Magnesium is an important intracellular cation that plays a key role in many cellular processes. Hypomagnesemia can result from reduced intake, malabsorption, renal losses due to drugs or conditions like Gitelman syndrome, while hypermagnesemia commonly occurs in renal failure or with magnesium-containing drugs. Both conditions can impact neuromuscular and cardiac function. Treatment of hypomagnesemia involves oral or IV magnesium supplementation while hypermagnesemia may require calcium, diuretics, or dialysis. Magnesium levels also influence PTH secretion and activity.

1. Magnesium

2. • major intracellular divalent cation
• 2ND MOST COMMON INTRACELLULAR CATION (AFTER POTASSSIUM)
• 4TH MOST COMMON CATION IN THE BODY

3. Serum magnesium
60 % Bones
1 % ECF
Rest Inside cells
Normal serum magnesium 1.4 to 2.2 mEq/l

4. ROLE OF MAGNESIUM
• Cardiovascular tone
• Neuromuscular junction
• Key complex with ATP and is an important cofactor for a wide range
of enzymes, transporters, and nucleic acids required for normal
cellular function, replication, and energy metabolism

5. excretion of approximately 40
mg in intestinal secretions
Urinary excretion of the approximately 100 mg (4.1 mmol)

6. EGF action is required for normal DCT apical
expression of TRPM6)

7. Determinant of serum magnesium
• The main determinant of Mg2+ balance is the serum [Mg2+] itself;
• hypomagnesemia stimulates renal tubular resorption of Mg2+
• hypermagnesemia inhibits this process
• In case of normal RFT Mg2+ will be excreted normally

8. • Regulation of serum magnesium concentrations is achieved mainly by
control of renal magnesium reabsorption

11. Magnesium reabsorption in the cTAL
increased by inhibited by
PTH hypercalcemia or
hypermagnesemiaactivate the CaSR in
this nephron segment

13. Hypermagnesemia
Serum magnesium > 2.2

14. Causes
• Iatrogenic
• Renal failure patients receiving magnesium containing antacids , laxative or
IVF
• Eclampsia rx with magnesium sulphate
• ARF with acute rhabdomyolyis
• DKA with out treatment
• tumor lysis syndrome

16. Signs
>2mmol/L
>4.8 mg/dL
• vasodilation Hypotension that is refractory
to vasopressors or volume
expansion may be an early
sign
• neuromuscular blockade
>4 mmol/L • gastrointestinal
hypomotility or ileus;
facial flushing; pupillary
dilation; paradoxical
bradycardia; prolongation
of PR, QRS, and QT
intervals;
10 mmol/L, • asystole

17. • Hypermagnesemiaacting via the CaSRboth parathyroid
suppression and impaired cTAL calcium reabsorptionhypocalcemia
and hypercalciuria

18. CF
Neuromuscular Cardiac ECG Hypocalcemia
• Muscular weakness
• Lethargy
• Muscular paresis
• Respiratory depression
• Respiratory failure
• hyporeflexia (usually
the first sign of
magnesium toxicity),
• Peripheral vasodilation
• Bradyaarhythmia
• Cardiac asystole
• Prolonged PR interval
• Increased QRS
duration
• Increased QT interval
• Completet heart block
Hypermagnesemia
decreased secretion of
PTH

19. Rx
• Eliminate source
• 10 % calcium gluconate
• 1 pint NS followed by Inj Lasix if RFT is normal
• HD if RFT is abnormal

21. Hypomagnesemia
< 1.3 mEq/L

22. CAUSES

23. Causes
Increased renal
excretion
Increased GI losses Drugs Poor intake others
increased renal
tubular
flow (as occurs with
osmotic diuresis) as
well as impaired
tubular function (as
seen with resolving
acute tubular
necrosis [ATN], loop
diuretics, and
Bartter’s
and Gitelman’s
syndromes)
• prolonged
diarrhea
• nasogastric
aspiration
• malnutrition, as
is common in
chronic
alcoholics
• malabsorption
syndrome
aminoglycosides,
amphotericin B,
cisplatin,
pentamidine, and
cyclo-
sporine.
• c/c alcoholic • Primary
aldosteronism
• Hypoparathyroidi
sm

24. DIETARY
• PPI UNKNOWN MECHANISM
• ALCOHOLISM
• Diarrhea or surgical drainage fluid
• Malabsorptive states
• compounded by vitamin D deficiency, can critically limit magnesium absorption and produce
hypomagnesemia despite the compensatory effects of secondary hyperparathyroidism
and of hypocalcemia and hypomagnesemia to enhance cTAL magnesium reabsorption
• primary infantile hypomagnesemiaselective intestinal magnesium
malabsorption
• hypomagnesemia with secondary hypocalcemia
• mutations in the gene encoding TRPM6, a protein that, along with TRPM7, forms a channel
important for both intestinal and distal-tubular renal transcellular magnesium transport.

