Electrolyte imbalances

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Questions and Answers

What is the primary reason for cerebral edema in hyponatremia?

Increased permeability of the blood-brain barrier

Rapid correction of sodium levels

Limited diffusion of solutes across the blood-brain barrier (correct)

Direct toxic effect of sodium on brain cells

What is the initial treatment approach for hyponatremia?

Administration of loop diuretics to increase sodium excretion

Fluid restriction, diuresis, and potential use of vasopressin receptor antagonists (correct)

Immediate correction of sodium levels to normal range

Aggressive sodium supplementation

What is a potential complication of rapid correction of hyponatremia?

Heart failure

Seizures

Cerebral hemorrhage

Central pontine myelinolysis (correct)

What is the recommended rate of sodium correction in hyponatremia?

1-2 mEq/L/hr Signup and view all the answers

What is the purpose of administering 3% saline in the treatment of hyponatremia?

To increase osmotic pressure and pull water out of the brain Signup and view all the answers

What symptoms would a patient with a sodium level of 128 likely exhibit?

Headache and lethargy Signup and view all the answers

A patient with a sodium level of 132 is likely to exhibit which of the following symptoms?

Little to no symptoms Signup and view all the answers

What is the likely sodium level of a patient experiencing nausea and malaise?

129-125 Signup and view all the answers

Which of the following is a consequence of excessive water absorption in the brain?

Brain cells swell and rupture Signup and view all the answers

What is the primary mechanism by which 3% saline helps to treat hyponatremia?

It shifts water from the brain into the bloodstream Signup and view all the answers

Which of the following is a characteristic of acute hyponatremia?

It is more likely to cause severe symptoms Signup and view all the answers

What is the primary goal of correcting sodium levels in hyponatremia?

To prevent seizures and cerebral edema Signup and view all the answers

Which of the following is a risk factor for developing cerebral edema due to hyponatremia?

Hypervolemia Signup and view all the answers

Which condition is associated with isotonic hyponatremia?

Hyperlipidemia Signup and view all the answers

What is the typical serum osmolality range in isotonic hyponatremia?

270-300 Signup and view all the answers

Which of the following is NOT a characteristic of hypertonic hyponatremia?

Decreased blood glucose levels Signup and view all the answers

What is the expected effect of mannitol therapy on serum osmolality?

Increase in serum osmolality Signup and view all the answers

What is the expected effect on serum osmolality in hypotonic hyponatremia?

Decreased serum osmolality Signup and view all the answers

Which of the following is a characteristic of hypotonic hyponatremia?

Decreased serum osmolality Signup and view all the answers

What is the significance of serum osmolality in diagnosing hyponatremia?

It helps to distinguish between hypotonic and hypertonic hyponatremia Signup and view all the answers

What is the formula to calculate free water deficit?

[(Na/140)-1]xTBW Signup and view all the answers

Which of the following conditions is associated with hypernatremia with low total body water and normal total body sodium?

Diabetes Signup and view all the answers

What is a potential cause of hypernatremia with increased total body sodium?

Hypertonic saline infusion Signup and view all the answers

Which of the following is NOT a cause of hypernatremia with dehydration and low total body sodium?

Cushing syndrome Signup and view all the answers

What is a common feature among Conn syndrome, Cushing syndrome, and hemodialysis?

Hypernatremia with increased total body sodium Signup and view all the answers

What is the typical clinical sign of a patient with a serum osmolality of 401-430?

Muscle twitching/spasm Signup and view all the answers

Which of the following symptoms is NOT typically seen in a patient with a serum osmolality of 350-375?

Ataxia Signup and view all the answers

What is the expected outcome of a patient with a serum osmolality above 430?

Coma and seizures Signup and view all the answers

Which of the following symptoms is typically seen in a patient with a serum osmolality between 376-400?

Ataxia and tremors Signup and view all the answers

What is the typical range of serum osmolality associated with confusion, restlessness, agitation, and headache?

350-375 Signup and view all the answers

What is the primary clinical manifestation of a patient with a serum osmolality of 401-430?

Hyperreflexia Signup and view all the answers

What is the expected outcome of a patient with a serum osmolality above 430 if left untreated?

Death Signup and view all the answers

What is the typical range of serum osmolality associated with ataxia, tremors, and weakness?

376-400 Signup and view all the answers

What is the primary clinical manifestation of a patient with a serum osmolality of 376-400?

Ataxia Signup and view all the answers

Which of the following potassium levels is a critical threshold for cardiac complications?

K > 5.5 Signup and view all the answers

What is the primary mechanism by which hypokalemia affects cardiac conduction?

Prolonged QT interval due to slowed repolarization Signup and view all the answers

What is the typical serum potassium level at which muscle weakness becomes apparent?

1.0 mEq/L Signup and view all the answers

What is the primary cause of potassium shift into cells in the treatment of hypokalemia?

Increased insulin levels Signup and view all the answers

What is the primary danger associated with hypokalemia?

Abnormal cardiac conduction Signup and view all the answers

What is the typical serum potassium level at which cardiac arrhythmias become apparent?

Less than 2.5 mEq/L Signup and view all the answers

What is the primary cause of potassium shift out of cells in hypokalemia?

pH imbalance Signup and view all the answers

What is the primary mechanism of action of IV infusion of calcium in hyperkalemia treatment?

Membrane stabilization Signup and view all the answers

What is the primary goal of administering IV infusion of glucose and insulin in hyperkalemia treatment?

Shifts potassium intracellularly Signup and view all the answers

What is the indication for immediate hemodialysis in hyperkalemia treatment?

Electrocardiographic evidence of impending arrest Signup and view all the answers

What is the duration of action of IV infusion of sodium bicarbonate in hyperkalemia treatment?

30-60 min Signup and view all the answers

What is the primary mechanism of action of K-binding resins in the GI tract in hyperkalemia treatment?

GI excretion Signup and view all the answers

What is the duration of action of IV infusion of calcium in hyperkalemia treatment?

5-10 min Signup and view all the answers

What is a potential cause of hyperkalemia due to increased potassium intake or absorption?

K supplements Signup and view all the answers

What is a potential cause of hyperkalemia due to impaired renal excretion?

Renal failure Signup and view all the answers

What is a potential cause of hyperkalemia due to transcellular shift?

Beta blockers Signup and view all the answers

What is a potential cause of hyperkalemia due to cellular injury?

Rhabdomyolysis Signup and view all the answers

What is a potential cause of hyperkalemia associated with adrenal disorders?

Addison's disease Signup and view all the answers

What is the primary function of parathyroid hormone in maintaining serum calcium levels?

Stimulation of calcium release from bone Signup and view all the answers

What is the effect of acidemia on serum calcium levels?

