Internal Medicine: UWorld Surg Shelf

Question 1

Metabolic alkalosis can be classified into what two broad categories?

Answer 1

1. Chloride-sensitive (hypochloremic, saline-responsive) metabolic alkalosis
2. Chloride-resistant (normochloremic, saline-unresponsive) metabolic alkalosis

Chloride-sensitive metabolic alkalosis is characterized by a urinary chloride level <20 mEq/day and signs of volume depletion. The common underlying pathophysiology in all causes of chloride-sensitive metabolic alkalosis involves ECF volume contraction. Volume contraction, causes increased mineralcorticoid action, which in turn causes bicarbonate retention, H+ loss, and K+ loss. The urinary chloride remains low due to avid renal retention of NaCl and water.

Question 2

What are some causes of chloride-sensitive metabolic alkalosis?

Answer 2

Thiazide or loop diuretics and loss of gastric secretions (surreptitious vomiting)

This condition is characterized by urinary chloride level <20 mEq/day and signs of volume depletion, and can be corrected with saline infusion to restore ECF volume.

Question 3

What are some causes of chloride-resistant metabolic alkalosis?

Answer 3

Primary hyperaldosteronism, Bartter syndrome, Gitelman’s syndrome, and excessive black licorice ingestion.

This is characterized by a urinary chloride level >20 mEq/day and ECF volume expansion and it is not corrected by saline infusion.

Question 4

Persistent diarrhea causes what acid-base disturbance?

Answer 4

Non-anion gap metabolic acidosis

Question 5

All forms of renal tubular acidosis cause what kind of acid-base disturbance?

Answer 5

Non-anion gap metabolic acidosis

Question 6

Aspirin toxicity causes what kind of acid-base disturbance?

Answer 6

Mixed respiratory alkalosis and metabolic acidosis

Aspirin directly stimulates the medullary respiratory center to cause tachypnea and respiratory alkalosis. Metabolic acidosis is due to increased production and decreased renal elimination of organic acids (e.g. lactic acid and ketoacids).

Question 7

An allergic reaction with stridor indicates what?

Answer 7

Laryngeal edema

This would impair ventilation and cause CO2 retention with resultatnt respiratory acidosis

Question 8

Asthma exacerbation usually leads to what acid-base disturbance?

Answer 8

Acute respiratory alkalosis

This is due to tachypnea. Most patients have a slightly decreased serum HCO_3-

Question 9

Persistent vomiting causes what acid-base disturbance?

Answer 9

Hypochloremic metabolic alkalosis

It causes volume contraction with H+ loss in gastric contents.

Question 10

Excessive diuresis causes what kind of acid-base disturbance?

Answer 10

Metabolic alkalosis

It causes volume contraction with an increased serum HCO_3-

Question 11

What is the appropriate solution for volume resuscitiation of a patient with contraction alkalosis (As with persistent vomiting)?

Answer 11

Normal saline with potassium supplementation

The pathogenesis of metabolic alkalosis resulting from vomiting can be separated into two phases: a generation phase and a maintenance phase. Initially, vomiting results in the loss of gastric fluids containing HCI, NaCl and water. The loss of H+ as HCl results in the unbalanced retention of HCO3-. Because of the loss of gastric acidity, there is no stimulus for HCO3- release by the pancreas. The HCO3- is instead retained in the blood leading to a metabolic alkalosis. This is the generation phase. Next, as a result of volume loss in the vomitus, the ECV volume is decreased leading to decreased renal perfusion pressure. This causes the kidneys to increase renin production, ultimately increasing aldosterone. Aldosterone acts to retain water at the expense of H+ and K+ in the urine. The action of aldosterone, which causes hypokalemia and a contraction alkalosis, accounts for the maintencance phase of metabolic alkalosis resulting from vomiting.

Question 12

What intravenous solution is given in severe forms of hypochloremic metabolic alkalosis to lower the pH of the ECF and urine?

Answer 12

Ammonium chloride

This intervention would worsen a patient’s volume contraction if used as a monotherapy and carries greater risk than normal saline due to its potential toxicity in liver failure.

Question 13

What is a rarely used emergency therapy to treat severe forms of metabolic alkalosis due to its risk of hemolysis and the availability of better invasive interventions?

