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FA17 Nephrology > Sodium Disorders > Flashcards

Sodium Disorders Flashcards

1
Q

isotonic solutions

A

0.9% normal saline
lactated ringer

stays in ECF/vasculature

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2
Q

hypotonic solutions

A

D5W
D5W + 0.45NS
D5W + 0.9 NS

hypotonic - goes into ALL spaces (essentially giving water)

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3
Q

normal fluid balance water movement

A

moves freely between intracellular space and intravascular space

responds to hydrostatic pressure

allows for osmotic equilibrium

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4
Q

normal fluid balance sodium movement

A

confined to extracellular space

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5
Q

kidney fluid balance

detect any hypo perfusion as _____

A

volume depletion

even if nonexistent

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6
Q

transfer water b/t vascular and interstitial compartments is governed by

A

osmotic balance

hydrostatic balance

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7
Q

major extracellular cation and anion

A

cat: Na
an: Cl, HCO3

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8
Q

major intracellular cation and anion

A

cat: K
an: protein

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9
Q

response to decreased ECF

A
  1. ADH release
  2. Decreases ANP
  3. Renin Release
  4. Stimulation of thirst
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10
Q

two systems that respond to decreased ECF

+ time

A

hemodynamically (immediate) via vasoconstriction (raises BP and HR)

renal (12-24hrs) via ADH release and RAAS activation

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11
Q

ADH

A

from posterior pituitary

closes aquaporin channels

decreased FREE water excretion

no effect on Na

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12
Q

ANP

A

decreased urinary sodium loss

released by atrial stretch receptors

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13
Q

aldosterone

A

RAAS activation stimulates release

decreasing sodium and water

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14
Q

effective hemostasis dependent on

A

functioning kidneys and afferent sensors

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15
Q

afferent sensors

A

found in: atria, pulmonary vasculature, carotid sinus, aortic arch, juxtaglomerular apparatus

responds to ECV

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16
Q

ECV

A

fullness and tension in arterial tree

should be = to ECF if no third spacing present

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17
Q

disorders of ECV

A

disorders of decreased CO or arterial HoTN

HFrEF (decreased pump and strength) 
Liver failure (third spacing, decreased liver protein production) 
Renal failure (third spacing, increased liver protein excretion)

body’s response to this is maladaptive

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18
Q

hypovolemia etiologies

A

renal water loss (nephrogenic DI)

extra renal loss of water (increase RR, sweating, v/d)

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19
Q

marker of hypovolemia

A

decreased urine output

HoTN

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20
Q

hypovolemia treatment

A

fluid replacement is mainstay of tx

0.9% NS or colloid (LR) bc fluids stay in ECF

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21
Q

hypervolemia

A

intake exceeds excretion, fluid shifts from intravascular to interstitial space due to high capillary hydrostatic pressure (third space)

primary or secondary

retention of Na, water

tx: volume restriction, diuretic

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22
Q

primary hypervolemia

A

increased ECV, caused by:

Oliguria 2/2 AKI, GN
severe CKD
Primary hyperaldosteronism
Cushings

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23
Q

secondary hypervolemia

A

decreased ECV

occurs in response to decreased ECV

found in CHF or cirrhosis

decreased perfusion = hold onto water

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24
Q

hypervolemia treatment

A

diuretics - block Na reabsorption at some point in kidney

TZDs can cause hyponatremia (bc works on last stop in tubule)

may need to use a combo to deal with electrolyte disturbances

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25
Q

site of action on tubule:

acetazolamide

A

proximal convoluted tubule

can cause metabolic acidosis (inhibits HCO3)

weak diuretic

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26
Q

site of action on tubule:

TZD

A

distal convoluted tubule

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27
Q

site of action on tubule:

spironolacton

A

aldosterone antagonists

collecting tubule

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28
Q

range of osmolarity

A

275-295

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29
Q

T or F

changes in osmolarity cause changes in both ECF and ICF

A

True!

