is nothing to suggest hypoxia in this patient.

Hypocapnia due to the effect of progesterone on respiratory center is a normal phenomenon of late pregnancy (Choice A).

Aspiration pneumonia (Choice D) would lead to hypocapnia secondary to tachypnea.

Educational Objective:
Hypercapnia in a patient with hyperemesis gravidarum is to due to compensatory respiratory compensation for the primary metabolic alkalosis.

Front 5

4-year-old Trey was left with a babysitter when he managed to grab his mother's aspirin and ingested an unknown number of tablets. He was brought to the ER in unconscious state about 12 hours after the accident. Which of the following is the most likely acid base status in this patient?

A. Primary metabolic alkalosis
B. Primary metabolic acidosis
C. Primary metabolic acidosis with compensatory respiratory alkalosis.
D. Primary metabolic acidosis with primary respiratory alkalosis
E. Normal acid base status.

Back 5

Aspirin toxicity can cause myriad of changes in acid base status. In adults, it causes respiratory alkalosis in acute stages and mixed metabolic acidosis and respiratory alkalosis in late stages.

However, in young children who have salicylate toxicity more frequently present with metabolic acidosis and a low pH because they are less likely to develop respiratory alkalosis. In such patents, there may be some decrease in PaCO2, which is suggestive of a compensatory respiratory alkalosis and not primary respiratory alkalosis.

A patient who has consumed substantial amounts of aspirin will never have a normal acid base status. (Choice E)

Adults, and not children with salicylate toxicity, will have both primary metabolic acidosis and primary respiratory alkalosis. (Choice D)

Primary uncompensated metabolic acidosis (Choice B) can be rarely seen in very early stages of salicylate toxicity but in this patient sufficient time passed for the respiratory compensation to occur. The onset of respiratory compensation mechanisms is very quick as opposed to the onset of renal compensation mechanisms.

Primary metabolic alkalosis (Choice A) does not occur with salicylate toxicity.

Educational Objective:
Children who have acute salicylate toxicity present with primary metabolic acidosis alone.

Front 6

A 5-year-old boy is brought to you with the history of severe vomiting for the last 3 days. On examination his skin is dry. His vitals are as follows: BP: 100/80 mmHg, PR: 88/min, supine and BP: 80/60 mmHg, PR: 102/min, on standing. His mother also complains of his decreased urine volume. Which of the following would best describe the expected acid base status of this patient?

pH, PaCO2(mmHg), HCO3-(meq/L)

A. 7.10, 80, 24
B. 7.40, 40, 24
C. 7.55, 50, 42
D. 7.62, 21, 21
E. 7.62, 30, 30

Back 6

Fluid-loss due to severe vomiting has caused hypovolemia in this patient as suggested by orthostatic hypotension and decrease in urine output.

Loss of gastric fluid leads to loss of HCL present in the gastric fluid and thus creates an acid deficit in the body leading to metabolic alkalosis.

In addition, loss of relatively large volumes of bicarbonate free fluid leads to contraction of extra cellular volume around the relatively constant quantity of extracellular bicarbonate leading to alkalosis called contraction alkalosis. In addition, the respiratory system is very quick to start its compensatory mechanisms leading to a respiratory acidosis. Therefore, we are expecting a metabolic alkalosis with respiratory compensation in this patient.

Choice (B) is a normal acid base status.

Choice (A) is suggestive of an acidotic condition.

Choice (C), (D) and (E), all have alkaline pH; however, Choice (D) has PaCO2 in the alkaline range suggestive of respiratory alkalosis. The compensation for primary metabolic alkalosis is respiratory acidosis not respiratory alkalosis. Choice (C) is the right answer because it has an alkaline pH with increase in HCO3- concentration and compensatory increase in PaCO2 suggestive of primary metabolic alkalosis with respiratory compensation.

Choice (E) has an alkaline pH but increase in bicarbonate and decrease in PaCO2 suggest mixed metabolic alkalosis and respiratory alkalosis. This combination of metabolic and respiratory alkalosis can result in extremes of pH.

Educational Objective:
Severe vomiting produces metabolic alkalosis due to loss of hydrogen ions present in the gastric fluid. Another contributor to alkalosis in such patients is contraction of ECF volume leading to contraction alkalosis.

Front 7

Which of the following is the most common acid base disorder seen in the hospitalized patients in United States?

A. Non anion gap metabolic acidosis.
B. Anionic gap metabolic acidosis.
C. Metabolic alkalosis.
D. Respiratory acidosis.
E. Respiratory alkalosis.

Back 7

Statistics show that metabolic alkalosis is the most common acid base disorder encountered in the hospitalized patient population. Metabolic alkalosis accounts for about 50% of all acid base disorders seen in the hospitalized patients. The most common causes of metabolic alkalosis are the use of diuretics and the external loss of gastric secretions, which account for about 90% of metabolic alkalosis seen in the hospitalized patients.

Furthermore, the causes of metabolic alkalosis can be classified into chloride-responsive alkalosis (urine chloride <20 mEq/L), chloride-resistant alkalosis (urine chloride >20 mEq/L).

Severe metabolic alkalosis (blood pH >7.55) is a serious medical problem. Mortality rates of 45% have been reported in patients with an arterial blood pH of 7.55 and 80% in patients with pH > 7.65.

Educational Objective:
Metabolic alkalosis is the most common acid base disorder encountered in the hospitalized patient population.

Front 8

A 46-year-old male is admitted for an acute exacerbation of COPD. He is a known patient of type-2 diabetes and is on metformin for the last 3 years. His arterial blood gases are:

Blood pH: 7.23
PaO2: 88 mmHg
PaCO2: 40 mmHg
HCO3-: 16 meq/L

Which of the following best describes the acid base status of this patient?


A. Metabolic acidosis
B. Respiratory acidosis
C. Mixed metabolic and respiratory acidosis
D. Mixed metabolic acidosis and respiratory alkalosis
E. Normal acid base balance

Back 8

Mixed acid-base disorders are defined as independently coexisting disorders and not merely compensatory responses. In order to diagnose mixed acid base disorders it is important to look for the blood pH first and decide the status of acid base balance. Second step would be to see if change in HCO3- or PaCO2 can explain the change in pH. Third step should be to see the degree of compensation possible for the disorder and if the values are not matching with the observed values, then a mixed acid base disorder is present. Mixed acid-base disorders may cause extreme pH abnormalities (metabolic and respiratory acidosis or metabolic and respiratory alkalosis) or can result in a normal pH (respiratory acidosis and metabolic alkalosis, metabolic acidosis and metabolic alkalosis, etc.).

The blood pH of the patient is 7.23 suggestive of acidosis. Next the HCO3-=16 meq/L is suggestive of metabolic acidosis. The metabolic acidosis in this patient is probably due to the chronic use of metformin and thus a respiratory compensation is expected.

With the respiratory compensation of metabolic acidosis the expected PaCO2 as calculated by Winter’s formula for this patient would be 1.5 (16) + 8 = 32 mmHg
[(PaCO2 = 1.5 (HCO3- ) + 8].

However, the observed PaCO2 is 40 mm Hg that though in a normal range is increased than the expected value suggestive of coexistent respiratory acidosis (Choice C) due to underlying COPD.

Educational Objective:
Know how to identify mixed acid base disorders.

Front 9

A 38-year-old woman with a previously diagnosed prepyloric peptic ulcer has had increased vomiting for 1 week. She is also complaining of muscular weakness, twitching, and cramps. She states she has not urinated for the last 20 hrs. Her vital signs are PR: 100/min; BP: 105/60 mm of Hg; RR: 12/min; Temperature 37.2 C (99F). Her oral mucosa is dry and skin turgor is decreased. Bowel sounds are hypoactive and abdomen is mildly tender to palpation in the epigastrium. Treatment with nasogastric suction and IV normal saline is started.

Labs showed:

Serum pH 7.52
Na 135
Cl 81
K 3.0
HCO3 40
Ca 2.2 mmol/L
Ca (ionized) 0.7 mmol/L (1.1-1.3 mmol/L)

Which of the listed agents should be added to the therapy?

A. Ammonium chloride
B. Potasium chloride
C. Calcium chloride
D. Furosemide
E. Clarithromycin

Back 9

This patient has gastric outlet obstruction due to complicated peptic ulcer disease (PUD). Unceasing vomiting and dehydration resulted in hypochloremic metabolic alkalosis. These are corrected with 0.9% NaCl. This type of alkalosis is frequently accompanied by hypokalemia. Note that NG suction doesn’t eliminate the potassium loss. Potassium supplementation is indicated whenever NG suction is done.

The tetany is due to the decrease of the ionized Ca because of the alkalosis. Total Ca is normal therefore no CaCl is needed at this moment.

Because of the dehydration this patient probably has functional oliguria. Diuresis is expected to improve from the volume repletion. Furosemide may worsen the volume deficit and is contraindicated now.

Educational Objective:
In a patient with hypochloremic metabolic alkalosis due to gastric outlet obstruction, potassium is usually low and needs to be supplemented.

Front 10

A 27-year-old male presents with profuse diarrhea that started 2 days ago. He just returned from a trip to Mexico. He also complains of abdominal pain. His lab profile is

Blood pH: 7.32
PaO2: 90 mmHg
PaCO2: 30 mmHg
HCO3-: 16 meq/L
Creatinine: 1.1 mg/dl
BUN: 20 mg/dl
Na+: 136 meq/L
K+: 3.2 meq/L
Cl-: 112 meq/L

What is the anion gap of this patient?

A. 10
B. 8
C. 12
D. 16
E. 6

Back 10

Anion gap (AG) is the measure of unmeasured anions in the plasma. The plasma AG is calculated by the following formula:

AG = Measured cations – Measured anions.

The major cation in the body is Na+ and the major anions in the body are Cl- and HCO3-. Therefore, the formula for AG can be modified to:

AG = Na+ - (HCO3- + Cl-)

Normal Anion gap is between 6-12 and it is primarily determined by negative charges on the plasma proteins, particularly albumin. Thus a rise in AG indicates presence of non-chloride containing acids that contain inorganic (phosphate, sulfate), organic (ketoacids, lactate, uremic organic anions), exogenous (salicylate or ingested toxins with organic acid production), or unidentified anions.

Some of the most common causes of increased anionic gap metabolic acidosis are:
1. Lactic acidosis
2. Ketoacidosis (diabetic, starvation or alcoholic)
3. Methanol ingestion
4. Ethylene glycol ingestion
5. Salicylate poisoning
6. Uremia (ESRD)

An increase in AG can rarely be due to a decrease in unmeasured cations (calcium, magnesium, potassium). Hyperalbuminemia can also cause an increase in AG.

