Electrolyte Flashcards

1
Q

Normal Na range

A

135-145 mEq/L

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2
Q

normal K range

A

3.5-5 mEq/L

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3
Q

normal Cl

A

98-106 mEq/L

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4
Q

normal CO2 “bicarb”

A

22-32 mEq/L

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5
Q

electrolyte panel CPT code

A

80051

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6
Q

what percent of Body weight is body water

A

60%

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7
Q

describe body water ie ICF and ECF composition

A

ICF: 2/3 body water
ECF: 1/3 body water - divided into interstitial (3/4 of ECF) and plasma (1/4 ECF)

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8
Q

What cations/anions are in ICF

A
  • ICF 2/3 body water
    anion: Protein, Phosphate
    cation: Na+, Mg2+, K+
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9
Q

What cations/anions are in the interstitial fluid of ECF

A
  • ECF 1/3 body water, interstitial = 3/4 of ECF*
    anion: HCO3-, Cl-
    cation: Na+
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10
Q

What cation/anions are in the plasma of ECF (*plasma has)

A
  • ECF 1/3 body water, plasma 1/4 ECF*
    anions: Protein, HCO3-, Cl-
    cation: Na+
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11
Q

What is the association be body water and obesity

A

body fat is free of water, so less total body water per weight ratio in obese
*inflants have more TBW and more in ECF space

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12
Q

define osmolality, normal range? (*note osmolality = tonicity)

A

solute or particle concentration of a fluid
normal range = 280-295 mOsm/kg
sx if >320 or <265

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13
Q

How do you calculate osmolality

A

2NA +GLU/18 + BUN/2.8

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14
Q

what are other osmotically active substances besides Na, GLU, BUN

A

mannitol and various proteins

ethanol, methanol, ethylene glycol (aka antifreeze)

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15
Q

what happens in isotonic fluid excess

A

increase in ECF volume/space; no shift into ICF bc isotonic

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16
Q

what happens in isotonic fluid deficit

A

decrease in volume of water in ECF space; no shifting out of ICF bc isotonic

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17
Q

What is hyponatremia and what happens in cell

A

Na deficit in ECF less than 135mEq/L (due to loss of sodium or gain in water). Results in water movement from extracellular to intracellular thus CELL SWELLS

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18
Q

What is hypernatremia and what happens in cell

A

Na excess in ECF (>145 mEq/L) due to gain of sodium or loss of water. Results in water movement from intracellular to extracellular space. CELL SHRINKS

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19
Q

clinical features of normovolemia

A

well being and alert, normal for vital, skin turgor, thirst, sweating and urination

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20
Q

clinical features hypovolemia

A

increased thirst, decrease sweating and skin turgor, dry mucus membrane, oliguria, CNS depression, weakness, cramps, decreased BP, increase pulse

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21
Q

clinical features hypervolemia

A

edema, SOB, orthopnea, PND, HTN, tachycardia, possible crackles on pulm exam, JCD, hepatojugular reflux

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22
Q

causes of Hypervolemia (increased total ECF): primary renal sodium retention (increased ECV)

A

acute or chronic renal failure, glomerulonephritis, nephrotic syndrome, cushings syndrome, primary hyperaldosteronism, liver disease

general: Increased ECF and increased ECV

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23
Q

causes of volume excess (increased total ECF): secondary renal sodium retention (decreased ECV)

A

HF, liver dz, nephrotic syndrome, pregnancy

General: increased ECF BUT decreased ECV

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24
Q

significance of ECV

A

aka intravascular volume; this is what homeostatic mechanisms respond to, NOT total ECF volume… thus can have ECF excess but low ECV = volume sensors promote salt/water retention (as in HF, Liver failure)

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25
Q

how to determine ECV

A

right heart cath to determine PCW (pulmonary capillar wedge) pressure aka CVP (central venous pressure)

JVD estimate less accurate

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26
Q

Decreased ECV signals afferent sensors to…

A
  • dec ANP (atrial natriuretic peptide) –> Na retention
  • increase catecholamines –> Na retention
  • increase renin –>inc angiotensin, aldosterone –> Na retention and incr thirst –> water retention
  • increase thirst and ADH –> water retention

note: ADH = vasopressin

27
Q

decreased ECV alters what physical factors in order to what..?

