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ABSITE (EVAN) > Chapter 9: Fluids and Electrolytes > Flashcards

Chapter 9: Fluids and Electrolytes Flashcards

1
Q

Water weight distribution

A

2/3: intracellular (mostly muscle)

1/3: extracellular

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2
Q

Extracellular water distribution

A

2/3: Interstitial

1/3: plasma

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3
Q

Determine plasma/interstitial compartment osmotic pressures

A

Proteins

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4
Q

Determines intracellular/extracellular osmotic pressure

A

Sodium

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5
Q

MCC is iatrogenic; first sign is weight gain

A

Volume overload

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6
Q

What is the first sign of volume overload?

A

Weight gain

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7
Q

Can release a significant amount of water

A

Cellular catabolism

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8
Q

Normal saline:

[Na], [Cl]

A 
[Na] = 154
[Cl] = 154
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9
Q

3% Normal saline

[Na], [Cl]

A 
[Na] = 513
[Cl] = 513
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10
Q

Lactated ringer’s

[Na], [K], [Ca], [Cl], [Bicarb]

A 
[Na] = 130
[K] = 4
[Ca] = 2.7
[Cl] = 109
[Bicarb] = 28
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11
Q

Calculate plasma osmolarity

A

(2Na) + (Glucose/18) + (BUN/2.8)

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12
Q

Normal plasma osmolarity

A

280 - 295

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13
Q

How does water achieve osmotic equilibrium?

A

Water shifts from areas of low solute concentration (low osmolarity) to areas of high solute concentration (high osmolarity) to achieve osmotic equilibrium.

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14
Q

Estimates of volume replacement

A

4 cc/kg/h for 1st 10kg
2cc/kg/h for 2nd 10kg
1 cc/kg/h for each kg after that

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15
Q

Best indicator of adequate volume replacement

A

Urine output

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16
Q

Fluid loss during abdominal operations

A

0.5 - 1.0 L/h unless there are measurable blood losses

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17
Q

When should you think about replacing blood?

A

> 500 cc

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18
Q

What are insensible fluid losses?

A

10 cc/kg/day; 75% skin, 25% respiratory, pure water

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19
Q

Replacement fluids after major adult gastrointestinal surgery:
1st 24 hours ->
After 24 hours ->

A

1st 24 hours: LR

After 24 hours: D5 1/2 NS with 20 mEq K+

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20
Q

Why switch to D5 1/2 after 24 hours with replacement fluids after major adult gastrointestinal surgery?

A
  • 5% dextrose will stimulate insulin release, resulting in amino acid uptake and protein synthesis (also prevents protein catabolism)
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21
Q

How much glucose does D5 1/2 NS @ 125/h provide?

A

150g glucose per day (525 kcal/day)

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22
Q

GI fluid secretion:

Stomach

A

1-2 L/day

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23
Q

GI fluid secretion:

Biliary system

A

500 - 1,000 mL/day

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24
Q

GI fluid secretion:

Pancreas

A

500 - 1,000 mL/day

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25
Q

GI fluid secretion:

Duodenum

A

500 - 1,000 mL/day

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26
Q

Normal K+ requirement

A

0.5 - 1.0 mEq/kg/day

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27
Q

Normal Na+ requirement

A

1 - 2 mEq/kg/day

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28
Q

Electrolyte loss: sweat

A

Hypotonic (Na concentration 35-65)

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29
Q

Electrolyte loss: saliva

A

K+ (highest concentration of K+ in body)

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30
Q

Electrolyte loss: stomach

A

H+ and Cl-

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31
Q

Electrolyte loss: pancreas

A

HCO3-

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32
Q

Electrolyte loss: bile

A

HCO3-

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33
Q

Electrolyte loss: small intestine

A

HCO3- and K+

34
Q

Electrolyte loss: large intestine

A

K+

35
Q

Replacement: gastric losses

A

Replacement is D5 1/2 NS with 20 mg K+

36
Q

Replacement: pancreatic / biliary / small intestine losses

A

Replacement is LR with HCO3-

37
Q

Replacement: large intestine losses (diarrhea)

A

Replacement is LR with K+

38
Q

Replacement: GI losses

A

Should generally be replaced cc/cc

39
Q

Replacement: Dehydration (eg marathon runner)

A

Replacement with normal saline

40
Q

Replacement: urine output

A

Should be kept at least 0.5 cc/kg/h; should not be replaced, usually a sign of normal postoperative diuresis

41
Q

Peaked t waves on EKG; often occurs with renal failure

Tx?

A

Hyperkalemia

  • Calcium gluconate (membrane stabilizer for heart)
  • Sodium bicarbonate (causes alkalosis, K enters cell in exchange for H)
  • 10U insulin, 1 amp D50 (K driven into cells with glucose)
  • Kayexalate
  • Dialysis if refractory
42
Q

T waves disappear (usually occurs in setting of overdiuresis)

A

Hypokalemia

- May need to replace magnesium before you can correct K+

43
Q

Usually from dehydration; restlessness, irritability, seizures
- Correct with D5 water slowly to avoid brain swelling

A

Hypernatremia

44
Q

Usually from fluid overload; headaches, n/v, seizures.