Decreased protein-bound calcium and increased ionized calcium Signup and view all the answers

What is the significance of measuring ionized calcium levels in critically ill patients?

It is less affected by changes in albumin levels Signup and view all the answers

What is the role of calcium in muscle contraction?

It plays a second messenger role in muscle contraction Signup and view all the answers

What is the percentage of calcium that is found in the bone?

99% Signup and view all the answers

What is the percentage of calcium in the ionized and physiologically active form?

50% Signup and view all the answers

What is the normal range of total serum calcium?

8.5-10.5 mg/dL Signup and view all the answers

What is the critical serum potassium level above which QRS widening can lead to sine waves, ventricular fibrillation, and cardiac arrest?

8 Signup and view all the answers

What is a potential cause of pseudohyperkalemia, which can be a lab artifact?

Leukocytosis Signup and view all the answers

What is the primary goal of treatment for hyperkalemia?

All of the above Signup and view all the answers

What is the primary mechanism of action of IV infusion of calcium in the treatment of hyperkalemia?

Stabilization of the cardiac membrane Signup and view all the answers

Which of the following conditions is associated with hypocalcemia due to PTH resistance?

Pseudohypoparathyroidism Signup and view all the answers

What is a common cause of hypocalcemia due to vitamin D insufficiency?

Malnutrition Signup and view all the answers

Which of the following is a cause of hypocalcemia due to calcium chelation?

Fluoride poisoning Signup and view all the answers

Which of the following conditions can cause secondary hypoparathyroidism?

Neck surgery Signup and view all the answers

What is a cause of hypocalcemia due to parathyroid hormone insufficiency?

Metastatic carcinoma Signup and view all the answers

Which of the following symptoms is most closely associated with cardiovascular manifestations of hypocalcemia?

Bradycardia Signup and view all the answers

Which of the following symptoms is most closely associated with neuromuscular manifestations of hypocalcemia?

Paresthesia Signup and view all the answers

Which of the following symptoms is most closely associated with pulmonary manifestations of hypocalcemia?

Bronchospasm Signup and view all the answers

Which of the following medications is most likely to cause hypercalcemia due to increased calcium ingestion?

Vitamin D Signup and view all the answers

What is the underlying mechanism of hypercalcemia in malignant disease?

All of the above Signup and view all the answers

Which of the following non-parathyroid endocrine disorders is associated with hypercalcemia?

Adrenal insufficiency Signup and view all the answers

What is the underlying mechanism of hypercalcemia in milk-alkali syndrome?

Increased calcium absorption Signup and view all the answers

What is a common neurological symptom of hypercalcemia?

Hypotonia Signup and view all the answers

What is a potential cardiovascular complication of hypercalcemia?

Short QT interval Signup and view all the answers

What is a common gastrointestinal symptom of hypercalcemia?

Nausea and vomiting Signup and view all the answers

What is a potential renal complication of hypercalcemia?

Nephrolithiasis Signup and view all the answers

Where is the majority of phosphate found in the body?

Bone Signup and view all the answers

What is the relationship between the concentration of phosphate and calcium in the plasma?

Inversely proportional Signup and view all the answers

What is the mechanism of treating hyperphosphatemia?

Aluminum hydroxide binding phosphate in the GI tract Signup and view all the answers

What is the role of phosphate in acid-base balance?

Acts as a buffer Signup and view all the answers

What is the role of phosphate in ATP production?

Acts as a component Signup and view all the answers

What is a potential cause of hypophosphatemia?

All of the above Signup and view all the answers

What is a common underlying condition associated with hyperphosphatemia?

Acute/chronic renal failure Signup and view all the answers

What is the normal range of magnesium in the body?

1.5-3.0 mEq/L Signup and view all the answers

Which of the following is a cause of hypomagnesemia?

Chronic diarrhea Signup and view all the answers

What is the primary function of magnesium in the body?

Regulation of enzymatic processes Signup and view all the answers

Which of the following medications can cause hypomagnesemia?

Diuretics Signup and view all the answers

What is the treatment for hypomagnesemia?

1-2 g IV magnesium sulfate over 5 minutes followed by 1-2 g/hr Signup and view all the answers

What is a potential benefit of administering IV magnesium sulfate in addition to treatment for hypomagnesemia?

Relieving bronchospasm Signup and view all the answers

What condition may occur due to overadministration during treatment of preeclampsia, preterm labor, ischemic heart disease, and dysrhythmias?

Hypermagnesemia Signup and view all the answers

What is the effect of magnesium on non-depolarizing neuromuscular blockers?

Potentiates their action Signup and view all the answers

What is the treatment for hypermagnesemia in urgent situations?

Administration of calcium gluconate 10-15 mg/kg Signup and view all the answers

At what serum magnesium level is respiratory paralysis likely to occur?

10 Signup and view all the answers

What is the likely outcome at a serum magnesium level of 10-20?

Heart block and cardiac arrest Signup and view all the answers

What is the primary mechanism by which magnesium improves symptoms in preeclampsia?

Vasodilation via direct effects and increasing concentrations of endogenous vasodilators Signup and view all the answers

What is the recommended treatment for torsade's de pointes?

Magnesium Signup and view all the answers

What is the primary mechanism by which magnesium produces analgesia?

Calcium and NMDA antagonism Signup and view all the answers

What is the effect of magnesium on the fetus when given to the mother?

Neonatal lethargy, hypotension, and respiratory depression Signup and view all the answers

What is the primary mechanism by which magnesium reduces catecholamine release in pheochromocytoma?

Inhibition of catecholamine release from the adrenal medulla Signup and view all the answers

Study Notes

Hyponatremia

ECV (extracellular fluid) is hypo-osmolar compared to ICV (intracellular fluid), causing water to move into the ICV.
The brain is confined within a fixed cranium, making cerebral edema the most significant effect of hyponatremia.
Limited diffusion of solutes across the BBB (blood-brain barrier) prevents equilibration of solutes among fluid compartments.

Initial Treatment of Hyponatremia

Initial treatment involves fluid restriction, diuresis, and potential use of vasopressin receptor antagonists (such as tolvaptan and conivaptan).

Correction of Hyponatremia

Rapid correction of hyponatremia can cause neurologic complications, including central pontine myelinolysis.
Correction should be limited to 1-2 mEq/L/hr using 3% saline at 1-2 mL/kg/hr.
The sodium level should not be raised more than 10-15 mmol/L in 24 hours.

Hyponatremia

ECV (extracellular fluid) is hypo-osmolar compared to ICV (intracellular fluid), causing water to move into the ICV, leading to cerebral edema.
The brain's fixed cranium and limited diffusion of solutes across the BBB (blood-brain barrier) prevent equilibration of solutes among fluid compartments, exacerbating cerebral edema.

