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Clin Med Exam 4 > Electrolytes Part 3 (Magnesium, Ca 2+ and Phosphate)-Paulson > Flashcards

Electrolytes Part 3 (Magnesium, Ca 2+ and Phosphate)-Paulson Flashcards

1
Q

Hypermagnesemia:

-plasma Mg=

A

> 2.5 mEg/L

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2
Q

Hypermagnesemia:

-how common?

A

Relatively rare other than in the setting of renal impairment

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3
Q

Hypermagnesemia:

pathophysiology?

A
  • Oral ingestion: Laxative abusers, accidental overdose of Epsom salts
  • Magnesium enemas

-Magnesium infusion:
Used for women with preeclampsia or eclampsia

  • Renal insufficiency:
  • -Magnesium is excreted renally–> levels rise as CKD worsens
  • -Antacids or laxatives in regular doses can provoke severe ↑ Mg
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4
Q

Hypermagnesemia:

-clinical features?

A
  • May be asymptomatic, esp. if level <4
  • Neuromuscular toxicity is most frequently observed
  • 4-6: nausea, flushing, headache, lethargy, drowsiness, ↓DTRs
  • 6-10: somnolence, hypocalcemia, absent DTRs, hypotension, bradycardia, EKG changes
  • > 10: Muscle paralysis–> flaccid quadriplegia, apnea, respiratory failure, complete heart block, cardiac arrest
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5
Q

Hypermagnesemia:

-Diagnostic labs?

A
  • Magnesium level
  • BMP
  • EKG
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6
Q

Hypermagnesemia:

-EKG findings?

A
  • Diminished conduction
  • Widened QRS
  • Prolonged PQ interval
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7
Q

Hypermagnesemia:

tx?

A
  • Normal renal function:
  • -Stop the offending agent
  • -May add diuretic to ↑ renal excretion of magnesium
  • Calcium gluconate given IV–>Helps stabilize cardiac membrane
  • Hemodialysis if severe + renal impairment
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8
Q

Hypomagnesemia=

A

Plasma magnesium levels < 1.8 mEq/L

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9
Q

Hypomagnesemia:

Most common causes?

A
  • **Chronic diuretic therapy (loop and thiazide)
  • Chronic alcoholism
  • **Chronic diarrhea
  • Hypoparathyroidism
  • Nutritional deficiencies (prolonged TPN, malnutrition)
  • Uncontrolled diabetes mellitus
  • **Chronic PPI usage
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10
Q

Hypomagnesemia:

-neurological features?

A
  • Tetany-may have a positive Trousseau and Chvostek sign, muscle spasm, muscle cramps
  • Seizures
  • Involuntary movements
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11
Q

Hypomagnesemia:

-Cardiovascular-EKG findings?

A
  • Widening of QRS & peaked T waves (moderate)
  • Prolonged PR interval, QRS widening, and diminished T wave (more severe)
  • Frequent PACs and PVCs, may develop sustained afib
  • Ventricular arrhythmias –> death
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12
Q

Hypomagnesemia:

-diagnostic labs?

A
  • These patients often have a concurrent **hypokalemia & hypocalcemia
  • If cause can’t be determined from HPI, 24 hour urine magnesium excretion or fraction excretion of magnesium on a random urine can help differentiate between GI and renal losses
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13
Q

Hypomagnesemia:

-tx of severe Sx?

A

Severe Sx ie tetany, arrhythmias, or seizures–>

  • IV magnesium sulfate
  • With continuous cardiac monitoring
  • Reduce dose in those with CrCl <30
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14
Q

Hypomagnesemia:

tx of Asymptomatic or minimal symptoms?

A

Oral replacement:

  • Magnesium chloride or magnesium oxide
  • **Diarrhea is a major side effect
  • Correct underlying disease if possible
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15
Q

Hypercalcemia=

A

Serum Calcium > 10.5 mEq/L

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16
Q

Normal serum Calcium=

A

9 to 10.5 mg/dL

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17
Q

Mild hypercalcemia=

A

10.5 to 12 mg/dL

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18
Q

Hypercalcemia:

-what serum Ca 2+ can be life threatening?

A

> 14 mg/dL

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19
Q

Hypercalcemia: CAUSES

-malignancy?