Answer 13

Hydrogen chloride (HCl)

Question 14

What is Winter’s formula when used to assess respiratory compensation in primary metabolic acidosis?

Answer 14

PaCO2 = (1.5 x bicarbonates) + 8 + 2

Question 15

What is Winter’s formula when used to assess respiratory compensation in primary metabolic alkalosis?

Answer 15

PaCO2 = (0.9 x bicarbonates) + 16 + 2

Question 16

Pregnancy causes what acid-base disturbance?

Answer 16

Primary respiratory alkalosis with metabolic compensation

Hypocapnia is a normal phenomenon of late pregnancy caused by a direct stimulatory effect of progesterone on the central respiratory center, leading to increased respiratory drive and exaggerated respiratory effort.

Question 17

What should be suspected in a diabetic patient with a non-anion gap metabolic acidosis, persistent hyperkalemia, and renal insufficiency?

Answer 17

Type 4 renal tubular acidosis

Renal insufficiency accompanied by hyperkalemia and a non-anion gap metabolic acidosis is consistent with type 4 renal tubular acidosis. Type 4 RTA is caused by aldosterone deficiency or renal tubular insensitivity to aldosterone. The lack of aldosterone effect in these patients leads to a failure to secrete acid as NH4+ and retention of potassium. Type 4 RTA may occur in the setting of diabetic nephropathy due to type I or II DM, and the condition can be worsened by drugs that inhibit the renin-angiotensin-aldosterone system such as ACE-Inhibitors and Angiotensin receptor blockers (ARBs).

Question 18

Chronic renal failure is a common cause of what acid-base disturbance?

Answer 18

Hypochloremic anion gap metabolic acidosis

This is due to the failure to excrete acid as NH4+ and accumulation of organic anions

Question 19

1. What is a normal anion gap?
2. How is it calculated?

Answer 19

1. 6-12 mEq/L
2. Anion gap = Na⁺ - (HCO₃^- + Cl^-)

The anion gap represents the concentration of unmeasured serum anions. In anion gap metabolic acidosis, the anion gap is increased by the abnormal presence of non-chlorinated acids in the serum.

Question 20

What are the most common causes of anionic gap metabolic acidosis [and their corresponding unmeasured anions that compose the anion gap]?

Answer 20

1. Lactic acidosis [lactate]
2. Ketoacidosis [beta-hydroxy butyrate, acetoacetic acid]
3. Methanol/formaldehyde ingestion [formic acid]
4. Ethylene glycol ingestion [glycolic acid, oxalic acid]
5. Slicylate poisoning [salicylic, lactic, sulfuric, and phosphoric acids]
6. Uremia (ESRD) [Impaired excretion of H+]

Question 21

What is the most common cause of hypernatremia?

Answer 21

Hypovolemia

Mild cases can be treated with 5% dextrose in 0.45% saline. Severe cases should be initially treated with 0.9% saline.

Question 22

What is the initial treatment of choice for treating mild hypovolemic hypernatremia?

Answer 22

5% dextrose in 0.45% saline

Question 23

What is the intial treatment of choice for severe cases of hypovolemic hypernatremia?

Answer 23

0. 9% saline
   * It acts to gradually correct the hyperosmolality while normalizing the patient’s volume status. Isotonic saline is usually hypoosmolar in comparison to the hypernatremic plasma. Once the volume deficit has been restored, such patients are then switched to half-normal (0.45%) saline in order to better replace the free water deficit. The goal rate of plasma sodium correction is no more than 1 mEq/L/h. A greater rate of correction may result in cerebral edema.*

Question 24

What is the treatment of choice for patients with euvolemic and hypervolemic hypernatremia?

Answer 24

5% dextrose in water (D5W)

Question 25

Chronic obstructive pulmonary disease (COPD) causes what acid-base disturbance?

Answer 25

Respiratory acidosis

Due to chronic CO₂ retention

Question 26

Although rare, glucocorticoids can cause what acid-base disturbance?

Answer 26

Metabolic alkalosis (and hypokalemia)

Glucocorticoids can increase the blood urea nitrogen (BUN) level due to the catabolic effect on body proteins but are unlikely to cause elevation of creatinine.

