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[Mine] core curric - 2016 > Ch 7.1: Fluids, Electrolytes > Flashcards

Ch 7.1: Fluids, Electrolytes Flashcards

1
Q

Water

A

50-60% total body weight

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2
Q

TBW

A

Total body water

Function of weight, age, sex, relative amount of body fat (least hydrated)

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3
Q

TBW distribution:

A
  • ICF (intracellular) = 2/3 of TBW
  • ECF (extracellular) = 1/3 of TBW
  • TCF (transcellular) = 3% of TBW
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4
Q

Why is ECF the most clinically important fluid department?

A

it contains intravascular and interstitial spaces

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5
Q

Major extracellular osmole holding water in the extracellular space

A

Sodium

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6
Q

Major intracellular osmole holding water within the cells

A

Potassium

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7
Q

Na-K-ATPase pumps

A

Maintenance of ECF/ICF compositions

Key role in regulating cell volume

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8
Q

D5W-IVF effect on ECF/ICF

A

Dextrose metabolized

Water distributed proportionally to all fluid compartments:
* ICF: 2/3 (667 mL)
* ECF: 1/3 (333 mL)

Within the ECF:
* Intravascular space: 25% (83 mL)
* Interstitial fluid: 75% (250 mL)

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9
Q

0.9% NaCl-IVF effect on ECF/ICF

A

0.9% NaCl is an isotonic saline

Distributed completely to ECF (sodium is major extracellular osmole)
* ICF: 0 mL
* ECF: 1000 mL
* 25% (250 mL) remains in intravascular space
* 75% (750 mL) - interstitial space

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10
Q

Which is more efficient at expanding the intravascular (plasma) space?

D5W or 0.9%-NaCl

A

Isotonic saline is 3x more efficient than 5% dextrose in water at expanding the intravascular space (plasma)

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11
Q

What effect does a hypertonic saline (3% NaCl) have?

A

Establishes osmotic gradient that results in movement of water out of the cells and into the ECF until osmotic equilibrium is obtained

Osmolality increases in both spaces:
* ECF – addition of NaCl
* ICF – water loss

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12
Q

Osmotic forces

A

determine the distribution of water between ICF and ECF spaces

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13
Q

Plasma oncotic and hydrostatic pressures

A

manage movement of fluid between plasma and interstitial fluid

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14
Q

Third spacing:

A

Caused by a disruption in oncotic and/or hydrostatic pressure → net flow of fluid from one compartment to another

Plasma-to-interstitial fluid shift → accumulation of excess fluid:
* Edema: interstitial space
* Effusion: potential fluid spaces

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15
Q

What can an acute reduction in blood volume cause?

During third-spacing

A

Can lead to severe volume depletion if not replaced

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16
Q

Third spacing in critical illness

A
  • Capillary permeability increases → leakage of albumin from plasma to interstitial space → reduced plasma oncotic pressure
  • Favors movement of fluid from intravascular → interstitial space
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17
Q

Third spacing can occur in the following scenarios:

A
  • Intestinal obstruction
  • Ileus
  • Pleural effusions or ascites
  • Severe acute pancreatitis
  • Peritonitis
  • Trauma
  • Bleeding
  • Obstruction of a major venous system
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18
Q

On average, healthy adults require _ _ _ mL/kg/d of fluid

A

30-40 mL/kg/d

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19
Q

Fluid losses - sensible vs insensible

A
  • Sensible (easily measurable) losses from GI tract and kidneys account for most fluid loss
  • Insensible losses from lungs/skin can contribute up to 1L/day
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20
Q

Additional fluid required in:

A
  • Severe diarrhea or emesis
  • Large draining wounds
  • Excessive diaphoresis
  • Constant drooling
  • Paracentesis losses
  • Persistent fevers
  • Drains
  • High gastric, fistula, and ostomy outputs
  • Lactation
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21
Q

Strategies to measure outputs that may otherwise not be collectable:

