Potassium

Question 1

What is the normal serum potassium range?

Answer 1

3.5–5.0 mEq/L.

Question 2

What is the definition of hypokalemia?

Answer 2

Serum potassium <3.5 mEq/L.

Question 3

What are the main categories of hypokalemia causes?

Answer 3

1. Extrarenal losses (GI losses), 2. Renal losses, 3. Redistribution, 4. Inadequate intake.

Question 4

What are the extrarenal causes of hypokalemia?

Answer 4

• Diarrhea
• Vomiting
• Loop diuretics
• Laxative abuse

Question 5

What is the expected urine potassium level in extrarenal hypokalemia?

Answer 5

Urine K+ <20 mEq/L (kidneys retain potassium to compensate for GI losses).

Question 6

What are the renal causes of hypokalemia?

Answer 6

Diuretics, diabetic ketoacidosis (DKA), hyperaldosteronism, renal tubular acidosis (RTA types 1 and 2).

Question 7

What is the expected urine potassium level in renal hypokalemia?

Answer 7

Urine K+ >20 mEq/L (kidneys excessively excrete potassium).

Question 8

What is the pathophysiology of renal tubular acidosis type 1 (distal RTA)?

Answer 8

Impaired H+ secretion in the distal tubule, leading to metabolic acidosis and hypokalemia.

Question 9

What are the causes of distal RTA (type 1)?

Answer 9

Autoimmune diseases (Sjogren’s, RA), amphotericin B toxicity, congenital anomalies.

Question 10

What is the pathophysiology of renal tubular acidosis type 2 (proximal RTA)?

Answer 10

Defective bicarbonate reabsorption in the proximal tubule, causing metabolic acidosis and hypokalemia.

Question 11

What are the causes of proximal RTA (type 2)?

Answer 11

Fanconi syndrome, multiple myeloma, Wilson’s disease, aminoglycosides.

Question 12

What is Bartter syndrome?

Answer 12

An autosomal recessive defect in the Na+/K+/2Cl- transporter in the thick ascending loop, mimicking a loop diuretic effect.

Question 13

What are the clinical features of Bartter syndrome?

Answer 13

Hypokalemia, metabolic alkalosis, normal to low blood pressure, hypercalciuria.

Question 14

What is Gitelman syndrome?

Answer 14

An autosomal recessive defect in the Na+/Cl- cotransporter in the distal tubule, mimicking a thiazide diuretic effect.

Question 15

What are the clinical features of Gitelman syndrome?

Answer 15

Hypokalemia, metabolic alkalosis, hypomagnesemia, hypocalciuria.

Question 16

What conditions cause redistribution hypokalemia?

Answer 16

Insulin excess, beta-adrenergic activation (e.g., epinephrine), metabolic/respiratory alkalosis.

Question 17

What are the main symptoms of hypokalemia?

Answer 17

• Muscle weakness
• Ileus (stasis of bowels)
• Cramps
• Fatigue
• Constipation
• Arrhythmias

Question 18

What are the ECG findings in hypokalemia?

Answer 18

Flattened T waves, U waves, prolonged PR interval, possible arrhythmias (PACs, PVCs, AV block).

Question 19

What is the treatment approach for mild hypokalemia (K+ >3.0 mEq/L)?

Answer 19

Oral potassium replacement.

Oral potassium replacement is recommended in patients able to tolerate oral intake. Parenteral potassium replacement is necessary in those unable to tolerate oral intake, those with a dysfunctional bowel and also in patients with cardiac or neurologic complications of hypokalemia.

Question 20

What is the treatment for severe hypokalemia (K+ <3.0 mEq/L or symptomatic)?

Answer 20

IV potassium replacement.

Oral potassium replacement is recommended in patients able to tolerate oral intake. Parenteral potassium replacement is necessary in those unable to tolerate oral intake, those with a dysfunctional bowel and also in patients with cardiac or neurologic complications of hypokalemia.

Question 21

Why should magnesium be corrected before potassium in hypokalemia?

Answer 21

Hypomagnesemia promotes potassium wasting via ROMK channels in the distal tubule.

Question 22

What potassium-sparing diuretics can be used in chronic hypokalemia?

Answer 22

Spironolactone, eplerenone, amiloride, triamterene.

Question 23

What is the definition of hyperkalemia?

Answer 23

Serum potassium >5.0 mEq/L.

Question 24

Upton initial assessment of hyperkalemia, what is the most important method for monitoring the patient?

Answer 24

After applying ABCDE, ensure the patient is on telemetry.

Question 25

What are the main causes of increased potassium load in patients?

Answer 25

- Increased intake - Cellular shifts - Decreased effective blood volume (redistribution) - Acute or Chronic kidney disease - Aldosterone resistance - Hyporeninemic Hypoaldosteronism - Adrenal insufficiency - Tissue breakdown (rhabdomyolysis, tumor lysis)

Question 26

How does kidney disease contribute to hyperkalemia?

Answer 26

Reduced potassium excretion due to decreased glomerular filtration and aldosterone dysfunction.

Question 27

What drugs can cause hyperkalemia?

Answer 27

- ACE inhibitors - ARBs - potassium-sparing diuretics - Calcineurin Inhibitors (Cyclosporine, tacrolimus) - NSAIDs - Heparin - Beta-blockers - Digoxin - Succinylcholine - Trimethoprim - Pentamidine

Question 28

What metabolic states leads to increased potassium?

Answer 28

Non-Anion Gap Metabolic Acidosis

Question 29

Which two conditions involving cellular destruction lead to hyperkalemia?

