Potassium Flashcards
What is the normal serum potassium range?
3.5–5.0 mEq/L.
What is the definition of hypokalemia?
Serum potassium <3.5 mEq/L.
What are the main categories of hypokalemia causes?
- Extrarenal losses (GI losses), 2. Renal losses, 3. Redistribution, 4. Inadequate intake.
What are the extrarenal causes of hypokalemia?
- Diarrhea
- Vomiting
- Loop diuretics
- Laxative abuse
What is the expected urine potassium level in extrarenal hypokalemia?
Urine K+ <20 mEq/L (kidneys retain potassium to compensate for GI losses).
What are the renal causes of hypokalemia?
Diuretics, diabetic ketoacidosis (DKA), hyperaldosteronism, renal tubular acidosis (RTA types 1 and 2).
What is the expected urine potassium level in renal hypokalemia?
Urine K+ >20 mEq/L (kidneys excessively excrete potassium).
What is the pathophysiology of renal tubular acidosis type 1 (distal RTA)?
Impaired H+ secretion in the distal tubule, leading to metabolic acidosis and hypokalemia.
What are the causes of distal RTA (type 1)?
Autoimmune diseases (Sjogren’s, RA), amphotericin B toxicity, congenital anomalies.
What is the pathophysiology of renal tubular acidosis type 2 (proximal RTA)?
Defective bicarbonate reabsorption in the proximal tubule, causing metabolic acidosis and hypokalemia.
What are the causes of proximal RTA (type 2)?
Fanconi syndrome, multiple myeloma, Wilson’s disease, aminoglycosides.
What is Bartter syndrome?
An autosomal recessive defect in the Na+/K+/2Cl- transporter in the thick ascending loop, mimicking a loop diuretic effect.
What are the clinical features of Bartter syndrome?
Hypokalemia, metabolic alkalosis, normal to low blood pressure, hypercalciuria.
What is Gitelman syndrome?
An autosomal recessive defect in the Na+/Cl- cotransporter in the distal tubule, mimicking a thiazide diuretic effect.
What are the clinical features of Gitelman syndrome?
Hypokalemia, metabolic alkalosis, hypomagnesemia, hypocalciuria.
What conditions cause redistribution hypokalemia?
Insulin excess, beta-adrenergic activation (e.g., epinephrine), metabolic/respiratory alkalosis.
What are the main symptoms of hypokalemia?
- Muscle weakness
- Ileus (stasis of bowels)
- Cramps
- Fatigue
- Constipation
- Arrhythmias
What are the ECG findings in hypokalemia?
Flattened T waves, U waves, prolonged PR interval, possible arrhythmias (PACs, PVCs, AV block).
What is the treatment approach for mild hypokalemia (K+ >3.0 mEq/L)?
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.
What is the treatment for severe hypokalemia (K+ <3.0 mEq/L or symptomatic)?
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.
Why should magnesium be corrected before potassium in hypokalemia?
Hypomagnesemia promotes potassium wasting via ROMK channels in the distal tubule.
What potassium-sparing diuretics can be used in chronic hypokalemia?
Spironolactone, eplerenone, amiloride, triamterene.
What is the definition of hyperkalemia?
Serum potassium >5.0 mEq/L.
Upton initial assessment of hyperkalemia, what is the most important method for monitoring the patient?
After applying ABCDE, ensure the patient is on telemetry.
What are the main causes of increased potassium load in patients?
- 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)
How does kidney disease contribute to hyperkalemia?
Reduced potassium excretion due to decreased glomerular filtration and aldosterone dysfunction.
What drugs can cause hyperkalemia?
- ACE inhibitors
- ARBs
- potassium-sparing diuretics
- Calcineurin Inhibitors (Cyclosporine, tacrolimus)
- NSAIDs
- Heparin
- Beta-blockers
- Digoxin
- Succinylcholine
- Trimethoprim
- Pentamidine
What metabolic states leads to increased potassium?
Non-Anion Gap Metabolic Acidosis
Which two conditions involving cellular destruction lead to hyperkalemia?
- Tumor Lysis Syndrome
- Rhabdomyolysis
What rare genetic disorder that causes hyperkalemia (possible paralysis) following exercise?
HYPERKALEMIC PERIODIC PARALYSIS
What is the workup for hyperkalemia when the patient is stable?
- Focused history and physical exam
- CMP
- ABG or VBG
- 12 lead ECG
How is hyperkalemia due to hypovolemia or congestive heart failure worked up?
Analysis of urine electrolytes
At what GFR would hyperkalemia be seen secondary to acute or chronic kidney disease?
- Less than 20.
- Urinary sodium will be increased (greater than 25 mM)
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.
Measure Aldosterone
When should hyporeninemic hypoaldosteronism be suspected for the cause of increased serum potassium?
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.
Which medications cause a decrease in aldosterone, but increase renin as a compensatory mechanism, still maintaining elevated potassium levels?
- Ace inhibitors
- ARBs
What are the neurological symptoms associated with hyperkalemia?
- Muscle weakness
- Paresthesias
- Flaccid paralysis
What are the symptoms of severe hyperkalemia (>7.0 mEq/L)?
- Muscle weakness
- Flaccid paralysis
- Life-threatening arrhythmias
What specific ECG findings are associated with hyperkalemia?
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)
What is a common cause for a falsely elevated potassium level?
Blood lysis.
** Warrants a repeat blood draw**
Does blood transfusion lead to a false or true elevation of serum potassium?
True.
** Warrants a repeat blood draw**
What is the first-line treatment for life-threatening hyperkalemia (>6.5 mEq/L or ECG changes)?
IV calcium gluconate to stabilize cardiac membranes.
What are the key treatments to shift potassium intracellularly in hyperkalemia?
- IV insulin + D5W (glucose)
- beta-agonists (albuterol)
- sodium bicarbonate (if acidosis present)
What is the role of sodium bicarbonate in hyperkalemia treatment?
- 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.
What are the treatments to remove potassium from the body in hyperkalemia following first-line medications?
- Sodium polystyrene sulfonate (Kayexalate)
- Patiromer
- Loop diuretics with IVFs (if kidney function is adequate)
- Hemodialysis (for renal failure)
When is hemodialysis required for hyperkalemia?
Severe hyperkalemia with renal failure or refractory to other treatments.
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?
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.