A
  • Weigh wound dressings before and after placement to determine losses from open wounds
  • Excessive diaphoresis that soaks the bed is usually = 1 liter of fluid
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22
Q

Heart failure

A
  • 20-25 mL/kg of estimated dry weight
  • Should take into consideration edema, fatigue, SOB
  • 2g sodium restriction (83 mEq/d)

**HF patients with significant overload should initially be treated with loop diuretics and sodium/fluid restrictions **

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23
Q

Maintenance Fluid Requirements

Weight and Age Based Formula

A
  • 18-55 years: 35 mL/kg/day
  • 56-75 years: 30 mL/kg/day
  • > 75 years: 25 mL/kg/day
  • Fluid-restricted adults: < 25 mL/kg/day

Based on 2023 NFM course

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24
Q

Maintenance Fluid Requirements

Energy based Formula

A

1 mL/kcal consumed or required

Not encouraged in >65 YOA

Based on 2023 NFM course

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25
Q

Maintenance Fluid Requirements

Holliday-Segar Formula

A

1500 mL for the first 20 kg of body weight, then ADD

  • 20 mL/kg remaining kg of BW

Based on 2023 NFM course

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26
Q

Maintenance Fluid Requirements

Adjusted Holliday-Segar Formula

A

1500 mL for the first 20 kg of body weight, then ADD

  • < 50 YOA: 20 mL/kg of remaining BW
  • > 50 YOA: 15 mL/kg of remaining BW

Based on 2023 NFM course

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27
Q

Disorders of Fluid Balance - Disturbance of Volume

Hypervolemia

A

Volume overload
Excessive gain of fluid

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28
Q

Disorders of Fluid Balance - Disturbance of Volume

Hypovolemia & Causes

A

Volume depleton
Excessive fluid loss

  • Often follows GI hemorrhage, vomiting, diarrhea, and diuresis
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29
Q

Disorders of Fluid Balance - Disturbance of Concentration

What is recognized by a change in serum sodium concentration and plasma osmolality?

A
  • Overhydration - Gain of water alone
  • Dehydration - Loss of water only
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30
Q

Disorders of Fluid Balance - Composition

Disturbance of Composition

A

Gain or loss of potassium, magnesium, calcium, phosphate, chloride, bicarbonate, or hydrogen ions

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31
Q

Electrolytes

Acute abnormality –
developed < 48 hours

A

Associated with symptoms requiring immediate treatment
* Ex: AMS with acute hyponatremia

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32
Q

Electrolytes

Chronic abnormality –
pt often asymptomatic

A

Patient may be harmed if disorder is corrected too rapidly
* Ex: chronic hyponatremia

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33
Q

What should you do if labs are inconsistent with trends?

A

Validate accuracy of specimen prior to treatment

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34
Q

Electrolyte above normal level – Potential treatments

A
  • Consider removing electrolyte supplementation from IVF or PN
  • Changing an enteral formulation containing the electrolytes to something else
  • D/c’ing medications that could contribute to electrolyte disorder
  • Manage acid-base abnormalities (e.g., metabolic acidosis)
  • Inducing renal or GI elimination of the electrolyte
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35
Q

How should patients with volume overload receive electrolyte repletions?

A

Patients with volume overload should receive volume-restricted electrolyte replacement, or PO therapy when able

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36
Q

Electrolytes

Why does peripheral administration have limits for volume and rate of administration?

A
  • Potassium/calcium especially
  • Exceeding limits can → tissue damage and potential patient harm
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37
Q

Sodium

Sodium disorders are a result of:

A

Alterations in water balance

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38
Q

Sodium

Adequate intake of sodium is
_ _ _ mg (_ _ mEq)
daily

A

Adequate intake (AI) is 1500 mg (65 mEq) daily

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39
Q

Sodium

Clinically relevant hyponatremia:

Lab value & what do you do in response?