In this patient the AG = 136-(112+16) = 8 (Choice B) This patient has non-anionic gap metabolic acidosis secondary to diarrheal loss of alkaline intestinal fluid.

Educational Objective:
Know how to measure and use the anion gap in the diagnosis of metabolic acidosis. The formula for measurement of anion gap (AG) is: AG = Na+ - (HCO3- + Cl-)

Front 11

A 52-year-old alcoholic is hospitalized with gross distention of his abdomen. He gives a history of esophageal varices for two years. On examination, he has bilateral pedal edema and spider angiomas over hands. Liver biopsy is clearly suggestive of alcoholic cirrhosis. Which type of acid base disorder is most common in this kind of liver disease?

A. Metabolic alkalosis.
B. Anion gap metabolic acidosis.
C. Non-anion gap metabolic acidosis.
D. Respiratory acidosis.
E. Respiratory alkalosis.

Back 11

This patient has a chronic liver disease with signs and symptoms suggestive of chronic liver failure. Patients with chronic liver disease most commonly have respiratory alkalosis. Chronic liver failure leads to accumulation of progesterone in the body. Progesterone has a stimulatory effect on the respiratory center, which leads to tachypnea causing respiratory alkalosis.

Other acid base disorders are also possible in a patient with liver diseases but their incidence is less than the respiratory alkalosis. Huge ascites in patients with liver failure can also cause respiratory alkalosis secondary to respiratory embarrassment.

Educational Objective:
Patients with chronic liver disease most commonly have respiratory alkalosis.

Front 12

A 58-year-old chronic alcoholic is hospitalized because of decompensated cirrhosis of liver. His lab panel shows:

Blood pH: 7.30 Na+: 140 meq/L
HCO3-: 12 meq/L Cl-: 104 meq/L
BUN: 80 mg/dl K+: 4.1 meq/L
S. Creatinine: 3.6 mg/dl

During hospitalization a NG tube is placed and his laboratory panel changes to:

Blood pH: 7.54 Na+: 138 meq/L
HCO3-: 25 meq/L Cl-: 92 meq/L
BUN: 80 mg/dl K+: 3.8 meq/L
S. Creatinine: 3.8 mg/dl

Which of the following explains the change in the profile of this patient?


A. Development of acute renal failure.
B. Development of metabolic alkalosis.
C. Development of metabolic acidosis.
D. Development of respiratory alkalosis.
E. Physiological compensation of acid base disorder.

Back 12

On admission, the patient’s laboratory profile shows a decrease in pH with a decrease in bicarbonate suggestive of metabolic acidosis. His AG is [140-(104+12)] = 24. He has AG metabolic acidosis.

During his stay in hospital there is a change in his ABG, which shows increase in pH. His bicarbonate is now 25 meq/L, which though in the normal range has increased significantly from the previous bicarbonate value. Change in pH to alkaline range with relative increase in bicarbonate concentration is suggestive of superimposed metabolic alkalosis.

In this patient this superimposed metabolic alkalosis is secondary to NG tube placements, which probably led to the loss of large amounts of acidic gastric fluid leading to contraction alkalosis.

Choice A: Patient has the same BUN and creatinine during his stay in the hospital as before so development of new acute renal failure is ruled out.

Choice C: Development of metabolic acidosis would have further lowered the pH and bicarbonate.

Choice D: Development of respiratory alkalosis would have lead to significant change in PaCO2 and not in a increase in his bicarbonate.

Choice E: Physiological compensation can never totally correct or overcorrect the underlying acid base disorder.

Educational Objective:
NG tube placements may lead to the loss of large amounts of acidic gastric fluid leading to contraction alkalosis, even in patients with preexisting metabolic acidosis. This phenomenon should not be confused with a normalization of the acid base status.

Front 13

A 32-year-old female is brought to the ER with weakness, tingling and numbness in her extremities. Her vitals are, PR: 90/min, RR: 14 /min; BP: 110/70 mm Hg. Physical examination is unremarkable. She is not on any medication. The laboratory profile shows:

Blood pH: 7.56
HCO3-: 37 meq/l
Urine Na+: 16 meq/L
Urine K+: 20 meq/l
Urine Cl-: 7 meq/L

Na+: 135 meq/l
K+: 2.9 meq/L
Cl-: 92 meq/l
BUN: 16 mg/dl
S. Creatinine: 0.9 mg/dl

Which of the following is the most likely cause of this patient’s condition?


A. Surreptitious vomiting
B. Acute renal failure
C. Gitelman syndrome
D. Bartter's syndrome
E. Hyperventilation syndrome.

Back 13

This patient is having alkaline pH with increased bicarbonate suggesting metabolic alkalosis. Next step would be to look for urinary chloride, which is less than 20 mg/dl suggestive of chloride sensitive metabolic alkalosis.

Metabolic alkalosis can be classified into two broad categories based on urinary chloride level:
1.Chloride sensitive metabolic alkalosis has urinary chloride < 20 meq/l that is suggestive of ECF contraction. It can be corrected with saline infusion and so is called chloride sensitive metabolic alkalosis. Some causes are thiazide or loop diuretics, loss of gastric secretion, ingestion of large dose of nonabsorbable antacids, cystic fibrosis, congenital chlorhydrorrheea, villous adenoma etc.
2.Chloride resistant metabolic alkalosis has urinary chloride >20 meq/l and generally has both generation and maintenance mechanisms related to persistent mineralocorticoid stimulation and hypokalemia. They are generally characterized by ECF expansion and HTN and thus are not corrected by saline infusion (so called chloride resistant). Some conditions are primary hyperaldosteronism, Cushing’s syndrome etc. It also includes conditions causing mineralocorticoid-independent acceleration of distal tubule Na+ reabsorption (Liddle’ s syndrome) as well as Bartter’s syndrome and Gitelman’s syndrome.

Choice C, D usually cause chloride resistant metabolic alkalosis (urinary chloride> 20 meq/L) so they are ruled out from the differential diagnosis.

Choice E: Hyperventilation syndrome causes respiratory alkalosis and not metabolic alkalosis.

Choice B: This patient has normal BUN and S. Creatinine, which rule out acute renal failure.

Choice A: This patient has chloride sensitive metabolic alkalosis secondary to surreptitious vomiting, which should be considered in the differential diagnosis of all patients with metabolic alkalosis.

Educational Objective:
Metabolic alkalosis can be classified into two broad categories based on urinary chloride level, which are chloride sensitive metabolic alkalosis and chloride resistant metabolic alkalosis.

Front 14

A 42-year-old male is found unconscious in a subway station. He is brought to the ER and emergency resuscitation is done. I.V glucose and thiamine are given. His lab profile shows:

Blood pH: 7.20
PaO2: 90 mmHg
PaCO2: 30 mmHg
HCO3-: 12 mEq/L

Which of the following would be the next best step in the diagnosis of the acid base status in this patient?


A. Calculate the anion gap.
B. Calculate the osmolar gap.
C. Calculate the urine anion gap.
D. Calculate the urine osmolar gap.
E. Do a brain CT scan.

Back 14

This patient has low blood pH with low bicarbonate suggestive of metabolic acidosis. In any case of metabolic acidosis the first step should be to calculate the anion gap. Anionic gap is the measure of unmeasured cations in the body. It is calculated by the following formula:

AG = Na - (HCO3 + Cl)

Normal anion gap is between 6-12. Thus, a rise in AG indicates presence of non-chloride-containing acids that contain inorganic, organic, exogenous, or unidentified anions. Some of the most common causes of anionic gap metabolic acidosis are:
1. Lactic acidosis
2. Ketoacidosis (diabetic, starvation or alcoholic)
3. Methanol ingestion
4. Ethylene glycol ingestion
5. Salicylate poisoning
6. Uremia (ESRD)

A patient is said to have a normal anion gap metabolic acidosis when he has decreased HCO3- but a normal AG. This is also called hyperchloremic metabolic acidosis.

Some of the common causes of a normal anion gap metabolic acidosis are:

1) Renal loss of bicarbonate

Renal tubular acidosis
Moderate renal failure (renal failure with GFR more than 20 ml/min will have a normal anion gap acidosis)
Carbonic anhydrase inhibitors

2) Gastrointestinal loss of bicarbonate

Diarrhea
Ureterosigmoidostomy
Pancreatic fistula

Osmolar gap (Choice B) should be calculated in selected cases of increased anion gap acidosis when substance toxicity is suspected.

Urine anionic gap (Choice C) is calculated in cases of normal anionic gap metabolic acidosis to know if the acidosis is due to renal or intestinal loss of bicarbonate.

Urine osmolar gap (Choice D) and Brain CT (Choice E) would not tell anything about the acid base status of this patient.

Educational Objective:
In any case of metabolic acidosis the first step should be to calculate the anion gap.

Front 15

A 68-year-old male is admitted for relapse of his myeloid leukemia. He is febrile and lethargic. Blood work showed systemic candidiasis. He is leukopenic and thrombocytopenic. He is given 2 units of red blood cells and started on intravenous amphotericin. After two weeks of therapy, the patient complains of palpitations. An ECG is obtained and reveals ‘U’ waves and flat ‘T‘ waves. He had no prior history of cardiac problems. The most likely cause is:


A. Hypocalcemia
B. Hyponatremia
C. Hyperkalemia
D. Hypokalemia
E. Leukemic myocarditis

Back 15

Amphotericin is a good drug for systemic fungal infections. The most consistent electrolyte deficiency associated with its use is development of hypokalemia. The agent can increase potassium-wasting secondary to tubular effects. Once hypokalemia occurs, the individual may have muscle weakness, ileus, polyuria, and ‘U’ waves in the ECG. Other ECG findings are increased ‘QT’ interval and flat ‘T’ waves.

Choice A: Hypocalcemia occurs in the setting of increased levels of parathyroid hormone, vitamin D deficiency, renal failure, malabsorption etc. Hypocalcemia can present with muscle spasms, depression, and psychosis. Chvostek or Trousseau’s sign are frequently positive. ECG will reveal prolonged QT interval but no ‘U’ Waves.

Choice B: Hyponatremia may be due to water excess, diabetes, lipidemia etc. Drugs known to release ADH will cause dilutional hyponatremia include morphine, tricyclics, nicotine, NSAIDs, etc. The individual will present with confusion, anorexia, lethargy and cramps. When sodium drops abruptly, seizures, hemiparesis and coma can develop.

