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Pharmacology III > Fluid and Electrolytes 2 > Flashcards

Fluid and Electrolytes 2 Flashcards

1
Q

What are a major cause of electrolyte abnormalities?

A

Diuretics

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2
Q

What are two conditions that no abnormality exists so there is no need to treat?

A

Pseudohyperkalemia from RBC lyses

Hypocalcemia from hypoalbumenia

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3
Q

What is used for K+ replacement?

A

No bolus of IV doses
Infusion rate should not exceed 10-20 Eq/hr
Usually have limitations on concentration for peripheral infusion (max 60 mEq/L)

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4
Q

When should IV calcium be used?

A

If cardiac sx exist for hyperkalemia or hypermagnesemia

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5
Q

When do low serum concentrations of K+, Mg2+, and PO4+?

A

Low serum concentrations can occur with refeeding syndrome, add higher than standard doses to PN and glucose containing IV solution if patient at risk

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6
Q

When do high serum concentrations of K+, Mg2+, and PO4+?

A

High serum concentrations can occur in renal failure, use reduced doses in PN and IV fluids

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7
Q

What occurs when calcium and phosphorous are mixed PN?

A
  • Increased risk for calcium-phosphorous precipitation if PN mixed with
  • Sodium bicarbonate when treating hyperkalemia
  • Infusions of calcium or phosphorous when treating deficiencies
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8
Q

What are the laboratory electrolyte tests?

A

Chem 7
Chem 10
Electrolyte panel
Need to order ionized calcium seperate

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9
Q

What drugs lead to hyperkalemia?

A

K+ sparing diuretics
ACE-I, NSAIDS
Beta-antagonists
Not drug related but be aware of the possibility of pseudohyperkalemia (lysis of RBC during collection)

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10
Q

What drugs lead to hypokalemia?

A

Diuretics (except K+ sparing)
Insulin, refeeding syndrome, treatment of DKA
Beta-agonist, glucocorticoids
Amphotericin B, aminoglycosides

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11
Q

What drugs lead to hypermagnesia?

A

Lithium

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12
Q

What drugs lead to hypomagnesemia?

A 
Diuretics
Amphotericin B, aminoglycosides
Cyclosporin, alcohol
Digoxin
Laxative abuse
Refeeding syndrome
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13
Q

What drugs lead to hypercalcemia?

A 
Thiazide diuretics (but not loop or K+ sparing)
Lithium, Vitamin A and D toxicity, calcium
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14
Q

What drugs lead to hypocalcemia?

A

Loop diuretics
Oral Phosphorus
Phenytoin, barbituates
Vitamin D deficiency

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15
Q

What drugs lead to hyperphosphatemia?

A

Phosphate- containing enemas

IV phosphorous to treat hypercalcemia

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16
Q

What drugs lead to hypophosphatemia?

A

Diuretics
Insulin, dextrose, refeeding syndrome, treatment of DKA
Sucralfate, antacids, calcium salts

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17
Q

What type of symptoms and treatment is associated with electrolyte abnormalities with a slow and chronic onset?

A

Electrolyte abnormalities with a slow and chronic onset usually have less severe symptoms and can be gradually corrected

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18
Q

What type of symptoms and treatment is associated with electrolyte abnormalities with an acute onset?

A

Electrolyte abnormalities with an acute onset may have more severe symptoms and should be treated more aggressively

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19
Q

What are the treatment goals of electrolyte abnormalities?

A
  • Treat or prevent severe life-threatening signs and symptoms
  • Improve or correct serum electrolyte concentration to within normal values
  • Do not overcorrect
  • Avoid undesirable effects of treatment
  • Correct cause for abnormality
  • Factors to consider: Presence and severity of symptoms, Acuteness of onset
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20
Q

What is the most abundant cation in the ICF?

A

Potassium

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21
Q

Is the serum K+ a good measure of total body potassium?

A

Intracellular; serum K+ not good measure of total body potassium
Clinical manifestations correlate well with serum potassium

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22
Q

What are the cardiac abnormalities associated with hyperkalemia?

