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Fluids and Electrolytes Flashcards

1
Q

What is the effect of small bowel fistula on acid-base balance?

A

Small bowel fistula leads to normal anion gap metabolic acidosis.

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2
Q

What is the sodium concentration in 3% NS?

A

3% NS has 513 Na.

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3
Q

What is the normal serum osmolarity range?

A

Normal serum osmolarity is 280-295.

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4
Q

How is serum osmolarity calculated?

A

Serum osmolarity is calculated as 2XNa + glucose/18 + BUN/2.8.

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5
Q

What does high serum osmolarity indicate?

A

High serum osmolarity indicates dehydration or diabetes insipidus.

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6
Q

What does low serum osmolarity indicate?

A

Low serum osmolarity indicates fluid overload or SIADH.

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7
Q

What is the normal urine specific gravity range?

A

Normal urine specific gravity is 1.002 to 1.028.

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8
Q

What does high urine specific gravity suggest?

A

High urine specific gravity suggests dehydration or SIADH.

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9
Q

What does low urine specific gravity suggest?

A

Low urine specific gravity suggests fluid overload or diabetes insipidus.

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10
Q

What fluid is used for sweat fluid loss?

A

Normal saline is used for sweat fluid loss.

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11
Q

What fluid is used for saliva fluid loss?

A

1/2 NS with 20 K is used for saliva fluid loss.

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12
Q

What is the effect of small bowel and pancreatic juice loss?

A

It causes hyponatremic, hypokalemic non-anion gap metabolic acidosis.

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13
Q

What metabolic condition is caused by sweating?

A

Sweating causes hypernatremic metabolic acidosis.

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14
Q

What are the characteristics of diabetes insipidus?

A

Diabetes insipidus is characterized by hypernatremia, low urine sodium, high UOP, low specific gravity, and high serum sodium and osmolarity.

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15
Q

What can cause diabetes insipidus?

A

Diabetes insipidus can occur with ETOH or head injury.

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16
Q

What is the treatment for central diabetes insipidus?

A

The treatment for central diabetes insipidus is DDAVP.

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17
Q

What is the treatment for nephrogenic diabetes insipidus?

A

Nephrogenic diabetes insipidus is treated with a low salt diet, thiazide diuretic, and D5 water.

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18
Q

What are the characteristics of SIADH?

A

SIADH is characterized by hyponatremia, high urine sodium >20, low UOP, high urine specific gravity, high urine Na, and low serum Na and osmolarity.

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19
Q

What causes hyponatremia in SIADH?

A

High levels of ADH lead to natriuretic peptide release, causing sodium loss in urine.

  • Can occur with head injury
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20
Q

What is the treatment for neurological symptoms in SIADH?

A

For neurological symptoms like seizure or lethargy, hypertonic saline is the treatment.

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21
Q

What is the initial treatment for mild symptoms of SIADH?

A

Fluid restriction is the initial treatment for mild symptoms of SIADH.

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22
Q

What is the treatment for SIADH due to brain injury?

A

For SIADH due to brain injury, 3% hypertonic saline is the treatment.

-fluid restriction can cause injury

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23
Q

What medications block ADH receptors in the kidney?

A

Conivaptan and demeclocycline block ADH receptors in the kidney.

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24
Q

What causes cerebral salt wasting?

A

Cerebral salt wasting is caused by excess release of atrial natriuretic peptide (released from right atrium)

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25
Q

What is the classic presentation of cerebral salt wasting?

A

Cerebral salt wasting is classically described as a patient with SAH, high urine output, and hyponatremic hypovolemia.

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26
Q

What is the key difference between SIADH and cerebral salt wasting?

A

The key difference is that in cerebral salt wasting, hyponatremia is caused by loss of sodium in urine, while in SIADH, it is due to water retention.

  • Means that the only difference between the two is intravascular status
  • CSW = Hypovolemic = key to diagnosis, while SIADH = Euvolemic or hypervolemic
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27
Q

What is the treatment for cerebral salt wasting?

A

The treatment for cerebral salt wasting is to replenish intravascular volume with normal saline.

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28
Q

What are the symptoms of hypercalcemia?

A

Hypercalcemia symptoms include nausea, vomiting, abdominal pain, AMS, ulcers, and kidney stones.

29
Q

How is corrected calcium calculated?

A

Corrected calcium = Serum calcium + 0.8(4 - serum albumin).

30
Q

What is the most common cause of hypercalcemia in outpatient settings?

A

The most common cause of hypercalcemia in outpatient settings is primary hyperparathyroidism (PHPT).

-in inpatient its cancer

31
Q

What is the most common cancer causing hypercalcemia? What are other cancers that can cause hypercalcemia?

A

The most common cancer causing hypercalcemia is breast cancer. Other cancers include squamous cell lung cancer and multiple myeloma.

32
Q

What are the PTH levels in cancer causing hypercalcemia?

A

PTH levels are low in cancer causing hypercalcemia.

33
Q

What is the main mechanism of high calcium in cancer?

A

The main mechanism is elevated calcium due to PTHrP, which resorbs calcium in the kidney and causes bone destruction.

  • Non-hematological malignancy: PTH-rp
  • Hematologic malignancy: Cause bone destruction causes increase in Ca, MC multiple myeloma
34
Q

What is the treatment for all hypercalcemia?

A

The treatment includes normal saline + bisphosphonate (zoledronic acid) as the initial treatment of choice.

35
Q

What to use if a patient with hypercalcemia has renal failure?

A

If renal failure is present, denosumab is used to reduce osteoclast activity instead of bisphosphonates.

36
Q

What are adjunct treatments for hypercalcemia?