Choice C: Hyperkalemia may be due to renal failure, hypoaldosteronism, muscle breakdown, hemolysis etc. The ECG manifestations of hyperkalemia have an affect on conduction of the heart and include peaked T waves, diminished R waves, wide QRS and prolonged PR interval. Hyperkalemia must be rapidly treated to avoid conduction problems.

Choice E: Leukemia does not affect the heart directly but can present with a pericarditis. In the later stages of leukemia, many patients will develop a pericardial effusion. It does not affect the conduction of the heart and no ECG changes occur on the basis of leukemia alone.

Educational objective:
Amphotericin use is associated with hypokalemia. Potassium levels should routinely be monitored when administrating this agent. The presence of ‘U’ waves in the ECG indicates hypokalemia.

Front 16

A 60-year-old male comes to you with dizziness, fatigue and weight loss. He mentions a past history of tuberculosis. On examination, he has BP: 102/64 mmHg and there is an increase in his skin pigmentation. His lab reports show, Na+: 126 meq/L, K+: 6.1 meq/L; Cl-: 102 meq/L. Morning serum cortisol level is 2.9 mg/dl. Which of the following acid base disturbance is expected in this patient?


A. Anionic gap metabolic acidosis.
B. Non-anionic gap metabolic acidosis.
C. Metabolic alkalosis.
D. Respiratory acidosis.
E. Respiratory alkalosis.

Back 16

This patient is having the signs and symptoms suggestive of adrenal failure (Addison’ s disease), probably secondary to tuberculosis. His morning serum cortisol level of 2.9 mg/dl confirms the adrenal insufficiency (Addison’s disease is also confirmed by high ACTH levels).

Addison’ s disease is characterized by decreased cortisol, adrenal sex hormones and aldosterone secretion. Normally aldosterone acts on the distal tubules of kidney to increase the reabsorption of sodium in exchange of potassium and hydrogen ions. If aldosterone is deficient, then the kidney loses more of the sodium and both potassium and hydrogen ions are retained in the body leading to mild non-anionic gap hyperkalemic, hyponatremic metabolic acidosis.

Choice A: AG metabolic acidosis is not seen with Addison’s disease as there is no increase in body unmeasured cations.

Choice C: Metabolic alkalosis occurs with hyperaldosteronism and not hypoaldosteronism.

Choice D and E: Respiratory acid base disorders are not common with hypoaldosteronism.

Educational Objective:
Aldosterone deficiency leads to a mild non-anionic gap hyperkalemic, hyponatremic metabolic acidosis.

Front 17

A 56-year-old white male comes to your clinic with symptoms of muscle weakness and fatigue for the past 2 months. He is a known diabetic for the past 20 years. His diabetes is being managed with diet, exercise, and oral hypoglycemic agents. Neurological examination showed mild weakness in lower limbs, depressed reflexes, and normal sensations.

Lab results:

Blood glucose 160 mg/dL
Hb A1C 9.0 gm/dl
K 6.1 meq/l
Na 140 meq/L
Cl 108 meq/dl

Urine analysis:
1 + protein
No leucocytes
2-3 RBC per HPF

TTPG (trans tubular potassium gradient) is < 5. EKG shows tall-tented T waves. What is your most appropriate next step in making the diagnosis?

A. Review his medications
B. Measure his renin and aldosterone level
C. Measure his urinary anion gap
D. Treat him with an ACE inhibitor

Back 17

This patient has hyperkalemia. His TTKG is < 5 which indicates that there is a defect in the excretion of potassium in the kidney. The next step would be to review the patient’s medications. In particular, ACE inhibitors, Angiotensin receptor blockers (which are not uncommonly seen in diabetics) and NSAIDs may cause hyperkalemia by blocking the aldosterone production.

Subsequently, the next step would be to calculate a urinary anion gap. This patient probably has RTA type 4. Hyperkalemia seen in distal type 4 RTA may be due to either hyporeninemic hypoaldosteronism or a chloride shunt (Gordon’s Syndrome).

If the patient had other features of adrenal insufficiency, you could measure the renin and aldosterone levels. If the renin level is increased with decreased aldosterone level, then this is a case of primary hypoaldosteronism or Addison’ s disease.

Knowledge of his blood pressure would be especially helpful if he had hypokalemia, in which case you should think of hyperaldosteronism if he is hypertensive and excess potassium loss if he was hypotensive.

An ACE inhibitor is contraindicated in a patient with hyperkalemia.

Educational Objective:
Know how to evaluate a patient with hyperkalemia.

Front 18

A 54-year-old hypertensive male comes to you with complaint of fatigue. Patient is taking magnesium hydroxide antacid and lisinopril regularly. His electrolyte panel shows Na+: 138 meq/L, K+: 5.9 meq/L, Cl-: 105 meq/L. His ECG shows normal rate and rhythm. You stop the lisinopril and prescribe him Kayexalate to control his hyperkalemia. Which of the following acid base disorder is most likely to develop in this patient because of your intervention?


A. Anionic gap metabolic acidosis.
B. Non-anionic gap metabolic acidosis.
C. Metabolic alkalosis.
D. Respiratory acidosis.
E. Respiratory alkalosis

Back 18

This patient is on a nonabsorbable antacid magnesium hydroxide and now you gave him a cation binging resin Kayexalate to correct his ACE inhibitor induced hyperkalemia. This can lead to development of metabolic alkalosis in this patient because of the interaction between Kayexalate and magnesium hydroxide.

Normally upon ingestion of magnesium hydroxide, its hydroxide anion binds to the hydrogen ions in the stomach whereas the cation portion binds with the bicarbonate in duodenum leading to loss of both hydrogen and bicarbonate and therefore no acid base disorder occurs. However, when a cation binding resin such as Kayexalate is given along with magnesium hydroxide the cation portion of the antacid will bind resin and so it will not be able to bind bicarbonate leading to bicarbonate excess and metabolic alkalosis.

Choice A, B, D and E is not possible with this drug interaction.

Educational Objective:
Be aware of the potential for the development of metabolic alkalosis in patients taking both Kayexalate and magnesium hydroxide.

Front 19

A 50-year-old chronic alcoholic patient is brought to the ER with massive hematemesis. In order to control his hematemesis the patient had to undergo a portocaval shunt. He is hemodynamically stable at present but in recovery room he is confused, tremulous and has changes in his sleep cycle. His labs are:

Na+: 146 meq/L WBC: 11,000/cmm
K+: 3.9 meq/L Cholesterol: 240 mg/dl
Cl-: 100 meq/L Ammonia: 40 mg/dl

Which of the following best represents the acid base status in this patient?

pH, PaCO2(mm Hg), HCO3-(meq/l)



A. 7.48, 40, 30
B. 7.40, 40, 24
C. 7.28, 40, 18
D. 7.60, 25, 27
E. 7.20, 40, 15

Back 19

This patient is an alcoholic, with portal hypertension, who undergoes portocaval shunt and develops hepatic encephalopathy as suggested by confusion, tremulousness and change in his sleep wake cycle. Hepatic encephalopathy occurs due to accumulation of ammonia in the blood, which is normally detoxified by the liver. The patient has the blood ammonia level of 40 mg/dl, which is suggestive of ammonia toxicity. Ammonia being a basic substance would lead to metabolic alkalosis in this patient. So we should be expecting a primary metabolic alkalosis in this patient.

Choice A has an alkaline pH with increase in bicarbonate and normal PaCO2 suggestive of uncompensated metabolic alkalosis. So choice A is the correct answer.

Choice B is normal acid base status.

Choice C is metabolic acidosis without respiratory compensation.

Choice D is suggestive of mixed metabolic and respiratory alkalosis.

Choice E is metabolic acidosis with no respiratory compensation.

Educational Objective:
Recognize metabolic alkalosis in the setting of uncompensated cirrhosis.

Front 20

A 45-year-old male was admitted to the hospital for acute pneumonia 2 days ago. His vitals are: Temperature: 38.3C(101F); RR: 28/min; BP: 120/80 mmHg; PR: 100/min. You are asked to evaluate him for severe diarrhea, which he developed while in the hospital. Which of the following acid-base values would best fit the profile of this patient?

PH, PaO2(mm Hg), PaCO2(mm Hg), HCO3-( eq/L)


A. 7.19, 58, 62, 23
B. 7.18, 83, 53, 19
C. 7.35, 86, 45, 24
D. 7.40, 51, 32, 18
E. 7.32, 85, 24, 12

Back 20

Mixed acid-base disorders are defined as independently coexisting disorders and not merely compensatory responses. In order to diagnose mixed acid base disorders it is important to look for the blood pH first and decide the status of acid base balance. Second step would be to see if change in HCO3- or PaCO2 can explain the change in pH. Third step should be to see the degree of compensation possible for the disorder and if the values are not matching with the observed values, then a mixed acid base disorder is present. Mixed acid-base disorders may cause extreme pH abnormalities (metabolic and respiratory acidosis or metabolic and respiratory alkalosis) or can result in a normal pH as in our patient (respiratory acidosis and metabolic alkalosis, metabolic acidosis and metabolic alkalosis, etc.).

This patient has an acute pneumonia with tachypnea so respiratory alkalosis is expected. The development of severe diarrhea, with loss of alkaline fluids, causes a metabolic acidosis. In consequence, he should have a decrease in HCO3- due to metabolic acidosis and a decrease in PaCO2 due to respiratory alkalosis. Thus, we can expect a mixed metabolic acidosis and respiratory alkalosis in this patient. Therefore, it is not surprising that the pH of the patient is in the normal range.

Choice (A) has an acidic pH with a marked increase in PaCO2 but a normal HCO3- concentration suggestive of acute uncompensated respiratory acidosis.

Choice (B) has acidic pH but both HCO3- and PaCO2 are in the acidic range suggestive of mixed respiratory and metabolic acidosis.

Choice (C) has acidic pH with PaCO2 in acidic range but normal HCO3- suggestive of uncompensated respiratory acidosis.

Choice (D) has normal pH but has decrease in HCO3- and decrease in PaCO2 suggestive of mixed metabolic acidosis and respiratory alkalosis. (Correct choice)

Choice (E) has acidic pH with decrease HCO3- and decrease PaCO2 suggestive of metabolic acidosis with respiratory compensation.

Educational Objective:
Know the correct diagnostic approach to mixed acid-base disorders.

