chapter 53 - Magnesium and Phosphate

Question 1

What percentage of total body magnesium is in the serum?

Answer 1

< 1%

Question 2

Which organs regulate magnesium homeostasis?

Answer 2

Intestines and kidneys

Question 3

What are the systems affected by hypomagnesemia and hypermagnesemia the most?

Answer 3

Cardiovascular and neuromuscular systems

Question 4

T/F Mg is the most abundant intracellular cation

Answer 4

F - K+ is

Question 5

Where is the vast majority of Mg?

Answer 5

Muscle (20%) and bone (60%) > heart and liver

Question 6

What are the main metabolic functions of Mg?

Answer 6

• Production and use of adenosine triphosphate
  (ATP)
• Coenzyme for the membrane bound
  sodium-potassium ATPase pump –> functions to maintain the sodium-potassium gradient across all membranes
• Coenzyme for calcium ATPase pump
• Coenzyme for proton pumps
• Protein and nucleic acid synthesis
• Regulation of vascular smooth muscle tone
• Cellular second messenger systems and signal transduction
• Influence on lymphocyte activation, cytokine production, and systemic inflammation

Question 7

What part of the kidney is the main site of magnesium reabsorption of the kidney?

Answer 7

Loop of Henle

Question 8

What are potential causes for hypomagnesemia (categories)?

Answer 8

• Decreased intake including IVF w/o Mg
• Increased loss (gastrointestinal, renal, lactation)
• Alterations in distribution (extracellular to intracellular shifts, chelation with circulating catecholamines or massive blood transfusion, sequestration with pancreatitis)

Question 9

What is the mechanism that explains the possible hypomagnesemia associated with pancreatitis?

Answer 9

Sequestration (insoluble soap formed) in areas of fat necrosis surrounding the pancreas

Question 10

What are the clinical signs associated with hypomagnesemia?

Answer 10

• Cardiac arrhythmias (atrial fibrillation, supraventricular tachycardia, ventricular tachycardia)
• Predisposition to digoxin-induced arrhythmias (increases uptake / inhibits the myocardial sodium-potassium ATPase pump, as does digoxin)
• Hypertension, coronary artery vasospasm, and platelet aggregation
• Generalized muscle weakness, muscle fasciculations, ataxia, and seizures
• Concurrent hypokalemia, hyponatremia, and hypocalcemia

Question 11

How should we supplement an azotemic patient with magnesium?

Answer 11

Because magnesium is excreted primarily by the
kidneys, the dosage should be reduced by 50% in azotemic patients and serum concentrations should be monitored frequently to prevent hypermagnesemia

Question 12

What are causes for hypermagnesemia?

Answer 12

• Renal failure, endocrinopathies, and iatrogenic overdose, especially in patients with impaired renal function
• Hypoadrenocorticism, hyperparathyroidism, and
  hypothyroidism (mechanism unknown)
• Improper dosing of magnesium replacement therapy

Question 13

What are clinical signs associated with hypermagnesemia?

Answer 13

Lethargy, depression, and weakness
Respiratory depression
Bradycardia, complete heart block and asystole

Question 14

Is ionized magnesium spensitive to detect hypomagnesemia? hypermagnesemia?

Answer 14

Hypomagnesemia - No

Hypermagnesemia - Yes

Question 15

What is a direct antagonist of magnesium at the neuromuscular junction and may be beneficial
in reversing the cardiovascular effects of hypermagnesemia?

Answer 15

Calcium

Question 16

What medication can be used to offset the neurotoxic effects of hypermagnesemia?

Answer 16

Anticholinesterase treatment -> physostigmine

Question 17

What are the roles of phosphorous?

Answer 17

• Production of ATP, guanosine triphosphate, cyclic adenosine monophosphate, and phosphocreatine, which function to maintain cellular membrane integrity, energy stores, metabolic processes, and biochemical messenger systems
• Maintenance of normal bone and teeth matrix
• Regulation of tissue oxygenation by way of 2,3-DPG
• Support of cellular membrane structure and ionic charge via phospholipids
• Mitochondrial production of ATP through the electron transport system by phosphoproteins
• Buffer

Question 18

Where is most of the phosphate in the body?

Answer 18

80-85% in the bone and teeth

Question 19

Give 3 causes for spurious hyperphosphatemia?

Answer 19

In vitro hemolysis or rupture of other blood cells, hypertriglyceridemia, and the presence of a monoclonal gammopathy

Question 20

Where is phosphate reabsorbed in the kidney (60-90% of filtered phosphate)?

Answer 20

Proximal convoluted tubule

Question 21

What is the effect of calcitriol on phosphate?

Answer 21

Increases intestinal absorption

Question 22

What is the effect of PTH on phosphate?

Answer 22

Increases phosphaturesis

Increased osteolysis

Question 23

What hormones increase phosphate tubular reabsorption?

Answer 23

Growth hormone, insulin, insulin-like growth factor 1, and thyroxine

Question 24

What would be a clinically significant hypophosphatemia?

Answer 24

<1 mg/dL

Question 25

From decreased intestinal absorption, transcellular shifts, or increased urinary excretion, which one is the most common?

Answer 25

transcellular shifts

Question 26

What conditions can cause transcellular shifting of phosphate?

Answer 26

alkalemia, hyperventilation, refeeding syndrome, parenteral nutrition, insulin administration, glucose administration, catecholamine administration or release, and salicylate toxicity.

Question 27

How does hyperventilation lead to transcellular shifting of phosphate?

Answer 27

Hyperventilation causes respiratory alkalosis, leading to rapid diffusion of carbon dioxide from the intracellular space to the extracellular space. The increase in intracellular pH activates phosphofructokinase and glycolysis, causing phosphate to rapidly shift into cells

Question 28

How can hyperadrenocorticism lead to hypophosphatemia?

Answer 28

Primary hyperaldosteronism causes renal loss of calcium, resulting in hypocalcemia, which stimulates secretion of PTH and may result in normal or low serum phosphate

Question 29

What are the clinical signs associated with severe hypophosphatemia?

Answer 29

Hemolysis, hypoxia (2,3-DPG), impaired chemotaxis, phagocytosis, and bactericidal activity of leukocytes, shortened platelet survival time, weakness, tremors, muscle pain, rhabdomyolysis, metabolic encephalopathy, GI upset

Question 30

Give 3 causes of transcellular shifts of phosphate leading to hyperphosphatemia

Answer 30

Tumor lysis syndrome, rhabdomyolysis, and hemolysis

Question 31

What are the clinical signs associated with hyperphosphatemia?

Answer 31

Anorexia, nausea, vomiting, weakness, tetany, seizures, and dysrhythmias