N15 - Electrolyte Disorders Flashcards

1
Q

What is hypokalemia?

A
  • definition: serum potassium (K+) is < 3.5mmol/L
  • clinical manifestations: hypertension, arrhythmia, sudden cardiac death, weakness, rhabdomyolysis, alterations in acid-base balance (metabolic alkalosis), paralytic ileus
  • long-term effects: mortality, risks of cardiovascular disease increases, renal cyst formation, renal fibrosis
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2
Q

What is the etiology for hypokalemia?

A

pseudohypokalemia
- artifact in blood sample
- ie. acutre leukemia (leukocytes take up potassium)

redistribution
- K+ shifts from the ECF to the ICF
- aldosterone increases, β2-adrenergic effects, anabolic state, insulin, alkalosis

extrarenal loss
- diarrhea, vomiting (alkalosis), sweating, laxative abuse

renal loss
- medication: thiazide, furosemide, piperacillin-tazobactam, aminoglycosides
- bicarbonaturia
- magnesium deficiency (increased ROMK-mediated K secretion)
- genetic diseases (Bartter syndrome, Gitelman syndrome)
- hormonal diseases (Liddle syndrome, Cushing syndrome, hyperaldosteronism)

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3
Q

What is the treatment for hypokalemia?

A

urgent therapy:
- in case of paralysis, AMI, ventricular ectopy
- max. speed: 5-10 mmol KCl in 20 mins
- monitor ECG
- avoid solution with dextrose (increase in insulin levels can worsen hypokalemia)

lack of severe symptoms:
- per os supplementation

magnesium depletion:
- magnesium supplementation

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4
Q

What is hyperkalemia?

A
  • definition: serum K+ > 5.5mmol/L
  • clinical manifestations: can be asymptomatic, mild or life-threatening; muscle weakness (diaphragmatic muscle-respiratory failure); metabolic acidosis; ECG changes (peaked T-waves, ST-depression, prolonged QRS, ventricular fibrillation etc.)
  • long-term effects: increased risk of mortality
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5
Q

What are ECG changes in hyperkalemia?

A
  • 6-7mmol/L K+: peaked T waves
  • 7-8mmol/L K+: flattened P wave, prolonged PR interval, depressed ST segment, peaked T wave
  • 8-9mmol/L K+: atrial standstill, prolonged QRS duration, further peaking T waves
  • >9mmol/L K+: sinusoid wave pattern
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6
Q

What is the etiology of hyperkalemia?

A

pseudohyperkalemia
- artifact in the blood sample
- ie. hemolysis, difficult phlebotomy

redistribution
- K+ moves from ICF to ECF, or there could be inhibition of ICF uptake of K+
- hyperglycemia, insulin resistance, acidosis, hyperosmolarity (mannitol), medications (digoxin, β2-antagonist)

excess intake (w/ damaged excretion)
- salt substitutes, enteral nutrition products, high-potassium diet

impaired renal excretion
- medication (ACEi, ARB, spironolactone)
- obstructive uropathy, other renal failure
- aldosterone deficiency/resistance, Addison’s disease, pseudohypoaldosteronism

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7
Q

What is the treatment for hyperkalemia?

A

if ECG changes, sever symptoms present:
- 10% Ca-gluconate (10ml/10min); for membrane stabilization and its effect lasts 20-60 mins
- insulin (4-10U/h) + 10% dextrose iv. (monitor serum glucose)
- hemodialysis
- β2 agonist by nebulizer (albuterol)

potassium removal:
- resin 15-60g/day (Na+/Ca+ polystyren-sulfonate, per os or as retention enema)
- diuretics: furosemide, thiazide

treatment of chronic hyperkalemia:
- in CKD, therapeutic goal is >5.5mM but >6.0mM is acceptable too
- review of medication
- dietary restrictions
- intermittent resin/Patiromer treatment
- Fludrocortisone (hypoaldosteronism)

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8
Q

What is hyponatremia?

A
  • definition: serum Na+ <135mmol/L (clinical signs usually begin <125mmol/L)
  • clinical manifestations: headache, yawning, lethargy, nausea, reversible ataxia, psychosis, seizures, cerebral edema, tentorial herniation, respiratory depression
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9
Q

What is the differential diagnosis for hyponatremia?

