Electrolyte Disorders PRE-CLASS - Calcium, Phosphorus, Magnesium

• Describe human pathophysiology of disorders of Ca, Ph, and Mg

• Use CORRECTED CALCIUM Equation to correct a serum calcium in someone with a serum albumin <4 g/dL

• Identify common causes of disorders of electroyltes

• Recognize disorders based on presentation

• Explain MOA of therapies used to treat HYPERCaclemia and HYPOcalcemia

• Design patient care plan for treatment regimen for calcium, Ph, and Mg

Learning Objectives

• Disorders of calcium homeostasis are related to calcium content in the ECF (extracellular fluids)

  • CA in ECF = 0.5%

  • Ca in bone = 99%

• 50% of calcium in the ECF is BOUND TO PLASMA protein (Albumin)

• Free calcium is the “active form”

Calcium Points

• Normal Serum Calcium points = 8.5-10.5

• Corrected calcium equation

  • Measured SCalcium + (0.8 x [4 g/dL - measured albumin])

Calcium Levels points

PTH, Vit. D, and Calcitonin

3 main things that can help with calcium homeostasis

• increases serum Ca stimulating calcium release from bone

• Increases renal tubular reabsorption of calcium

• Increases absorption of calcium in the GI tract secondary to increased 1,25 Vit D in kidney

How does PTH help regulate calcium homeostasis?

• Increases serum Ca and Phosphorous by increasing GI absorption

• Increases calcium release from bone and reduce renal excretion of calcium (indirectly)

How does Vit D help regulate calcium homeostasis?

• Inhibits osteoclastic bone resorption

How does Calcitonin help regulate calcium homeostasis?

1. Low calcium / High Phosphorous

2. Parathyroid glands secrete PTH to the kidneys

3. Kidneys reabsorb calcium and secrete Phosphorous (increase Calcium/ Decrease Ph)

• Kidneys then secrete Vit D (1, 25) to GUT and cause increase in Ca and Ph

Steps of How ParaThyroid increases calcium reabsorption via KIDNEYS/GUT

1. Low calcium / High Phosphorous

2. Parathyroid glands secrete PTH to the bones

3. Bone resorption results in increase in Calcium AND Phosphorous

Steps of How ParaThyroid increases calcium reabsorption via BONES

FGF23

Increase in phosphorous signals bones to release _____ which in turn lowers phosphorous and regulates levels

hypercalcemia definition

• serum calcium > 10.5

• Ionized calcium > 5.6

Mild (10.5-11.9 // 5.6-8)

Moderate (12-13.9 // 8-10)

Severe (14-16 // 10-12)

Hypercalcemia pathophysiology

One or combo of the following:

• increase in bone resorption

• Increase in GI absorption

• Increase tubular reabsorption by kidney

Hypercalcemia ETIOLOGY

Important ones to know:

• Cancer

• Primary hyperthyroidism

• Thiazide AND lithium medications

Hypercalcemia clinical presentation

CNS:

• AMS

GI

• ABD pain

Kidney

• Volume depletion

Cardiac

• Shortened QT interval

HyPOcalcemia definition

Serum calcium < 8.5 and Ionized <4.4 (when albumin is > 4)

HYPOcalcemia parhophysiology

• Vit D deficiency

• Parathyroidectomy (surgery)

• Loop diuretics (drug induced)

Just know these ones!

HyPOcalcemia clinical presentation

Cardiac

• PROLONGED QT interval

Neuromuscular

• tetany

• Muscle cramps

Phosphorous points

Phosphate is the major intracellular anion

Role of phosphorus

• Cellular metabolism and energy production
  (ATP!)

Muscle contractility

Oxygen delivery

• Electrolyte transport

• Neurologic function

Normal serum phosphorus range:

• 2.5 - 4.5 mg/dL (0.9 - 1.45 mmol/L)

Phosphorous homeostasis points

• Typical western diet includes 800-1600 mg Ph

• 60-80% absorbed in GI tract

• Steady state serum concentrations of Ph regulated by

  • GI tract

  • Kidney

  • Bone

Hyperphosphatemia

Serum Phosphate > 4.5

HYPERphosphatemia pathophysiolot and etiology

• CKD or AKI

• Tumor lysis syndrome (tissue catabolism)

only these are important fro exam

Hyperphosphatemia clinical presentation

Lethargy (CNS)

N/V/D ( GI)

Calciphylaxis (Vascular)

HYPOphosphatemia definition

Serum Phos < 2.5

2-2.4(mild)

1-2 (moderate)

<1 (severe)

HYPOphosphatemia Pathophysiology/etiology

• Phosphate binding drugs (low GI absorption)

• Referring syndrome

• Alcoholism

HYPOphosphatemia clinical presentation

• Arrhythmias (cardiac)

• Weakness, numbness, confusion (CNS)

Magnesium points

Fourth most abundant extracellular cation

Second most abundant intracellular cation, after potassium

Role of magnesium

• Cellular function
  Glucose metabolism

• Parathyroid hormone secretion
  Magnesium distribution

• Bone (67%)
  Muscle (20%)
  Normal serum magnesium range:

•1.7 - 2.4 mg/dL (1.4 - 2 mEq/L)

Magnesium homeostasis steps

Hypermagnesemia

Mg > 2.4

Hypermagnesemia pathophys/etiology

• AKI

• Severe CKD with exogenous intake

• Lithium drugs

HyPOmagensemia definition

Mg < 1.7

Hypomagnesemia pathophys/etiology

• Reduced GI absorption

• Drug induced in kidney

• Chronic alcoholism

Hypomagnesemia clinical presentation

1. Tetany and tremors/trousseau signs (Neuro)

2. EKG abnormalities

Key concept summary

1. When albumin is < 4g/dL it is important to calculate corrected calcium to determine the true serum calcium level

2. Serum calcium is closely regulated by the interaction of parathyroid hormone
   (PTH), phosphorous, vitamin D, and calcitonin

Serum phosphorus is regulated by the Gl tract, kidneys, and bone Magnesium homeostasis depends on the balance between intake and output Electrolyte disorders are diagnosed by lab values, and signs and symptoms of these electrolyte disorders are relatively non-specific; the presence of symptoms helps to determine severity, clinical treatment, and monitoring

Hypermagnesemia clinical presentation

• Lethargy and Muscle weakness (neuro)

• Arrhythmias