A

Ventricular fibrillation
Asystole
ECG: peaked T waves

**Life threatening

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23
Q

What are the muscle abnormalities associated with hyperkalemia?

A

Weakness

Paralysis

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24
Q

What is hyperkalemia defined as?

A

Defined as serum K+ >5mEq/L

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25
Q

What are the causes of hyperkalemia?

A

Increased potassium intake (be aware of potassium sparing diuretics)
Decreased potassium excretion
Potassium release from intracellular space

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26
Q

What are the treatment goals of hyperkalemia?

A

Antagonize adverse cardiac effects (only needs to be done if having cardiac effects, needs to be done first)
Reverse other sx
Return serum concentrations to normal

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27
Q

What are the treatment approaches for hyperkalemia?

A

Antagonism of K+ if cardiac abnormalities exist (only if cardiac effects are present)
Promote intracellular redistribution
Remove K+ from the body

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28
Q

If cardiac effects are present (peaked T-waves, widened QRS) what are the treatment options?

A

IV calcium gluconate

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29
Q

IV calcium gluconate

A
  • Only restores normal conduction of heart
  • Does not reduce or redistribute serum K+
  • Onset 1-2 minutes; duration 10-30 minutes
  • May need to repeat dose if symptoms return
  • Calcium gluconate 10% (1 ampule) over 5-10 minutes, repeat every 30-60 minutes until ECG normalizes
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30
Q

What is the first line therapy of hyperkalemia treament for the correction of intracellular redistribution as long as acidosis is not present?

A

Regular insulin
5-10 units IV or SubQ
Onset 30 minutes; duration 2-6 hours

If not hyperglycemic, give dextrose
D10W, 1L over 1-2 hours
D50W, 50ml over minutes
Insulin promotes cellular uptake of K+
Glucose enhances exogenous insulin release and prevents hypoglycemia
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31
Q

What is the second line therapy for hyperkalemia treatment for the correction of intracellular redistribution?

A

Albuterol (B2-agonist) is second line therapy
Use if patient unresponsive to insulin/glucose after 30-60 minutes
10-20mg (high dose) nebulized over 10 minutes
Onset 30 min; duration 1-2 hours

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32
Q

What is the treatment used for hyperkalemia due to acidosis for correction of intracellular redistribution?

A

Sodium Bicarbonate
Use only when hyperkalemia due to acidosis
50-100 mEq IV over 2-5 minutes
Onset 30 min; duration 2-6 hours
Do not infuse through same IV line as parenteral nutrition or other calcium & phosphorous solution

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33
Q

What are the treatment options for removal of K+ from the body in a patient with hyperkalemia?

A

Furosemide (Lasix) if normal renal function
20-40 mg IV

Sodium polystyrene sulfonate (Kayexalate)
15-60 grams orally or rectally
Oral route more effective and better tolerated
Onset 1 hour or more; duration variable
Exchanges Na+ for K+
This could potentially lead into another problem. Depends on sodium levels of the patient.

Hemodialysis

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34
Q

What are the cardiac abnormalities associated with hypokalemia?

A 
EKG changes- flattened T waves, presence of U wave
Bradycardia
PVCs
Heart Block
Atrial flutter/ventricular fibrillation
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35
Q

What are the muscle abnormalities associated with hypokalemia?

A

Myalgia
Muscle weakness
Cramps
Paralysis

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36
Q

What are the causes of hypokalemia?

A

GI losses (V/D, NG suction)
Inadequate K+ intake
Alkalosis
Meds

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37
Q

What are the meds that can cause hypokalemia?

A

Cellular redistribution- these are options for treating hyperkalemia so remember they can then cause hypokalemia.
B2-agonists
Insulin

Renal wasting
Loop and thiazide diuretics (not sparing but dumping it out)
High dose antibiotics ie PCN

Depletion of magnesium diminishes intracellular K+ -> K+ wasting
AmphoB, foscarnet

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38
Q

When should you treat hypokalemia?