A

Adjunct treatments include calcitonin, cinacalcet, and steroids.

37
Q

When should steroids be given in hypercalcemia?

A

Steroids should be given for lymphoma secreting calcitriol.

38
Q

What is the role of loop diuretics in hypercalcemia?

A

Loop diuretics have fallen out of favor as they worsen electrolytes.

39
Q

What does cinacalcet do?

A

Cinacalcet decreases PTH production and is used in secondary hyperparathyroidism, ectopic PTH, and parathyroid cancer to decrease calcium.

Cinacalcet is not used in malignant hypercalcemia because PTH is suppressed.

40
Q

What is the fluid production by saliva?

A

Saliva produces about 1500 ml.

41
Q

What is the fluid production by the stomach?

A

The stomach produces about 1000-2000 ml.

42
Q

What is the fluid production by the biliary system?

A

The biliary system produces about 500 ml.

43
Q

What is the fluid production by pancreatic juice?

A

Pancreatic juice produces about 1500 ml.

44
Q

What is the fluid production by the small bowel?

A

The small bowel produces about 1500 ml.

45
Q

What is tumor lysis syndrome characterized by?

A

Tumor lysis syndrome is characterized by high uric acid, potassium, phosphate, and low calcium, along with metabolic lactic acidosis and AKI.

46
Q

What should be avoided in tumor lysis syndrome?

A

Calcium should be avoided as it causes calcium-phosphate crystal deposition in the kidney, leading to renal injury.

47
Q

What is the treatment for tumor lysis syndrome?

A

The treatment is hydration, and dialysis if refractory.

48
Q

What is the most common cause of metabolic alkalosis?

A

The most common cause of metabolic alkalosis is contraction alkalosis (NGT to suction, vomiting, GOO, pyloric stenosis).

49
Q

What do gastric losses cause in metabolic alkalosis?

A

Gastric losses cause low chloride and hydrogen, leading to hypochloremic alkalosis.

50
Q

What is the treatment for metabolic alkalosis?

A

The treatment is fluid resuscitation with normal saline.

51
Q

What are the two forms of metabolic alkalosis?

A

The two forms are chloride responsive alkalosis and chloride resistant alkalosis.

52
Q

What characterizes chloride responsive alkalosis?

A

Chloride responsive alkalosis is characterized by temporary loss of chloride that can be replaced, with low chloride in urine <10.

  • Examples: gastric loss, NGT, vomiting, diuretic use
  • these you treat by giving NS
53
Q

What characterizes chloride resistant alkalosis?

A

Chloride resistant alkalosis is characterized by hormonal mechanisms where chloride cannot be replaced, with high chloride in urine >20.

-Examples: Conn syndrome, secondary hyperaldosteronism, cushings

54
Q

How is total free water deficit calculated for males?

A

Total free water deficit = 0.6 (male) × weight (kg) × [(Serum Na+/140) - 1].

55
Q

How is total free water deficit calculated for females?

A

Total free water deficit = 0.5 (female) × weight (kg) × [(Serum Na+/140) - 1].

56
Q

How much of the total free water deficit should be replaced in the next 24 hours?

A

Half of the total free water deficit should be replaced in the next 24 hours.

57
Q

What is plasma osmolarity?

A

Plasma osmolarity = (2 X Na) + (glucose/18) + (BUN/2.8). Normal is 280-295.

58
Q

What can cause pseudohyponatremia?

A

Hyperglycemia can cause pseudohyponatremia; for each 100 glucose over normal, add 2 Na.

59
Q

What can cause pseudohypocalcemia?

A

Low albumin can cause pseudohypocalcemia; corrected calcium = Serum Ca + 0.8 × [4 - albumin].

For every 1 g of decrease in albumin, add 0.8 to Ca

60
Q

What is the formula for anion gap?

A

Anion gap = Na - (HCO3 + Cl); normal is <12.

61
Q

What is the delta anion gap used for?

A

Delta anion gap checks if CO2 responded appropriately in high anion gap metabolic acidosis.

  • = (change in anion gap from normal – change in CO2 from normal)
  • < 1 = also has Non-gap metabolic acidosis, >1 also has metabolic alkalosis
62
Q

What does FeNa indicate?

A

FeNa = (Urine Na/Cr) / (Plasma Na/Cr); it helps assess kidney function.

63
Q

What characterizes contrast-induced nephropathy?

A

Contrast-induced nephropathy is characterized by intrinsic kidney injury with FeNa <1%, normal UOP, rise in Cr, and muddy brown casts.

64
Q

What do brown casts indicate?

A

Brown casts indicate acute tubular necrosis (ATN).

65
Q

Paradoxical acuduria

A

Kidney reabsorbed Na in exchange for K. Na/K pump (aldosterone)  hypokalemia
K/H exchanger in kidney  absorbs K  paradoxical aciduria
Tx: Fluid resuscitation with normal saline!!!

66
Q

Acid-base abnormality associated with high ouput fistula/stoma

A

-Metabolic acidosis with a normal anion gap
-Normal anion gap because loos of HCO3- with compensatory increase in Cl-
-Hyperchloremic because negatively charged Cl- displaced to extracellular space with loss of bicarb

67
Q

Metabolic acidosis in vomiting (gastric outlet obstruction, congenital hypertrophic pyloric stenosis)

A

Hypokalemic, hypchloremic metabolic alkalosis

68
Q

Medical treatment of caclicum channel blocker toxicity

A

-IV calcium gluconate or chloride
-High-dose insuilin
-Atropine if bradycardic
-Norepinephrine if suspected vasodilatory shock
-Dobutamine or epinephrine if suspected cardiogenic shock

Intubate if GCS less than 8

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