A
  • Serum sodium <130 mEq/L
  • Determine serum sodium concentration and volume status
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40
Q

Role of sodium in the body

A
  • Major osmotic determinant in regulating ECF volume and water distribution in the body
  • Determines membrane potential of cells
  • Active transport of molecues across cell membranes (Na-K-ATPase pumps)
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41
Q

Sodium

When are clinical manifestations of hyponatremia more likely to occur?

Lab value

A

Na <125 mEq/L

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42
Q

Sodium

Hypertonic hyponatremia

A
  • Serum osmolarity >295 mOsm/L
  • Caused by presence of osmotically active substances other than sodium in the ECF
  • Common causes: hyperglycemia, mannitol
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43
Q

Sodium

Formula to correct serum sodium in setting of hyperglycemia

A

Corrected Na = serum Na + 0.016 (serum glucose – 100)

Hypertonic hyponatremia

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44
Q

Sodium

Why do you not want to correct sodium too quickly?

A

To prevent osmotic demyelination

Target rate of sodium correction for hyponatremia should not exceed
* Acute: 10-12 mEq/L/d
* Chronic/unknown duration: 6-8 mEq/L/d

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45
Q

Sodium

Isotonic hyponatremia

A
  • Serum osmolarity in normal range: 280-295 mOsm/L
  • Rarely observed with recent advances in lab analysis
  • Fraction of serum that is composed of water is reduced = excess of plasma proteins or lipids
  • Isotonic infusions: dextrose, mannitol
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46
Q

Sodium

What is pseudohyponatremia caused by?

A

hypertriglyceridemia; hyperproteinemia

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47
Q

Sodium

Hypotonic hyponatremia:

A
  • serum osmolarity <280 mOsm/L
  • Requires detailed assessment of volume status and urine sodium osmolality
  • Check urine osmolality: >100 mOsm/kg = inappropriate renal dilution
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48
Q

Sodium

Hypovolemic hypotonic hyponatremia

Include sodium / TBW

A

↓↓ total body Na; ↓ TBW
* Patients lose more sodium in relation to water
* Critical to identify source of fluid loss
* Urine osmolality > serum osmolality = concentrated urine + body’s attempt to retain fluid

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49
Q

Sodium

What can cause hypovolemic hypotonic hyponatremia?

A

Cerebral salt wasting 2/2 SAH can → hypovolemic hyponatremia

Extrarenal losses:
Diarrhea, GI fistula output, excessive sweating, burns, open wounds, and fluid drains (peritoneal, pleural, biliary, or pancreatic)

Renal losses:
Diuretics, osmosis diuresis,

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50
Q

Sodium

Hypovolemic state:

Determine ECF volume & treatment

A
  • ECF volume status: Tachycardia, low BP, poor skin turgor
  • Treatment: isotonic fluids to expand ECF volume
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51
Q

Sodium

Euvolemic hypotonic hyponatremia

Include sodium / TBW

A

+/= total body Na; ↑ TBW

  • Urine osmolality > serum osmolality & Urine Na+ > 20 mEq/L
  • Indicates kidneys are inappropriately concentrating urine (would be dark urine)
  • Volume status is adequate
  • Urine osmolality > serum osmolality AND urine Na >20 = kidneys inappropriately concentrating urine
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52
Q

Sodium

What can cause euvolemic hypotonic hyponatremia?

A

Commonly associated with SIADH

  • Hypothyroidism
  • Drug-induced
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53
Q

Sodium

Euvolemic state
Determine ECF volume & treatment

A
  • ECF volume status: Normal pulse, BP, skin turgor; no edema
  • Treatment (additional causes): correct the underlying disorder + fluid restriction

SIADH
* Fluid restriction 500-1000 mL/d
* Concentrate PN
* Ensure at least isotonic fluids (PN concentration = 154 mEq Na/L)
* NaCl tablets
* Urea
* Vaptan

Deficiency
* Glucocorticoids

Hypothyroid
* Thyroid hormone replacement

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54
Q

Sodium

Hypervolemic hypotonic hyponatremia

Include sodium / TBW

A

↑ total body Na; ↑↑ TBW
* Pts have some element of end-organ damage (renal failure, hepatic failure w/ ascites, HF)
→ fluid retention or third spacing
* Patients retain more water > sodium

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55
Q

Sodium

Hypervolemic state

Determine ECF volume & treatment

A
  • ECF volume status: Edema
  • Treatment: fluid and sodium restrictions; concentrate PN, diuretics, vaptans
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56
Q

Sodium

SIADH

Cause, what happens, what contributes to it, what does pt present w/?

