Electrolyte/Acid Base Disorders Flashcards

1
Q

Functions of the kidney?

A
  1. Primarily responsible for regulation of fluid and electrolyte balance (maintenance and regulation)
  2. Secretion of hormones that participate in regulation of systemic/renal hemodynamics, RBC production, Metabolism of Ca++, phosphorus & bone
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2
Q

Maintenance of the kidney?

A

Maintains constant extracellular environment so cells can function

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3
Q

Regulation of kidney?

A

Regulates excretion of water and solutes (Na+, K+, H+)

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4
Q

Hormones secreted by kidney for regulation of hemodynamics?

A

Renin, prostaglandins, bradykinin, erythropoietin

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5
Q

Common electrolytes in electrolyte disorders?

A

Na+, K+, Mg, Ca+, Phosphorus (P), Chloride (Cl), Bicarb (HCO3)

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6
Q

Where are electrolytes found?

A

Serum

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7
Q

What are electrolytes?

A

Chemicals that are dissolved in water –> producing ions that enable flow of electrical signals through body

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8
Q

What do ions aid in?

A

Nerve excitability, endocrine secretion, membrane permeability, body fluid buffering, controlling movement of fluid between compartments

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9
Q

How do ions enter the body?

A

Digestive tract (90%)

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10
Q

How are ions excreted?

A

Kidneys (small amount lost through sweat/feces)

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11
Q

What does serum osmolality measure?

A

Body’s electrolyte-water balance (measured by labs)

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12
Q

What are the primary circulating solutes?

A

Sodium salts (Cl, HCO3), glucose, urea

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13
Q

The osmolality of extracellular fluid and intracellular fluid are approximately ______?

A

Equal

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14
Q

What is tonicity a measure of?

A

Effective osmotic pressure gradient; the water potential of two solutions separated by semipermeable cell membrane
(relative concentration of solutes dissolved in solution that determine direction/extent of diffusion)

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15
Q

Tonicity is influenced only by what solutes?

A

Solutes that cannot cross the cell membrane (exert an effective osmotic pressure)

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16
Q

What are the three classifications of tonicity?

A

Hypertonic, Hypotonic, Isotonic
*used to compare osmolarity of cell to osmolality of extracellular fluid around it

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17
Q

Hypertonic fluid/electrolyte disorders cause what?

A

Fluid/H2O to flow out of cell (dehydrate)

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18
Q

Hypotonic fluid/electrolyte disorders cause what?

A

Fluid/H2O to flow into cell (overhydrate)

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19
Q

What happens to fluid/electrolyte balance in dehydration?

A

Serum osmolality increases leading to:
Hypertonic dehyration or Hypotonic dehydration or Isotonic dehydration

BY release of ADH

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20
Q

What happens to fluid/electrolyte balance in excessive water intake?

A

Serum osmolality decreases leading to: hypervolemia

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21
Q

What is the anion gap?

A

Difference between measured cations and anions in serum, plasma, or urine

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22
Q

Serum anion gap formula?

A

Serum AG = measured cations - measured anions
OR
Serum AG = Na - (Cl + HCO3)

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23
Q

Serum anion gap (AG) is used in the differential diagnosis of what?

A

Metabolic acidosis

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24
Q

What does a high/increased AG indicate?

A

Metabolic acidosis**, hyperalbuminemia, hyperphosphatemia, lab error

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25
Q

What does a low/decreased AG indicate?

A

Lab error**, hypoalbuminemia, hyperkalemia, hypercalcemia, hypermagnesia, lithium toxicity

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26
Q

Sodium is a ______ _______ of ECF?

A

Major cation

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27
Q

Sodium is responsible for 50% of the osmotic pressure gradient existing between what?

A

ICF and ECF

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28
Q

How is Na+ excreted?

A

Kidneys

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29
Q

How much sodium is typically consumed daily in the western diet?

A

130-160 mmol

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30
Q

What occurs in hyponatremia?