A

GFR, RBF, peritubular starling forces –> Na retention

28
Q

What is more important to maintain.. blood volume or osmotic changes

A

loss of blood volume takes precedence over osmotic changes

29
Q

where is ADH produced and where does it travel

A

decreased blood volume signals hypothalamus –> posterior pituitary –> blood –> reabsorption of water by kidney

30
Q

what effect does aldosterone have (RAS)

A

increases renal Na REABSORPTION

increases renal K SECRETION

31
Q

what is renal activity EXCRETION

A

sum of the processes of filtration, reabosrption and secretion in nephron

32
Q

What is a normal saline solution

A

0.9% NaCL
308 mOsm/soln kg
154 Na, 154 Cl

33
Q

What is serum sodium in regards to body distribution?

A

principle cation in ECF (90-95%) total body sodium located here

34
Q

Hypernatremia lab indication and features

A

> 145 mEq/L serum sodium
clinical features due to brain shrinkage secondary to increased ECF osmolality - thirst, dehydration, alt mental status/weakness, tics/termors, focal neuro deficits, seizures or coma

*condition gradual onset = less dramatic sx

35
Q

etiology of Hypernatremia

A
  • GI loss (common in elderly, infants w/ diarrhea)
  • skin loss: sweating, fever etc.
  • renal loss: OSMOTIC DIURESIS due to HYPERGLYCEMIA in DM pt –> obligatory water loss –> see glucosuria and hyperglycemia (can cause Hyperosmolar nonketotic coma)
  • drug related: diuretics, lithium (induces nephrogenic diabetes insipidus)
36
Q

Hypernatremia can be… (volume)

A

Hypervolemic, euvolemic, hypovolemic

37
Q

Hypervolemic hypernatremia causes

A
  1. admin of hypertonic saline or sodium bicarb
  2. Hypertonic dialysis
  3. hypertonic feedings
  4. primary hyperaldosteronism
  5. cushing syndrome
38
Q

Euvolemic Hypernatremia causes

A
  1. Diabetes inspidus (central or nephrogenic) (may be hypovolemic)
  2. hypodipsia
  3. insensible dermal and skin losses (if hypodipsic)
39
Q

causes of Hypovolemic Hypernatremia

A
  1. GI losses
  2. Renal losses (diuretics, osmotic diuresis,renal tubular acidosis, diabetes insipidus)
  3. skin/respiratory losses
  4. Sequestration without external fluid loss (intestinal obstrution, rhabdomyolysis)
40
Q

Hypovolemia vs hypervolemia homeostatic response

A

hypovolemia sensed by baroreceptors –> increase ADH
hypervolemia sensed by osmoreceptors –> decreased ADH secretion

*overall ECV volume overrides osmolarity

41
Q

how does the body normally respond to hypernatremia

A
  1. create thirst and increase fluid intake

2. Maximally concentrate urine to prevent further water loss

42
Q

what is most important for body to maintain… volume, electrolyes or pH. Put in order most important to least

A

Volume, pH, then electrolytes

43
Q

What is Diabetes Insipidus

A

nonosmotic urinary water loss despite elevated serum sodium: urine dilute when should be concentrated bc CD impermeable to water so water is not reabsorbed

44
Q

Central vs nephrogenic diabetes insipidus

A

central is due to impaired ADH secretion

nephrogenic is a lack of kidney response to ADH.. water loss even lot pt low on water and adequate ADH is present

45
Q

what tx for central diabetes insipidus

A

dAVP nasal spray (ADH analogue) bc central neurogenic DM is due to inadequate ADH secretion

46
Q

Hx of Nephrogenic DIabetes Insipidus

A
  • may be genetic or aquired
  • acquired = chronic renal insufficiency, tubulointerstitial dz, amyloidosis, lithium toxicity, hypercalcemia or hypokalemia
47
Q

tx for nephrogenic DI

A

varied. . goal is to increase renal responsiveness to ADH
- thiazide diuretics
- amiloride (K sparing diuretic)
- chlorpropamide (antidiabetic oral agent)
- NSAIDS (incl indomethacin)

48
Q

Tx Hypernatremia

A
  • if severe, hospitalization
  • stop water loss
  • replace water deficit (orally, NG tube, or IV of hypotonic fluid) *do not replace too rapidly or rapid shift into brain causing seizure/brain damage/ central pontine myelinolysis with quadriplegia and coma
    it is OK to correct more rapidly if hypernatremia developed recently; otherwise correct over 48-72 hr
49
Q

What is hyponatremia, what is the danger zone and what are sx?

A

disorder due to serum sodium below 135 mEq/L
danger zone if Na below 125
sx: weakness, lethargy, somnolence, anorexia N/V, muscle cramp, seizures, coma, death

50
Q

what is the most common electrolyte abnormality in hospitalized patients? BOARD Question!!!!