Front 21

A 35-year-old male is brought to the ER with a gunshot wound in his right arm. He went to the operating room for the removal of the bullet. On postoperative day 4, he develops a swinging fever and tachypnea. On examination, he has altered sensorium and hypotension with oliguria. A diagnosis of septic shock is made. His laboratory profile shows:

Blood pH: 7.20
PaO2: 80 mm Hg
PaCO2: 32 mmHg
HCO3-: 12 mEq/L

Which of the following would be the most appropriate treatment for this patient’s acidosis?

A. I.V sodium bicarbonate, and broad spectrum antibiotics
B. I.V normal saline and I.V bicarbonate
C. Oral sodium bicarbonate, vasopressors, and antibiotics
D. IV normal saline, vasopressors, and antibiotics

Back 21

This patient has septic shock secondary to a gun shot injury. His ABG is suggestive of metabolic acidosis (decreased pH with decrease bicarbonate). In this case, the metabolic acidosis is due to accumulation of blood lactate secondary to tissue hypoxia and anaerobic respiration due to septic shock. It is very important to correct the underlying cause and restore the tissue perfusion first. IV fluids and vasopressor therapy to maintain the intravascular pressure and antibiotics to correct the underlying infection are the most important steps in the management.

Choice A, B and C: Use of bicarbonate in treatment of lactic acidosis is very controversial and is recommended only in severe acute acidosis with pH < 7.2. Bicarbonate should be given only to correct the pH up to 7.2. Full correction with bicarbonate should not be sought. In addition, in the case of lactic acidosis, bicarbonate treatment may paradoxically depress cardiac performance and exacerbate acidosis by enhancing lactate production (HCO3- stimulates phosphofructokinase).

Educational Objective:
IV fluids and vasopressor therapy to maintain the intravascular pressure and antibiotics to correct the underlying infection are the most important steps in the management of lactic acidosis from septic shock.

Front 22

A 50-year-old male is found unconscious on the street, when paramedics arrive and start giving him advanced cardiac life support (ACLS). After coming to the ER, he is resuscitated. On examination, his BP: 90/60 mmHg; PR: 60/min. His lab panel shows:

Blood pH: 7.20
PaO2 : 65 mmHg
PaCO2: 63 mmHg
HCO3-: 19 mEq/L

Which of the following is the most appropriate treatment for this patient’s acidosis?

A. Give him I.V bicarbonate.
B. Ventilate the patient.
C. Give him oral bicarbonate.
D. Give him I.V HCL.
E. Ask the patient to breathe in a closed bag.

Back 22

The patient is having cardiac depression, as suggested by his hypotension and bradycardia. Hypoxia, and not acidosis, accounts for most of the cardiac depression. However, acidosis also produces an immediate and profound cardiac depression. This patient has ABG suggestive of hypoventilation. Thus increasing the ventilation (Choice B) should be used as a primary means of correcting his respiratory acidosis.

In general, the management of respiratory acidosis depends on its severity and rate of onset. Acute respiratory acidosis, like in this patient, can be life threatening and measures should be taken to correct the underlying cause along with measures to improve the ventilation.

There is a great controversy in use of bicarbonate (Choice A and C) for treatment of acidosis. However, it is almost never indicated in treatment of respiratory acidosis as a first measure unless ventilation fails to correct the acidosis. Although the cardiac function is depressed by the acidic pH, the determining factor is the intracellular pH and not the extracellular pH and so use of bicarbonate is more controversial.

I.V HCL (Choice D) and breathing in a closed bag (Choice E) are the treatment modalities for alkalosis and not acidosis.

Educational Objective:
In cases of respiratory acidosis CO2 washout is achieved by providing ventilation either in the form of non-invasive (BiPAP) or invasive (intubation).

Front 23

A 48-year-old type 1 diabetic female is on a trip to her daughter's home but forgets to bring her insulin. She thinks it would be fine without it for a few days, as she has been very regular in taking it. On third day of her trip she develops abdominal pain, severe nausea, and vomiting. She is brought to the ER the next day and on examination her Temperature: 36.7C (98.2F); PR: 90/min; RR: 30/min; BP: 140/80 mm Hg. Her blood glucose is 360 mg/dl and her urine is positive for ketones. What is the most likely cause of her tachypnea?

A. Hyperglycemia itself
B. Dehydration due to vomiting
C. Metabolic acidosis
D. Anxiety
E. Hypoglycemia

Back 23

All the primary acid base disorders lead to a compensatory phenomenon in the body in order to correct the acid base imbalance. The respiratory acid base imbalances are compensated by renal mechanisms and the metabolic acid base disorders are compensated by respiratory mechanisms.

This is a classic presentation of diabetic ketoacidosis. She is having anion gap metabolic acidosis due to accumulation of ketoacids in the body. The body tries to compensate for the acidosis by increasing the respiratory rate, which will decrease the PaCO2 and try to bring the pH back to normal. Thus, the tachypnea seen in this patient is a part of respiratory compensation of metabolic acidosis. (Choice C)

Hyperglycemia (Choice A) itself has no effect on the respiratory center and would not cause tachypnea.

The dehydration, due to vomiting, (Choice B) would lead to metabolic alkalosis, which would rather decrease the respiratory rate as compensation.

This patient has symptoms suggestive of hyperglycemia and not hypoglycemia (Choice E) or anxiety (Choice D).

Educational Objective:
All the primary acid base disorders lead to a compensatory phenomenon in the body in order to correct the acid base imbalance. The respiratory acid base imbalances are compensated by renal mechanisms and the metabolic acid base disorders are compensated by respiratory mechanisms.

Front 24

A 55-year-old white female is suffering from osteoarthritis in her left knee for the past 6 years. She is on ibuprofen, because of the knee arthritis, for the past 1 year. She comes to you with the main complaint of vomiting for the last three days. She gives a history of epigastric pain and distress for the past six months. Her laboratory reports are as follows:

Blood pH 7.55
PaO2 100 mmHg
PaCO2 48 mmHg

Na+ 132 meq/L
K+ 3.0 meq/L
Cl- 88 meq/L
HCO3- 32 meq/L
BUN 15 mg/dl
Creatinine 1 mg/dl

Which of the following would describe her primary acid base status?

A. Normal profile
B. Metabolic acidosis
C. Metabolic alkalosis
D. Respiratory acidosis
E. Respiratory alkalosis

Back 24

In healthy subjects, blood pH is maintained at 7.39-7.41. PH is calculated by the equation pH = - log10 [H+]. As pH is the negative logarithm of [H+], an increase in pH indicates a decrease in [H+] and vice versa. Thus a pH more the 7.41 is considered as alkalosis and pH less than 7.39 is considered as acidosis. However, mixed acid base disorders can exist with pH in a normal range therefore it is very necessary to study the HCO3 and PaCO2 to get the correct acid base diagnosis.

The normal HCO3- is 24 meq/L and normal PaCO2 is 35-40 mm Hg. A deviation from these normal values is indicative of an acid base disorder. Metabolic acid base disorders are due to a primary change in the concentration of HCO3 whereas respiratory acid base disorders are due to a primary change in PaCO2. A primary rise in arterial PaCO2 (respiratory acidosis) or fall in plasma HCO3 (metabolic acidosis) reduces the pH, whereas a primary fall in arterial PaCO2 (respiratory alkalosis) or a rise in plasma HCO3 (metabolic alkalosis) increases the pH.

In deciding the acid base status always look at the pH first to decide whether it is acidosis or alkalosis. Next step is to look whether PaCO2 or HCO3- correlates with the status indicated by pH to decide whether it’s a metabolic or a respiratory condition.

This patient has a blood pH of 7.55 indicative of alkalosis (so Choices A, B, D are incorrect). Next the patient has an increase in his HCO3, which explains the alkalosis, thus the patient has metabolic alkalosis (Choice C).

The cause of metabolic alkalosis in this patient is vomiting secondary to NSAIDs induced gastritis. Gastric secretions are rich in HCl, however in the absence of vomiting this does not lead to alkalosis because when acid enters the duodenum it stimulates the secretion of pancreatic bicarbonate which balances the H + loss. However, in vomiting the gastric secretions do not reach the duodenum to stimulate the pancreatic secretions so there is deficit of H + in the body leading to alkalosis.

Educational Objective:
The main causes of metabolic alkalosis can be classified into following 4 main categories:
1. Exogenous administration of alkali.
2. Removal of gastric secretions due to vomiting or NG tube aspiration.
3. Renal hydrogen loss e.g. primary or secondary mineralocorticoid excess
4. Contraction alkalosis.

Front 25

A 42-year-old male is brought to ER immediately after a seizure episode. Family gives a history suggestive of grand mal seizures. Jim was on phenytoin for the past 10 years for his seizure disorder until he stopped it, six months ago. He had no seizures for the past nine years. On examination, patient is confused and lethargic. His vitals are, BP: 136/88 mm Hg, RR: 18/min, PR: 96/min. His laboratory report shows:

Blood pH: 7.24 L
PaO2: 98 mm Hg
PaCO2: 29 mm Hg
HCO3-: 12 meq/l

Na+: 140 meq/
K+: 4.5 meq/L
Cl-: 102 meq/L
BUN: 11 mg/dl
Creatinine: 0.9mg/dl

Which of the following is the most appropriate treatment for his metabolic acidosis?


A. Give bicarbonate I.V bolus.
B. Give oral bicarbonate.
C. Give bicarbonate I.V drip.
D. Observe and repeat the labs after 2 hours.
E. Hemodialysis.

Back 25

This patient has an acidic pH with a decrease in his bicarbonate concentration suggestive of metabolic acidosis. His AG is 140-(102+12) = 26.

The patient had an epileptic seizure due to non-compliance with the medication. A post-seizure increased anion gap metabolic acidosis is suggestive of lactic acidosis. This is caused by accelerated production of lactic acid in muscle and reduced hepatic lactate uptake. However, this post-ictal lactic acidosis is transient and resolves without treatment within 60 to 90 minutes. Therefore, the best intervention in this patient is to observe him and repeat his ABG after 2 hours to see if the acidosis has resolved. If it does not resolve, then look for other potential cause of metabolic acidosis.

Choice A, B and C: Use of bicarbonate in the treatment of lactic acidosis is very controversial and is recommended only in severe acute acidosis with pH < 7.2. Bicarbonate should be given only sufficient to correct the pH up to 7.2 and full correction with bicarbonate should not be sought. In addition, in a case of lactic acidosis, bicarbonate treatment may paradoxically depress cardiac performance and exacerbate acidosis by enhancing lactate production (HCO3- stimulates phosphofructokinase).

