Chem: Mg

  1. Where is most of the Mg found in our bodies?
    ICF, about half found in muscles
  2. How much Mg found in the plasma?
  3. Normal Value?
    1.8-2.5 mg/dl 1.5-1.9 mEq/L
  4. How much of the Mg is ionized?
    • 55% ionized
    • 30% bound to protein
    • 15% bound to anions
  5. What do we use Mg for?
    • Enzyme synthesis
    • DNA and protein synthesis
    • energy metabolism
    • glucose utilization
    • Fatty acid synthesis and breakdown
  6. Name some of the channel/pump that Mg influences?
    • Na/K ATPase pump
    • Na/Ca ATPase pump
    • Ca leak channel
    • others
  7. Why is Mg referred to as an endogenous antagonist of Ca?
    • maintenance of Ca leak channels=norm vascular tone
    • prevention of vasospasm
    • prevention of Ca overload in tissue
  8. Is Mg involved in enzyme reactions?
    Yes, it is often a Co-factor
  9. What interaction does Mg have with PTH?
    • PTH partially responsible for the absorption of Mg
    • controls end organ sensitivity to both PTH and Vit D
  10. Why will abnormalities in Mg result in abnormalities of Ca metabolism?
    Mg is responsible for control of Vit D
  11. What role in K metabolism does Mg have?
    regulation of the Na/k ATPase pump particularly in K depleted states
  12. Does Mg help regulate cell membranes?
  13. Where is Mg found as a structural component?
    Cell membranes and bones
  14. How does hypo Mg effect axonal transmission?
    Mg stabilizes neural fiber. In low Mg stated transmission speed is increased and more excitable
  15. How does Mg effect the release of nuerotransmitters?
    competition with Ca inhibits Ca entry into presynaptic terminal
  16. How will the muscles react to a low Mg state?
    contract more to a smaller stimulus, this leads to tetany
  17. When would hypermagnesemia be used theraputically?
    • Premature labor
    • Pre-eclampsia & eclampsia
    • Torsades
    • Prevents vasospasm via blocking release of catechols
  18. Most pt's will begin to show symptoms of a Mg level below?
    1.2 mg/dl
  19. Will low levels of Mg increase Dig toxicity?
  20. How is it that levels are usually low?
    • excessive loss via GI tract
    • failure of kidneys to conserve Mg
  21. How many of hospitalized alcoholic pt's will have low levels of Mg?
  22. What drug can lower Mg levels?
    • aminoglycosides
    • chemo
    • cardiac glycosides
    • diuretics
  23. When might an intracellular shift of phos be noted?
    • Thyroid hormones
    • insulin
  24. Why would low levels of Mg cause Dig tox?
    Mg regulates the Na/K ATPase pump thereby decreasing the effectiveness. This could lead to K wasting in the kidneys and Low K increases dig tox.
  25. If a pt is hypo Mg and hypo K is it likely that you would have to replace both lytes?
  26. If we were going to treat Mg with IV bolus what dose would we give?
    8-16 mEq in bolus over an hour, followed by 2-4 mEq/hr, followed by 1 mEq/min
  27. When replacing Mg do we need to use a monitor?
  28. What is the most common cause of hyperMg?
    • Iatrogenic: Antacids, enemas, parenteral nutrition
    • Renal failure
  29. what are some of the less common causes of HyperMg?
    • Addsions disease
    • lithium tox
    • hypothyroidism
  30. Why would we see a depressed musculoskeletal function in lieu of hyperMg?
    Mg is a competitive inhibitor of Ca, so more Mg would mean that there is less Ca to help with the release of acetylcoline
  31. How does hyperMg effect the muscle relaxants that we might use?
    • it potentates the effect of the nondepolarizing musc relaxants
    • reduces the release of K when used with Succ
  32. How would we treat acute neuro and cardiac toxicities associated with hyperMg?
    5-10mEq Ca IV, ECF fluid expansion and lasix to increase secretion,dyalysis
  33. Is the emergency treatment of hyperMg with Ca a definitive treatment?
    not really, only buys us time to work on underlying cause
Card Set
Chem: Mg
BC Boston College chem:lytes