Question 27

What should be suspected in a patient with the triad of fever, tinnitus, and tachypnea?

Answer 27

Aspirin intoxication

Adults with aspirin toxicity develop a mixed respiratory alkalosis and anion gap metabolic acidosis.

Question 28

Mineralcorticoid deficiency has what effect on serum water, sodium, and potassium?

Answer 28

Wasting of sodium and water, but increased serum potassium.

Question 29

Chronic alcoholism has what effect on serum potassium, magnesium, and phosphate?

Answer 29

Decreases all 3

Hypomagnesemia causes refractory hypokalemia, therefore it is important to correct the magnesium along with the potassium levels to be able to correct the electrolyte abnormalities of such patients. Mg is an important cofactor for potassium uptake and maintenance of intracellular potassium levels.

Question 30

What electrolyte disturbance can result in weakness, rhabdomyolysis, paresthesias, and respiratory failure in severe cases?

Answer 30

Hypophosphatemia

Question 31

What agents can be used to shift potassium intracellularly?

Answer 31

1. Insulin and glucose
2. Sodium bicarbonate
3. Beta-2 agonists (Albuterol)

Question 32

What electrolyte disturbance is usually asymptomatic, but can cause muscle weakness, and in severe cases, flaccid paralysis, and life-threatening arrhythmias?

Answer 32

Hyperkalemia

This causes QRS prolongation with peaked T waves.

Question 33

What is the first step in management of a patient with hyperkalemia and EKG changes?

Answer 33

Emergent administration of IV calcium gluconate to stabilize the cardiac membrane

The next step is to lower serum potassium by driving potassium intracellularly. Finally, the excess potassium should be eliminated from the body.

Question 34

What is the earliest symptom of hyperkalemia?

Answer 34

Weakness

Severe hyperkalemia may cause flacced paralysis, respiratory insufficiency and cardiac toxicity, which may precipitate a sine wave on ECG and ventricular fibrillation.

Question 35

What 2 causes of hypoxemia is associated with a normal A-a gradient and respiratory acidosis?

Answer 35

1. Hypoventilation
2. Reduced inspired oxygen tension

Question 36

What antibiotic can cause hyperkalemia due to blockade of the epithelial sodium channel in the collecting tubule, and also competitively inhibits renal tubular creatinine secretion and may cause an artificial increase in serum creatinine without affecting the glomerular filtration rate?

Answer 36

Trimethoprim

Patients treated with high-dose trimethoprim require serial monitoring of potassium to avoid serious complications.

Question 37

What are the 3 steps in therapy for hyperkalemia?

Answer 37

1. Membrane stabilization (with calcium)
2. Shifting potassium intracellularly (with insulin and glucose is quickest)
3. Decreasing the total body potassium content (with diuretics)

Question 38

What is a potassium-binding resin that decreases total body potassium content by catharsis in the gut?

Answer 38

Sodium polystyrene sulfonate (Kayexalate)

Sodium is exchanged for potassium. Sodium polystyrene sulfonate takes at least 1-2 hours to work.

Question 39

What is the most definitive way to remove potassium from the body in patients with renal failure?

Answer 39

Hemodialysis

However, it often takes at least 1 hour to set up in a patient who has dialysis catheter or fistula in place.

Question 40

What is the treatment for acute, symptomatic hyponatremia?

Answer 40

Prompt increase in the serum sodium concentration with 3% or hypertonic saline

This should be done at a rate of no more than 0.5 mEq/L/hr to avoid causing central nervous system osmotic demyelination syndrome. Rapid correction of hyponatremia results in increased water movement out of brain tissue and so would contribute to the formation of hydrocephalus. Hydrocephalus can be either obstructive (noncommunicating) or nonobstructive (communicating), resulting from excess cerebrospinal fluid production or impaired cerebrospinal fluid absorption.

Question 41

What acid-base disturbance is common during pregnancy?

Answer 41

Physiologic chronic compensated respiratory alkalosis

This is due to the stimulatory effect of progesterone on the medullary respiratory center, leading to tachypnea. During pregnancy, serum progesterone concentration is high.