Treatment of Hyponatremia

Initial treatment involves fluid restriction, diuresis, and potential use of vasopressin receptor antagonists (e.g., tolvaptan and conivaptan).
Rapid correction of hyponatremia should be avoided to prevent neurologic complications, including central pontine myelinolysis.
Correction should not exceed 1-2 mEq/L/hr with 3% saline at 1-2 mL/kg/hr, and not raised more than 10-15 mmol/L in 24 hours.

Sodium Levels and Physiologic Manifestations

135-130 mEq/L: Little to no symptoms, with possible mild neurologic signs.
129-125 mEq/L: Nausea and malaise.
124-115 mEq/L: Headache, lethargy, and altered level of consciousness (LOC).

Hyponatremia

ECV is hypo-osmolar compared to ICV, causing water to move into ICV
Most significant effect is cerebral edema due to the brain being confined within the fixed cranium
Limited diffusion of solutes across the BBB prevents equilibration of solutes among fluid compartments

Treatment of Hyponatremia

Initial treatment involves fluid restriction, diuresis, and potential use of vasopressin receptor antagonists (tolvaptan and conivaptan)
Rapid correction of hyponatremia can cause neurologic complications including central pontine myelinolysis
Correction rate: no more than 1-2 mEq/L/hr with 3% saline at 1-2 mL/kg/hr, not raised more than 10-15 mmol/L in 24 hours

Sodium Levels and Physiologic Manifestations

135-130 mmol/L: little to no symptoms, may see mild neurologic signs
129-125 mmol/L: nausea, malaise
124-115 mmol/L: headache, lethargy, altered level of consciousness

Hyponatremia

ECV is hypo-osmolar compared to ICV, causing water to move into ICV
Most significant effect is cerebral edema due to the brain being confined within the fixed cranium
Limited diffusion of solutes across the BBB prevents equilibration of solutes among fluid compartments

Treatment of Hyponatremia

Initial treatment involves fluid restriction, diuresis, and potential use of vasopressin receptor antagonists (tolvaptan and conivaptan)
Rapid correction of hyponatremia can cause neurologic complications including central pontine myelinolysis
Correction rate: no more than 1-2 mEq/L/hr with 3% saline at 1-2 mL/kg/hr, not raised more than 10-15 mmol/L in 24 hours

Sodium Levels and Physiologic Manifestations

135-130 mmol/L: little to no symptoms, may see mild neurologic signs
129-125 mmol/L: nausea, malaise
124-115 mmol/L: headache, lethargy, altered level of consciousness

Classification of Hyponatremia

Isotonic Hyponatremia (Pseudohyponatremia) is characterized by a serum osmolality of 270-300.
Causes of Isotonic Hyponatremia include: • Hyperlipidemia • Hyperproteinemia • Multiple myeloma • Excess isotonic nonelectrolyte solutions

Hypertonic Hyponatremia

Hypertonic Hyponatremia is characterized by a serum osmolality greater than 300.
Causes of Hypertonic Hyponatremia include: • Hyperglycemia • Mannitol excess • Glycerol therapy

Hypotonic Hyponatremia

Hypotonic Hyponatremia is characterized by a serum osmolality less than 270.

Classification of Hyponatremia

Isotonic Hyponatremia (Pseudohyponatremia) is characterized by a serum osmolality of 270-300.
Causes of Isotonic Hyponatremia include: • Hyperlipidemia • Hyperproteinemia • Multiple myeloma • Excess isotonic nonelectrolyte solutions

Hypertonic Hyponatremia

Hypertonic Hyponatremia is characterized by a serum osmolality greater than 300.
Causes of Hypertonic Hyponatremia include: • Hyperglycemia • Mannitol excess • Glycerol therapy

Hypotonic Hyponatremia

Hypotonic Hyponatremia is characterized by a serum osmolality less than 270.

Hyponatremia

ECV (extracellular fluid) is hypo-osmolar compared to ICV (intracellular fluid), causing water to move into the ICV.
The most significant effect of hyponatremia is cerebral edema, which occurs because the brain is confined within the fixed cranium.
Limited diffusion of solutes across the BBB (blood-brain barrier) prevents equilibration of solutes among fluid compartments.

Treatment of Hyponatremia

Initial treatment involves fluid restriction, diuresis, and potential use of vasopressin receptor antagonists (tolvaptan and conivaptan).
Rapid correction of hyponatremia can cause neurologic complications, including central pontine myelinolysis.
Correction of hyponatremia should be limited to 1-2 mEq/L/hr with 3% saline at 1-2 mL/kg/hr, and not raised more than 10-15 mmol/L in 24 hours.

Sodium Levels and Physiologic Manifestations

135-130 mEq/L: Little to no symptoms, may see mild neurologic signs.
129-125 mEq/L: Nausea, malaise.
124-115 mEq/L: Headache, lethargy, altered LOC.

Classification of Hyponatremia

Isotonic Hyponatremia (Pseudohyponatremia): Serum osmolality 270-300 mEq/L, caused by hyperlipidemia, hyperproteinemia, multiple myeloma, or excess isotonic nonelectrolyte solutions.
Hypertonic Hyponatremia: Serum osmolality >300 mEq/L, caused by hyperglycemia, mannitol, or excess glycerol therapy.
Hypotonic Hyponatremia: Serum osmolality <270 mEq/L.

Hyponatremia

ECV is hypo-osmolar compared to ICV, so water moves into ICV, causing cerebral edema due to the confined space of the cranium.
Limited diffusion of solutes across the BBB prevents equilibration of solutes among fluid compartments.

Treatment of Hyponatremia

Initial treatment involves fluid restriction, diuresis, and potential use of vasopressin receptor antagonists (tolvaptan and conivaptan).
Rapid correction of hyponatremia can cause neurologic complications, including central pontine myelinolysis.
Correction should be no more than 1-2 mEq/L/hr with 3% saline at 1-2 mL/kg/hr, and not raised more than 10-15 mmol/L in 24 hours.

Sodium Levels and Physiologic Manifestations

135-130 mEq/L: Little to no symptoms, may see mild neurologic signs.
129-125 mEq/L: Nausea, malaise.
124-115 mEq/L: Headache, lethargy, altered level of consciousness.

Classification of Hyponatremia

Isotonic Hyponatremia (Pseudohyponatremia): Serum osmolality 270-300, caused by hyperlipidemia, hyperproteinemia, multiple myeloma, and excess isotonic nonelectrolyte solutions.
Hypertonic Hyponatremia: Serum osmolality >300, caused by hyperglycemia, mannitol excess, and glycerol therapy.
Hypotonic Hyponatremia: Serum osmolality <270, caused by excessive water intake, heart failure, liver failure, and nephrotic syndrome.

