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Comprehensive Prep > Chapter 9: Fluids and Electrolytes > Flashcards

Chapter 9: Fluids and Electrolytes Flashcards

1
Q

Water distribution

A
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2
Q

Determines intracellular/extracellular osmotic pressure

A

Sodium

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3
Q

MCC is iatrogenic; first sign is weight gain

A

Volume overload

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4
Q

What is the first sign of volume overload?

A

Weight gain

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5
Q

Can release a significant amount of water

A

Cellular catabolism

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6
Q

Normal saline: [Na], [Cl]

A

[Na] = 154 [Cl] = 154

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7
Q

3% Normal saline [Na], [Cl]

A

[Na] = 513 [Cl] = 513

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8
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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9
Q

Calculate plasma osmolarity

A

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

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10
Q

Normal plasma osmolarity

A

280 - 295

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11
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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12
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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13
Q

Best indicator of adequate volume replacement

A

Urine output

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14
Q

Fluid loss during abdominal operations

A

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

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15
Q

When should you think about replacing blood?

A

> 500 cc

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16
Q

What are insensible fluid losses?

A

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

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17
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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18
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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19
Q

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

A

150g glucose per day (525 kcal/day)

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20
Q

GI fluid secretion: Stomach

A

1-2 L/day

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21
Q

GI fluid secretion: Biliary system

A

500 - 1,000 mL/day

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22
Q

GI fluid secretion: Pancreas

A

500 - 1,000 mL/day

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23
Q

GI fluid secretion: Duodenum

A

500 - 1,000 mL/day

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24
Q

Normal K+ requirement

A

0.5 - 1.0 mEq/kg/day

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25
Q

Normal Na+ requirement

A

1 - 2 mEq/kg/day

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26
Q

Electrolyte loss: sweat

A

Hypotonic (Na concentration 35-65)

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27
Q

Electrolyte loss: saliva

A

K+ (highest concentration of K+ in body)

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28
Q

Electrolyte loss: stomach

A

H+ and Cl-

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29
Q

Electrolyte loss: pancreas

A

HCO3-

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30
Q

Electrolyte loss: bile

31
Q

Electrolyte loss: small intestine

A

HCO3- and K+

32
Q

Electrolyte loss: large intestine

33
Q

Replacement: gastric losses

A

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

34
Q

Replacement: pancreatic / biliary / small intestine losses

A

Replacement is LR with HCO3-

35
Q

Replacement: large intestine losses (diarrhea)

A

Replacement is LR with K+

36
Q

Replacement: GI losses

A

Should generally be replaced cc/cc

37
Q

Replacement: Dehydration (eg marathon runner)

A

Replacement with normal saline

38
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

39
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

40
Q

T waves disappear (usually occurs in setting of overdiuresis)

A

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

41
Q

First-line treatment for hyponatremia

A

Water restriction, then diuresis

42
Q

Why correct sodium slowly?

A

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

43
Q

How does sugar affect sodium?

A

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

44
Q

How does SIADH affect sodium?

A

SIADH: syndrome of inappropriate antidiuretic hormone can cause hyponatremia

45
Q

MC malignant cause of hypercalcemia

A

Breast cancer

46
Q

MC benign cause of hypercalcemia

A

Hyperparathyroidism

47
Q

Tx: hypercalcemia - General disease - Malignant disease

A
  • General: NS at 200-300 cc/h and Lasix - Malignant: mithramycin, calcitonin, alendrotnic acid, dialysis
48
Q

Why no LR or thiazide diuretics in hypercalcemia?

A

LR: contains calcium Thiazide diuretics: retain calcium

49
Q

Hypocalcemia: S&S

A

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

50
Q

Hypermagnesemia: S&S, treatment

A

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

51
Q

Hypomagnesemia: S&S

A

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

52
Q

Calculate anion gap

A

Na = (HCO3 + Cl) Normal:

53
Q

DDx: high anion gap acidosis

A

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

54
Q

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

A

Normal anion gap acidosis

55
Q

Tx: normal anion gap acidosis

A

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

56
Q

Usually a contraction alkalosis

A

Metabolic alkalosis

57
Q

Electrolyte changes: nasogastric suction

A

Hypochloremic, hypokalemic, metabolic alkalosis, and paradoxical aciduria

58
Q

Pathophysiology: 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
59
Q

Tx: electrolyte disturbance s/t nasogastric suction

A

Normal saline (need to correct the Cl- deficit)

60
Q

Time: respiratory compensation

A

Minutes (CO2 regulation)

61
Q

Time: renal compensation

A

Hours-days (HCO3- regulation)

62
Q

Best test for azotemia

63
Q

Calculation: FeNa

A

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

64
Q

Dx: prerenal azotemia - FeNa - Urine Na - BUN/Cr ratio - Urine osomolality

A

Prerenal azotemia: - FeNa 20 - Urine osmolality > 500 mOsm

65
Q

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

A

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

66
Q

Prevent renal damage secondary to contrast dyes

A

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

67
Q

Myoglobin and renal toxicity

A

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

68
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

69
Q

Converts uric acid in inactive metabolite allantoin

A

Rasburicase

70
Q

Decreases uric acid production

A

Allopurinol

71
Q

Vitamin D (cholecalciferol) synthesis

A
  • 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
72
Q

Vitamin D: function

A

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

73
Q

Transporter of iron

A

Transferrin

74
Q

Storage form of iron

Comprehensive Prep (45 decks)

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