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Boards.CP.Chemistry > Electrolytes > Flashcards

Electrolytes Flashcards

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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
Q

What happens to free calcium in Alkalosis?

A

Decreases

26
Q

Presentation of pt. with Hypercalcemia. (4)

A
  • CNS depression
  • N/V/Constipation
  • Peaked T waves on ECG
  • Nephrolithiasis
27
Q

Hypercalcemia increases the risk of what? (2)

A
  • Pancreatitis

- Peptic ulcer disease

28
Q

What is calciphylaxis and what causes it?

A

Metastatic calcification of vessel walls and soft tissue

-Long term hypercalcemia with concomitant hyperphosphatemia (increased Ca x phosphate product)

29
Q

Primary hyperparathryoidism lab findings. (5)

A
  • Increased PTH
  • Increased Ca++
  • Decreased Phosphate
  • Increased Cl-/PO4- ratio
  • Increased urinary cAMP
30
Q

Define Secondary Hyperparathyroidism.

A

Excessive secretion of PTH in response to hypocalcemia of any cause.

31
Q

MCC of secondary hyperparathyroidism.

A

Chronic Renal Failure

32
Q

What malignancy are most commonly associated with Hypercalcemia (PTHrP)? (3)

A
  • SCC (Lung, Head/Neck, Skin, Cervix, Esphagus)
  • Breast
  • T-cell Lymphoma
33
Q

T/F: Hypervitaminosis D leads to increased calcium and phosphate.

A

True

34
Q

MCC of primary hyperparathryoidism.

A

Parathyroid adenoma

35
Q

Familial hypocalciuric hypercacemia gene/chr.

A

CASR gene on chr3

36
Q

Which forms of PTH have biologic activity, what is their T1/2?

A
  • Intact PTH
  • N-terminal PTH

*T1/2 - 5 minutes

37
Q

PTH forms that do not have biologic activity and T1/2.

A
  • Mid-region PTH
  • C-terminal PTH

*T1/2 - 36 hours

38
Q

What causes CNS excitabitility (low or high Ca++)?

A

Hypocalcemia

39
Q

Hypocalcemia presentation and classic exam findings. (5)

A
  • 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
Q

Hypocalcemia Cardiac manifestations. (3)

A
  • QT prolongation
  • Low-voltage T waves
  • Dysrhythmias
41
Q

F/T: Primary hypoparathyroidism is most often iatrogenic.

A

True

Boards.CP.Chemistry (17 decks)

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