Free Water Deficit Calculation

Free water deficit can be calculated using the formula: [(Na/140)-1]xTBW

Classification of Hypernatremia

Hypernatremia can be classified into three types based on total body water and sodium levels

Hypernatremia with Dehydration and Low Total Body Sodium

Characterized by low total body water and low total body sodium
Causes include:
- Vomiting
- Diarrhea
- Continuous gastrointestinal suctioning
- Osmotic diuresis

Hypernatremia with Low Total Body Water and Normal Total Body Sodium

Characterized by low total body water and normal total body sodium
Causes include:
- Diabetes
- Neurogenic disorders
- Renal disease
- Sickle cell disease
- Aminoglycosides

Hypernatremia with Increased Total Body Sodium

Characterized by high total body sodium
Causes include:
- Hypertonic saline infusion
- Cushing syndrome
- Conn syndrome
- Hemodialysis

Clinical Signs of Hypernatremia with Increased Serum Osmolality

At a serum osmolality of 350-375, symptoms include confusion, restlessness, agitation, and headache
At a serum osmolality of 376-400, symptoms escalate to ataxia, tremors, and weakness
At a serum osmolality of 401-430, symptoms further progress to hyperreflexia, muscle twitching, and muscle spasm
At a serum osmolality above 430, severe and life-threatening symptoms occur, including coma, seizures, and ultimately, death

Clinical Signs of Hypernatremia with Increased Serum Osmolality

At a serum osmolality of 350-375, symptoms include confusion, restlessness, agitation, and headache
At a serum osmolality of 376-400, symptoms escalate to ataxia, tremors, and weakness
At a serum osmolality of 401-430, symptoms further progress to hyperreflexia, muscle twitching, and muscle spasm
At a serum osmolality above 430, severe and life-threatening symptoms occur, including coma, seizures, and ultimately, death

Hyponatremia

Hyponatremia occurs when the ECV is hypo-osmolar compared to the ICV, causing water to move into the ICV.
This leads to cerebral edema, as the brain is confined within the fixed cranium, and limited diffusion of solutes across the BBB prevents equilibration of solutes among fluid compartments.

Initial Treatment of Hyponatremia

Initial treatment involves fluid restriction, diuresis, and potential use of vasopressin receptor antagonists (tolvaptan and conivaptan).
Rapid correction of hyponatremia can cause neurologic complications, including central pontine myelinolysis.
Correction should be done at a rate of 1-2 mEq/L/hr with 3% saline at 1-2 mL/kg/hr, and not raised more than 10-15 mmol/L in 24 hours.

Sodium Levels and Physiologic Manifestations

Sodium levels of 135-130 mmol/L: little to no symptoms, may see mild neurologic signs.
Sodium levels of 129-125 mmol/L: nausea, malaise.
Sodium levels of 124-115 mmol/L: headache, lethargy, altered LOC.

Classification of Hyponatremia

Isotonic Hyponatremia (Pseudohyponatremia): serum osmolality 270-300 mmol/L, caused by hyperlipidemia, hyperproteinemia, multiple myeloma, and excess isotonic nonelectrolyte solutions.
Hypertonic Hyponatremia: serum osmolality >300 mmol/L, caused by hyperglycemia, mannitol excess, and glycerol therapy.
Hypotonic Hyponatremia: serum osmolality <270 mmol/L, calculated using the formula: free water deficit = [(Na/140)-1]xTBW.

Hypernatremia

Hypernatremia can be classified into three types:
- Hypernatremia with dehydration and low total body sodium, caused by vomiting, diarrhea, continuous gastrointestinal suctioning, and osmotic diuresis.
- Hypernatremia with low total body water and normal total body sodium, caused by diabetes, neurogenic, renal disease, sickle cell disease, and aminoglycosides.
- Hypernatremia with increased total body sodium, caused by hypertonic saline infusion, Cushing syndrome, Conn syndrome, and hemodialysis.

Clinical Signs of Hypernatremia

Serum osmolality of 350-375 mmol/L: confusion, restlessness, agitation, and headache.
Serum osmolality of 376-400 mmol/L: ataxia, tremors, and weakness.
Serum osmolality of 401-430 mmol/L: hyperreflexia, muscle twitching/spasm.
Serum osmolality >430 mmol/L: coma, seizures, and death.

Hyponatremia

Hyponatremia occurs when ECV is hypo-osmolar compared to ICV, causing water to move into the ICV and resulting in cerebral edema.
Cerebral edema is the most significant effect due to the brain being confined within the fixed cranium.
Limited diffusion of solutes across the BBB prevents equilibration of solutes among fluid compartments.

Treatment of Hyponatremia

Initial treatment involves fluid restriction, diuresis, and potential use of vasopressin receptor antagonists (tolvaptan and conivaptan).
Rapid correction of hyponatremia can cause neurologic complications, including central pontine myelinolysis.
Correction should be done at a rate of 1-2 mEq/L/hr with 3% saline at 1-2 mL/kg/hr, and not raised more than 10-15 mmol/L in 24 hours.

Sodium Levels and Physiologic Manifestations

135-130 mmol/L: Little to no symptoms, may see mild neurologic signs.
129-125 mmol/L: Nausea, malaise.
124-115 mmol/L: Headache, lethargy, altered LOC.

Classification of Hyponatremia

Isotonic Hyponatremia (Pseudohyponatremia): Serum osmolality 270-300, caused by hyperlipidemia, hyperproteinemia, multiple myeloma, and excess isotonic nonelectrolyte solutions.
Hypertonic Hyponatremia: Serum osmolality >300, caused by hyperglycemia, mannitol excess, and glycerol therapy.
Hypotonic Hyponatremia: Serum osmolality <270, caused by free water deficit.

Hypernatremia

Classification:
- Hypernatremia with dehydration and low total body sodium, caused by vomiting, diarrhea, continuous gastrointestinal suctioning, and osmotic diuresis.
- Hypernatremia with low total body water and normal total body sodium, caused by diabetes, neurogenic, renal disease, sickle cell disease, and aminoglycosides.
- Hypernatremia with increased total body sodium, caused by hypertonic saline infusion, Cushing syndrome, Conn syndrome, and hemodialysis.

Clinical Signs of Hypernatremia

350-375 mmol/L: Confusion, restlessness, agitation, headache.
376-400 mmol/L: Ataxia, tremors, weakness.
401-430 mmol/L: Hyperreflexia, muscle twitching/spasm.
>430 mmol/L: Coma, seizures, death.