A

pseudohyponatremia:
- serum Na+ ↓, serum osmolarity is normal
- solid phase of serum increases (ie. hypertriglyceridemia, paraproteinemia)

translocational hyponatremia
- serum Na+ ↓ and serum osm. ↑
- movement of water from ICF to ECF due to osmotically active substances (ie. glucose, mannitol, glycine, maltose)

real/hypotonic hyponatremia:
- serum Na+ ↓ and serum osm. ↓

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10
Q

What is the etiology of hyponatremia?

A

assess volume status, first!!

hypovolemia
- hypovolemia as a result of decreased TBW, and consequently very low total body Na+
- if urine Na ≥ 20mM, then it is due to renal losses
- if urine Na < 20mM, the it is due to extrarenal losses

euvolemia
- TBW increased with normal total body Na+
- urine Na > 20mM

hypervolemia
- TBW is very high and total body Na increases too
- if urine Na ≥ 20mM, then it is due to renal loss w/ water retention
- if urine Na < 20mM, the it is due to water retention

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11
Q

What renal volume loss can cause hypovolemic hyponatremia?

A
  • diuretics (thiazide!)
  • mineralocorticoid deficiency
  • salt-losing nephropathy
  • bicarbonaturia (renal tubular acidosis, metabolic alkalosis)
  • osmotic diuresis
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12
Q

What extrarenal volume loss can cause hypovolemic hyponatremia?

A
  • vomiting
  • diarrhea
  • burns, trauma
  • pancreatitis
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13
Q

What are the possible causes of euvolemic hyponatremia?

A
  • glucocorticoid deficiency
  • hypothyroidism
  • medication, drugs
  • SIAD
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14
Q

What renal volume loss w/ water retention can cause hypervolemic hyponatremia?

A

acute or chronic kidney injury

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15
Q

What are the possible causes of water retention?

A
  • cardiac failure
  • cirrhosis
  • nephrotic syndrome
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16
Q

What is SIAD?

A

SIAD: syndrome of inappropriate antidiuresis
- a defect in osmoregulation causes vasopressin (AVP/ADH) to be inappropriately stimulated

diagnostic criteria
- serum osm. ↓, urine osm. > 100mOsm/kgH2O, urin Na > 20mmol/L
- euvolemia
- diagnosis by exclusion: absence of adrenal, thyroid, pituitary, or renal insufficiency; or absence of diuretic use

supplementary criteria
- abnormal water-load test result (inability to excrete, failure to dilute urine)
- serum Na is almost not corrected with any volume expansion
- serum uric acid ↓, fractional excretion of uric acid ↑

17
Q

What medication/drugs cause hyponatremia?

A
  • thiazide (-like) diuretics
  • SSRI, tricyclic antidepressants, haloperidol
  • vasopressin analogs (desmopressin, oxytocin)
  • carbamazepine
  • NSAID (nonsteroidal anti-inflammatory drugs)
  • clofibrate
  • cyclophosphamide
  • iv. immune globulin (IVIG)
  • vincristine
  • nicotine
  • metamphetamin (ecstasy)
18
Q

How is acute hyponatremia treated?

A
  • acute (symptoms within 48 hours)
  • 1-2 mL/kg 3% NaCl infusion in 1 hour ± furosemide (to reach serum Na+ of 4-6mmol/L
  • SLOW correction to normal level
19
Q

How is chronic hyponatremia treated?

A
  • chronic: (>48h symptoms or unknown duration)
  • in case of severe symptoms, same treatment as acute hyponatremia
  • in case of moderate symptoms, 0.9% NaCl infusion w/ furosemide
  • in case its asymptomatic, no immediate correction is needed but identify the cause
20
Q

How is chronic hypovolemic hyponatremia treated?

A
  • 0.9% NaCl infusion, per os fluids
  • increase per os Na intake
  • stop diuretics
21
Q

How is hypervolemic chronic hyponatremia treated?

A
  • usually in case of heart failure or cirrhosis
  • water and salt restriction
  • furosemide, V2-R antagonists (vaptans)
22
Q

How is euvolemic chronic hyponatremia treated?

A
  • water restriction: 500-1500mL/day w/ furosemide
  • increase in per os Na intake, V2-R antagonists (vaptans)
23
Q

What to be cautious of when treating hyponatremia?

