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Silverstein & Hopper (+ West) > chapter 53 - Magnesium and Phosphate > Flashcards

chapter 53 - Magnesium and Phosphate Flashcards

1
Q

What percentage of total body magnesium is in the serum?

A

< 1%

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2
Q

Which organs regulate magnesium homeostasis?

A

Intestines and kidneys

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3
Q

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

A

Cardiovascular and neuromuscular systems

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4
Q

T/F Mg is the most abundant intracellular cation

A

F - K+ is

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5
Q

Where is the vast majority of Mg?

A

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

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6
Q

What are the main metabolic functions of Mg?

A
  • 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
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7
Q

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

A

Loop of Henle

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8
Q

What are potential causes for hypomagnesemia (categories)?

A
  • 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)
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9
Q

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

A

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

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10
Q

What are the clinical signs associated with hypomagnesemia?

A
  • 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
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11
Q

How should we supplement an azotemic patient with magnesium?

A

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

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12
Q

What are causes for hypermagnesemia?

A
  • 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
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13
Q

What are clinical signs associated with hypermagnesemia?

A

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

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14
Q

Is ionized magnesium spensitive to detect hypomagnesemia? hypermagnesemia?

A

Hypomagnesemia - No

Hypermagnesemia - Yes

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15
Q

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

A

Calcium

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16
Q

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

A

Anticholinesterase treatment -> physostigmine

17
Q

What are the roles of phosphorous?

A
  • 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
18
Q

Where is most of the phosphate in the body?

A

80-85% in the bone and teeth

19
Q

Give 3 causes for spurious hyperphosphatemia?

A

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

20
Q

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

A

Proximal convoluted tubule

21
Q

What is the effect of calcitriol on phosphate?

A

Increases intestinal absorption

22
Q

What is the effect of PTH on phosphate?

A

Increases phosphaturesis

Increased osteolysis

23
Q

What hormones increase phosphate tubular reabsorption?

A

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

24
Q

What would be a clinically significant hypophosphatemia?

A

<1 mg/dL

25
Q

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

A

transcellular shifts

26
Q

What conditions can cause transcellular shifting of phosphate?

A

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

27
Q

How does hyperventilation lead to transcellular shifting of phosphate?

A

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

28
Q

How can hyperadrenocorticism lead to hypophosphatemia?

A

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

29
Q

What are the clinical signs associated with severe hypophosphatemia?

A

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

30
Q

Give 3 causes of transcellular shifts of phosphate leading to hyperphosphatemia

A

Tumor lysis syndrome, rhabdomyolysis, and hemolysis

31
Q

What are the clinical signs associated with hyperphosphatemia?

A

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

Silverstein & Hopper (+ West) (84 decks)

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