A
  • Any low serum K+ if patient symptomatic
  • Underlying cardiac conditions that predisposes them to arrhythmias (cardiac therapies arent used unless there are cardiac sx)
  • Receiving digoxin therapy
  • Consider for patients receiving diuretics
  • Laxative abuse
  • Any patient with serum K+ < 3.0 mEq/L
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39
Q

What are the dietary sources that can be used for non-pharmacologic therapy?

A

Fresh fruits
Vegetables
Meats

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40
Q

A condition that causes a loss of potassium might also cause a loss of?

A

Chloride

Caused by: Diuretic therapy, vomiting, diarrhea

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41
Q

What are the non-pharmacologic therapy options for hypokalemia?

A
  • some salt substitutes
  • Dietary sources- fresh fruits, vegetables, and meats
  • Dietary potassium is usually in form of potassium phosphate versus potassium chloride
  • Most conditions cause loss of potassium and chloride so both need replacing
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42
Q

What is involved with pharmacologic therapy for hypokalemia?

A
  • Pharmacological replacement therapies should accompany dietary potassium
  • Administration orally in divided doses over several days until replete
  • Fatalities have occurred from IV potassium replacement
  • Caution with dosing in patients with renal insufficiency
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43
Q

Oral potassium

A
  • Oral potassium is available as chloride, phosphate, and bicarbonate salts
  • -KCl most commonly used
  • -KPO4 used if depleted in both K+ and PO4-
  • -KHCO3 if patient acidotic (otherwise not usually used)
  • Available as elixir, effervescent tablet, microencapsulated particles, wax-matrix extended release
  • -Microencapsulated particles preferred because better taste and GI tolerability
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44
Q

What are the oral doses involved with hypokalemia treatment?

A
  • Prevent hypokalemia with 20 mEq/day (Good prophylaxis dose. Used if starting a patient on something like digoxin.)
  • Treat mild hypokalemia with 40-100 mEq total dose
  • Treat severe deficiency with 120 mEq total dose
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45
Q

When should IV treament be used for treatment of hypokalemia?

A

If oral route not feasible or life-threatening symptoms

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46
Q

What are the guidelines for IV therapy for hypokalemia?

A

Usually 10 – 20 mEq diluted with 100ml NS
Usually safe for peripheral administration

Administered over 1 hour, no bolus!!!!!!
Institution specific guidelines usually stipulate administration issues for example
Infusion rate not to exceed 10 to 20 mEq/hr
Max concentration for peripheral administration 60 mEq/L

47
Q

What should IV therapy for hypokalemia be diluted with?

A

Dilute dose with saline containing solution, avoid dextrose containing solutions
Dextrose promotes insulin release
Insulin shifts potassium intracellularly

48
Q

What should be monitored if infusing a patient for hypokalemia?

A

ECG monitoring if rate > 10 mEq/hr

Measure serum concentration after each 30 to 40 mEq increment for adults

49
Q

What is the second most abundant ICF cation?

A

Magnesium

NOT part of the standard chem panel…needs to be ordered separate.

50
Q

What is hypermagnesemia defined as?

A

> 2.4mg/dL

51
Q

What are the neuromuscular sx associated with hypermagnesemia?

A

Neuromuscular blockade
Muscle weakness
Respiratory muscle paralysis- this would be in an extreme situation but can be fatal

52
Q

What are the cardiovascular sx associated with hypermagnesemia?

A

Calcium channel blockade
Hypotension
Sinus bradycardia
asystole

53
Q

What are the causes of hypermagnesemia?

A

Renal failure in conjunction with magnesium-containing meds (cathartics, antacids, magnesium supplements) and lithium therapy

54
Q

What is the treatment for hypermagnesemia?

A

-DC all magnesium supplements or mag-containing meds
-Elemental calcium 100 to 200 mg IV
Antagonizes neuromuscular and cardiovascular effects of magnesium
Rapid onset, transient duration of action
Requires repeated doses
-Add loop diuretics (furosemide) and saline if normal renal function
Wont help if the person has kidney failure
-Hemodialysis if renal disease
-May require mechanical ventilation, vasopressors, and cardiac pacemakers until serum concentrations decrease

55
Q

What is hypomagnesemia defined as?