changes in extracellular osmolality cause changes in intracellular volume

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30
Q

calculating osmolality

A

gives idea of concentration of a toxin (osmolar gap)

uses serum electrolytes

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31
Q

Receptors at work to regulate osmolality

A
  1. osmoreceptors

2. baroreceptors

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32
Q

osmoreceptors

A

located in third ventricle of brain

monitor osmolality of blood in internal cards

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33
Q

when serum osmolality rises, osmoreceptors … (2)

A

stimulation thirst

stimulate ADH release from posterior pituitary

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34
Q

baroreceptors

A

atrial and venous circulation sense decrease in ECF

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35
Q

ADH release is stimulated by

A

10% decrease in ECF

regardless of serum osmolality

once volume is replaced or osmolality is restored, ADH and thirst are suppressed

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36
Q

hyponatremia

A

low SERUM sodium concentration (<135)

can be found in normal, low, or high total body sodium content OR low, normal, high, serum osmolality

typically a water issue

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37
Q

primary symptoms of hyponatremia

A

neurological bc

decreased plasma sodium = movement of water into cells

THEREFORE:

swelling of neurons = decreased function

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38
Q

s/s 125-130 Na level

A

nausea malaise

39
Q

s/s 115-125 Na level

A

HA, lethargy worsening confusion

40
Q

s/s <115 Na level

A

worsening LOC to eventual obtundaiton

seizures

respiratory arrest

41
Q

what influences progression of symptoms

A

speed of sodium loss/progression

sodium level

42
Q

CNS adaptation to chronic hyponatremia

A

cerebral cell edema forces ECF out of brain and into CSF

neuron begins to extrude osmolytes not essential for function (this decreases swelling in neuron)

reuptake of osmolytes will occur if

43
Q

worst complication of hyponatremia

A

cerebral herniation

rapid loss of Na causes swelling that literally pushes the brain out of the skull

44
Q

MC patients who get cerebral herniation

A
  1. women and children with acute post-op hyponatremia
  2. hyper acute hyponatremia caused by massive water ingestion (psychosis, marathon running, ecstasy)
  3. hyponatremic pts with intracranial pathology
45
Q

s/s of chronic hyponatremia

A

gradually developing = asymptomatic (even if severely slow)

if they DO develop - non-specific (gait disturbance, forgetfulness, dizziness, weakness, malaise, muscle cramps)

46
Q

diagnostic approach to hyponatremia

A

typically due to a water imbalance, not sodium issue

  1. historical information: body weight change, fluid intake, UO, thirst
  2. serum electrolytes and osmolality and urine sodium
  3. determine if hyper, hypo, or isotonic
  4. IF hyponatremic and hypotonic = asses volume status
47
Q

hypertonic hyponatremia

+ tx

A

INCREASED serum osmolality and DECREASED Na

dilution hyponatremia

tx: get rid of underlying solute, use math formulas to determine if due to solute or true Na loss

48
Q

hypertonic hyponatremia path

A

osmotically active solute (i.e. glucose) causes FREE WATER to leave intracellular compartment toward ECF

increased water then dilutes concentration of Na = hyponatremia

49
Q

isotonic hyponatremia

A

NORMAL osmolality, LOW Na

may be pseudo-, due to absorption of large quantities of isosmolar solution in OR procedures

tx: 0.9% NS

50
Q

causes of pseudohyponatremia

A
  1. hyperlipidemia (TGs)
  2. hyperproteinemia causes laboratory error

leads to a false lab report of isotonic hyponatremia

51
Q

procedures that cause isotonic hyponatremia

A

non-conducting solution used in electrocautery in OR

TURP/Bladder Sx
Hysteroscopy
Laprascopy

absorption of large quantities cause dilution

52
Q

hypotonic hyponatremia types

A

must asses volume status via BP and urine output, check lungs for crackers, JVD

hypovolemic hypotonic hyponatremia
hypervolemic hypotonic hyponatremia
euvolemic hypotonic hyponatremia

53
Q

hypotonic hyponatremia

A

DECREASED osmolality, DECREASED Na

can be due to excessive consumption of free water or improper retention of free water in kidney