Question 42

What are the most important steps in the management of lactic acidosis from septic shock?

Answer 42

1. Intravenous normal saline + vasopressor therapy to maintain the intravascular pressure
2. Antibiotics to correct the underlying infection

Question 43

What is used to rapidly expand intravascular volume at the expense of extravascular volume?

Answer 43

Hypertonic (3%) saline

This occurs by drawing fluid out of the extravascular compartment into the intravascular compartment.

Question 44

What treatment of lactic acidosis is controversial and only recommended in severe acute acidosis (pH < 7.2)

Answer 44

Intravenous sodium bicarbonate

Question 45

When are vasopressors indicated for the treatment of hypotension in states of shock?

Answer 45

Only after intravenous fluids have failed to restore normotension

Question 46

What is a contraindication of succinylcholine?

Answer 46

Hyperkalemia

Succinylcholine is a depolarizing neuromuscular blocker that can cause life-threatening hyperkalemia. It should not be used in patients with or at high risk for hyperkalemia, such as burn and crush injury patients and patients with prolonged demyelination.

Question 47

What are 3 potential side effects of loop diuretics?

Answer 47

1. Hypokalemia
2. Metabolic alkalosis
3. Prerenal kidney failure

Question 48

Opioids may cause what acid-base disturbance?

Answer 48

Respiratory acidosis

This is because opioid medication may result in hypoventilation.

Question 49

Hypocalcemia with concordant changes of serum calcium and phosphate levels is usually caused by what?

Answer 49

Vitamin D deficiency

Chronic alcoholism can predispose patients to malabsorption of vitamin D due to chronic pancreatitis. Vtamin D malabsorption causes hypocalcemia accompanied with hypophosphatemia, because 1,25-dihydro cholecalciferol (the active form of vitamin D) raises the serum level of both calcium and phosphate. The other cause of concordantly decreased serum calcium and phosphate levels is acute pancreatitis.

Question 50

What lab value can differentiate between saline-resistant and saline-responsive metabolic alkalosis?

Answer 50

Urine chloride

• Saline-resistant metabolic alkalosis has excess mineralcorticoid causing hydrogen and potassium loss and increased sodium retention leading to increased extracellular volume. The kidneys respond by excreting both sodium and chloride to result in high urine chloride.*
• Saline-responsive metabolic alkalosis has low urine chloride (<20mEq/L) due to hypovolemia and hypochloremia.*

Question 51

What must always be determined in patients with metabolic acidosis in order to narrow the differential diagnosis?

Answer 51

Anion gap

The anion gap (AG) represents the unmeasured anions in the body. Normal AG = 6 to 12 mEq/L

Question 52

When is the urine anion gap calculated?

Answer 52

When there is a normal anion gap metabolic acidosis

The urine anion gap helps determine if such acidosis is due to the renal or intestinal bicarbonate losses. Renal losses of bicarbonate occur in renal tubular acidosis or carbonic anhydrase inhibitor use. GI loss of bicarbonate occurs classically in diarrhea.

Question 53

When is a plasma osmolar gap calculated?

Answer 53

In select cases of increased anion gap metabolic acidosis, such as when ethanol, methanol, or ethylene glycol toxicity is suspected.

It is calculated by determining the difference between the measured and calculated serum osmolality.

Question 54

What causes hyponatremia in hypovolemic hyponatremic patients?

Answer 54

High levels of antidiuretic hormone

Volume depletion increases the plasma osmolality and activates antidiuretic hormone release from the pituitary to absorb more water in the collecting ducts of the kidney. Hypovolemia also decreases the effective arterial volume to the kidney, resulting in increased renin and angiotensin levels. This results in increased aldosterone activity, which works on the distal tubules to increase sodium reabsorption (with low urinary sodium excretion), increase potassium excretion causing hypokalemia, and increase hydrogen excretion causing a metabolic alkalosis.

Question 55

What are the classic causes of metabolic acidosis?

Answer 55

“MUDPILES”

1. Methanol
2. Uremia (renal failure)
3. Diabetic ketoacidosis
4. Propylene glycol
5. Isoniazid
6. Lactic acidosis
7. Ethylene glycol
8. Salicylates