A

Dec. serum osmolality: water moves from ECF to ICF

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31
Q

Hyponatremia is typically associated w/ what?

A

Excess water accumulation (dilutes Na+) or diuretic use (inc. water and Na+ excretion)

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32
Q

Early clinical manifestations of acute hyponatremia?

A

Nausea and malaise (125-130 mEq/L)

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33
Q

Delayed clinical manifestations of acute hyponatremia?

A

Headache, lethargy, obtundation, seizure, resp. arrest (115-120 mEq/L)

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34
Q

Severity of symptoms of hyponatremia reflects what?

A

Degree of cerebral involvement/over-hydration and edema

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35
Q

What is a concern with excessive cerebral edema as a result of hyponatremia?

A

Herniation of the brain

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36
Q

Clinical manifestations of chronic hyponatremia?

A

cerebral adaptation allows for pts to be relatively asx
If sx: fatigue, N/V, dizziness, gait disturbance, confusion, lethargy

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37
Q

Causes of Hyponatremia?

A

Diuretic use**, diarrhea, CHF, Liver and renal dz, SIADH
Chronic diseases that cause retention of sodium and fluid: body retains more water than Na+ (dilutes Na+ conc.)

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38
Q

Diagnostic testing for Hyponatremia?

A

CBC, CMP, urine osmolality (24 hrs), Mg, Phos

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39
Q

Treatment of hyponatremia depends on what?

A

The cause

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40
Q

Treatment of hyponatremia?

A

H2O restriction, Sodium and water repletion SLOWLY
-Vaptans: nonpeptide vasopressin antagonist (interfered w ADH) *useful for hypervolemic, hyponatremia secondary to CHF/Liver failure

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41
Q

What is hypernatremia?

A

Inc. serum osmolality, water movement from ICF to ECF
*most often d/t water depletion

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42
Q

Clinical manifestations of hypernatremia?

A

Early/mild: thirst, weakness, nausea, loss of appetite
Severe: confusion, lethargy, muscle twitching, intracerebral hemorrhage

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43
Q

Causes of hypernatremia?

A

Vomiting, diarrhea, DI (unreplaced water loss), dehydration (pts w/ dementia, end of life/failure to thrive), severe exercise or seizure (water loss into cells), overload of Na+/hypertonic solution

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44
Q

Hypernatremia is seen in those with impaired ability to do what?

A

Impaired ability to obtain water or experience thirst

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45
Q

Treatment of hypernatremia?

A

If due to water loss (dehydration) or hypovolemia (Na+ and water loss): determine etiology, calculate water deficit, fluid repletion (D5W)

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46
Q

How to calculate water deficit?

A

Plasma Na = (total body Na + total body K)/TBW

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47
Q

Potassium is a major ________ _______?

A

Intracellular cation

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48
Q

What does Potassium help establish?

A

Resting membrane potential in neurons and muscle fibers

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49
Q

Effect of potassium on osmotic pressure?

A

Very little effect (unlike Na+)

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50
Q

What maintains potassium gradients between ICF and ECF?

A

Sodium-potassium pumps in cell membranes

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51
Q

How is potassium excreted?

A

Kidneys

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52
Q

Recommended adult daily consumption of potassium?

A

4700mg

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53
Q

Hypokalemia typically results from what?

A

Unreplenished GI or urinary loss of K+

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54
Q

Symptom severity of hypokalemia is directly related to what?

A

Degree/duration of K+ reduction

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55
Q

Clinical manifestations of hypokalemia (<3.0mEq/L)?

A

Muscle weakness (LE to UE), muscle cramps, rhabdo, N/V/D and ileus, Cardiac arrhythmias/EKG abnormalities***

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56
Q

Cardiac arrhythmias with hypokalemia?

A

PAC’s, PVC’s, sinus brady, AV block, Vtach, Vfib

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57
Q

Characteristics EKG findings associated with hypokalemia?

A

ST depression, decreased T wave amplitude, increased amplitude of U wave, prolonged QT interval

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58
Q

Causes of hypokalemia?