A

<1.5mg/dL

56
Q

What are the neuromuscluar sx associated with hypomagnesemia?

A

Hyperreflexia/tetany
Tremors
seizures

57
Q

What are the cardiac sx associate with hypomagnesemia?

A

Tachycardia
Ventricullar fibrillation
Torsade de pointes
EKG changes: increased PR interval and OT interval; prolonged QRS

58
Q

What are other clinical presentations of hypomagnesemia?

A

Metabolic alkalosis
Hypocalcemia
Digoxin toxicity
Strong relationship between hypo-K+ and hypo-Mg

59
Q

What are the inadequate intake causes of hypomagnesemia?

A

ETOH

Dietary restriction

60
Q

What are the inadequate absorption causes of hypomagnesemia?

A

Steatorrhea
cancer
malabsorption syndrome
excessive ca or P in GI tract

61
Q

What are the excessive GI loss causes of hypomagnesemia?

A

Diarrhea
Laxative abuse
NG suctioning
Acute pancreatitis

62
Q

What are the excessive urinary loss causes of hypomagnesemia?

A

Primary hyperaldosteronism
DKA
Renal disease

63
Q

What are the medication causes of hypomagnesemia?

A 
Aminoglycosides
AmphoB
Cisplatin
Insulin
Loop and thiazide diuretics
Cyclosporin
64
Q

What is the treatment for hypomagnesemia?

A

Magnesium concentration doesn’t correlate with body stores; administer empirically
Magnesium
Intravenous magnesium sulfate
Oral magnesium

65
Q

Magnesium

A

IV route if severe (1.0 mEq/L) and symptomatic

66
Q

IV magnesium sulfate

A

Avoid rapid bolus injection – associated with flushing and sweating
Dilute administration to avoid pain and venosclerosis
IM injection painful; use only if peripheral access nor available
Major limitation, even in face of severe depletion, 50% of IV dose immediately cleared by kidneys
Need to gradually replace deficit over days

67
Q

Oral magnesium

A
  • MOM (milk of magnesia), Mg2+-containing antacids, magnesium oxide
  • These are all drugs that are given for constipation.
  • Diarrhea main limiting factor
  • Frequent dosing required due to small quantity of magnesium in products
  • Reduce dose with renal insufficiency
68
Q

What is calciums role and where is it found?

A

99% total body calcium in bone
<1% ECF and ICF
Role in transmission of nerve impulses, skeletal muscle contraction, myocardial contractions, maintenance of cellular permeability and formation of bones and teeth

69
Q

What does serum caclium have a reciprocal relationship with?

A

Reciprocal relationship between serum Ca and serum phosphate concentration that is regulated by complex interaction between parathyroid hormone, Vit D, and calcitonin
½ protein bound and ½ free ionized form

70
Q

How is hypercalcemia defined?

A

> 10.2 mg/dL

71
Q

What is the clinical presentation of acute hypercalcemia?

A

Inability to concentrate urine
Acute renal failure
Coma
Ventricular arrhythmias

72
Q

What are the sx associated with chronic hypercalcemia?

A

Metastatic calcification
Nephrolithiasis
Chronic renal insufficiency

73
Q

What are the causes of hypercalcemia?

A 
Hyperparathyroidism
Malignancy
Paget’s disease
Granulomatous diseases (TB, sarcoidosis)
Hyperthyroidism
Immobilization; multiple bony fractures
Acidosis
Meds
74
Q

What are the medication causes of hypercalcemia?

A 
Thiazide diuretics
Estrogens
Lithium
Tamoxifen
VIt A and D
Calcium supplements
75
Q

What is the treatment for hypercalcemia if the condition involves life-threatening sx, functioning kidneys?

A

Saline rehydration, loop diuretics, hemodialysis, calcitonin, glucocorticoids, IV PO4 if low

76
Q

What is the treatment for hypercalcemia if the condition involves life-threatening symptoms and renal failure?