A
  • A disorder of impaired water excretion caused by the inability to suppress the secretion of antidiuretic hormone (ADH)
  • If water intake exceeds the reduced urine output, the ensuing water retention leads to the development of hyponatremia
  • ADH: increases water reabsorption by the kidney
  • Retain water (hypotonic hyponatremia); low UOP
  • Presents with excessive thirst
57
Q

SIADH essential diagnostic criteria:

Includes lab value

A
  • Serum osmolality = < 275 mOsm/kg
  • Urine osmolality = double to serum osmolality
  • Urine sodium = >20
  • No adrenal, thyroid, pituitary or renal insufficiency
  • No recent diuretic use
58
Q

SIADH causes

A

Respiratory (small cell lung cancer, pneumonia, abscess, tuberculosis)

Neurologic (tumors, trauma, meningitis, abscess, subarachnoid hemorrhage, pain, anxiety, nausea)

Medications
* Anticancer agents: cyclophosphamide, ifosfamide, vincristine, cisplatin, carboplatin
* Anticonvulsants: carbamazepine, oxcarbazepine
* Antidepressants: SSRIs, TCADs, MAOI, venlafaxine
* Antidiabetic agent: chlorpropamide
* Antipsychotics: phenothiazines, haloperidol
* Miscellaneous: opiates, 3,4-methylenedioxy-methamphetamine, NSAIDs
* Vasopressin analogs: desmopressin, oxytocin, terlipressin, vasopressin

59
Q

Sodium

Hypernatremia - levels > _ _ _ mEq/L are associated with a significant increase in mortality

A

Levels >160 mEq/L associated with a significant increase in mortality

60
Q

Sodium

Symptoms of hypernatremia

A
  • Lethargy
  • Twitching
  • Weakness
  • Seizures
  • Confusion
  • Coma
  • Restlessness
  • Death
  • Irritability
61
Q

Sodium

How to address hypernatremia:

A
  1. Assess volume status
  2. Correct water deficit: administer 50% within first 24 hours, remainder over next 24-48 hours
  3. Limit serum Na correction to 8-10 mEq or mmol / Liter per day → prevention of cerebral edema
62
Q

Sodium

Equation for free water deficit

A

Water deficit (L) = TBW x [(serum Na – 140)/ 140]

TBW =
* 0.6 x weight (males)
* 0.5 x weight (females)

63
Q

Sodium

Hypovolemic hypernatremia & causes

A

↓ Na / ↓↓ water

  • Above normal serum osmolality

Causes:
* Osmotic or solute diuresis
* Post-obstructive diuresis
* Vomiting
* Diarrhea or excess laxative use
* High insensible losses

64
Q

Sodium

Hypovolemic hypernatremia - treatment

A
  • Replace free water deficit (oral water, enteral water flushes, dextrose 5% in water, 0.45% NaCl, addition of sterile water to PN)
  • Insulin (hyperglycemia)
  • Amino acid dose reduction (solute diuresis)
65
Q

Sodium

Euvolemic hypernatremia & causes

A

WNL Na / ↓ water

Water losses exceed sodium losses

Common causes:
* Central diabetes insipidus → impairment of ADH secretion
—- DI also presents with extreme thirst like SIADH; polydipsia
* Nephrogenic DI → kidneys cannot respond to ADH circulating in serum
—- Hypercalcemia, hypokalemia, amphotericin B, cidofovir, foscarnet, demeclocycline, lithium