Potassium Imbalance and Hyponatremia

Patients with potassium levels >5.5 mmol/L or hyponatremia are at risk of complications.
ECV (extracellular fluid) is hypo-osmolar compared to ICV (intracellular fluid), causing water to move into the ICV and leading to cerebral edema.
The brain's confinement within the fixed cranium exacerbates the edema.
Limited diffusion of solutes across the BBB (blood-brain barrier) prevents equilibration of solutes among fluid compartments.

Treatment of Hyponatremia

Initial treatment involves fluid restriction, diuresis, and potential use of vasopressin receptor antagonists (tolvaptan and conivaptan).
Rapid correction of hyponatremia can cause neurologic complications, including central pontine myelinolysis.
Correction should be limited to 1-2 mEq/L/hr with 3% saline at 1-2 mL/kg/hr, and not raised more than 10-15 mmol/L in 24 hours.

Sodium Levels and Physiologic Manifestations

Sodium levels between 135-130 mmol/L: little to no symptoms, with possible mild neurologic signs.
Sodium levels between 129-125 mmol/L: nausea, malaise.
Sodium levels between 124-115 mmol/L: headache, lethargy, altered level of consciousness.

Hyponatremia Classification

Isotonic Hyponatremia (Pseudohyponatremia): serum osmolality 270-300 mmol/L, caused by hyperlipidemia, hyperproteinemia, multiple myeloma, or excess isotonic nonelectrolyte solutions.
Hypertonic Hyponatremia: serum osmolality >300 mmol/L, caused by hyperglycemia, mannitol excess, or glycerol therapy.
Hypotonic Hyponatremia: serum osmolality <270 mmol/L, caused by free water excess.

Hypernatremia Classification

Hypernatremia with dehydration and low total body sodium: caused by vomiting, diarrhea, continuous gastrointestinal suctioning, or osmotic diuresis.
Hypernatremia with low total body water and normal total body sodium: caused by diabetes, neurogenic, renal disease, sickle cell disease, or aminoglycosides.
Hypernatremia with increased total body sodium: caused by hypertonic saline infusion, Cushing syndrome, Conn syndrome, or hemodialysis.

Clinical Signs of Hypernatremia

Serum osmolality 350-375 mmol/L: confusion, restlessness, agitation, headache.
Serum osmolality 376-400 mmol/L: ataxia, tremors, weakness.
Serum osmolality 401-430 mmol/L: hyperreflexia, muscle twitching/spasm.
Serum osmolality >430 mmol/L: coma, seizures, death.

Potassium Imbalance and Hyponatremia

Hyponatremia occurs when serum sodium (Na) level is <135 mmol/L
In hyponatremia, ECV is hypo-osmolar compared to ICV, causing water to move into the ICV
Most significant effect is cerebral edema due to limited diffusion of solutes across the BBB
Initial treatment involves fluid restriction, diuresis, and potential use of vasopressin receptor antagonists (tolvaptan and conivaptan)
Rapid correction of hyponatremia can cause neurologic complications, including central pontine myelinolysis

Sodium Levels and Physiologic Manifestations

135-130 mmol/L: Little to no symptoms, may see mild neurologic signs
129-125 mmol/L: Nausea, malaise
124-115 mmol/L: Headache, lethargy, altered LOC

Hyponatremia Classification

Isotonic Hyponatremia (Pseudohyponatremia): Serum osmolality 270-300, caused by hyperlipidemia, hyperproteinemia, multiple myeloma, or excess isotonic nonelectrolyte solutions
Hypertonic Hyponatremia: Serum osmolality >300, caused by hyperglycemia, mannitol, or excess glycerol therapy
Hypotonic Hyponatremia: Serum osmolality <270, caused by free water excess or deficient solute intake

Hypernatremia Classification

Hypernatremia with dehydration and low total body sodium: caused by vomiting, diarrhea, continuous gastrointestinal suctioning, or osmotic diuresis
Hypernatremia with low total body water and normal total body sodium: caused by diabetes, neurogenic, renal disease, sickle cell disease, or aminoglycosides
Hypernatremia with increased total body sodium: caused by hypertonic saline infusion, Cushing syndrome, Conn syndrome, or hemodialysis

Clinical Signs of Hypernatremia

350-375 mmol/L: Confusion, restlessness, agitation, headache
376-400 mmol/L: Ataxia, tremors, weakness
401-430 mmol/L: Hyperreflexia, muscle twitching/spasm
>430 mmol/L: Coma, seizures, death

Potassium Imbalance

Patients with K > 5.5 are at risk of potassium imbalance
Hypokalemia occurs when serum potassium levels are low

Hyponatremia

Serum osmolality is hypo-osmolar compared to intracellular volume (ICV)
Water moves into the ICV, causing cerebral edema due to the brain's fixed cranium
Initial treatment involves fluid restriction, diuresis, and potential use of vasopressin receptor antagonists (tolvaptan and conivaptan)
Rapid correction can cause neurologic complications, including central pontine myelinolysis
Correction should be limited to 1-2 mEq/L/hr with 3% saline at 1-2 mL/kg/hr and not raised more than 10-15 mmol/L in 24 hours

Sodium Levels and Physiologic Manifestations

135-130: Little to no symptoms; may see mild neurologic signs
129-125: Nausea, malaise
124-115: Headache, lethargy, altered LOC

Classification of Hyponatremia

Isotonic Hyponatremia (Pseudohyponatremia): Serum osmolality 270-300; associated with hyperlipidemia, hyperproteinemia, multiple myeloma, and excess isotonic nonelectrolyte solutions
Hypertonic Hyponatremia: Serum osmolality > 300; associated with hyperglycemia, mannitol, and excess glycerol therapy
Hypotonic Hyponatremia: Serum osmolality < 270; associated with free water deficit, calculated as [(Na/140)-1]xTBW

Hypernatremia

Classification:
- Hypernatremia with dehydration and low total body sodium; associated with vomiting, diarrhea, continuous gastrointestinal suctioning, and osmotic diuresis
- Hypernatremia with low total body water and normal total body sodium; associated with diabetes, neurogenic disease, renal disease, sickle cell disease, and aminoglycosides
- Hypernatremia with increased total body sodium; associated with hypertonic saline infusion, Cushing syndrome, Conn syndrome, and hemodialysis

Clinical Signs of Hypernatremia

350-375: Confusion, restlessness, agitation, and headache
376-400: Ataxia, tremors, and weakness
401-430: Hyperreflexia, muscle twitching/spasm
>430: Coma, seizures, and death

Guidelines for Hyperkalemia Treatment

Clinical Features

Electrocardiographic evidence of impending arrest (loss of P wave and QRS widening) requires immediate therapy
Peaked T waves indicate potassium deficit and prompt therapy is necessary