A

Vomiting, diarrhea, diuretics (non-K+ sparing), DKA

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59
Q

Diagnostics for hypokalemia?

A

Hypo-K and Hypo-Mg concurrent loss, CMC, CMP, Mg, Phos, EKG, ABG, serum ketones

60
Q

Assume what with hypokalemia tx?

A

Intracellular and extracellular K+ is equal

61
Q

Management methods for hypokalemia?

A

-Careful monitoring in repletion to avoid hyperkalemia (overcorrection risk increases w/ renal insuff.)
-Determine Cause & replete IV or PO

62
Q

Preparations for repletion of K+ in hypokalemia?

A

Potassium chloride preferred in most cases (IV, PO)

63
Q

Treatment for mild-mod hypokalemia (3.0-3.4 mEq/L)?

A

K+ 10-20 mEq BID (tabs, liquid, or K+ rich foods)
+/- potassium sparing diuretic

64
Q

Treatment for severe hypokalemia (<2.9mEq/L)?

A

Admit
K+ 20 mEq PO
10-20 mEq/hr in 100-200mL saline (K-rider)

65
Q

What is transient correction of hypokalemia?

A

OK for several hours and then drops (most exogenous K+ taken into cells)

66
Q

What is hyperkalemia?

A

-Impaired urinary K+ excretion by CKD, meds
-Inc. K+ release from cells (DKA)

67
Q

Hyperkalemia is rare in most healthy individuals due to what?

A

Cellular and urinary response mechanisms to prevent excess K+ accumulation in ECF

68
Q

Clinical manifestations of hyperkalemia (>7.0 mEq/L)

A

Muscle weakness/paralysis, cardiac arrhythmias/EKG changes

69
Q

Characteristic EKG changes with hyperkalemia?

A

Peaked T-waves, Shortened QT interval

70
Q

Causes of hyperkalemia?

A

Inc. potassium release from cells: DKA***, succinylcholine, exercise, rhabdo, crush injury
Reduced urinary excretion: acute & chronic kidney disease

71
Q

Diagnostic testing for hyperkalemia?

A

EKG, CBC, CMP, Mg, Phos, consider ABG and serum ketones

72
Q

Management of hyperkalemia?

A

-Calcium antagonizes membrane actions of hyperkalemia (stabilizes cardiac tissue)
-Insulin (w/ IV glucose) drives extracellular K+ into cells
-Inhaled beta-agonists (Albuterol)
-Remove K+ from body: IV diuretics (+/- IV saline), Polystyrene sulfonates (Kayexalate PO), hemodialysis (ESRD)

73
Q

Hypomagnesemia occurs in what % of hospitalized populations?

A

12%

74
Q

Symptoms of hypomagnesemia are typically associated with what?

A

Concurrent hypokalemia, hypocalcemia and/or metabolic acidosis

75
Q

Causes of hypomagnesemia?

A

GI loss/diarrhea, chronic PPI use, Renal loss (loop/thiazide diuretics, nephrotoxic drugs), alcohol (secondary to urinary excretion, diarrhea, dietary deficiency), Hypercalcemia

76
Q

Most of the body’s magnesium stores are where?

A

Intracellular, 60% in bone

77
Q

Extracellular magnesium can be ionized (free) or bound to what?

A

Protein

78
Q

Magnesium helps to maintain what?

A

Normal nerve and muscle function, blood glucose control, BP regulation, contributes to construction of bone

79
Q

Magnesium is required for what?

A

Energy production

80
Q

What does magnesium help transport across cell membranes?

A

Calcium and potassium

81
Q

Diagnostic testing for hypomagnesemia?

A

EKG, CMC, CMP, Mg, Phos, consider ETOH

82
Q

Treatment for hypomagnesemia?

A

Identify cause, IV/PO repletion

83
Q

Hypermagnesemia is uncommon in the absence of what?

A

Mg+ repletion or kidney disease

84
Q

Clinical manifestations of hypermagnesemia?