A

HYPONATREMIA is the most common electrolyte abnormality in hospitalized patients

51
Q

what are the risks of chronic hyponatremia

A

serum sodium 120-132

9X higher risk of falls due to gait and balance problems (improves if hyponatremia corrected)

52
Q

What are the 3 main categories of hyponatremia? subcategories?

A
  1. hyponatremia hyperosmolar (hyperglycemia)
  2. Hyponatremia hypoosmolar (then broken down by hypervolemic, Euvolemic, or Hypovolemic)
  3. Hyponatremia with iso-osmolar (pseudohyponatremia due to hyperlipid or hyperpro)
53
Q

What 2 situations do you need to r/o with hyponatremia (think hyperosmolar and iso-osmolar)

A

r/o pseudohyponatremia (serum Na <135 but normal osmolarity due to hyperlipidemia or hyperproteinemia)

r/o hyponatremia due to hyperglycemia) - increaed glu in ECF causes shift of water from ICF to ECF. Na drops 1.5 mmole/L for every 100mg/dl rise in plasma glucose

54
Q

What are causes of hyperosmolar hyponatremia?

A

hyperglycemia, hypertonic mannitol

*low in sodium but high in other osmolar substances

55
Q

What conditions result in iso-osmolar Hyponatremia

*low Na but normal osmolality

A
  1. pseudohyponatremia (hyperlipid or hyperproteinemia)

2. Post transurethral hyster/prostatectomy

56
Q

What are the different categories of hypoosmolar hyponatremia and their causes
**think volume differences

A
  1. Hypervolemia/^ECF:
    can be dec ECV (renal failure) OR incr ECV (HF, liver dz, sepsis, prenancy, anaphylaxis)
  2. Euvolemic:
    (SIADH, drugs, hypothyroid, primary polydipsia, glucocorticoid def, poor osmolar intake, positive pressure ventilation)
  3. Hypovolemic:
    (decreased ECF, decreased ECV) - diuretics, diabetes insipidus, osmotic diuresis, GI losses, sequestration ie rhabdo…)
57
Q

what is Hyponatremia with Hypervolemia and what clinical findings are there

A
  • fluid overload condition: CHF, nephrotic syndrome, renal failure, hepatic dz
  • clinical findings: pedal edema, pulmonary crackles, JVD; anemia; other signs heart/lever/renal disease
58
Q

what findings are there for hyponatremia with euvolemia **BOARD… ddx?

A

NO evidence of fluid overload, volume depletion or dehydration

ddx: 
Hypothyroidism
SIADH (most common cause euvolemic hyponatremia; impaired water excretion)
Diuretic use (w/o vol depletion)
Adrenal insufficiency
59
Q

what are the etiologies and 4 characteristics of SIADH (most common cause of euvolemic hyponatremia)

A

Etiology: neuropsychiatric disorders, malignancy, pulm disorders (small cell lung CA), drug induced (carbamazepine, TCA, narcotic)

Characteristics:

  1. low serum osmolality below 275
  2. Inappropriately concentrated urine
  3. euvolemia (clinically)
  4. normal renal, adrenal, thyroid function
60
Q

How should you treat SIADH? (the most common cause of euvolemic hyponatremia)

A

determine underlying cause: CT/MRI heck to check CNS disorder and CXR to check lung tumor/infection

tx dependent on cause

61
Q

What can cause hyponatremia with hypovolemia and what clinical characteristic is manifest with hyponatremia with hypovolemia?

A
  • Due to renal or nonrenal causes (get rid of water and salt)
    a) renal: diuretics; osmotic diuresis, addisons dz
    b) Nonrenal: external GI (vomiting, diarrhea, fistula); internal GI (Pancreatitis, peritonitis, internal fistula

results in clinical characteristics of dehydration

62
Q

What are the various txs of hyponatremia *** know this!

A

a) symptomatic or Na <125: hospitalize
b) tx underlying cause
* If hypervolemic or euvolemic: restrict fluid
* if hypovolemic, replace fluid usually with NS (.9%) - cautiously to avoid CNS damage ie central pontine myelinolysis (demylination
c) traditional tx CHRONIC hyponatremia: Declomycin which induces nephrogenic DI (decreases kidney response to ADH)
d) new class: v2 receptor antagonists conivaptan or tolvaptan

63
Q

Tx of hyponatremia continued (NEW Tx)

A
New class of drugs for chronic hyponatremia: vasopressin/ADH antagonists "aquaretics" or "V2 receptor antagonists"
 *conivaptan, tolvaptan