Therapy

IV infusion of calcium (10 mL of 10% calcium chloride over 10 min or 10 mL 10% calcium gluconate over 3-5 min) for membrane stabilization
IV infusion of sodium bicarbonate (50-100 mEq over 10-20 min) to shift potassium intracellularly
Glucose and insulin infusion (IV infusion of 50mL of D50W and 10 units of regular insulin, monitor glucose) to shift potassium intracellularly
Immediate hemodialysis for 30 min to 4-6 hours to shift potassium intracellularly
K-binding resins in GI tract to promote GI excretion
Diuretic (furosemide 40mg IV) to promote renal potassium excretion

Onset and Duration of Action

Calcium: 1-3 min onset, 30-60 min duration
Sodium bicarbonate: 1-3 min onset, 30-60 min duration
Glucose and insulin: 1-2 hours onset, 4-6 hours duration
Hemodialysis: 30 min to 4-6 hours duration
K-binding resins: 1-2 hours onset, 2-3 hours duration
Diuretic: 15-30 min onset, 4-6 hours duration

Causes of Hyperkalemia

Increased K Intake/Absorption

K supplements can cause hyperkalemia
Salt substitutes can contribute to increased potassium intake
Stored blood transfusions can lead to hyperkalemia
Certain medications containing potassium can increase K levels

Impaired Renal Excretion

Renal failure can cause hyperkalemia due to reduced K excretion
Tubular defects can impair renal potassium excretion
Nephropathy, obstructive uropathy, and nephritis can lead to hyperkalemia
Pyelonephritis, a kidney infection, can cause hyperkalemia
K-sparing diuretics can reduce potassium excretion
Hypoaldosteronism, a condition characterized by low aldosterone levels, can cause hyperkalemia
Systemic lupus erythematosus (SLE) can lead to hyperkalemia
Addison's disease, a condition characterized by adrenal insufficiency, can cause hyperkalemia
Adrenal hyperplasia, a condition characterized by adrenal gland overgrowth, can lead to hyperkalemia
Certain drugs can impair renal potassium excretion

Transcellular Shift

Acidosis, a condition characterized by high blood acidity, can cause potassium to shift out of cells
Hypertonicity, a condition characterized by high blood osmolarity, can lead to potassium shift
Insulin deficiency, common in diabetes, can cause potassium to shift out of cells
Beta blockers, a type of medication, can cause potassium shift
Digitalis, a medication used to treat heart conditions, can lead to potassium shift
Succinylcholine, a medication used in anesthesia, can cause potassium shift
Exercise, particularly strenuous exercise, can cause potassium shift
Hyperkalemic periodic paralysis, a rare genetic disorder, can cause potassium shift

Cellular Injury

Rhabdomyolysis, a condition characterized by muscle breakdown, can cause potassium release
Severe intravascular hemolysis, a condition characterized by red blood cell destruction, can lead to potassium release
Acute tumor lysis syndrome, a condition characterized by rapid tumor cell destruction, can cause potassium release
Burns and crush injuries can cause potassium release from injured cells

Calcium Distribution

99% of calcium is stored in bones as hydroxyapatite, while 1% is found in plasma and cells.

Calcium Levels

Total serum calcium levels range from 8.5-10.5 mg/dL.
Serum levels are primarily maintained by Parathyroid hormone.

Calcium Forms

Calcium is found in three forms:
Ionized and physiologically active form (50%)
Bound to anions (10%)
Bound to proteins (40%)

Factors Affecting Calcium Levels

Total amount of calcium is largely dependent on albumin concentration.
Measuring ionized calcium is preferred, especially in patients with critical illness or hypoalbuminemia.

Effect of pH on Calcium

Acidemia decreases protein-bound calcium and increases ionized calcium.
Conversely, alkalosis increases protein-bound calcium and decreases ionized calcium.

Physiological Roles of Calcium

Calcium acts as a second messenger in many cellular responses.
It plays a role in:
- Muscle contraction
- Release of neurotransmitters and hormones
- Blood coagulation
- Myocardial contractility

Calcium Distribution

99% of calcium is stored in bones as hydroxyapatite, while 1% is found in plasma and cells.

Calcium Levels

Total serum calcium levels range from 8.5-10.5 mg/dL.
Serum levels are primarily maintained by Parathyroid hormone.

Calcium Forms

Calcium is found in three forms:
Ionized and physiologically active form (50%)
Bound to anions (10%)
Bound to proteins (40%)

Factors Affecting Calcium Levels

Total amount of calcium is largely dependent on albumin concentration.
Measuring ionized calcium is preferred, especially in patients with critical illness or hypoalbuminemia.

Effect of pH on Calcium

Acidemia decreases protein-bound calcium and increases ionized calcium.
Conversely, alkalosis increases protein-bound calcium and decreases ionized calcium.

Physiological Roles of Calcium

Calcium acts as a second messenger in many cellular responses.
It plays a role in:
- Muscle contraction
- Release of neurotransmitters and hormones
- Blood coagulation
- Myocardial contractility

Hyperkalemia

Serum level > 5 mmol/L
Occurs less frequently than hypokalemia
At potassium levels > 8 mmol/L, ECG changes can lead to:
- QRS widening
- Sine waves
- Ventricular fibrillation (V fib)
- Cardiac arrest
Treatment should rule out pseudohyperkalemia, a lab artifact caused by:
- Hemolysis of the blood sample
- Leukocytosis
- Thrombocytosis
- Prolonged clenching of the fist during blood draw
Treatment goals:
- Stabilize the cardiac membrane
- Drive potassium from the extracellular compartment (ECV) to the intracellular compartment (ICV)
- Remove potassium from the body

Causes of Hypocalcemia

Parathyroid Hormone Insufficiency

Primary hypoparathyroidism can be caused by congenital syndromes or maternal hyperparathyroidism
Secondary hypoparathyroidism can be caused by neck surgery, metastatic carcinoma, infiltrative disorders, or certain conditions such as hypo/hypermagnesemia, sepsis, pancreatitis, burns, or exposure to chemotherapy agents, ethanol, or cimetidine

Vitamin D Insufficiency

Causes of vitamin D insufficiency include congenital rickets, malnutrition, malabsorption, liver disease, or renal disease (acute/chronic failure, nephrotic syndrome)
Certain conditions can also contribute to vitamin D insufficiency, such as hypomagnesemia, sepsis, or taking anticonvulsants like phenytoin or primidone

PTH Resistance States

Pseudohypoparathyroidism is a condition of PTH resistance

Calcium Chelation

Calcium chelation can cause hypocalcemia due to hyperphosphatemia, citrate, free fatty acids, alkalosis, or fluoride poisoning

