Electrolytes Flashcards

1
Q

What causes Spurious Hyponatremia?

A

Blood is drawn proximal to IV infusion or central line

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2
Q

When can you see Pseudohyponatremia?

A

Instruments that use “indirect” method, sample is prediluted before analysis

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3
Q

How do analyzers that use the “indirect” method of calculating Soldium work?

A

Calculate the plasma/serum sodium on the assumption that the H20 content of plasma is 93%.

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4
Q

When might the assumption that the H20 content of plasma is 93% be incorrect?

A
  • Hypertriglyceridemia
  • Hypercholesterolemia
  • Hyperproteinemia

*Water content in original sample is LOWER

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5
Q

How does Hyperglycemia affect Sodium?

A
  • Shift in Na+ into Extracellular space

* True hyponatremia, but unrelated to any intrinsic defect in sodium homeostasis

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6
Q

Formula used to assess the degree of change in sodium concentration attributable to glucose

A

1.6 X (serum glucose - 100) / 100

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7
Q

What does Hypertonic (>295 mOsm/kg) Hyponatremia suggest?

A
  • Hyperglycemia (marked)

- Mannitol (reduce ICP)

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8
Q
Hypotonic Hyponatremia (<280 mOsm/kg):
-Hypovolemic (Renal Loss) (5)
A

Increased Urine Sodium

  • Diuretics
  • Renal medullary dz
  • Addison dz (primary adrenal insuff.)
  • RTA type I
  • Cerebral salt wasting syndrome
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9
Q
Hypotonic Hyponatremia (<280 mOsm/kg):
-Hypovolemic (Extrarenal loss) (2)
A

Low Urine Sodium

  • GI (V/D)
  • 3rd spacing (peritonitis/pleuritis)
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10
Q
Hypotonic Hyponatremia (<280 mOsm/kg):
-Euvolemic (9)
A
  • SIADH
  • Psychogenic polydipsia
  • HypOthroidism
  • Addison Dz
  • ADH/Vasopressin-like drugs
  • Desmopressin
  • SSRis
  • TCAs
  • MDMA
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11
Q
Hypotonic Hyponatremia (<280 mOsm/kg):
-Hypervolemic (3)
A
  • CHF
  • Cirrhosis
  • Nephrotic syndrome
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12
Q

When do you most commonly see Hypernatremia?

A

Excess water loss and inability to respond to thirst response (Infants, ICU, debilitated)

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13
Q

Hypernatremia:

-Central Diabetes Insipidus

A

Damage to hypothalamus or nuerohypophysis

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14
Q

Hypernatremia:

-Nephrogenic (5)

A
Diseases that affect Medullary space:
-Sickle Cell, Tubulointerstitial nephritis
Electrolyte disturbances:
-HypOKalemia and HyperCalcemia
Renal Tubular Acidosis
Fanconi Syndrome
Drugs:
-Lithium, democlocyline, colchicine, AmptoB, gentamicin, furosemide
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15
Q

General causes of Hypokalemia. (3)

A
  • Renal loss
  • GI loss
  • Transcellular shift
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16
Q

Hypokalemia:

-Renal loss (10)

A

Urinary K+ >30mEq/day

  • Diuretics
  • Hypomagensemia
  • Abx
  • Minearlocorticoid excess
  • RTA types I and II
  • CAH
  • Bartter syndrome
  • Liddle syndrome
  • Gitelmand syndrome
  • Licorice (glyceyrrhizin)
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17
Q

Hypokalemia:

-GI loss (4)

A
  • Vomiting
  • NG tube suction
  • Diarrhea
  • Villous Adenoma
18
Q

Hypokalemia:

-Transcellular shift (2)

A
  • Metabolic Alkalosis

- Correction of DKA

19
Q

What happens to Potassium in DKA?

A
  • Initial Hyperkalemia
  • Profound Hypokalemia with correction of DKA

*Must give supplemental K+

20
Q

What happens to Potassium in Acidotic states?

A

HyperKalemia

21
Q

What are the acidotic states that are NOT associated with hyperkalemis?

A

RTA types I and II (hypokalemia)

22
Q

T/F: 50% of serum calcium is bound to protein.

A

True; primarily Albumin

23
Q

What are Calcium levels in a patient with Hypoalbuminemia?

A
  • Total calcium LOW

- Free (ionized) calcium is Normal

24
Q

What happens to Calcium in acidosis?

A
  • Decreases binding of calcium to Albumin

- Increases the proportion of free calcium

25
What happens to free calcium in Alkalosis?
Decreases
26
Presentation of pt. with Hypercalcemia. (4)
- CNS depression - N/V/Constipation - Peaked T waves on ECG - Nephrolithiasis
27
Hypercalcemia increases the risk of what? (2)
- Pancreatitis | - Peptic ulcer disease
28
What is calciphylaxis and what causes it?
Metastatic calcification of vessel walls and soft tissue | -Long term hypercalcemia with concomitant hyperphosphatemia (increased Ca x phosphate product)
29
Primary hyperparathryoidism lab findings. (5)
- Increased PTH - Increased Ca++ - Decreased Phosphate - Increased Cl-/PO4- ratio - Increased urinary cAMP
30
Define Secondary Hyperparathyroidism.
Excessive secretion of PTH in response to hypocalcemia of any cause.
31
MCC of secondary hyperparathyroidism.
Chronic Renal Failure
32
What malignancy are most commonly associated with Hypercalcemia (PTHrP)? (3)
- SCC (Lung, Head/Neck, Skin, Cervix, Esphagus) - Breast - T-cell Lymphoma
33
T/F: Hypervitaminosis D leads to increased calcium and phosphate.
True
34
MCC of primary hyperparathryoidism.
Parathyroid adenoma
35
Familial hypocalciuric hypercacemia gene/chr.
CASR gene on chr3
36
Which forms of PTH have biologic activity, what is their T1/2?
- Intact PTH - N-terminal PTH *T1/2 - 5 minutes
37
PTH forms that do not have biologic activity and T1/2.
- Mid-region PTH - C-terminal PTH *T1/2 - 36 hours
38
What causes CNS excitabitility (low or high Ca++)?
Hypocalcemia
39
Hypocalcemia presentation and classic exam findings. (5)
- Perioral tingling (paresthesia) - Muscle spasm - Hyperreflexia - Chvostek sign (twitching of the facial muscles in response to tapping over the area of the facial nerve) - Trousseau sign (carpopedal spasm that results from ischemia)
40
Hypocalcemia Cardiac manifestations. (3)
- QT prolongation - Low-voltage T waves - Dysrhythmias
41
F/T: Primary hypoparathyroidism is most often iatrogenic.
True