25. magnesium-wasting syndromes
DCT NaCl co-transporter (Gitelman’s syndrome)
cTAL Na-K-2Cl transport (Bartter’s syndrome)
claudin 16 or claudin19 autosomal recessive renal hypomagnesemia with
hypercalciuria
DCT Na + ,K + -ATPase γ-subunit autosomal dominant renal hypo-
magnesemia with hypocalciuria
DCT K+ channels (Kv1.1, Kir4.1)
mitochondrial gene encoding a tRNA
Activating mutations
of the CaSR.
hypomagnesemia as well as hypocalcemia

26. Neurologic manifestation Cardiac
• lethargy, confusion, tremor, fasciculations,
• ataxia, nystagmus, tetany, and seizures
• Atrial & ventricular arrhythmia
• prolonged PR and QT interval with a widened QRS.
Torsades de pointes is the classically associated
arrhythmia

27. • Other electrolyte abnormalities often seen with hypomagnesemia,
• hypocalcemia (with hypocalciuria)
• hypokalemia
Causes of hypocalcemia in hypomagnesemia
• concurrent vitamin D deficiency
• impaired synthesis of 1,25(OH)2D,
• cellular resistance to PTH
• a defect in PTH secretion

30. Rx of hypermagnesemia
If ECG changes + If asymptomatic and no ECG changes
1–2 g MgSO4 (1 g MgSO4 = 96 mg elemental Mg2+
= 8 mEq Mg2+) IV over 15 min, followed by an
infusion of 6 g MgSO4 in 1 L IV fluid over 24 hrs
Mild
hypomagnesemia:
240 mg PO elemental
Mg2+per day in divided doses
Severe 720 mg PO elemental
Mg2+per day in divided doses
MgSO4
the sulfate anions may bind calcium in serum
and urine and aggravate hypocalcemia

31. • Serum magnesium should be monitored at intervals of 12–24 h
during therapy, which may continue for several days because of
impaired renal conservation of magnesium (only 50–70% of the
daily IV magnesium dose is retained) and delayed repletion of
intracellular deficits, which may be as high as 1–1.5 mmol/kg (2–3
meq/kg)

32. • In severely hypomagnesemic patients with concomitant
hypocalcemia and hypophosphatemia,
• administration of IV magnesium , due to rapid stimulation of PTH
secretion worsen hypophosphatemia, provoking neuromuscular
symptoms or rhabdomyolysis.
• administering both calcium and magnesium

33. Magnesium

34. • Normal serum magnesium = 1.4 to 2.2 mEq/l
• Important role in neuromuscular function
• Maintenance of cardiovascular tone
• Approximately 60% of body magnesium is stored in bone, and most of
the remainder is found in cells. Only 1% is in the ECF

35. • Magnesium is required for PTH secretion and for PTH action

36. • Serum Ca and Serum Mg level always go parallel in the body.
• The notable exceptions
• CRF (Hypocalcemia and Hypermagnesemia),
• Gitelman syndome (Normocalcemia and hypomagnesemia)

37. Decreased intestinal absorption Increased renal excretion Drugs
• malnutrition
• Chronic alcoholics
• any malabsorption syndrome.
• prolonged diarrhea and
• nasogastric aspiration
• Loop diuretic
• Osmotic diuretics
• ATN
• Bartter’s syndrome
• Gitelman’s syndromes
• aminoglycosides,
• amphotericin B,
• cisplatin,
• pentamidine, and
• cyclosporine

38. • Causes of hypomagnesemia
• 1. Reduce intake especially common in alcoholic patient and on TPN
• 2. GI losses - chronic diarrhea
• 3. Kidney loss – diuretics, Gitelman syndrome.
• 4. Acute pancreatitis
• 5. Drugs - Foscarnet (It is an anti herpes group of drug used generall in zoster
ophthalmitis).

39. Neuromuscular Cardiovascular Metabolic
• Lethargy
• Confusion
• tremor
• Fasciculation
• Ataxia
• Tetany
• Seizures
• Aggarvated digitalis toxicity with
hypomagnesemia
• Prolonged PR & QT interval
• Hypocalcemia
 Mg deficiency leads to decrease
in PTH secretion & end organ
resistance to PTH
• Hypokalemia
 Mg deficiency enhances renal
excretion of K

40. Rx
• Magnesium supplement

42. Hypermagnesemia

43. Causes
• ARF with rhabdomyolysis
• CRF
• Addison disease
• Magnesium containing drugs.
• Hemolysis

44. CF
• Occur due to vasodilatation and neuromuscular blockage.
• There is paradoxical Bradycardia, Hypotension, Altered sensorium,
respiratory depression

45. • Treatment:
• 1. Injection calcium gluconate for heart
• 2. Diuretics (Frusemide)
• 3. Dialysis

47. effects of magnesium on PTH secretion
hypermagnesemia
suppresses
PTH secretion.
MILD HYPOMAGNESEMIA

48. • MILD HYPOMAGNESEMIA  INCREASE PTH
SECRETION
• SVERE  SUPPRESS PTH SECRETION
• severe, chronic hypomagnesemia intracellular
magnesium deficiency, which interferes with
secretion and peripheral responses to PTH. The
mechanism of the cellular abnormalities caused by
hypomagnesemia is unknown, although effects on
adenylate cyclase (for which magnesium is a
cofactor) have been proposed

49. HYPOMAGNESEMIA
Diminished peripheral responsiveness to PTHimpaired PTH secretion