Neuromuscular Symptoms

Paresthesia, muscle weakness, and muscle spasms occur due to hypocalcemia
Tetany is a characteristic symptom of hypocalcemia
Chvostek's sign is a facial or eye muscle twitching that indicates hypocalcemia
Trousseau's sign is a carpopedal spasm that occurs in hypocalcemic patients
Hyperreflexia is another notable symptom of hypocalcemia

Cardiovascular Symptoms

Hypocalcemia can cause bradycardia (slow heart rate)
Angina, hypotension, and congestive heart failure (CHF) are cardiovascular complications of hypocalcemia
Cardiac arrest can occur in severe cases of hypocalcemia
Hypocalcemia can lead to digitalis insensitivity, making digoxin therapy less effective
QT prolongation is a cardiac symptom of hypocalcemia

Pulmonary Symptoms

Bronchospasm and laryngospasm are respiratory complications of hypocalcemia

Psychiatric Symptoms

Anxiety, depression, irritability, and confusion can occur due to hypocalcemia
Psychosis and dementia are rare but possible psychiatric symptoms of hypocalcemia

Causes of Hypercalcemia

Primary hyperparathyroidism is a cause of hypercalcemia
Malignant diseases can cause hypercalcemia through: • Production of parathyroid hormone-related protein • Ectopic production of 1,25-dihydroxyvitamin D • Release of bone-resorbing substances • Osteolytic bone metastasis
Certain medications can cause hypercalcemia, including: • Thiazide diuretics • Lithium • Estrogens • Vitamin D toxicity • Vitamin A toxicity • Calcium ingestion

Granulomatous Disorders

Granulomatous disorders can cause hypercalcemia, including: • Sarcoidosis • Tuberculosis • Coccidioidomycosis • Berylliosis • Histoplasmosis • Leprosy

Non-Parathyroid Endocrine Disorders

Certain endocrine disorders can cause hypercalcemia, including: • Hyperparathyroidism • Adrenal insufficiency • Pheochromocytoma • Acromegaly • Vasoactive intestinal polypeptide-producing tumor

Miscellaneous Causes

Other causes of hypercalcemia include: • Milk-alkali syndrome • Immobilization • Idiopathic hypocalcemia of infancy

Neurological Symptoms of Hypercalcemia

Fatigue, weakness, and lethargy may occur due to hypercalcemia
Confusion and seizures are potential neurological symptoms
Hypotonia, characterized by decreased muscle tone, can be a sign of hypercalcemia
Diminished deep tendon reflexes may indicate hypercalcemia
In severe cases, hypercalcemia can lead to coma

Cardiovascular Symptoms of Hypercalcemia

Hypercalcemia can cause hypertension
Electrocardiogram changes include ST segment elevation, sinus bradycardia/arrest, and AV block
A short QT interval is a potential cardiac symptom
Bundle branch block (BBB) can occur in hypercalcemia
Ventricular dysrhythmias, including ventricular tachycardia and fibrillation, are potential complications
Hypercalcemia can potentiate digoxin toxicity

Renal Symptoms of Hypercalcemia

Polyuria (excessive urine production) and polydipsia (excessive thirst) are common symptoms
Dehydration can occur due to excessive urine production
Electrolyte imbalance and loss of electrolytes are potential complications
Prerenal azotemia, a type of kidney failure, can occur in hypercalcemia
Nephrolithiasis, the formation of kidney stones, is a potential complication
Nephrocalcinosis, the deposition of calcium in the kidneys, can occur in hypercalcemia

Gastrointestinal Symptoms of Hypercalcemia

Nausea and vomiting are common gastrointestinal symptoms
Anorexia, or loss of appetite, can occur in hypercalcemia
Peptic ulcers, which are sores in the lining of the stomach or duodenum, can be a complication
Pancreatitis, or inflammation of the pancreas, can occur in hypercalcemia
Constipation and ileus, a condition in which the intestine fails to function, can be gastrointestinal symptoms

Phosphate Distribution

85% of phosphate is found in the bone, with a small amount in the plasma

Phosphate Forms in Plasma

Phosphate exists in plasma as:
- Phospholipids
- Phosphate esters
- Inorganic phosphate (ionized form)

Intracellular Phosphate Functions

Component of ATP
Component of 2,3 DPG
Acts as a buffer in acid-base balance

Phosphate Regulation

Phosphate concentration in plasma is inversely proportional to calcium concentration
Regulated by same mechanisms as calcium, including:
- PTH (parathyroid hormone)
- Vitamin D
- Calcitonin

Treatment of Phosphate Imbalances

Hypophosphatemia: treated with oral or IV supplementation
Hyperphosphatemia: treated with aluminum hydroxide, which binds phosphate in the GI tract

Hypophosphatemia

Defined by a blood phosphorus level of 4.7 mg/dL or lower
Causes include:
- Acute or chronic renal failure
- Treatment of metastatic tumor
- Long-term use of laxatives or enemas containing phosphates
- Hypoparathyroidism
Complications include:
Symptoms related to hypocalcemia
- Chronic calcification of soft tissues
- Affected tissues include:
  - Joints
  - Lungs
  - Kidneys

Hypomagnesemia (Low Magnesium Levels)

Normal range of magnesium levels in the body is 1.5-3 mEq/L.
Regulation of magnesium levels occurs in the intestines and kidneys.
Magnesium plays a crucial role in various bodily functions, including enzymatic processes, Na/K pump, protein synthesis, and nerve-muscle excitability.

Causes of Hypomagnesemia

Renal loss: renal failure, postobstructive diuresis, tubular necrosis, glomerulonephritis, interstitial nephropathy, transplant.
GI loss: chronic diarrhea, NG suction, short-bowel syndrome, protein-calorie deficit, bowel fistula, TPN, pancreatitis.
Endocrine disorders: DM, hyperaldosteronism, hyperthyroidism, hyperparathyroidism, acute porphyria.
Medications: aminoglycosides, amphotericin, beta-agonists, cisplatin, cyclosporine, diuretics, foscarnet, pentamidine, PPI, theophylline.
Congenital: familial hypomagnesemia, maternal diabetes, maternal hypothyroidism, maternal hyperparathyroidism.
Miscellaneous: pregnancy, excessive alcohol intake, citrate binding with blood administration.

Symptoms and Treatment of Hypomagnesemia

Symptoms: inhibits Na/K pump, decreasing ICV K, N/V, tetany, flat T-waves, U-waves, prolonged QT, wide QRS, arrhythmias.
Treatment: 1-2 g IV magnesium sulfate over 5 minutes, followed by 1-2 g/hr. IV infusions can also relieve severe bronchospasm, arrhythmias, and decrease post-operative pain.