A

Hyponatremia

45
Q

First-line treatment for hyponatremia

A

Water restriction, then diuresis

46
Q

Why correct sodium slowly?

A

Avoid central pontine myelinosis (no more than 1 mEq/h)

47
Q

How does sodium affect sugar?

A

Hyperglycemia can cause pseudohyponatremia - for each 100 increment of glucose over normal, add 2 points to the sodium value

48
Q

How does SIADH affect sodium?

A

SIADH: syndrome of inappropriate antidiuretic hormone can cause hyponatremia

49
Q

MC malignant cause of hypercalcemia

A

Breast cancer

50
Q

MC benign cause of hypercalcemia

A

Hyperparathyroidism

51
Q

Tx: hypercalcemia

  • General disease
  • Malignant disease
A
  • General: NS at 200-300 cc/h and Lasix

- Malignant: mithramycin, calcitonin, alendrotnic acid, dialysis

52
Q

Why no LR or thiazide diuretics in hypercalcemia?

A

LR: contains calcium

Thiazide diuretics: retain calcium

53
Q

Hyperrelfexia, Chovstek’s sign, perioral tingling and numbness, Trousseau’s sign, prolonged QT

A

Hypocalcemia

54
Q

Dx: hypercalcemia

A

Ca usually > 13 or ionized > 6-7 for symptoms (causes lethargy)

55
Q

Dx: hypocalcemia

A

Ca usually

56
Q

Causes lethargic state; usually in renal failure patients taking supplements.
Tx: calcium

A

Hypermagnesemia

57
Q

Usually occurs with massive diuresis, chronic TPN without mineral replacement or ETOH abuse; signs similar to hypocalcemia

A

Hypomagnesemia

58
Q

Calculate anion gap

A

Na = (HCO3 + Cl)

Normal:

59
Q

DDx: high anion gap acidosis

A

MUDPILES

Methanol, uremeia, DKA, paraldehydes, isoniazid, lactic acidosis, ethylene glycol, salicylates

60
Q

Acidosis usually secondary to loss of Na/HCO3- (ileostomies, small bowel fistulas).

A

Normal anion gap acidosis

61
Q

Tx: normal anion gap acidosis

A

Tx: underlying cause, keep pH > 7.20 with bicarbonate, severely decreased pH can affect myocardial contractility.

62
Q

Usually a contraction alkalosis

A

Metabolic alkalosis

63
Q

Electrolyte changes: nasogastric suction

A

Hypochloremic, hypokalemic, metabolic alkalosis, and paradoxical aciduria

64
Q

Pathophys: electrolyte changes nasogastric suction

A
  • Low Cl/H: NGT suction (hypochloremia, alkalosis)
  • Low H2O: kidneys reabsorb Na in exchange for K, (Na/K ATPase) thus losing K (hypokalemia)
  • Na/H exchange to reabsorb H2O with K/H to reabsorb K -> paradoxical aciduria
65
Q

Tx: electrolyte disturbance s/t nasogastric suction

A

Normal saline (need to correct the Cl- deficit)

66
Q

Time: respiratory compensation

A

Minutes (CO2 regulation)

67
Q

Time: renal compensation

A

Hours-days (HCO3- regulation)

68
Q

Best test for azotemia

A

FeNa

69
Q

Calculation: FeNa

A

(urine Na/Cr)/(plasma Na/Cr)

70
Q

Dx: prerenal azotemia

  • FeNa
  • Urine Na
  • BUN/Cr ratio
  • Urine osomolality
A

Prerenal azotemia:

  • FeNa 20
  • Urine osmolality > 500 mOsm
71
Q

%: renal mass damaged before you see increased Cr and BUN

A

70% of renal mass must be damaged before you see changes

72
Q

Prevent renal damage secondary to contrast dyes

A

Prehydration best prevents renal damage; HCO3- and N-acetylcysteine

73
Q

Converted to ferrihemate in acidic environment, which is toxic to renal cells.
Tx: alkalinize urine.

A

Myoglobin

74
Q
  • Release of purines and pyrimidines leads to increased phosphate and uric acid and decreased calcium.
  • Can result in increased BUN/Cr (from renal damage), EKG changes
A

Tx: hydration (best), rasburicase (converts uric acid in inactive metabolite allantoin), allopurinol (decreases uric acid production), diuretics, alkalization of urine

75
Q

Converts uric acid in inactive metabolite allantoin

A

Rasburicase

76
Q

Decreases uric acid production

A

Allopurinol

77
Q
  • Made in skin (UV sunlight converts 7-dehydrocholesterol to cholecalciferol)
  • Goes to liver for (25-OH), then kidney for (1-OH). This creates the active form
A

Vitamin D (cholecalciferol)

78
Q

Increases calcium-binding protein, leading to increased intestinal calcium absorption

A

Active form of vitamin D

79
Q
  • Decreased active vitamin D (decreased 1-OH hydroxylation) -> decreased calcium reabsorption from gut (decreased calcium-binding protein)
  • Anemia: from low erythropoietin
A

Chronic Renal Failure

80
Q

Transporter of iron

A

Transferrin

81
Q

Storage form of iron

A

Ferritin

ABSITE (EVAN) (35 decks)

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