54
Q

hypovolemic hypotonic hyponatremia

Labs, patho, tx

A

LOW serum Na, reduced total body sodium, DECREASED ECF

low ECV which causes baroreceptors to stimulated ADH, thirst

increased free water intake and free water retention despite low osmolality

volume replacement: 0.9% NS

55
Q

hypovolemic hypotonic hyponatremia occurs due to

A
  1. GI loss of salt (emesis, diarrhea, dehydration) LOW urine Na levels
  2. Na loss via medications (diuretics, ACE) HIGH urine Na levels
  3. sodium loss due to disease (adrenal insufficiency, cerebral salt wasting) HIGH urine Na levels
56
Q

hypervolemic hypotonic hyponatremia

A

HIGH ECF (low ECV), LOW osmolality, LOW Na

occurs with severe HF, advance Liver or kidney dz, cirrhosis, nephrotic syndrome

low ECV sensed by baroreceptors and ADH is released, prompting free water and sodium retention (to fix ECV)

57
Q

hypervolemic hypotonic hyponatremia tx

A

improve underlying condition

fluid restriction (1L or less) - volume control

loop diuretics (may worsen hyponatremia) - comume control (CAN’T INCREASE FREE WATER)

58
Q

euvolemic hypotonic hyponatremia

labs and causes (9)

A

normal ECF/volume, LOW osmolality, LOW Na

  1. hyponatremia following IV therapy
  2. SIADH
  3. psychogenic polydipsia
  4. hypothyroidism
  5. beer potomania
  6. exercise associated hyponatremia
  7. adrenal insufficiency
  8. HIV
  9. Ecstasy
59
Q

hyponatremia following IV therapy

A

euvolemic hypotonic hyponatremia

exacerbated by inappropriate ADH secretion due to pain

HYPERtonic urine

60
Q

SIADH euvolemic hypotonic hyponatremia

A

ADH secreted without physiological stimulus

inappropriately hypertonic urine and free water retention (hold on to too much H2O, so excretion is highly concentrated with Na)

mc due to pain, malignancy, reset osmostat

61
Q

psychogenic polydipsia

A

euvolemic hypotonic hyponatremia

large amounts of free water are ingested due to anti-cholinergic meds or intentionally

62
Q

beer potomania

A

excessive amounts of beer (low Na, K, protein) consumed = just enough carbohydrate to suppress protein breakdown

also a “tea and toast” diet

can’t excrete excessive free water bc low solute intake limits ability to make enough urine

63
Q

exercise associated hyponatremia

A

euvolemic hypotonic hyponatremia

large volumes of low solute fluid over long endurance event WITH inappropriately elevated ADH levels (intense exercise, n/v, NSAID)

hypernatremia is more common

64
Q

making the diagnosis of euvolemic hypotonic hyponatremia

A

evaluation of urine sodium levels and urine osmolality

differentiates between SIADH and psychogenic polydipsia/beer potomania

65
Q

urine osmolality and urine sodium are ____ in SIADH

A

inappropriately concentrated (increased Na, increased osmolality)

hold onto water so that you release lots of solute with limited water

66
Q

urine osmolality and urine sodium are ____ in psychogenic polydipsia/beer potomania

A

LOW

attempting to get rid of water, maximally diluted urine

67
Q

distinguishing SIADH and reduced ECV

A

both have concentrated urine osmolality

reduced ECV: LOW urine sodium and HIGH BUN and uric acid (hypovolemia, no fluid to dilute0

SIADH: urine sodium is normal to elevated, BUN/uric acid LOW (free H2o stays in vascular space to dilute)

68
Q

risk stratification in hyponatremia

A

hyperacute (few hours, h2o intoxication)

acute (24 hrs)

subacute (24-48 hrs)

chronic (>48, duration unknown)

69
Q

mild-moderate symptoms hyponatremia

A

HA, n/v, gait changes, fatigue confusion

NOT associated with herniation

121-135

70
Q

severe symptoms of hyponatremia

A

<120

seizures, obtundation, coma, respiratory arrest

71
Q

immediate sodium correction in hyponatremia if

A
  1. severe symptoms
  2. acute hyponatremia w/symptoms (even mild)
  3. hyperactive hyponatremia, even if asymptomatic