Choice E: Hemodialysis for the treatment of acidosis is reserved for acute life threatening acidosis.

Educational Objective:
Post-ictal lactic acidosis is transient and resolves without treatment within 60 to 90 minutes.

Front 26

A 34-year-old female comes to you with the complaints of headache and fatigue for the last four days. On examination she has BP: 102/74 mmHg; PR: 112/min on supine; BP: 86/60 mm Hg; PR: 130 on sitting. Her laboratory panel shows:

Blood pH: 7.28
PaO2: 105 mm Hg
PaCO2: 24 mm Hg
HCO3-: 11 meq/l

Na+: 135 meq/L
K+: 3.4 meq/L
Cl-: 102 meq/L
BUN: 31 mg/dl
Creatinine: 1.6 mg/dl

Her acid base status can be best described as?


A. Anionic gap metabolic acidosis.
B. Non-anionic gap metabolic acidosis.
C. Combination of anionic gap and non-anionic gap metabolic acidosis.
D. Combination of metabolic acidosis and respiratory acidosis.
E. Normal acid base status.

Back 26

The patient is having acidic pH 7.23 (normal range is 7.39 to 7.41). His bicarbonate is decreased (normal is 24 meq/L). This combination is suggestive of primary metabolic acidosis. The body will try to compensate for this metabolic acidosis by washing out of PaCO2 by increasing the respiratory rate. The expected compensation can be calculated by Winter’s formula

PaCO2 = 1.5 (HCO3) + 8
= 1.5 (11) + 8
= 24.5

Observed PaCO2 is same as calculated PaCO2 suggestive of complete respiratory compensation of metabolic acidosis.

Next step in the evaluation of metabolic acidosis is to calculate the anionic gap.

AG of this patient is [135-(102+11)] = 22 (normal = 6-12)

The patient has AG metabolic acidosis (Choice A)

Next step in evaluation of AG metabolic acidosis is to calculate the ∆-∆ equation to look for coexisting acid base disorders.

∆-∆ equation = ∆ AG / ∆ Bicarbonate
= 14/14
= 1 (normal)

Thus, this patient is having an AG metabolic acidosis.

Educational Objective:
Know how to approach the interpretation of arterial blood gases suggestive of anion gap metabolic acidosis.

Front 27

A 32-year-old male is brought to ER with nausea and abdominal pain, of 2 days duration. He is a known type 1 diabetic. He had some flu-like symptoms for the past 4 days but no frank fever or chills. His appetite was markedly diminished over this period, therefore he decreased his insulin to half the dose for the past 3 days. His vitals are, Temperature: 37.6C(99.7F); BP: 122/86 mmHg, RR: 25/min, PR: 88/min. His lab values are:

Blood pH: 7.31
PaO2: 90 mmHg
PaCO2: 29 mmHg
HCO3-: 14 meq/L
Blood glucose: 350 mg/dl
Urine ketones: Positive.

Na+: 132 meq/l
K+: 4.6 meq/l
Cl-: 85 meq/l
BUN: 19 mg/dl
Creatinine: 1.1 mg/dl

Which of the following best describes his acid base status?


A. Primary metabolic acidosis with respiratory compensation.
B. Primary metabolic acidosis without compensation.
C. Respiratory acidosis with compensation.
D. Primary metabolic acidosis with renal compensation.
E. Normal acid base status.

Back 27

This patient is a type 1 diabetic who stopped taking his insulin and developed diabetic ketoacidosis as suggested by the increase in his blood sugar and the presence of urinary ketones. An anion gap acidosis is the most common acid base disorder in this situation due to the accumulation of ketoacids in the blood.

The patient has an acidic pH with a decrease in HCO3- suggestive of metabolic acidosis. The anion gap of the patient is 132-(85+14) = 33. Thus, the patient has anion gap metabolic acidosis.

There should be a respiratory compensation of this metabolic acidosis. If he was fully respiratory compensated the expected PaCO2 would be 1.5 (14) + 8 = 29 [Winter's formula is PaCO2 = 1.5 (HCO3-) + 8]. The observed PaCO2 is the same suggestive of full respiratory compensation of metabolic acidosis (Choice A). The respiratory compensation is also suggested by the tachypnea, which is called Kussmaul’s breathing (deep and rapid).

Educational Objective:
An anion gap acidosis is the most common acid base disorder in a type 1 diabetic who stops taking his insulin. This is due to diabetic ketoacidosis.

Front 28

Carolina is a 28-year-old female with history of hyperventilation syndrome and diabetes. She was started on insulin therapy 3 years ago. She went for a driving test, and became acutely ill. She was brought to the ER with confusion, chest pain and paresthesias in her hands. On examination her vitals are, Temperature: 36.7C(98.2F); PR: 98/min; RR: 23/min. Her arterial blood gas analysis is shown below:

Blood pH: 7.54
PaO2: 90 mmHg
PaCO2: 22 mmHg
HCO3-: 18 meq/L

What is the most likely cause of her paresthesias?


A. Respiratory alkalosis.
B. Diabetic ketoacidosis.
C. Insulin toxicity.
D. Hypocalcemia due to primary hypoparathyroidism.
E. Diabetic neuropathy.

Back 28

The patient has a history of hyperventilation syndrome and she is experiencing an acute attack. Her tachypnea leads to a primary respiratory alkalosis suggested by the appropriate changes in her ABG (alkaline pH with low PaCO2). One of the very common complications of acute alkalosis is development of hypocalcemia (due to binding of serum Ca++ to the negative HO- ions) leading to tetany like symptoms. This patient is most likely to be having symptoms of hypocalcemia due to fall in ionized calcium in her plasma. Crampy pain, paresthesias and carpopedal spasm all are important clinical features of hypocalcemia. Plasma calcium exists in three forms that include ionized calcium 45%, calcium bound to albumin40% and calcium bound to inorganic and organic anions15%. Ionized calcium is physiologically active.

Acute respiratory alkalosis by increasing extracellular pH causes increase in affinity of serum albumin to calcium resulting in decrease in plasma ionized calcium and increase in calcium bound to albumin. Decrease in plasma ionized calcium will result in the clinical manifestations of hypocalcemia. Total plasma calcium is normal in such cases.

Diabetic ketoacidosis (Choice B) and insulin toxicity (Choice C) are not associated with such kind of symptoms.

Diabetic neuropathy (Choice E) can cause such symptoms but the onset is never so acute.

Primary hypoparathyroidism (Choice D) can lead to hypocalcemia and tetany but again the onset is not so acute. Her history is more suggestive for (Choice A).

Educational Objective:
Hyperventilation causes acute respiratory alkalosis (incresaed pH) which increases the affinity of albumin to calcium and as a result serum ionzed calcium falls and clinical features of hypocacemia are seen.

Front 29

A 56-year-old male is brought to your office with the chief complaint of fever and chest pain for the past 3 days. He also gives a history of purulent sputum for the past 2 days. On examination he is drowsy and cyanotic. His vitals are as follows: Temperature: 38.8C(102F); RR: 27/min; PR: 90/min. His arterial blood gas (ABG) analysis is

Blood pH: 7.53
PaO2: 80 mmHg
PaCO2: 30 mmHg
HCO3-: 22 mEq/L

Which of the following best describes his acid base status?


A. Respiratory acidosis
B. Respiratory alkalosis
C. Metabolic acidosis
D. Metabolic alkalosis
E. Normal acid base status

Back 29

In deciding the acid base status always look at the pH first to decide whether it is acidosis or alkalosis. Next step is to look at whether PaCO2 or HCO3- correlates with the status indicated by pH, to decide whether it is a metabolic or a respiratory condition.

This patient has a pH of 7.53 suggestive of alkalosis (Choice A, C, E are incorrect). Next, his PaCO2 = 30 mmHg explains the alkalosis suggested by the pH change. Thus this patient has respiratory alkalosis. (Choice B)

This patient has some lung infection, which caused tachypnea, thus more CO2 is lost from the body leading to decrease in PCO2 and thus respiratory alkalosis.

Any conditions that cause an increase in the respiratory rate can lead to primary respiratory alkalosis. Some of these conditions are:
1. Anxiety.
2. Primary CNS disorder that leads to inappropriate respiratory center stimulation.
3. Liver insufficiency (due to stimulation of respiratory center by increase in progesterone concentration).
4. Pregnancy.
5. Hypoxia (conditions like pneumonia, pulmonary embolism, fat embolism, pulmonary fibrosis, asthma etc.).

Educational Objective:
Patients with respiratory alkalosis have incresaed pH and decreased PaCO2.

Front 30

A 45-year-old hypertensive male comes with periorbital edema, fatigue, nausea and anorexia. On examination, he has a bruit in his abdominal region. His blood studies are suggestive of hypokalemia and normocytic normochromic anemia. His GFR is 40 ml/min. Which of the following is the expected acid base status of the patient?


A. Normal anion gap acidosis.
B. Increase anion gap acidosis.
C. Metabolic alkalosis.
D. Respiratory acidosis.
E. Respiratory alkalosis.

Back 30

This patient’s history and clinical findings are suggestive of mild to moderate renal failure, secondary to renal artery stenosis, which also causes hypertension. Hypokalemic metabolic alkalosis is found in 20% of patients with hypertension due to renal artery stenosis. This is due to a hyperreninemic mineralocorticoid excess induced by renal artery stenosis. This causes increased salt reabsorption, volume expansion(hence HTN), increased potassium excretion and increased ammonia excretion.

The primary mechanism for acidosis in advanced renal failure is reduced ammonia genesis secondary to loss of functioning renal mass, leading to an inability of the kidney to excrete the normal daily acid load. This patient has a mild to moderate renal failure as suggested by his GFR of 40 ml/min. At this stage, the renal acid handling is usually preserved(Choices A, B).

In advanced renal failure (GFR < 20 ml/min), the acidosis can be associated with a high anion gap. Poor filtration and reabsorption of organic anions contribute to the pathogenesis.

Educational Objective:
20% of patients with renovascular hypertension have hypokalemic metabolic alkalosis due to hyperreninemic mineralocorticoid excess.