A
  • Ectopic secretion of PTH by tumor
  • Multiple myeloma
  • Bone mets
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20
Q

Hypercalcemia: CAUSES

-endocrine?

A
  • **Hyperparathyroidism
  • MEN (multiple endocrine neoplasias)
  • Hyperthyroidism
  • Pheochromocytoma
  • Adrenal insufficiency
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21
Q

Hypercalcemia: CAUSES

-ex’s of granulomatous diseases

A 
Sarcoidosis
TB
Histoplasmosis
Berylliosis
Coccidiomycosis
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22
Q

Hypercalcemia: CAUSES

-drugs?

A
  • Vitamins A and D
  • **Thiazide diuretics
  • Estrogens
  • Milk-alkali syndrome
  • Lithium
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23
Q

Hypercalcemia: CAUSES

-miscellaneous?

A
  • Dehydration
  • Prolonged immobilization
  • Iatrogenic
  • Rhabdomyolysis
  • Familial
  • Lab error
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24
Q

Hypercalcemia: CAUSES

-which 2 causes are the MOST important to remember?

A

-MALIGNANCY -HYPERPARATHYROIDISM

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25
Q

Hypercalcemia: presentation

Sx?

A
  • Symptoms: often vague and nonspecific
  • Non-focal abdominal pain
  • Constipation
  • Fatigue
  • Diffuse body aches
  • Anorexia
  • Nausea/Vomiting
  • Signs of intravascular volume depletion (tachycardia, orthostatic hypotension)
  • Anxiety, depression, confusion, hallucinations
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26
Q

Hypercalcemia: presentation

severe?

A
  • Lethargy, altered mental status, seizures, coma

- Cardiac conduction abnormalities

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27
Q

Ex’s of cardiac conduction abnormalities associated with hypercalcemia

A 
Bradyarrhythmias
Sinus arrest
AV blocks
AF
VT
LBBB or RBBB
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28
Q

Hypercalcemia:

-other possible EKG findings?

A
  • ST segment elevation

- Short QT interval – “classic” finding but not reliably seen in most patients (KNOW shortened QT interval)

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29
Q

Hypercalcemia: presentation

-rhyme to help remember the Sx?

A 
Painful BONES
Renal STONES
Abdominal GROANS
Psychic MOANS
(or psychiatric overtones)
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30
Q

Hypercalcemia: diagnostic labs?

-ionized Ca vs total Ca:

A

-The serum total calcium represents both bound and unbound calcium

  • Can measure IONIZED CALCIUM as a separate lab test, or can estimate:
  • -Account for albumin levels (next slide)
  • -May also check a 24 hour urine collection
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31
Q

slide 27

A

?

32
Q

Pts with hypercalcemia might have a “normal” calcium level if their ______ is low and vice versa

A

albumin

  • **Need to correct for albumin levels
  • **Or measure ionized calcium levels
33
Q

Corrected calcium =

A

measured total calcium + [0.8 x (4-albumin)]

34
Q

hypercalcemia:

-Additional Labs?

A

After confirming hypercalcemia:

-Serum PTH
If high–> Likely primary hyperparathyroidism

If low –> Check vit D level & PTHrP

35
Q

Hypercalcemia: tx?

A
  • Patients in hypercalcemic crisis are usually dehydrated
  • IV access and cardiac monitoring
  • Infuse NS “wide open” until BP and perfusion normalize
36
Q

For treatment of hypercalcemia, the routine use of __________ is no longer recommended

A

furosemide
–>Furosemide can actually worsen hypercalcemia if given to patients who are not yet volume replete; can adversely affect hemodynamics and renal status

37
Q

Hypercalcemia tx:

  • Other tx methods?
  • what is the last resort tx method for severe hypercalcemia?
A
  • *Osteoclast-inhibiting therapies:
  • Bisphosphonates (often used in hypercalcemia of malignancy)
  • Calcitonin
  • Glucocorticoids

-If severe, may need dialysis (last resort)

38
Q

Hypercalcemic crisis resulting from primary hyperparathyroidism: treatment?

A

*urgent parathyroidectomy is potentially curative

39
Q

EKG findings:

-Hypercalcemia

A

shortened QT

40
Q

EKG findings:

-hypocalcemia?