A

Nausea, flushing, headache, lethargy, comnolence, hypocalcemia, absent deep tendon reflexes, hypotension, bradycardia, muscle paralysis, apnea, resp. failure, heart block

85
Q

Causes of hypermagnesemia?

A

Kidney disease/failure (no Mg regulation other than urinary excretion), Mg infusion/repletion

86
Q

Diagnostic testing for hypermagnesemia?

A

EKG, CBC, CMP, Mg, Phos

87
Q

Treatment of hypermagnesemia?

A

Determine cause, prevention, improve renal elimination by loop diuretics and IV saline or hemodialysis

88
Q

99% of calcium is found where?

A

Bone and teeth

89
Q

1% of calcium is in the serum and is required for what?

A

Vascular function, muscle function, nerve transmission

90
Q

Serum calcium is regulated and does not fluctuate with what?

A

Dietary intake

91
Q

The body uses what as a reservoir to maintain constant Ca concentration?

A

Bone

92
Q

45% of calcium in the serum is bound to what?

A

Albumin

93
Q

The 40% of calcium in the serum not bound to albumin is ____ _____ ______?

A

Ionized free calcium (not bound to proteins)

94
Q

Average recommended daily intake of calcium varies with what?

A

Age (most adults 1000-1300mg)

95
Q

Hypocalcemia values must be corrected if patients have what?

A

An abnormal albumin level

96
Q

How to calculate corrected calcium?

A

Corrected calcium = measured total Ca + 0.8 (4.0 - serum albumin)

97
Q

Clinical manifestations of acute hypocalcemia?

A

Tetany** (HALLMARK), fatigue, hyperirritability, anxiety, QT prolongation
Trousseau’s and Chvosteks’s signs

98
Q

What is Trousseau’s sign?

A

Induction of carpal spasm by inflation of BP cuff

99
Q

What is Chvosteks’s sign?

A

Contraction of the ipsilateral facial muscles elicited by tapping facial nerve anterior to the ear

100
Q

Causes of hypocalcemia?

A

Vitamin D/ phosphate influence on serum calcium, hypoalbuminemia (pseudo-hypocalcemia), Hypoparathyroidism due to excision, Vit D deficiency, CKD, Sepsis

101
Q

Diagnostics for hypocalcemia?

A

EKG, CBC, CMP, Mg, Phos, Ionized Ca

102
Q

Treatment of hypocalcemia?

A

Determine cause
Severe: IV calcium gluconate (over 10-20 min*** NEVER FASTER)
Mildly symptomatic/chronic: PO calcium gluconate

103
Q

Is hypercalcemia common?

A

No, relatively uncommon

104
Q

Causes of hypercalcemia?

A

Primary hyperparathyroidism and malignancy (90% of cases), Drug-induced hypercalcemia

105
Q

Clinical manifestations of hypercalcemia?

A

No specific manifestation, depends on cause

106
Q

Diagnostics for hypercalcemia?

A

Confirm dx, Measure PTH, Vit D levels

107
Q

Treatment of hypercalcemia?

A

Tx underlying cause

108
Q

If normal or low PTH with hypercalcemia, assume what dx?

A

Malignancy

109
Q

Phosphorous is an essential mineral and makes up what % of someone’s total body weight?

A

1%

110
Q

Phosphorous is present in which cells?

A

All of them

111
Q

85% of phosphorous is found where?

A

Bones & teeth, DNA, RNA

112
Q

Phosphorous and what ion are interrelated?

A

Calcium

113
Q

Phosphorous and calcium metabolism is regulated by what?

A

Vit. D and PTH

114
Q

Phosphorous is excreted by what?

A

Kidneys (w/ renal failure levels rise)

115
Q

Where is phosphorous absorbed?

A

Small intestines

116
Q

Phosphorous can be found in many ____ and _____?

A

Foods and additives

117
Q

Causes of hyperphosphatemia?

A

Acute or chronic kidney disease, acute phosphate load: tumor lysis, rhabdo, exogenous phosphate

118
Q

Treatment of hyperphosphatemia?