Front 31

A 33-year-old Hispanic female is admitted to the hospital for severe vomiting for the last 2 days. On examination, her vitals are, Temperature: 36.7C(98.2F); PR: 90/min; RR: 14 /min; BP: 100/70 mmHg, supine. Her laboratory profile shows:

Blood pH: 7.49
PaO2: 100 mmHg
PaCO2: 41 mm Hg
HCO3-: 30 meq/L

Na+: 138 meq/L
K+: 3.0 meq/L
Cl-: 95 meq/L

Which of the following is the most appropriate treatment for her alkalosis?


A. I.V ammonium chloride and potassium
B. IV HCL and IV potassium
C. Oral ammonium chloride
D. I.V normal saline and potassium
E. Dialysis

Back 31

Vomiting leads to loss of gastric fluid containing HCL, NaCl and water. This leads to retention of bicarbonate in body by the following mechanisms:
1.Generation phase of metabolic alkalosis is characterized by entry of bicarbonate in the blood due to secretion of HCL by stomach, which is lost in vomitus and so does not stimulate compensatory alkaline pancreatic secretions.
2.Loss of NaCl and water in vomitus leads to volume contraction and Cl depletion. This increases the renin, aldosterone and angiotensin II level, which in turn lead to increased reabsorption of bicarbonate and loss of H+. (Contraction alkalosis).

Thus, correction of the contracted ECF volume with NaCl would correct the acid base disorder. Normal saline will reverse all the factors driving bicarbonate reabsorption in kidney by correcting the volume contraction and Cl deficit. Correction of potassium deficit should be considered and it can be added to NS.

Choice A, B, C, E: They are all inappropriate for this patient as the primary treatments of alkalosis. In this patient, her volume contraction can be easily corrected with saline, and alkalosis is not so severe to require treatment with acids.

Educational Objective:
Know how to manage a patient with hypochloremic metabolic alkalosis due to vomiting.

Front 32

A 55-year-old male comes with the complaints of abdominal pain after meals. He is known to have hypertension and had two previous myocardial infarctions. He was advised to undergo cardiac bypass surgery but he is reluctant to do so. His laboratory profile shows

Blood pH: 7.37
PaO2: 100 mmHg
PaCO2: 32 mm Hg
HCO3-: 18 meq/l

Na+: 140 meq/L
K+: 5 meq/L
Cl-: 100 meq/L
Cholesterol: 300 mg/dl
LDL cholesterol: 240 mg/dl

Which of the following is the most likely cause of acid base disorder in this patient?


A. Diabetic ketoacidosis.
B. Unrecognized bowel ischemia.
C. Hyperlipidemia.
D. Small bowel infection.
E. Peptic ulcer perforation.

Back 32

The patient has an acidic pH with a decrease in the bicarbonate concentration and a compensatory decrease in the PaCO2 suggestive of metabolic acidosis. His AG is [140-(100+20)] = 20. Thus he has an AG metabolic acidosis.

Patient’s history is suggestive of severe atherosclerotic disease with two previous myocardial infarctions. His complain of epigastric pain after meals in presence of severe atherosclerotic diseases suggest bowel ischemia. Unrecognized bowel ischemia (Choice B) is one of the common causes of lactic acidosis in patients with severe atherosclerotic disease. Lactic acidosis is secondary to tissue hypoxia.

Choice A: Diabetic ketoacidosis can cause anion gap acidosis but this patient has no signs or symptoms suggestive of DKA. DKA can also present with abdominal pain but the onset is acute and also it has no relationship to meals.

Choice C: Hyperlipidemia is a risk factor for atherosclerotic disease, which is causing bowel ischemia.

Choice D: A small bowel infection can cause lactic acidosis secondary to septic shock but the patient would have hypotension, fever, tachycardia and other signs of septic shock.

Choice E: Peptic perforation has an acute onset with severe abdominal pain and is a medical emergency.

Educational Objective:
Unrecognized bowel ischemia is one of the common causes of lactic acidosis in patients with severe atherosclerotic disease.

Front 33

The laboratory reports of a patient are as follows:

Blood pH: 7.43
PaO2: 100 mm Hg
PaCO2: 25 mmHg
HCO3-: 16 meq/L

Na+: 137 meq/L
K+: 4.5 meq/L
Cl-: 108 meq/L

Which of the following patients is most likely to have these laboratory values?


A. 42-year-old female with aspirin toxicity.
B. 52-year-old lady on chemotherapeutic agent with severe vomiting.
C. 62-year-old patient with end stage renal disease.
D. 36-year-old patient with Bartter’s syndrome.
E. 14-year-old boy with cystic fibrosis.

Back 33

This patient has an alkaline pH with decreased PaCO2 suggestive of primary respiratory alkalosis. However, his bicarbonate is below the normal value instead of being elevated, which suggests mixed metabolic acidosis and respiratory alkalosis. (Choice A)

Aspirin intoxication in adults initially causes increased respiratory drive leading to respiratory alkalosis and then uncouples oxidative phosphorylation leading to metabolic acidosis.

Choice B would have chloride sensitive metabolic alkalosis.

Choice C would have anion gap metabolic acidosis.

Choice D would have chloride resistant metabolic alkalosis.

Choice E would have chloride sensitive metabolic alkalosis.

Educational Objective:
Aspirin intoxication in adults initially causes increased respiratory drive leading to respiratory alkalosis and then uncouples oxidative phosphorylation leading to metabolic acidosis.

Front 34

A 55-year-old diabetic is brought to ER with confusion and vomiting. His chemistry panel shows:

Blood pH: 7.26
PaO2: 98 mm Hg
PaCO2: 30 mm Hg
HCO3-: 14 mEq/L
U. Ketones: positive

Na+ 132 mEq/L
K+ 3.8 mEq/L
Cl- 90 mEq/L
Blood sugar 380 mg/dL

Accumulation of which of the following is responsible for acidosis in this patient?


A. Glucose.
B. Lactic Acid.
C. Beta hydroxy butyrate.
D. Alcohol.
E. Salicylic acid.

Back 34

The patient has an acidic pH with decreased bicarbonate and AG of 132 – (90 + 14) = 28, suggestive of increased anionic gap metabolic acidosis. Increased anionic gap metabolic acidosis in the presence of high blood sugar and positive urine ketones is highly suggestive of diabetic ketoacidosis.

Increased anionic gap metabolic acidosis is due to accumulation of unmeasured cations in the body. In case of diabetic ketoacidosis it is due to accumulation of ketoacids. These ketoacids are beta hydroxy butyrate (Choice C), acetoacetate, and acetone.

Accumulation of glucose in body (Choice A) causes metabolic acidosis in patients secondary to accumulation of ketoacids.

Accumulation of lactic acid (Choice B) would cause metabolic acidosis in conditions causing severe tissue hypoxia leading to anaerobic metabolism and thus lactic acid accumulation.

Alcohol intoxication (Choice D) leads to metabolic acidosis secondary to accumulation of ketoacids primarily and also lactic acid.

Salicylate intoxication (Choice E) would cause initially a respiratory alkalosis due to a direct stimulating effect on the respiratory center and eventually a metabolic acidosis secondary to uncoupling of oxidative phosphorylation pathways and accumulation of lactic acid.

Educational Objective:
Increased anionic gap metabolic acidosis in the presence of high blood sugar and positive urine ketones is highly suggestive of diabetic ketoacidosis. Ketoacids responsible for diabetic ketoacidosis include beta hydroxy butyrate, acetoacetate, and acetone.

Front 35

A 45-year-old chronic alcoholic is brought to ER in a stuporous state. On examination, he is agitated and disoriented. His vitals are, Temperature: 37.2C(99F); RR: 20/min; PR: 90/min; BP: 110/70 mm of Hg. His lab findings are:

Blood pH: 7.21
PaO2: 100 mmHg
PaCO2: 30 mmHg
HCO3-: 13 meq/L
Osmolarity: 400 mOsm/L
Blood Glucose: 92 mg/dl.

Na+: 141 meq/L
K+: 5.9 meq/L
Cl-: 100 meq/L
BUN: 70mg/dl
Creatinine: 7 mg/dl

His urine shows the presence of rectangular, envelope shaped crystals. What is the most likely cause of this lab abnormality in this patient?


A. Diabetic ketoacidosis.
B. Ethylene glycol poisoning.
C. Methyl alcohol poisoning.
D. Uremic acidosis.
E. Lactic acidosis.

Back 35

The patient has a pH of 7.21 and HCO3- = 13 meq/L suggestive of metabolic acidosis. Next step is to calculate the anion gap, which is [141- (100+13)] = 28. Thus, the patient has a high anion gap metabolic acidosis.

All of the given choices can cause anion gap metabolic acidosis. When the anion gap is markedly elevated, in the absence of uremia you should calculate the osmolar gap. The calculated osmolarity is POsm = [2Na + Glu/18 + BUN/2.8] which for this patient is [2(141) + 92/18 + 70/2.8] = 312.

Osmolar gap = observed osmolarity - calculated osmolarity. (Normal is less than 10)

Osmolar gap in this patient is 88. Thus, the patient has a high osmolar anion gap metabolic acidosis (Choice A, D, E are incorrect as they do not cause increase in osmolar gap). Osmotic gap metabolic acidosis is seen with acute methanol, ethanol or ethylene glycol poisoning.

Next, the key point is that the patient’s urine shows rectangular, envelope shaped crystals, which are pathognomonic of calcium oxalate crystals seen in patients with ethylene glycol (anti-freeze) poisoning. (Choice B is correct).

Educational Objective:
Calcium oxalate crystals (rectangular, envelope shaped crystals) are seen in patients with ethylene glycol (anti-freeze) poisoning.

Front 36

A 55-year-old chronic smoker undergoes cystectomy for bladder carcinoma. A urinary diversion, in form of a ileal conduit, is made. However, three months later the patient comes to the ER with tachypnea and confusion. His laboratory studies show a pH of 7.3. Which of the following acid base disorder is most likely expected in this patient?


A. Hyperchloremic metabolic acidosis.
B. Hyperchloremic metabolic alkalosis.
C. Hypochloremic metabolic acidosis.
D. Normochloremic metabolic acidosis.
E. No acid base disorder.

Back 36

Up to 80% of patients who undergo a urinary diversion procedure, especially an ileal conduit, can develop hyperchloremic metabolic acidosis due to the following reasons:
1.Exchange of chloride for bicarbonate through apical Cl-/HCO3-exchanger in the intestinal mucosa leading to significant loss of HCO3-, with a concurrent increase in serum Cl- concentration.
2.The colon can also reabsorb ammonium, which is derived both from the urine and from urea-splitting bacteria in the colon; mechanism is not clear. Absorbed ammonium is metabolized in liver to NH3 and H+. It is usually detoxified but in patients with severe hepatic impairment, it can cause encephalopathy picture.