A

acute, severe hyponatremia can be life threatening
- cerebral edema
- herniation

rapid correction of serum Na is life threatening
- central pontine myelinolysis (CPM); osmotic demyelination
- symptoms: encephalopathy, behavioral changes, cranial nerve palsies, progressive weakness, quadriplegia, “locked-in” syndrome

treatment efficacy is not predictable
- frequently check serum Na (every 2 hours)
- max. 8mmol/L per 24hours (1-1.5mM/hour)
- in case of rapid correction: iv. dextrose, desmopressin

24
Q

What is hypernatremia?

A
  • definition: serum Na >145mmol/L
  • clinical manifestations: altered mental status, lethargy, irritability, restlessness, seizures, muscle twitching, hyperreflexia, spasticity, fever, nausea, vomitin, labored breathing
  • at risk: elderly, infants, hypertonic infusions, feeding tubes, mechaical ventilation, uncontrolled DM, polyuric disorders
25
Q

What is the etiology of hypernatremia?

A

assess volume first!!

hypovolemia
- TBW is very low and total body Na is low
- if urine Na ≥ 20mM: renal losses
- if urine Na < 20mM: extrarenal losses

euvolemia
- TBW is low but total boday Na is variable
- urine Na is variable: renal or extrarenal losses

hypervolemia
- TBW is high and total body Na is very high
- urine Na >20mM: sodium gains

26
Q

What renal losses can lead to hypovolemic hypernatremia?

A
  • diuretics (loop and osmotic)
  • postobstruction (polyuria)
  • osmotic diuresis (DM)
  • intrinsic renal disease
27
Q

What extrarenal losses can lead to hypovolemic hypernatremia?

A
  • excess sweating
  • diarrhea
  • burns
  • fistulas
28
Q

What renal losses lead to euvolemic hypernatremia?

A
  • diabetes insipidus
  • hypodipsia
29
Q

What extrarenal losses lead to euvolemic hypernatremia?

A
  • respiratory loss
  • dermal loss
30
Q

What sodium gains can lead to hypervolemic hypernatremia?

A
  • primary hyperaldosteronism
  • cushing’s syndrome
  • NaCl tablets
  • hypertonic infusions (NaHCO3, NaCl)
  • hypertonic dialysis
31
Q

What is the treatment for hypovolemic hypernatremia?

A
  1. correction of volume deficit (0.9% NaCl), treatment of the cause
  2. correction of water deficit (0.45% NaCl, 5% dextrose, per os water)
32
Q

What is the treatment for euvolemic hypernatremia?

A
  1. correction of water deficit (0.45% NaCl, 5% dextrose, per os water)
  2. long-term therapy (diabetes insipidus, vasopressin analog)
33
Q

What is the treatment for hypervolemic hypernatremia?

A
  1. treatment of cause
  2. removal of Na: furosemide, hemodialysis as needed (renal failure)
34
Q

What is the maximum speed of correction for hypernatremia?

A

2mmol/L/hour, 10mmol/L/day

caution: cerebral edema

35
Q

Overview of hypermagnesemia

A
  • normal Mg level: 0.75 - 1.0 mmol/L
  • causes: renal failure; Mg supplements; familial hypocalciuric hypercalcemia; acromegaly; adrenal insufficiency
  • symptoms: deep tendon reflexes decrease (>3mM), paralysis (>5mM)
  • treatment: Ca-gluconate iv.
36
Q

Overview of hypomagnesemia

A
  • normal Mg level: 0.75 - 1.0 mmol/L
  • causes: decreased intake, malabsorption; increased excretion; medication; acute pancreatitis; chronic alcoholism; idiopathic
  • symptoms: weakness, hyperreflexia, tremor, spasm, ECG changes
  • treatment: MgSO4 iv., per os Mg-salts
37
Q

What can lead to increased excretion of Mg?

A
  • polyuric disease
  • prolonged infusion with excessive Na
  • primary aldosteronism
  • metabolic acidosis
  • phosphate deficiency
  • hyperthyroidism
  • Gitelman syndrome
38
Q

What medications can lead to hypomagnesemia?

A

aminoglycosides, calcineurin inhibitors, cisplatin, amphotericin, thiazide

39
Q

What are the ECG changes in hypomagnesemia?

A
  • prolonged QT interval
  • ST depression
  • risk of arrythmias increases