Answer 29

- Tumor Lysis Syndrome - Rhabdomyolysis

Question 30

What rare genetic disorder that causes hyperkalemia (possible paralysis) following exercise?

Answer 30

**HYPERKALEMIC PERIODIC PARALYSIS**

Question 31

What is the workup for hyperkalemia when the patient is stable?

Answer 31

- Focused history and physical exam - CMP - ABG or VBG - 12 lead ECG

Question 32

How is hyperkalemia due to hypovolemia or congestive heart failure worked up?

Answer 32

Analysis of urine electrolytes

Question 33

At what GFR would hyperkalemia be seen secondary to acute or chronic kidney disease?

Answer 33

- Less than 20. - Urinary sodium will be **increased** (greater than 25 mM)

Question 34

In cases of hyperkalemia, when urine sodium is increased (meaning above 25 mM, pathologic), but the GFR is adequate (above 20), what would be the first approach to determining the underlying cause for hyperkalemia.

Answer 34

Measure **Aldosterone**

Question 35

When should hyporeninemic hypoaldosteronism be suspected for the cause of increased serum potassium?

Answer 35

Hyporeninemic Hypoaldosteronism leads to hyperkalemia due to impaired renin and aldosterone secretion, which reduces potassium excretion by the kidneys. It is commonly seen in diabetes and CKD and presents with hyperkalemia and a mild metabolic acidosis, however the GFR is usually greater than 20.

Question 36

Which medications cause a decrease in aldosterone, but increase renin as a compensatory mechanism, still maintaining elevated potassium levels?

Answer 36

- Ace inhibitors - ARBs

Question 37

What are the neurological symptoms associated with hyperkalemia?

Answer 37

- Muscle weakness - Paresthesias - Flaccid paralysis

Question 38

What are the symptoms of severe hyperkalemia (>7.0 mEq/L)?

Answer 38

- Muscle weakness - Flaccid paralysis - Life-threatening arrhythmias

Question 39

What specific ECG findings are associated with hyperkalemia?

Answer 39

Progressively: - Peaked T waves (**earliest**) - Flattened p-waves - Prolonged PR interval - Absent p-waves, Widened QRS, and Sine wave pattern in severe cases (**latest change**)

Question 40

What is a common cause for a falsely elevated potassium level?

Answer 40

Blood lysis. ** Warrants a repeat blood draw**

Question 41

Does blood transfusion lead to a false or true elevation of serum potassium?

Answer 41

True. ** Warrants a repeat blood draw**

Question 42

What is the first-line treatment for life-threatening hyperkalemia (>6.5 mEq/L or ECG changes)?

Answer 42

IV calcium gluconate to stabilize cardiac membranes.

Question 43

What are the key treatments to shift potassium intracellularly in hyperkalemia?

Answer 43

- IV insulin + D5W (glucose) - beta-agonists (albuterol) - sodium bicarbonate (if acidosis present)

Question 44

What is the role of sodium bicarbonate in hyperkalemia treatment?

Answer 44

- Used in metabolic acidosis to shift potassium intracellularly. - This is a second-line medication that is used as a temporizing treatment following IV Calcium gluconate.

Question 45

What are the treatments to remove potassium from the body in hyperkalemia following first-line medications?

Answer 45

- Sodium polystyrene sulfonate (Kayexalate) - Patiromer - Loop diuretics with IVFs (if kidney function is adequate) - Hemodialysis (for renal failure)

Question 46

When is hemodialysis required for hyperkalemia?

Answer 46

Severe hyperkalemia with renal failure or refractory to other treatments.

Question 47

A 55-year-old man with a past medical history of essential hypertension for 10 years presents to the clinic for follow-up. The patient's blood pressure has been consistently elevated despite being on a thiazide diuretic, a calcium channel blocker, and an angiotensin-converting enzyme inhibitor. He reports medication compliance and adherence to a low sodium diet. He does not use tobacco, alcohol, or other recreational drugs. BMI is 23 kg/m?. Temperature is 36.7°C (98.1°F), blood pressure is 156/96 mmHg, heart rate is 85/min, respiratory rate is 16/min, and oxygen saturation is 98% on room air. Physical examination reveals a well-nourished male in no distress. Cardiovascular examination is normal without evidence of heart failure. No abdominal bruits are heard. Laboratory results are shown below. What particular lab findings is most likely to be seen on this patient's evaluation?

Answer 47

Primary hyperaldosteronism, which presents with resistant hypertension, hypokalemia, and metabolic alkalosis, is a common cause of secondary hypertension. This patient presents with resistant hypertension despite taking three antihypertensive medications and implementing lifestyle modifications. In addition, he has evidence of hypokalemia and metabolic alkalosis on laboratory evaluation. This clinical presentation is suggestive of primary hyperaldosteronism, which is a common cause of secondary hypertension. It can be diagnosed with a plasma aldosterone concentration to plasma renin activity ratio >20 and a PAC >15 ng/dL. Primary hyperaldosteronism, also known as Conn syndrome, is characterized by overproduction of aldosterone from the adrenal glands. Overproduction can be due to an adrenal adenoma (aldosterone-producing adenoma [APA]) or bilateral adrenal hyperplasia. This results in hypertension, hypokalemia, and metabolic alkalosis. The most appropriate screening test for primary hyperaldosteronism is the plasma aldosterone concentration (PAC) to plasma renin activity (PRA) ratio. A PAC:PRA ratio > 20 along with a PAC > 15 ng/dL is suggestive of primary hyperaldosteronism. If the ratios are sufficiently elevated, then confirmatory testing should be done with an adrenal CT scan to distinguish between an aldosterone-producing adrenal adenoma and bilateral adrenal hyperplasia.