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Acute Care I > Electrolytes > Flashcards

Electrolytes Flashcards

1
Q

Free water movement ensures that Na concentration in ECF will = what?

A

K concentration in ICF

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2
Q

Na is principle determinant of ECF volume & ultimately shifting of what?

A

fluid b/t ECF & ICF comparments

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3
Q

Major cation in ECF?

A

Na

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4
Q

Major cation in ICF?

A

K

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5
Q

Major anions in ECF?

A

Cl & HCO3

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6
Q

Negatively charged molecules in ECF (Cl, HCO3) maintain electroneutrality with?

A

positively charged cations in ICF

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7
Q

small changes in osmolality or tonicity are detected by what?

A

osmoreceptors in the hypothalamus

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8
Q

Under normal circumstances, the kidney increases or decreases H2O excretion & is mediated by?

A

antidiuretic hormone (ADH)/vasopressin from pituitary

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9
Q

Increased ADH secretion happens in response to what?
Decreased secretion?

A

volume contraction
Volume expansion

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10
Q

Under normal circumstances, the kidney responds to altered Na level in ECF & increases or decreases Na reabsorption due to impulses from what mechanisms?

A

carotid baroreceptors
atrial stretch receptors
intrarenal mechanisms

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11
Q

Normal “set point” for plasma osmolality is appox?

A

285 mOsm/kg

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12
Q

Minimum urine osmolality?
Maximum urine osmolality?

A

appox 50 mOsm/kg
approx 1200mOsm/kg

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13
Q

With rise in plasma osmolality >295mOsm/kg what two responses occur?

A

thirst centers of the hypothalamus are stimulated & signals individual to drink
ADH levels rise until osmolality returns to normal

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14
Q

ADH is also released in response to what even if plasma osmolality is low?

A

hypotension or decreased effective arterial volume

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15
Q

Maintenance IVFs needed if NPO, how much volume per day?

A

30-35 ml/kg/d

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16
Q

Maintenance IVFs needed if NPO, how much UOP is necessary to excrete daily solute load consumed?

A

> 500 ml/d

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17
Q

Maintenance IVFs needed if NPO, how much dextrose is necessary to minimize protein catabolism and ketoacidosis?

A

100-150 gm/d

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18
Q

Volume losses to consider when prescribing IVFs
Stool?

A

typically lose 200 ml/d

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19
Q

Volume losses to consider when prescribing IVFs
Insensible losses from skin, respiratory tract?

A

400-500ml/d

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20
Q

Volume losses to consider when prescribing IVFs
Fever?

A

losses increase by 100-150 ml/d for each degree > 37C

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21
Q

Volume losses to consider when prescribing IVFs
minimum volume/d =?

A

1400 ml or 60ml/hr

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22
Q

Volume losses to consider when prescribing IVFs
What may cause patients to require more?
What may cause patients to require less?

A

burns/open wounds
CHF patients

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23
Q

Reduced ECF volume in r/t capacity
May/may not have decreased ___ level.
May appear hypovolemic d/t increased capacitance of ECF or intravascular compartment (relative hypovolemia).
What can cause this appearance?

A

Na
Vasodilation: meds (vasodilators), sepsis, pregnancy
Generalized edema: CHF, cirrhosis, nephrotic syndrome
3rd spacing: sequestered compartment-SQ tissue, RP/peritoneal space, GI tract-not in equilibrium with ECF

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24
Q

Absolute hypovolemia results in what effect on Na level?

A

deficit in Na level

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25
Q

Absolute Hypovolemia
Renal causes?

A

inhibit or disrupt Na reabsorption
diuretics
tubule dysfunction (AKI-disrupts)
Endocrine disorders (AI, hyperaldosteronism-disrupts)

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26
Q

Absolute Hypovolemia
Extrarenal causes?

A

bleeding
losses from GI, skin, respiratory systems

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27
Q

Clinical presentation of hypovolemia depends on?

A

rate of loss

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28
Q

Clinical presentation of hypovolemia
Lab results for…
BUN (BUN:Cr ratio)
UOP
CVP/JVP
Specific gravity & urine osmolality
Urine Na
Fractional excretion of Na (FeNa)

A

elevated (>20:1)
decreased
low
high
< 15mEq (or may be higher in setting of diuretics)
< 1%

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29
Q

Equation for Fractional Excretion of Na?

A

(urine Na x serum Cr) / (urine Cr x serum Na) x 100

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30
Q

Clinical presentation of hypovolemia
Symptoms expected?