66
Q

Sodium

Euvolemic hypernatremia- treatment

A
  • Desmopressin (central diabetes insipidus)
  • Remove offending agent, potassium replacement, thiazide diuretics, Na restriction (nephrogenic diabetes insipidus)
67
Q

Sodium

Hypervolemic hypernatremia
& causes

A

↑↑ Na / ↑ water

Common causes:
* Hypertonic saline or Na bicarbonate infusions
* Hyperaldosteronism

68
Q

Sodium

Hypervolemic hypernatremia - treatment

A
  • Loop diuretic
  • Hypotonic fluids (Na overload)
  • Spironolactone/adrenalectomy (hyperaldosteronism)
69
Q

What is the role of potassium in the body?

A
  • Critical role in cell metabolism (protein and glycogen synthesis)
  • Also maintains resting membrane potential with ratio between ECF and cell
70
Q

What is the most important component in daily regulation of potassium balance?

A

Na-K-ATPase pump

impacts plasma potassium concentration

71
Q

Additional impacts on potassium distribution:

A
  • Insulin and catecholamines;
  • exercise,
  • extracellular pH,
  • cellular breakdown
72
Q

Symptoms of hypokalemia:

mild, mod, severe

A
  • Mild depletion (3.0-3.5) → asymptomatic
  • Lower serum levels → nonspecific sx: generalized weakness, lethargy, constipation
  • Severe deficiency/consequences → muscle necrosis, ascending paralysis, arrhythmias, and death
73
Q

What is hypokalemia often the result of?

A

Abnormal losses via urine or stool

74
Q

What are two additional causes of hypokalemia?

A
  • Can develop from transcellular shift of potassium from ECF → cells,
  • Inadequate PO intakes
75
Q

What are potential causes of transcellular shifts of potassium into the cells?

A
  • Metabolic alkalosis
  • Increases in insulin and catecholamines (epi, norepi)
76
Q

Potassium

What are potential causes of extracellular shift

A
  • glucagon
  • metabolic acidosis
  • aldosterone (allows renal elimination)
77
Q

Drug-induced hypokalemia - Increased renal potassium loss

A

Diuretics
* Acetazolamide (glaucoma tx)
* Thiazides (↑ excretion of Na/Cl; Increased reabsorption of calcium)
* Indapamide
* Metolazone (inhibits resorption of sodium and chloride in the proximal convoluted tubule)
* Bumetanide (loop; decreased reabsorption of Ca2+ and Mg2+)
* Furosemide (loop)
* Torsemide (loop)

Fludrocortisone

Hydrocortisone

Drugs associated with magnesium depletion:
* Aminoglycosides (antibiotics)
* Cisplatin (chemotherapy)
* Foscarnet (antiviral)
* Amphotericin B (antifungal)
* Posaconazole (antifungal; used in weakened immune states)

78
Q

Drug-induced hypokalemia - Excess potassium loss in stool

A
  • Patiromer (binds with potassium in the gut)
  • Phenolphthalein (laxative; increased fecal sodium/potassium loss)
  • Sodium polystyrene sulfonate (kayexelate, same as patiromer)
  • Sorbitol
79
Q

Drug-induced hypokalemia - Potassium shift from ECF to ICF

A

Beta-2 adrenergic agonists (respiratory dz: asthma, copd)
* Epinephrine
* Albuterol
* Terbutaline
* Pirbuterol
* Salmeterol
* Isoproterenol
* Ephedrine
* Pseudoephedrine

Theophylline (Bronchodilator)
Caffeine
Verapamil intoxication (calcium channel blocker)
Insulin (all types)

80
Q

Generalized causes of losses

body systems

A
  • Kidney losses- diuretics, hyperaldosteronism, amphotericin, aminoglycosides
  • GI tract losses
  • –Diarrhea (10 mEq/L)
  • –Emesis / NG losses (up to 50 mEq/L)
  • Skin losses – burns, strenuous exercise on hot humid day
  • Altered distribution – alkalosis, catecholamine surge, excessive insulin
  • Dietary – inadequate intake, large volumes of IV saline, pica
81
Q

Liquid and slow release potassium supplementation

A
82
Q

At what rate of potassium infusion…
1) does a patient require cardiac monitoring
2) should a central line be used, and why?