A

prolonged QT

41
Q

Hypocalcemia:

-defined as serum calcium of ____ or ionized calcium of _______

A

Serum calcium (corrected) <8.5 mg/dL or ionized calcium of <4.6 mg/dL

42
Q

Hypocalcemia: pathophysiology

-Hypoparathyroidism?

A
  • Genetic disorder
  • Postsurgical or Radiation-induced damage
  • Hungry bone syndrome
  • Infiltration of the parathyroid gland (ie: mets)
  • Autoimmune destruction
43
Q

Hypocalcemia: pathophysiology

-drugs?

A
  • Bisphosphonates & meds used to treat hypercalcemia
  • Calcium chelators (EDTA, citrate, phosphate)
  • Phenytoin
  • Fluoride poisoning
44
Q

Hypocalcemia: pathophysiology

-other causes?

A
  • **Hypomagnesemia
  • Vitamin D deficiency
  • PTH resistance
  • Renal disease
  • Loss of calcium from circulation
45
Q

Hypocalcemia: pathophysiology

-describe the etiology of loss of calcium from circulation

A
  • Tumor lysis
  • Acute pancreatitis
  • Osteoblastic metastases
  • Sepsis or acute severe illness
46
Q

Hypocalcemia: classic clinical features (KNOW! hint: 2 signs)

A
  • Trosseau sign

- Chvostek sign

47
Q

Trosseau sign=

A

carpal tunnel spasm after BP cuff is applied for 3 minutes

48
Q

Chvostek sign=

A

Spasm of facial muscle after tapping facial nerve in front of ear

49
Q

Hypocalcemia: clinical features (list ex’s)

A
  • May be asymptomatic
  • Muscle spasm or muscle cramps
  • Tetany
  • Paresthesias (perioral and peripheral)
  • Confusion
  • Seizures
  • Dry skin, brittle nails, coarse hair
  • Carpopedal spasm or tetany
  • Anxiety, depression, dementia
  • Laryngospasm or bronchospasm
  • EKG: Prolonged QT or ST flattening
50
Q

Hypocalcemia: diagnostic labs?

A
  • Total serum calcium (corrected for albumin) or ionized calcium
  • Serum phosphate
  • Vitamin D level
  • Serum PTH
  • Magnesium level
  • BMP
  • EKG
51
Q

Hypocalcemia: tx

-acute OR severely symptomatic?

A

IV calcium gluconate

–>Treat any emergent cardiovascular issues

52
Q

Hypocalcemia: tx

-mild?

A
  • **can be treated outpatient with oral calcium + vit D (calcitriol preferred)
  • **Treat any concurrent hypomagnesemia 1st to effectively treat the hypocalcemia
53
Q

Hyperphosphatemia:

-defined as serum phosphate of _____

A

> 4.5 mg/dL

54
Q

Hyperphosphatemia:

Pathophysiology- Acute causes (list 6)

A
  • **Acute renal failure (ARF)
  • Rhabdomyolysis
  • **Tumor lysis syndrome
  • Acute phosphate load
  • Hypoparathyroidism (acquired)
  • Extracellular shift of phosphate
55
Q

Describe acute phosphate load

A

=Excess phosphate in TPN, rapid administration of phosphate-rich drugs (ie: fosphenytoin), phosphate-containing laxatives given in prep for colonoscopy, vitamin D toxicity

56
Q

Describe the MC causes of hypoparathyroidism (acquired)

A

-**Parathyroidectomy, infiltration of parathyroid glands, metal overload (ie: hemochromatosis, Wilson disease, thalassemia)

57
Q

Describe the MC causes of extracellular shift of phosphate

A

Lactic acidosis, ketoacidosis, respiratory acidosis, crush injuries

58
Q

Hyperphosphatemia:

-list Ex’s of chronic causes

A
  • CKD **
  • Hypoparathyroidism (congenital or hereditary)–> Autoimmune, gene mutations
  • Pseudohypoparathyroidism
59
Q

Hyperphosphatemia:
clinical Sx?
-acute severe hyperphosphatemia can lead to accompanying ________

A

-*Most asymptomatic

  • Acute, severe hyperphosphatemia can lead to accompanying hypocalcemia:
  • -Tetany, muscle cramps, perioral numbness or tingling, seizures
  • -Trousseau or Chvostek sign, hyperreflexia, carpopedal spasm, seizure
60
Q

Hyperphosphatemia:

-other Sx?