A

tachycardia
hypotension
lactic acidosis
hemoconcentration if not bleeding
cold extremities (unless septic)

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31
Q

Clinical presentation of hypovolemia
in what setting is hypernatremia expected?

A

H2O deficit

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32
Q

Management of hypovolemia
Deficit can be difficult to estimate and requires what?

A

frequent assessment

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33
Q

Management of hypovolemia
Goal?

A

HD stability, replenish intravascular volume

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34
Q

Management of hypovolemia
Use what type of fluids for resusitation?

A

Isotonic IVF (NS/LR)

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35
Q

Management of hypovolemia
Isotonic IVF contain what?

A

small molecules that diffuse freely throughout ECF compartment

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36
Q

Management of hypovolemia
Because 2/3 of ECF is interstitial, a similar proportion is interstitial; meaning IVFs do what?

A

follow the same distribution with approx. 2/3 of IVF distributed to interstitial space

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37
Q

Management of hypovolemia
To acutely expand intravascular space what is often required?

A

1-2L bolus

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38
Q

Colloids (albumin) contain what?

A

large, poorly diffusible molecules that create osmotic pressure to keep H2O intravascular

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39
Q

Colloids are more effective than crystalloids at what?

A

Expanding intravascular volume

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40
Q

Considerations about crystalloids
cost?
availability?
side effect?
effectiveness of expanding intravascular volume?
survival compared to colloids?
mortality, ICU/hospital LOS, MV days, or days of renal-replacement tx compared to colloids?

A

inexpensive
readily available
edema formation
need for increased volumes to = that of colloids
have been associated with survival advantage compared to colloids
Have been associated with no difference in mortality, ICU/hospital LOS, MV days, or days of renal-replacement tx compared to colloids

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41
Q

Infusion of large volumes of NS can result in what?

A

metabolic acidosis (hyperchloremic acidosis)

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42
Q

NS usually has what kind of adverse consequences?

A

usually none

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43
Q

LR contains what? what can this affect?

A

Calcium
may bind to certain meds/reduce effectiveness

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44
Q

LRs effect on serum lactate levels in critically ill or those with hepatic insufficiency?

A

not known

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45
Q

Cost of colloids vs crystalloids
NS/LR
5% albumin
25% albumin

A

$1.46/L
$30.63/250ml
$30.63/50ml

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46
Q

What advantages do colloids have over crystalloids?

A

remain intravascular longer & provide more plasma volume expansion than crystalloids

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47
Q

Albumin is what?
Available in what % solutions?

A

heat-treated preparations of human serum albumin
5% (50g/L)
25% (250g/L)

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48
Q

Hypervolemia results in what kind of Na balance?

A

surplus of total body Na

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49
Q

Hypervolemia/Na retention is secondary to?

A

renal disease (AKI, glomerular disease)
Endocrine d/o (excess mineralocorticoid action)

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50
Q

Hypervolemia/Na retention d/t renal disease occurs because?

A

Limited ability to excrete Na & H2O
Disruption of capillary Starling forces result in shifting of fluid from intravascular space to interstitium & activation of RAAS
May be secondary to hypoalbuminemia

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51
Q

Hypervolemia/Na retention d/t endocrine d/o
usually presents as?
May have what electrolyte abnormality?

A

HTN
hypokalemia

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52
Q

Secondary renal response to…
Reduced effective arterial blood volume resulting in?

A

renal Na retention, expanded ECF

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53
Q

Secondary renal Na retention results in?

A

enhanced sympathetic activity, RAAS activation
CHF (from low CO)
Cirrhosis synthetic dysfunction & hypoalbuminemia

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54
Q

Hypervolemia/Na retention clinical presentation

A

Edema
effusions
rales
elevated JVP/CVP
hepatojugular reflux
S3
HTN
Low urine Na (<15mEq/L

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55
Q

Hypervolemia/Na retention symptoms

A

dypnea
abd distention
edema

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56
Q

Management of Hypervolemia/Na retention primary goals?

A

address underlying problem
limit Na intake (20-40mmol/d)

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57
Q

Management of Hypervolemia/Na retention
What medication should be used?

A

Diuretics

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58
Q

Diuretics enhance renal Na excretion by what mechanism?

A

blocking various sites along nephron

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59
Q

Proxmial tubule diuretic to use in management of Hypervolemia/Na retention?

A

Diamox

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60
Q

Loop Diuretic to use in management of Hypervolemia/Na retention?

A

lasix

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61
Q

Distal tubule diuretic to use in management of Hypervolemia/Na retention

A

HCTZ

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62
Q

Collecting duct diuretic to use in management of Hypervolemia/Na retention?