A

If infusion >10 mEq/h → continuous cardiac monitoring required
* CVC to avoid phlebitis and burning

83
Q

Empiric potassium dose in PN for normal renal function and impaired renal function?

A
  • Empiric potassium dose in PN: 1-2 mEq/kg/day
  • 10 mEq of K intravenously increases serum K by ~0.1 mEq/L
  • Decrease dose by 50% in renal impairment
84
Q

What type of solutions do you want to avoid in hypokalemia when repleting?

A

Avoid dextrose solutions; can worsen hypokalemia 2/2 insulin stimulation → ITC shift

85
Q

What electrolyte can cause refractory hypokalemia?

A

Hypomagnesemia

Can result in refractory hypokalemia 2/2 accelerated renal potassium loss or impairment of Na-K-ATPase pump activity

86
Q

Clinical manifestations of hyperkalemia:

A
  • changes in neuromuscular and cardiac function
  • Muscle weakness, paralysis
  • ECG changes
  • Arrhythmias
87
Q

In hyperkalemia, pts are often asymptomatic until >_ _ _ mEq/L

A

> 5.5 mEq/L

88
Q

Etiology of hyperkalemia

A
  • Traumatic blood draw – hemolyzed specimen
  • Excessive intake – usually IV administration
  • Altered distribution – acidosis, succinylcholine
  • Massive cellular breakdown – intravascular hemolysis, burns, crush injuries, tumor lysis syndrome

Impaired renal excretion ** most often occurs in CKD **
* AKI, CKD 4/5
* ACEI, ARBs, K-sparing diuretics, aldosterone antagonists, NSAIDs, trimethoprim, tacrolimus

89
Q

Meds:

Treatment of hyperkalemia (>6) or changes in ECG:

Stabilize myocardium

A

Calcium gluconate

Does NOT remove potassium

90
Q

Meds:

Treatment of hyperkalemia (>6) or changes in ECG:

Shift potassium intracellularly

A
  • Insulin +/- 50% dextrose
  • Sodium bicarb
  • Albuterol
91
Q

Meds:

Treatment of hyperkalemia (>6) or changes in ECG:

Remove potassium

A
  • Furosemide
  • Sodium polystyrene sulfonate
  • Patiromer (not for acute use)
  • Sodium zirconium cyclosilicate (not for acute use)
  • HD
92
Q

Where is Magnesium found?

A

Mostly found in ICF (second most abundant intracellular cation)

93
Q

Where is Magnesium absorbed?

A

Distal jejunum and ileum

94
Q

How is magnesium regulated/excreted?

A

Regulated by GI tract, kidney, and bone

95
Q

What are some of magnesium’s functions?

A
  • Enzyme cofactor: glucose metabolism, fatty acid synthesis and breakdown, and DNA and protein metabolism
  • Maintenance of Na-K-ATPase pump / cell membrane action potential
  • Neuromuscular transmission
  • Cardiovascular tone
  • Muscle contraction
96
Q

Concomitant electrolyte abnormalities in hypomagnesemia:

A

Potassium and calcium

  • Both refractory to treatment until magnesium deficit is corrected
97
Q

How can hypomagnesemia impact insulin and glucose?

A
  • May reduce insulin sensitivity and glucose cellular uptake
  • Impair insulin secretion
  • Reduce lipoprotein lipase
98
Q

Etiology of hypomagnesemia:

A
  • Poor PO intake
  • Malabsorption or GI losses
  • –Small bowel diseases, gastric bypass, alcoholism, laxatives, diarrhea
  • Intracellular shift with insulin, refeeding, DKA, MI, hyperthyroidism
  • Increased renal excretion
  • CRRT
99
Q

_ _ _ mEq of IV Mg increases serum Mg by _ _ _ mg/dL

A

8 mEq of Mg IV increases serum Mg by ~0.1 mg/dL

In healthy individuals

100
Q

Parenteral IV Magnesium:
what is the max rate and why?