A

Hemodialysis, calcitonin, glucocorticoids

77
Q

What is the treatment for hypercalcemia if the condition involves non-life threatening sx and >12 mg/dL?

A

Saline rehydration, loop diuretics, calcitonin (gets the calcium into the bone), glucocorticoids, IV bisphosphonate (wont work quickly), mithramycin
Still treat the patient but can treat them slower

78
Q

What is the treatment for hypercalcemia if the condition involves being asymptomatic and >12 gm/dL?

A

Observe, correct reversible causes

79
Q

In hypercalcemia what might vomiting cause and how do you fix it?

A

Vomiting and inability to concentrate urine may cause dehydration and intravascular depletion
NS rehydration therapy
200-300 ml/hr initially, decrease to maintenance rate (e.g., 100 ml/hr) after volume status improved

80
Q

Loop Diuretics- In treating hypercalcemia

A
  • Initiate after rehydration completed
  • MOA: inhibits Ca2+ reabsorption from thick ascending LOH
  • Prevent volume overload that may occur with NS rehydration
  • 40-80 mg furosemide IV q 1 to 4 hours
  • Monitor for hypokalemia and hypomagnesemia
81
Q

Calcitonin- In treating hypercalcemia

A
  • hormone that counters effects of PTH
  • Inhibits osteoclast activity; promotes renal excretion of calcium
  • onset 1-2 hours
  • unpredictable effects
  • Tachyphylaxis- sudden decrease in a drug response after administration
82
Q

Glucocorticoid- In treating hypercalcemia

A
  • interference with Vitamin D metabolism
  • prednisone 40 to 60 mg/day
  • slow onset
  • many ADRs
  • add to calcitonin to prolong effect
83
Q

Phosphates- In treating hypercalcemia

A

Phosphates- doesn’t work very good
minimally effective in chronic treatment
calcium-phosphorus crystals may precipitate in tissue

84
Q

What is the long term therapy hypercalcemia?

A

oral phosphates if hyperparathyroid
glucocorticoids
Bisphosphonate
Bottom two are good long term therapy options

85
Q

If a patient is asymptomatic and hypoalbuminemic with hypercalcemia what do you treat with?

A

No tx is required

86
Q

How do you calculate a corrected serum total calcium?

A

Corrected Ca= serum calcium +
0.8 * (NL albumin - Pt’s albumin)
If the corrected calcium concentration is within the reference range, no treatment is needed

87
Q

What is hypocalcemia defined as?

A

<6.5 mg/dL

88
Q

What is the clinical presentation for hypocalcemia?

A

Neuromuscular- tetany, muscle cramps
Cardiovascular- hypotension, decreased contractility, heart failure
CNS-seizures, areflexia
Other-rickets, osteomalacia

89
Q

What are the inadequate intake causes of hypocalcemia?

A

Vitamin D deficiency

ETOH

90
Q

What are the excessive losses causes of hypocalcemia?

A

Hypoparathyroidism, renal failure, alkalosis, pancreatitis

91
Q

What are the medication causes of hypocalcemia?

A

Phosphate replacement products, loop diuretics, phenytoin, phenobarbital, corticosteroids, aminoglycosides

92
Q

What is the treatment for acute symptomatic hypocalcemia?

A

-Bolus with 100 to 300 mg of elemental calcium IV over 5 to 10 minutes
1 g chloride or 2 to 3 grams of gluconate salt
-Continuous infusion of 0.5 to 2 mg/kg/hr, decrease to 0.3 to 0.5 mg/kg/hr elemental Ca2+ after improvement of serum calcium
-Monitor serum calcium every 4 to 6 hours

93
Q

What is the IV administration treatment for hypocalcemia?

A
  • Rate NTE 60 mg/min to avoid cardiac ADR
  • Do not add to bicarbonate or phosphate containing solutions-may cause precipitation
  • Calcium gluconate causes less phlebitis
  • Calcium chloride requires smaller volume and more ionized fraction available
94
Q

How is hypocalcemia treated after acute sx are treated?