A

-May have s/s of uremia:
Fatigue, n/v, AMS, pruritis, SOB, sleep disturbances

-May have painful masses around joints, skin ulcerations, irritated conjunctiva–> Ectopic calcifications

61
Q

Hyperphosphatemia:

-diagnostic labs?

A
  • Serum phosphorous
  • PTH to see if this is the cause
  • Serum calcium
  • Vit D level to look for toxicity
  • ?Renal ultrasound
62
Q

Hyperphosphatemia: tx?

A

**Treat underlying Cause

63
Q

Tx of Acute hyperphosphatemia and normal renal function

A

Saline + diuresis (loop diuretic) forces phosphaturia

64
Q

Tx of Acute hyperphosphatemia 2/2 to hypoparathyroidism

A

Calcium + Vit D supplementation to correct hypocalcemia

65
Q

Tx of Acute hyperphosphatemia 2/2 AKI

A
  • **Phosphate binders when level is > 6:
  • -If serum ionized calcium low: use a calcium based binder: calcium carbonate or calcium acetate
  • -If serum ionized calcium high, use a non-calcium-based binder: sevelamer, aluminum hydroxide, lanthanum carbonate

-** Dialysis if severe (serum phosphate > 12) or symptomatic

66
Q

Tx of Acute hyperphosphatemia 2/2 CKD

A

-Start tx when levels above normal range

  • Restrict dietary phosphate to 800-1000 mg
  • ->Dark colas, oysters, cheese, milk, organ meats, ice cream, chocolate, nuts/seeds
  • Phosphate binders to ↓ intestinal phosphate absorption
  • Dialysis to remove excess phosphate
67
Q

Hypophosphatemia is defined as a serum phosphate of _____

A

Serum phosphate < 2.5 mg/dL

68
Q

Hypophosphatemia: pathophysiology?

A
  • Respiratory alkalosis (causes a rapid redistribution of phosphate from serum into intracellular space)
  • Sepsis
  • Refeeding syndrome
  • Alcohol withdrawal
  • Renal transplantation
  • Hypercalcemia of malignancy
  • Hyperparathyroidism
  • Hereditary rickets
  • Vitamin D deficiency
  • Inhibition of phosphate absorption (antacids, phosphate binders, niacin)
  • Inadequate intake
69
Q

Hypophosphatemia: clinical Sx?

A
  • Rarely symptomatic unless serum phosphorous is <1 mg/dL
  • Metabolic encephalopathy
  • Proximal myopathy
  • Impaired myocardial contractility
  • Respiratory failure
  • Dysphagia
  • Rhabdomyolysis
  • Hemolysis
70
Q

Hypophosphatemia: diagnostic labs?

A

-Serum phosphorous

  • Urinary phosphorous excretion (24 hour or random specimen + calculate fractional excretion of filtered phosphate)
  • -Excreting < 100 mg or FEPO4 <5% –> low renal phosphate excretion

–Excreting >100 mg or FEPO4 >5% shows renal phosphate wasting

71
Q

What is the likely cause of hypophosphatemia when the Pt is excreting < 100 mg or FEPO4 <5% (low renal phosphate excretion) ?

A

Likely cause is internal redistribution or ↓ intestinal absorption

72
Q

What is the likely cause of hypophosphatemia when the Pt is excreting >100 mg or FEPO4 >5% (shows renal phosphate wasting) ?

A

Likely cause: hyperparathyroidism, vit D deficiency, renal tubular defect

73
Q

Hypophosphatemia: Asymptomatic + serum phosphate <2.0 mg/dL

-Tx?

A

**Oral phosphate therapy

74
Q

Hypophosphatemia:
symptomatic
-tx?

A
  • ** 1.0-1.9: Oral phosphate (but IV if rhabdo, CNS sx present, or hemolysis)
  • ** <1.0: IV phosphate, then switch to PO once serum phosphate is >1.5
75
Q

Hypophosphatemia:
urinary phosphate wasting
-tx?

A
  • More difficult to treat
  • Dipyridamole QID helps to ↑ phosphate levels
  • -Increases renal phosphate reabsorption

Clin Med Exam 4 (14 decks)

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