HYPERMAGNESEMIA

Occurs due to overadministration during treatment of preeclampsia, preterm labor, ischemic heart disease, and dysrhythmias
Potentiates the action of nondepolarizing neuromuscular blockers (NMB)

Treatment of HYPERMAGNESEMIA

Involves stopping the magnesium infusion (if given)
In urgent situations, calcium gluconate 10-15 mg/kg can be given as an antagonist

HYPERMAGNESEMIA Causes and Manifestations

Caused by renal failure, excessive magnesium administration, and adrenal insufficiency
Manifestations vary by serum level:
- 4-5 mmol/L: decreased deep tendon reflexes (DTR)
- 5-7 mmol/L: hypotension
- 10 mmol/L: respiratory paralysis and coma
- 10-20 mmol/L: heart block and cardiac arrest

Magnesium Uses

Preeclampsia

Improves symptoms by systemic, vertebral, and uterine vasodilation via direct effects and increasing concentrations of endogenous vasodilators
Typically administered as 4 g IV load over 15 minutes, followed by 1 g/hr for 24 hours
Crosses the placenta, potentially causing neonatal lethargy, hypotension, and respiratory depression

Dysrhythmias

Blocks calcium influx, decreasing SA node activity and prolonging AV conduction time
Recommended for treating torsade's de pointes

Analgesia

Functions as a calcium and NMDA antagonist

Asthma

Induces bronchodilation via calcium inhibition in smooth muscle

Pheochromocytoma

Reduces catecholamine release and dilates vasculature

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Questions and Answers

What is the primary reason for cerebral edema in hyponatremia?

What is the initial treatment approach for hyponatremia?

What is a potential complication of rapid correction of hyponatremia?

What is the recommended rate of sodium correction in hyponatremia?

What is the purpose of administering 3% saline in the treatment of hyponatremia?

What symptoms would a patient with a sodium level of 128 likely exhibit?

A patient with a sodium level of 132 is likely to exhibit which of the following symptoms?

What is the likely sodium level of a patient experiencing nausea and malaise?

Which of the following is a consequence of excessive water absorption in the brain?

What is the primary mechanism by which 3% saline helps to treat hyponatremia?

Which of the following is a characteristic of acute hyponatremia?

What is the primary goal of correcting sodium levels in hyponatremia?

Which of the following is a risk factor for developing cerebral edema due to hyponatremia?

Which condition is associated with isotonic hyponatremia?

What is the typical serum osmolality range in isotonic hyponatremia?

Which of the following is NOT a characteristic of hypertonic hyponatremia?

What is the expected effect of mannitol therapy on serum osmolality?

What is the expected effect on serum osmolality in hypotonic hyponatremia?

Which of the following is a characteristic of hypotonic hyponatremia?

What is the significance of serum osmolality in diagnosing hyponatremia?

What is the formula to calculate free water deficit?

Which of the following conditions is associated with hypernatremia with low total body water and normal total body sodium?

What is a potential cause of hypernatremia with increased total body sodium?

Which of the following is NOT a cause of hypernatremia with dehydration and low total body sodium?

What is a common feature among Conn syndrome, Cushing syndrome, and hemodialysis?

What is the typical clinical sign of a patient with a serum osmolality of 401-430?

Which of the following symptoms is NOT typically seen in a patient with a serum osmolality of 350-375?

What is the expected outcome of a patient with a serum osmolality above 430?

Which of the following symptoms is typically seen in a patient with a serum osmolality between 376-400?

What is the typical range of serum osmolality associated with confusion, restlessness, agitation, and headache?

What is the primary clinical manifestation of a patient with a serum osmolality of 401-430?

What is the expected outcome of a patient with a serum osmolality above 430 if left untreated?

What is the typical range of serum osmolality associated with ataxia, tremors, and weakness?

What is the primary clinical manifestation of a patient with a serum osmolality of 376-400?

Which of the following potassium levels is a critical threshold for cardiac complications?

What is the primary mechanism by which hypokalemia affects cardiac conduction?

What is the typical serum potassium level at which muscle weakness becomes apparent?

What is the primary cause of potassium shift into cells in the treatment of hypokalemia?

What is the primary danger associated with hypokalemia?

What is the typical serum potassium level at which cardiac arrhythmias become apparent?

What is the primary cause of potassium shift out of cells in hypokalemia?

What is the primary mechanism of action of IV infusion of calcium in hyperkalemia treatment?

What is the primary goal of administering IV infusion of glucose and insulin in hyperkalemia treatment?

What is the indication for immediate hemodialysis in hyperkalemia treatment?

What is the duration of action of IV infusion of sodium bicarbonate in hyperkalemia treatment?

What is the primary mechanism of action of K-binding resins in the GI tract in hyperkalemia treatment?

What is the duration of action of IV infusion of calcium in hyperkalemia treatment?

What is a potential cause of hyperkalemia due to increased potassium intake or absorption?

What is a potential cause of hyperkalemia due to impaired renal excretion?

What is a potential cause of hyperkalemia due to transcellular shift?

What is a potential cause of hyperkalemia due to cellular injury?

What is a potential cause of hyperkalemia associated with adrenal disorders?

What is the primary function of parathyroid hormone in maintaining serum calcium levels?

What is the effect of acidemia on serum calcium levels?

What is the significance of measuring ionized calcium levels in critically ill patients?

What is the role of calcium in muscle contraction?

What is the percentage of calcium that is found in the bone?

What is the percentage of calcium in the ionized and physiologically active form?

What is the normal range of total serum calcium?

What is the critical serum potassium level above which QRS widening can lead to sine waves, ventricular fibrillation, and cardiac arrest?

What is a potential cause of pseudohyperkalemia, which can be a lab artifact?

What is the primary goal of treatment for hyperkalemia?

What is the primary mechanism of action of IV infusion of calcium in the treatment of hyperkalemia?

Which of the following conditions is associated with hypocalcemia due to PTH resistance?

What is a common cause of hypocalcemia due to vitamin D insufficiency?

Which of the following is a cause of hypocalcemia due to calcium chelation?

Which of the following conditions can cause secondary hypoparathyroidism?

What is a cause of hypocalcemia due to parathyroid hormone insufficiency?

Which of the following symptoms is most closely associated with cardiovascular manifestations of hypocalcemia?

Which of the following symptoms is most closely associated with neuromuscular manifestations of hypocalcemia?

Which of the following symptoms is most closely associated with pulmonary manifestations of hypocalcemia?

Which of the following medications is most likely to cause hypercalcemia due to increased calcium ingestion?

What is the underlying mechanism of hypercalcemia in malignant disease?

Which of the following non-parathyroid endocrine disorders is associated with hypercalcemia?

What is the underlying mechanism of hypercalcemia in milk-alkali syndrome?

What is a common neurological symptom of hypercalcemia?