A

Determine cause, IV normal saline, May require dialysis

119
Q

Causes of hypophosphatemia?

A

Increased insulin secretion (when treating DKA), poor absorption (anorexia, alcoholism, chronic diarrhea, short gut synd.), Hyperparathyroidism, Vit D deficiency

120
Q

Treatment of hypophosphatemia?

A

Determine cause (may only require tx of underlying cause), repletion often not necessary

121
Q

What is the physiology of acid-base status?

A

Humans generate large amounts of acids daily –> must be excreted, expired, metabolized, or buffered

122
Q

Acid-base is maintained by what?

A

Normal pulmonary excretion (CO2), Metabolic utilization of acid, Renal excretion of acid

123
Q

Acid-base is aseessed by measuring what?

A

Components of bicarb-carbon dioxide buffer system in the blood

124
Q

Measuring pH is measuring which ions?

A

H+ ions (balance = regulation of H+ ions)

125
Q

Concentration of H+ ions in the body has a ____ range for optimal cellular function?

A

narrow *small deviations in either direction carries significant morbidity and mortality

126
Q

Buffer system defense mech. of the body in acid-base balance?

A

HCO3

127
Q

Respiratory system defense mech. of the body in acid-base balance?

A

CO2 (expire)

128
Q

Renal system defense mech. of the body in acid-base balance?

A

Reabsorbs HCO3, excretes H+

129
Q

CO2 formed during cellular respiration combines with H2O to form what?

A

Carbonic acid

130
Q

What are carbonic acid disscoates?

A

HCO3 and H+ ion (pH)

131
Q

a pH of <7.35 (acidemia) and inc. PaCO2 indicates what?

A

Resp. Acidosis

132
Q

a pH of <7.35 (acidemia) and dec. HCO3- indicates what?

A

Metabolic Acidosis

133
Q

a pH of >7.45 (alkalemia) and dec. PaCO2 indicates what?

A

Resp. Alkalosis

134
Q

a pH of >7.45 (alkalemia) and inc. HCO3- indicates what?

A

Metabolic Alkalosis

135
Q

How to measure acid-base?

A

ABG (arterial or venous)
1. identify/monitor acid-base
2. measure PaO2 and PaCO2
3. assess response to tx
4. detect abnormal hemoglobins**

136
Q

Contraindications of measuring acid-base w/ ABG?

A

Local infection, thrombus, abnormal anatomy, severe PVD, anti-coagulation pts (relatively C/I)

137
Q

How to interpret ABG?

A

Look at pH (acidotic, alkalotic, normal?), look at HCO3 and CO2 –> determine if metabolic or resp.

138
Q

Low pH w/ High CO2 ABG?

A

respiratory

139
Q

Low pH w/ Low HCO3 ABG?

A

metabolic

140
Q

High pH w/ Low CO2 ABG?

A

respiratory

141
Q

High pH w/ High HCO3 ABG?

A

metabolic

142
Q

What indicates compensation?

A

If CO2 and HCO3 are both high or both low
if pH normal: full compensation
if pH abnormal: partial compensation

143
Q

Causes of metabolic acidosis?

A

Lactic acidosis (DKA), Ketoacidosis (ETOH), Ingestions (methanol, ethylene glycol, ASA), Loss of HCO3 (diarrhea), Dec. renal excretion (CKD)

144
Q

Causes of metabolic alkalosis?

A

GI loss (excess vomiting/diarrhea, laxative abuse), Renal loss (diuretics)

145
Q

Causes of respiratory acidosis?

A

Dec. central respiratory drive (overdose, encephalitis, CVA), Dec. NM respiratory drive (metabolic disorders), Short/shallow breathing (PE, pulm vascular dz, COPD, interstitial lung disease)

146
Q

Causes of respiratory alkalosis?

A

CNS (pain, hyperventilation, anxiety/panic, drug withdrawal), Pulmonary (COPD, interstitial lung disease, pneumothorax, pneumonia), High altitude