Educational Objective:
Recognize hyperchloremic metabolic acidosis in a patient who just had a urinary diversion procedure.

Front 37

A 56-year-old diabetic male is brought to the ER with nausea and vomiting. You think that the determination of his acid base status is important in determining the etiology of his problem and planning the treatment. Which of the following pair of laboratory values will help to get the best picture of the acid base status of the patient?


A. pH and PaCO2.
B. pH and PaO2.
C. PaO2 and PaCO2.
D. Urinary pH and PaCO2.
E. Urinary pH and HCO3-.

Back 37

Acid Base disturbances are characterized by changes in either the bicarbonate or dissolved carbon dioxide components of the buffer pair. Classically the acid base status is expressed by the Henderson Hasselbalch equation, which has three variables (pH, PaCO2 and HCO3-) and two constants and is expressed as follows:
pH = 6.10 + log ([HCO3-]/0.03 X PaCO2)

In the determination of arterial blood gases by the clinical laboratory, both pH and PaCO2 are measured, and the [HCO3-] is calculated from the Henderson-Hasselbalch equation. (Choice A).

Thus, knowing two of the three variables in Henderson Hasselbalch equation would help us to find the third one with the equation.

Educational Objective:
PH and PaCO2 are the two lab values that provide us with the best picture of the acid base status of any patient.

Front 38

A 36-year-old patient is brought to emergency room by the family with the complaints of confusion, nausea, and diminished vision. Patient gives the history of heavy consumption of alcohol in a party 5 hours ago. On examination his vitals are, Temperature: 36.7C(98.2F); RR: 22/min; PR: 86/min. The ABG and serum electrolyte results show:

pH: 7.21
HCO3-: 12 meq/L
PaO2: 96 mmHg
PaCO2: 30 mm Hg
Creatinine: 1 mg/dl

Na+: 140 meq/L
K+: 4 meq/L
Cl-: 98 meq/L
BUN: 15 mg/dl

What is the most likely primary acid base disorder in this patient?


A. Non-anionic gap metabolic acidosis.
B. Anion gap metabolic acidosis.
C. Metabolic alkalosis.
D. Respiratory alkalosis.
E. Respiratory acidosis.

Back 38

This patient has blood pH of 7.26 suggestive of acidosis (so Choice C and D are incorrect). Also his HCO3- is 12 meq/L, which is less than normal of 24 meq/L, is suggestive of metabolic acidosis (so Choice E is incorrect).

Next step is to calculate the anion gap, which is given by the formula:
AG = Na - (Cl+ HCO3).

AG is the measure of unmeasured anions in the plasma. Normal anion gap is between 6-12. Thus a rise in AG indicates presence of non-chloride-containing acids that contain inorganic (phosphate, sulfate), organic (ketoacids, lactate, uremic organic anions), exogenous (salicylate or ingested toxins with organic acid production), or unidentified anions.

Some of the most common causes of anionic gap metabolic acidosis are:
1.Lactic acidosis.
2.Ketoacidosis (diabetic, starvation or alcoholic).
3.Methanol ingestion.
4.Ethylene glycol ingestion.
5.Salicylate poisoning.
6.Uremia (ESRD).

Increase in AG can rarely be due to a decrease in unmeasured cations (calcium, magnesium, potassium). Hyperalbuminemia can also cause an increase in AG.

For this patient the AG is equal to 140-98-12 = 30, which is higher than normal. Therefore, this patient has high anion gap metabolic acidosis (Choice B).

Educational Objective:
Know how to recognize anion-gap metabolic acidosis.

Front 39

A 42-year-old male develops sudden onset of pain in his right eye associated with blurring of vision and haloes around light. A diagnosis of acute angle closure glaucoma is made and I.V acetazolamide is given to the patient. Several hours later, he develops confusion and tachypnea and his lab report shows:

Blood pH: 7.28
PaO2: 100 mm Hg
PaCO2: 32 mm Hg
HCO3-: 16 meq/l

Na+: 140 meq/l
K+: 3.6 meq/L
Cl-: 114 meq/l
BUN: 9 mg/dl
Creatinine: 1 mg/dl

Which of the following is the most likely cause of his acid base disorder?


A. Diabetic nephropathy.
B. Diabetic ketoacidosis.
C. Acute methanol poisoning.
D. Acute acetazolamide toxicity.

Back 39

This patient has low pH with decrease in bicarbonate suggestive of metabolic acidosis. His anionic gap is [140- (114+16)] =10. Thus, the patient has a normal anionic gap metabolic acidosis.

The patient was given I.V acetazolamide for acute glaucoma. Acetazolamide is a mild diuretic, which inhibits the carbonic anhydrase enzyme in the proximal tubules of kidney, interfering with the absorption of bicarbonate at this site, therefore leading to a normal anionic gap metabolic acidosis due to renal loss of bicarbonate. Acetazolamide is also used in edematous patients with metabolic alkalosis, as loss of bicarbonate can cause metabolic acidosis and can compensate the acid base status (Choice D).

Diabetic ketoacidosis (Choice B) and methanol poisoning (Choice C) would cause an increased anionic gap acidosis.

DM nephropathy (Choice A) can cause normal anion gap metabolic acidosis secondary to renal tubular acidosis (RTA) but it is unlikely in this patient with normokalemia and normal BUN and creatinine.

Educational Objective:
Acetazolamide causes a normal anionic gap metabolic acidosis due to renal loss of bicarbonate.

Front 40

A 45-year-old white female comes to you with complaints of gritty sensation in her eyes and dry mouth for several months. She even complains of arthralgia in her hands. On examination, she has pruritic plaques on her calves and knuckles. Her laboratory studies show pH of 7.35, PaCO2 of 30 mm Hg, HCO3- of 16 meq/L, Na+ of 140 meq/L, K+ of 3.0 meq/L, and Cl- of 114 meq/L. Her abdominal x-ray is suggestive of nephrolithiasis. Her urine pH is 6. Which of the following is the most likely diagnosis?


A. RTA type 1
B. RTA type 2
C. RTA type 3
D. RTA type 4
E. Uric acid nephropathy

Back 40

This patient has signs and symptoms suggestive of Sjogren’s syndrome (gritty sensation in eyes, dry mouth, arthralgia, and pruritic plaques). Her ABG is suggestive of a normal anionic gap metabolic acidosis (low pH with low bicarbonate and AG= [140 – (114 + 16)] = 10). Also she has a low potassium and urine pH>6 which is suggestive of RTA type 1 (Choice A)

RTA is a term used to describe those conditions in which normal AG metabolic acidosis occurs from decreased net renal acid secretion. There are three important types of renal tubular acidosis.

RTA type 1 (distal tubular acidosis): It is characterized by decreased distal tubular capacity for hydrogen ion secretion and therefore the inability to generate new bicarbonate. Type 1 RTA should be suspected in any patient with non-AG metabolic acidosis and a urine pH greater than 5.5. Serum potassium, classically, is low in patients with distal RTA. Causes include Sjogren’s syndrome, SLE, Amphotericin toxicity, Wilson’s disease, Sickle cell disease, Fabry’ s diseases etc. It is commonly associated with nephrolithiasis (just like in this patient).

RTA type 2 (proximal tubular acidosis): The hallmark of type 2 RTA is impairment in proximal tubular HCO3- reabsorption leading to excessive urinary excretion of bicarbonate. Patients have urinary pH<5.5 when there is low body bicarbonate. There is normokalemia or mild hypokalemia. The most common causes are heavy metal poisoning, Wilson’s disease, multiple myeloma, amyloidosis, cystinosis etc. The diagnosis of type 2 RTA should be suspected in patients who have a normal-AG metabolic acidosis with a serum HCO3- usually around 15 mEq/L and acid urine (pH <5.0). It is associated with osteomalacia.

RTA type 4 (Hyperkalemic RTA): This is the most common form of RTA in adults and results from aldosterone resistance or deficiency. Almost everyone with type 4 RTA manifest varying degrees of hyperkalemia, which commonly is asymptomatic. Some common causes of type 4 RTA are diabetes mellitus, conditions causing aldosterone resistance or deficiency, cyclosporine etc. Type 4 RTA should be suspected in any patient with a mild non-AG metabolic acidosis and hyperkalemia.

Educational Objective:
Type 1 RTA should be suspected in any patient with non-AG metabolic acidosis, urine pH greater than 5.5 and low serum potassium.

Front 41

A 44-year-old obese female undergoes an open cholecystectomy. Post operatively on day 4, her vitals are: Temperature: 36.7C(98.2F); RR: 10/min; BP: 110/80 mm Hg, PR: 92/min. Her arterial blood gases are:

Blood pH: 7.28
PaO2: 62 mmHg
PaCO2: 54 mmHg
HCO3-: 30 mEq/L

What is the most likely cause of acidosis in this patient?


A. Alveolar hypoventilation
B. Acute pulmonary embolism
C. Atelectasis
D. Pulmonary edema
E. Pleural effusion

Back 41

This patient has a blood pH suggestive of acidosis and her PaCO2=54 mmHg is suggestive of respiratory acidosis. However, her PaO2 =62 mmHg is also lower than normal. A low PaO2 and high PaCO2 are highly suggestive of alveolar hypoventilation (Choice A). PaCO2 is a better indicator of alveolar ventilation than PaO2. Some common causes of respiratory acidosis are:

1. Pulmonary diseases like emphysema, pneumoconiosis, barotrauma, bronchitis etc. COPD is very commonly associated with chronic respiratory acidosis. Obstructive airway lesions like asthma can also cause respiratory acidosis.
2. Neuromuscular diseases: Any condition causing weakness or paralysis of respiratory muscles e.g. Myasthenia gravis, poliomyelitis, muscular dystrophies or kyphoscoliosis.
3. Drug induced hypoventilation. E.g. anesthetics, morphine, sedatives.
4. Primary CNS dysfunction like a brain stem lesion, infections, stroke.

Acute pulmonary embolism (Choice B), atelectasis (Choice C), pulmonary edema (Choice D) and pleural effusion (Choice E) can cause a decrease in PaO2, but they all will also cause decrease in PaCO2 due to tachypnea.

Educational Objective:
Patients with respiratory acidosis have decreased pH and increased PaCO2. Alveolar hypoventilation is an important cause of respiratory acidosis.