A
  • Do not exceed 1 g/hr (8 mEq/h)
    → 50% of dose can be lost in urine
  • Adverse effects – phlebitis, injection site pain
101
Q

How much should you reduce magnesium dosing in renal insufficiency?

A

Reduce empirical dose by 50% in renal impairment to avoid causing hypermagnesemia

102
Q

What long term medication use may be associated with hypomagnesemia?

A

Long term PPI use may be associated with hypomagnesemia

  • May not correct even with magnesium supplementation
  • H2 blockers do not have this effect
103
Q

Hypermagnesemia

A

Typically associated with renal dysfunction and Mg intake

104
Q

Calcium is essential for;

A
  • Normal muscle contraction
  • Nerve function
  • Blood coagulation
  • Bone formation
105
Q

Metabolically active form of calcium:

A

Iionized fraction of calcium

  • Ionized calcium – most accurate method to assess calcium abnormalities
  • Important in critical illness
106
Q

How is calcium excreted?

A

Excess calcium is excreted in the urine

107
Q

Calcium regulation:
* Vitamin D
* PTH
* Calcitonin
* Phosphorous
* pH
* Metabolic alkalosis

A
  • Vitamin D (increases)
  • Parathyroid hormone (increases)
  • Calcitonin (decreases)
  • Phosphorus (decreases ionized calcium level)
  • pH (affects albumin binding)
  • Metabolic alkalosis (decreases ionized calcium level)
108
Q

Hypocalcemia occurrences:

A

Frequently occurs 2/2 hypoalbuminemia

Common in:
* Critically ill patients
* Sepsis
* Rhabdomyolysis
* Massive blood transfusions

109
Q

How do massive blood transfusions affect calcium levels?

A

Xfusions 2/2 citrate preservative in blood bank binding with serum calcium

110
Q

What is a side effect of PO calcium?

A

Constipation

111
Q

Calcium chloride may cause:

A

Tissue necrosis if extravasation occurs

112
Q

Management of hypocalcemia

A
  • Correct hypomagnesemia if present (reduced parathyroid hormone)
  • Hyperphosphatemia may require phos binders prior to calcium repletion to reduce the risk of soft tissue calcification
  • Oral vitamin D therapy
  • Parenteral calcium therapy
113
Q

Causes of hypercalcemia:
acute vs chronic

A
  • Acute > hypercalcemia of malignancy
  • Chronic > primary hyperparathyroidism
114
Q

Why does severe hypercalcemia (>14 mg/dL) require immediate treatment?

A

→ acute renal failure, obtundation, ventricular arrhythmias, coma, death

115
Q

First step in treating hypercalcemia

A

Aggressive IV hydration – reverse volume depletion caused by hypercalcemia

116
Q

Additional steps in treating hypercalcemia

A
  • Calcitonin – rapid onset; tachyphylaxis ~ 48 hours
  • HD – life threatening or in CKD
  • Bisphosphonates – slower onset (4-10 days), longer duration / maintenance therapy
  • Steroids – decreases calcitriol production and reduces intestinal calcium absorption
  • Surgery (primary hyperparathyroidism)

Tachyphylaxis: acute, sudden decrease in response to a drug after admin

117
Q

What medication is controversial in tx of hypercalcemia?