A

-Correct contributing electrolyte abnormalities
-Oral calcium
1 to 3 grams per day elemental in divided doses
ADR: hypercalciuria, nephrolithiasis
treat patients at risk for stones with thiazides

Vitamin D as needed
individualize dose
may need to use active Vitamin D
1,25-dihydroxyvitamin D3

95
Q

Where is phosphorus found?

A

Primarily in bone (80-85%); ICF 15-20%; ECF (1%)
Major anion
Distribution doesn’t reflect total body stores

96
Q

How is hyperphoshatemia defined?

A

> 4.5mg/dL

97
Q

What are the signs of hyperphosphatemia due to?

A

Signs of hyperphosphatemia are due to hypocalcemia and precipitation of salt crystals
deposition of crystals in joints, soft tissue, kidney

98
Q

When is crystal formation likely to occur in hyperphosphatemia?

A

Crystal formation is likely to occur when product of the serum calcium and phosphate concentrations exceed 50-60

99
Q

What are the impaired secretion causes of hyperphosphatemia?

A

Renal failure

Hypoparathyroidism

100
Q

What are the redistribution to ECF causes of hyperphosphatemia?

A

Acid-base imbalance (the body will redistribute from the bone into the ECG and ICF). Rhabdomyolysis, tumor lysis during chemo

101
Q

What are the increase intake causes of hyperphosphatemia?

A

Due to medications

P containing enemas and supplements, Vit D supplements, bisphosphonates

102
Q

What is the treatment for hyperphosphatemia?

A

Severe symptomatic
IV calcium salts
Less severe
oral phosphate binders to decrease GI absorption
These would be able to bind to the phosphorus and keep it in the GI for excretion rather than allowing it to be into the serum
Ca2+, Mg2+, Al3+ salts

103
Q

What is hypophosphatemia defined as?

A

<2.5mg/dL

104
Q

What are the CNS sx associated with hypophosphatemia?

A

Seizures

105
Q

What are muscle weakness sx associated with hypophosphatemia?

A

Diaphragm muscle fatigue and failure
Decreased cardiac contractility
Skeletal muscle weakness

106
Q

What are the increased distribution to ICF causes of hypophosphatemia?

A

Hyperglycemia, insulin therapy, malnutrition

107
Q

What are the decreased absorption causes of hypophosphatemia?

A

Starvation, excessive use of p-binding antacids (absorbs phosphate), Vit D deficiency, diarrhea, laxative abuse

108
Q

What are the increased renal loss causes of hypophosphatemia?

A

DKA (getting insulin therapy), ETOH, diuretic use, burns, hyperparathyoidism

109
Q

What are the medication causes of hypophosphatemia?

A

Diuretics, antacids, foscarnet, phenytoin, phosphate binders, calcium acetate

110
Q

What clinical situations should you be aware of where hypophosphatemia might occur?

A

Alcoholism
Diabetic ketoacidosis treatment
Glucose infusion
Refeeding syndrome

111
Q

What are the treatments for hypophosphatemia if its severe and symptomatic?

A

Severe (<1 mg/dL) and symptomatic (true no matter what to cause is)
IV phosphorous
0.25 mmol/kg lean body weight
Infuse over 4 to 6 hours to avoid precipitation

112
Q

What are the treatments for hypophasphatemia if its moderate?

A

Moderate (1 to 2.5 mg/dL)
Oral phosphorous
1.5 to 2.0 grams (50-60 mmol) per day in 3 to 4 divided doses
Doses recommended in many drug references are often inadequate to replete, repeated doses and higher doses often needed

113
Q

What should you consider with treatment for hypophosphatemia?

A

-Reduce doses in renal insufficiency
-Add larger dose than standard dose in TPN or glucose-containing solution if refeeding syndrome a concern
Monitor serum phosphorous, magnesium, potassium and calcium
-Monitor serum phosphorous every 6 hours during first 48 to 72 hours after starting therapy

Pharmacology III (19 decks)

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