GOAL: raise serum Na by 4-6/hr w/hypertonic saline

72
Q

strategies for patient with normal sodium at baseline but now hyponatremia (6)

A
  1. treat underlying dz
  2. fluid restriction (<1L/day)
  3. oral salt tablets (1gm Nacl/tab)
  4. administration of 0.9 NS
  5. Vasopression receptor antagonist
  6. demeclocycline or lithium
73
Q

sodium correction goal

A

0.5 meq/L/hr

** shoot for 9 (10 realistic) in first 24 hrs ***
if >/= 12 start worrying

4-6 over several hours

74
Q

vasopressin receptor antagonists used (2)

A

Tolvaptan (Samsca)

Conivaptan (Vaprisol)

hospitalized, pos <125 Na

75
Q

conivaptan

A

selective V1A and V2 receptor agonists

increased urine water excretion, activation of vasoconstriction

CANT be used in HF, liver, renal dz

76
Q

tolvaptan (Samsca)

A

selective V2 receptor agonists

urine water excretion (free water loss w/o Na loss)

can be used in euvolemic and hypervolemic

no CI but $$$$

77
Q

if urgent partial correction of sodium is needed

A

100 cc bolus of 3% hypertonic solution can be given over 10 min then raise up over next few ours

two more may be given but levels must be measured hourly

78
Q

TOC of euvolemic hypotonic hyponatremia

A

free water restriction

oral salt tablets CAN be used bc likely will not listen

79
Q

TOC for hypervolemic hypotonic hyponatremia

A

sodium and fluid restriction + loop diuretics

correct underlying cause

consider captain agent

80
Q

hypovolemic hypotonic hyponatremia TOC

A

isotonic 0.9% NS to replace volume

this will turn off ADH secretion = more rapid correction of hyponatremia than desired

81
Q

too rapid correction of fluid may cause

A

hyponatremia develops

cells of brain respond by extruding osmolytes = osmotic demyelination syndrome

82
Q

why don’t we give everyone NS?

A

euvolemic SIADH will excrete all the sodium they give bc of normal aldosterone and ANP response and water will be retained

this lowers concentration of sodium and worsens hyponatremia

83
Q

osmotic demyelination syndrome

A

2-6 days following sodium correction

irreversible

dysarthria, dysphagia, parapheresis, behavioral disturbance, coma, seizures

common in pre-menopausal women

prevention by monitoring sodium

84
Q

hypernatremia causes

A

due to excess water loss rather than sodium gain

  1. high insensible loss
  2. osmotic diuresis
  3. diabetes insipidus
85
Q

hypernatremia s/s

A

dehydration

delerium

hyperthermia

coma

86
Q

dehydration symptoms in hypernatremia

A

decreased skin turgor

dry mucous membranes

decreased urine output

87
Q

tx of hypernatremia

A

gradual correction over 48hrs

0.5 mEq/L/hr no more than 9-10 /day

monitor closely bc math is only an estimate

88
Q

hypovolemic hypernatremia

euvolemic hypernatremia

A

hypo: 0.9% NS first to expand intravascular volume
eu: D5W or .45 NS

corrected too rapidly and seizures and cerebral edema will result

89
Q

SIADH

A

ASH screened without appropriate stimulus

following volume expansion, body will have inappropriately hypertonic urine

90
Q

etiologies of SIADH (7)

A
  1. paraneoplastic syndrome
  2. reset osmostat
  3. major sx/cardiac cath
  4. medications
  5. pulmonary disease
  6. transphenoid pituitary sx
  7. other
91
Q

reset osmostat

A

osmotic threshold for ADH secretion is slower

secreted at normal osmolalities causing water retention

92
Q

meds that INCREASE SDH production

A

antidepressants

carbamezepine

ecstasy

93
Q

meds that potentiate ADH

A

carbamezepine

NSAIDS
amiodarone

94
Q

cerebral salt wasting

A

depletion due to loss of sodium in urine

occurs following CNS event

volume depletion (HoTN)

isotonic saline TOC

FA17 Nephrology (13 decks)

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