Front 42

A 52-year-old male patient has been diagnosed with diabetic nephropathy 6 years ago. He is in moderately severe renal failure and is taking ACE inhibitors for this. During a routine follow-up, his laboratory panel shows:

Blood pH:


7.29

HCO3-:


15 mEq/L

Na+:


135 mEq/L

K+:


6.0 mEq/L

Cl-:


110 mEq/L

BUN:


40 mg/dL

S. Creatinine:


2.2 mg/dL

Which of the following is the principal cause of acidosis in this patient?


A. Loss of HCO3- in urine.
B. Increase in aldosterone
C. Impaired excretion of tritrable acids
D. Decrease filtration of hydrogen ions
E. Impaired ammonium excretion

Back 42

This patient has an acidic pH with decreased serum bicarbonate and normal AG (10) suggestive of a non-AG metabolic acidosis. This, the fact that he is diabetic and the hyperkalemia are suggestive of RTA type 4.

In normal individuals the kidney helps in maintaining the normal acid base status thru the following mechanisms:
1.Reabsorption of filtered HCO3-
Excretion of fixed acid by the following two mechanisms:
2.Excretion of titratable acid (H2PO4-)
3.Excretion of H+ as NH4+
In adults, the metabolism of dietary protein generates approximately 1 meq/kg per day of H+. This H+ is excreted primarily by renal mechanisms to maintain neutral acid-base balance. Although, in a majority of patients with chronic renal disease the urine can be acidified normally, these patients have a reduced ability to produce ammonium ion (NH4+) (Choice E). This is partially due to limited ATP utilization, resulting from diminished Na+ reabsorption in the proximal tubule. As a result, the use of glutamine as an energy source is limited, which in turn limits proximal tubular ammonia production.

Loss of bicarbonate (Choice A) and impaired excretion of titratable acids (Choice C) do occur with ESRD but these are not the principal mechanisms for metabolic acidosis in chronic renal disease.

Increase in aldosterone (Choice A) would cause alkalosis and not acidosis.

Educational Objective:
Impaired ammonia excretion is the principal mechanism of metabolic acidosis in chronic renal disease.

Front 43

A 40-year-old African American male comes to your clinic with a 3x3cm lipoma on the back of his neck. You discuss the options with the patient and decide to excise the mass. You ordered serum electrolytes and serum glucose. His serum calcium level is 12.5 meq/L. You suspect primary hyperparathyroidism and find that his PTH level is increased. 99m TC sestambi scan is done and solitary adenoma is located in the inferior parathyroid gland. What is the most appropriate next step?


A. Neck exploration for parathyroidectomy
B. No treatment since he is asymptomatic
C. Calcitonin
D. Oral phosphate

Back 43

Parathyroidectomy is the only effective treatment for primary hyperparathyroidism. The progressive loss of bone mass and increased risk of fracture are the main concerns, but the likelihood of these outcomes appear to be low. Many people who are asymptomatic have a benign course, but currently it is impossible to predict which patient will develop complications.
The indications for surgery include:
1)Symptoms due to hypercalcemia
2)Nephrolithiasis
3)Reduced bone mass (More than 2 standard deviation below mean for the age)
4)Serum calcium in excess of 12 mg/dl
5)Younger than 50 year of age
6)Not eligible for long-term follow-up.
Surgery is a reasonable choice in healthy persons even if they do not meet these criteria because it has a high success rate with low morbidity and mortality.

Educational Objective:
Parathyroidectomy is the only effective treatment for primary hyperparathyroidism.

Front 44

A 70-year-old man is admitted to the hospital with a hip fracture. He was previously diagnosed with multiple myeloma. He is being treated with melphalan and prednisone. He complains of anorexia, nausea, vomiting, and constipation. He is slightly stuporous. ECG shows shortened QT interval. His serum calcium level is 13.5 meq/dl. His BUN is 50 mg/dl and serum creatinine is 2.0 mg/dl. What is the most appropriate next step in management?


A. Hydrochlorothiazide
B. 0.9 % saline
C. Pamidronate
D. Calcitonin
E. IV furosemide

Back 44

Extra cellular fluid (ECF) volume restoration with 0.9 % saline constitutes initial therapy in severely hypercalcemic patients who usually are dehydrated. The goal of the therapy is restoration of the normal GFR. Saline diuresis with 0.9 % saline infusion promotes calcium excretion after ECF volume is restored. Therapy should be monitored carefully with frequent evaluation for heart failure.

Furosemide is used if there is clinical evidence of heart failure. It could worsen the condition if given before the correction of ECF volume. Most of the patients can be managed with IV fluids alone. Patient should be adequately hydrated before giving diuretics other wise his prerenal azotemia will worsen.

Pamidronate inhibits bone resorption. IV pamidronate is given monthly to reduce fracture in patients with significant bone disease. This patient may benefit from IV pamidronate after his acute hypercalcemia is corrected. Bisphosphonates are safe and effective in more than 95 % of the patients with hypercalcemia due to malignancy. Also, in this patient who is bed ridden, it is safe to give IV pamidronate rather than any other bisphosphonates which usually require the patient to sit up right after the dose to reduce reflux esophagitis.

Thiazides can actually cause hypercalcemia and worsen the situation.

Educational Objective:
Know the importance of fluid replacement in the treatment of acute hypercalcemia. Loop diuretics are indicated only after adequate rehydration.

Front 45

A 36-year-old diabetic female comes to you with chest pain, fever and cough with purulent expectoration. A chest x-ray shows a right lobar pneumonia. She is started on empirical antibiotics until the sputum culture reports become available. While on treatment, she develops severe nausea, vomiting and abdominal pain. On examination, she has PR: 96/min, RR: 24/min. Her blood glucose is 350 mg/dl and her urine is positive for ketones. Her laboratory report shows

Blood pH: 7.53
PaO2: 90 mm Hg
PaCO2: 30 mm Hg
HCO3-: 24 meq/L

Na+: 138 meq/L
K+: 3.3 meq/L
Cl-: 85 meq/L
BUN: 18 mg/dl
Creatinine: 1 mg/dl

The acid base status of this patient can be best described as:


A. Normal acid base profile.
B. Mixed metabolic acidosis and alkalosis.
C. Triple disorder with metabolic acidosis, metabolic alkalosis, and respiratory alkalosis.
D. Mixed metabolic acidosis and respiratory alkalosis.
E. Primary metabolic acidosis.

Back 45

This patient is having an alkaline pH with low PaCO2 suggestive of respiratory alkalosis. She also has an AG of [138-(85+24)] = 31, suggestive of primary AG metabolic acidosis. In patients with only AG acidosis the change in anion gap should be equal to the change in bicarbonate. However, she is having a normal bicarbonate concentration, which is suggestive of a coexistent metabolic alkalosis.

The patient is suffering from lobar pneumonia and has tachypnea thus she is likely to have a primary respiratory alkalosis. In addition, she develops severe nausea and vomiting predisposing her to metabolic alkalosis. Due to severe infection and stress, she even develops diabetic ketoacidosis predisposing her to metabolic acidosis. Thus, she is likely to have a triple disorder, which is primary metabolic acidosis, primary metabolic alkalosis and primary respiratory alkalosis.

Educational Objective:
Mixed acid-base disorders are very complex independently coexisting disorders and not merely compensatory responses. They are sometimes seen in patients in critical care units and can lead to dangerous extremes of pH.

Front 46

An 87-year-old Caucasian female with multiinfarct dementia, who lives at local nursing home, is brought to the ER for evaluation of altered mental status. They deny any history of new symptoms. She has multiple medical problems including HTN, stroke, CAD, severe degenerative joint disease, chronic atrial fibrillation, constipation and urinary incontinence. Her medications include aspirin, acetaminophen, atenolol, nitroglycerine, multivitamins, pravastatin, docusate, senna, digoxin, and glucosamine. Her vital signs are: BP 110/70 mmHg, PR 98/min, RR 16/min, and temperature 36.1C(97F). On examination, she has dry mucus membranes and skin turgor is decreased. There are no new focal neurologic deficits. Which of the following is most likely to be present in this patient?


A. Hyponatremia
B. Hypokalemia
C. Hypernatremia
D. Hyperkalemia
E. Anion gap acidosis

Back 46

Eighty to ninety percent of all the sodium in the body is extracellular and total Na content of body is a reflection of ECF volume. Normally, physiological regulatory responses ensure that Na+ loss balances Na+ gain. However, in the absence of this regulation, state of Na excess or deficit is seen, which manifests as edematous or hypovolemic states, respectively.

Plasma concentration greater than 145 meq/L is termed as hypernatremia. Hypernatremia is a state of hyperosmolality as sodium and its accompanying anions are the major effective ECF osmoles.

The underlying pathophysiology of hypernatremia includes primary Na gain or water deficit. Physiological response to hypernatremia includes stimulation of the thirst center and increased secretion of AVP.

The degree of hyperosmolality associated with hypernatremia is particularly severe in cases of impaired thirst mechanism or when access to water is denied. The latter is the case in this vignette and is usually seen in infants, the physically handicapped, patients with impaired mental status, in the postoperative state and in intubated patients in the Intensive Care Unit.

The major causes of altered mental status in an elderly patient include electrolyte disturbances (hypernatremia, hyponatremia), stroke, cardiac events and infection. The elderly are at increased risk of dehydration due to an impaired thirst mechanism.

The above patient clearly has signs of dehydration which is a very common finding in nursing home patients. So, her altered mental status is most likely from hypernatremia resulting from dehydration.

(Choice A) Hyponatremia resulting from SIADH is usually found in patients with stroke; they are usually euvolemic rather than hypovolemic. The other common cause of hyponatremia in elderly patients is the use of diuretics, particularly hydrochlorothiazide.

(Choice D) Hyperkalemia itself does not cause mental status changes. It is often associated with renal failure and uremic encephalopathy.

Other electrolyte abnormalities that can produce altered mental status (encephalopathy) include hypo- or hypercalcemia, hypomagnesemia and hypophosphatemia. Hypoglycemia is another important cause of alerted mental status.

Educational Objective:
Recognize the common causes of alerted mental status in elderly patients. The major causes include:

Hyponatremia and hypernatremia.
Hypocalcemia and hypercalcemia.
Hypomagnesemia.
Hypophosphatemia.
Hypoglycemia.
Stroke.
Cardiac events.
Infections (chest-x ray and urinalysis is routine).

*Since altered mental status is one of the common causes of hospitalization in the United States, USMLE expects you to know everything possible.