A

Loop diuretics

  • Enhance renal calcium excretion
  • Requires vigilant monitoring to avoid further volume depletion
118
Q

Phosphorous funtions:

A
  • Essential part of nucleic acids, phospholipid membranes and nucleoproteins
  • Key role in macronutrient metabolism
  • Provides energy-rich bonds in ATP
  • Bone and cell membrane composition
  • Muscular function – especially myocardium and diaphragm
119
Q

Primary causes of ITC shifts of phos

A

CHO and insulin, catecholamines, alkalosis

120
Q

Release of Phos from cell → ECF:

A

cellular destruction, and acidosis

121
Q

Hypophosphatemia symptoms:

A

Symptoms: neurologic, neuromuscular, cardiopulmonary, hematologic

122
Q

Etiologies of hypophosphatemia

A
  • Poor PO intake
  • Critical illness
  • Alcoholism
  • Respiratory and metabolic alkalosis
  • Poor absorption
  • Phosphate binders, vitamin D deficiency, laxatives, diarrhea
  • Increased renal excretion
  • RRT
  • Intracellular shifts
123
Q

Why are dosing recommendations of phosphorous empirical?

A

Because serum phosphorous concentrations may not accurately reflect total body stores

124
Q

Infusion rate shouldn’t exceed _ _ _ mmol/hr

Why?

A

Infusion rate shouldn’t exceed 7 mmol/hr

Faster infusion rates can cause thrombophlebitis and soft tissue calcium-phosphate deposition

125
Q

Hyperphosphatemia

A

Rare, typically associated with renal dysfunction / CKD

126
Q

Additional causes of hyperphosphatemia

A
  • Endogenous release of phos into ECF from cellular destruction
  • Massive trauma
  • Cytotoxic agents - esp in tx of lymphomas and leukemias with large tumor burden
  • Hypercatabolism
  • Hemolysis
  • Rhabdomyolysis
  • Malignant hyperthermia
  • Transcellular shifts of phos from ICF to ECF 2/2 respiratory or metabolic acidosis
127
Q

Respiratory or Metabolic Acidosis + Phosphorous

A

Hyperphosphatemia

shifts of phos from ICF to ECF

128
Q

Respiratory or Metabolic Alkalosis + Phosphorous

A

Hypophosphatemia

shifts of phos from ECF → cell

129
Q

Treatment of hyperphosphatemia:

A

Reduced intake, phosphate binders

130
Q

Gastric fluid loss replacement

A

0.45% NaCl (1/2 Normal Saline) + 10-20 mEq KCl/L

131
Q

Stomach
mEq/L
sodium, chloride, potassium, bicarb

A
  • Na: 60 mEq
  • Cl: 130 mEq
  • K: 15 mEq
  • HCO3: 0 mEq
132
Q

Duodenum
mEq/L
sodium, chloride, potassium, bicarb

A
  • Na: 140 mEq
  • Cl: 80 mEq
  • K: 5 mEq
  • HCO3: 0 mEq
133
Q

Pancreas
mEq/L
sodium, chloride, potassium, bicarb

A
  • Na: 140 mEq
  • Cl: 75 mEq
  • K: 5 mEq
  • HCO3: 115 mEq
134
Q

Bile
mEq/L
sodium, chloride, potassium, bicarb

A
  • Na: 145 mEq
  • Cl: 100 mEq
  • K: 5 mEq
  • HCO3: 35 mEq
135
Q

Ileum
mEq/L
sodium, chloride, potassium, bicarb

A
  • Na: 140 mEq
  • Cl: 104 mEq
  • K: 5 mEq
  • HCO3: 30 mEq
136
Q

Colon
mEq/L
sodium, chloride, potassium, bicarb

A
  • Na: 60 mEq
  • Cl: 40 mEq
  • K: 30 mEq
  • HCO3: 0 mEq
137
Q

Small bowel fluid loss replacement

A
  • Balanced crystalloid (e.g., Ringers Lactate, Plasmalyte)
  • Bicarbonate or acetate-based customized fluid
  • 0.9% NaCl (Normal Saline)
138
Q

Rapid infusion of phosphate can result in tetany due to

ASPEN self assessment - PN

A

an abrupt decrease in serum calcium concentration

139
Q

Thiazide diuretics

A
  • act solely in the distal tubules
  • do not interfere with urinary concentration and the ability of antidiuretic hormone to promote water retention
  • use can cause hyponatremia in older patients

[Mine] core curric - 2016 (22 decks)

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