A

Spironolactone

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63
Q

Which is the most potent diuretic to use in management of Hypervolemia/Na retention?

A

lasix

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64
Q

How does spironolactone work?

A

competes with aldosterone

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65
Q

How does spironolactone improve survival of those with Left Ventricular Dysfunction?

A

competitive blockade of nonepithelial mineralocorticoid receptors in heart and other vascular structures reducing fluid/Na retention

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66
Q

Hyponatremia results from?

A

processes that limit elimination of H2O or expands volume around fixed Na content

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67
Q

Antidiuretic hormone secretion leads to hyponatremia how?

A

either appropriate secretion in response to low circulating volume or inappropriate d/t neuro d/o, pulmonary disease, malignancy

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68
Q

Hyperosmolar Hyponatremia occurs when plasma osmolality is what?

A

> 295 mOsm/kg

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69
Q

Hyperosmolar hyponatremia is d/t?

A

hyperglycemia

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70
Q

Hyperosmolar hyponatremia causes increased ECF resulting in?

A

dilution of Na content

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71
Q

Hyperosmolar hyponatremia
For every 100 mg/dL rise in plasma glucose Na falls by?

A

1.6-2.4 mEq/L

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72
Q

Pseudohyponatremia Osmolality is?
Cause?

A

280-295 mOsm/kg
Lab phenomenon in which high concentrations of plasma proteins, lipids expand non-aqueous portion of plasma sample

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73
Q

Diagnostic approach to hyponatremia
Isotonic Hyponatremia 280-295 mOsm/kg?

A

Pseudohyponatremia

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74
Q

Diagnostic approach to hyponatremia
Hypertonic Hyponatremia >295 mOsm/kg

A

Hyperglycemia
Hypertonic fluid admin

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75
Q

Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg first step?

Second step?

A

Assessment of volume status
hypovolemic
euvolemic
hypervolemic

Check urine sodium

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76
Q

Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Hypovolemic: urine sodium > 20 mEq/L

A

Renal solute loss

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77
Q

Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Hypovolemic: urine sodium </= 20 mEq/L

A

Extrarenal solute loss

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78
Q

Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Euvolemic: urine sodium always >20 mEq/L

A

SIADH
Endocrinopathies (Glucocorticoid deficiency)
Potassium depletion (diuretic use)

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79
Q

Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Hypervolemic: urine sodium > 20 mEq/L

A

Renal failure

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80
Q

Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Hypervolemic: urine sodium </= 20 mEq/L

A

Edematous d/o’s
Heart failure
Cirrhosis
Nephrotic Syndrome

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81
Q

Hyponatremic Clinical presentation

A

Neurologic abnormalities d/t cerebral edema from shifting of H2O from ECF to ICF

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82
Q

Hyponatremic Clinical Presentation
neurologic abnormalities severity depends on?

A

magnitude & rapidity of fall

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83
Q

Hyponatremic Clinical Presentation
Acute: timeframe?
symptoms?

A

<2 days
nausea
malaise
H/A
lethargy
confusion
obtundation

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84
Q

Hyponatremic Clinical Presentation
Na 115 mEq/L results in?

A

stupor
seizures
coma

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85
Q

Hyponatremic Clinical Presentation
Chronic: timeframe?
symptoms?

A

> 3 days
minimization of increased ICF/symptoms

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86
Q

Management of Hyponatremia is determined by?

A

ECV (extracellular volume): low, normal, high
Presence of neuro symptoms

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87
Q

Symptomatic hyponatremia requires more rapid correction, however no greater increase in plasma Na than what rate?
not to exceed what level?
or how much Na mEq/L/d?
why?

A

0.5mEq/L/hr
130 mEq/L
>12 mEq/L/d
possible occurrence of central pontine myelinolysis (CPM) from neuronal damage from rapid osmotic shifts

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88
Q

Management of Hyponatremia for low ECV?

A

hypertonic saline 3% if symptomatic
NS if asymptomatic

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89
Q

Management of Hyponatremia for normal ECV?

A

lasix
hypertonic saline if symptomatic
NS if asymptomatic

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90
Q

Management of Hyponatremia for high ECV?

A

lasix
hypertonic saline if symptomatic
lasix if asymptomatic
water restriction

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91
Q

Formula for expected change in Na?

A

[(Na conc in IVF + K conc in IVF) - serum Na] / (kg x 0.6 +1)

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92
Q

ADH is secreted by and transmitted to?

A

hypothalamus
posterior pituitary

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93
Q

ADH is released in response to?

A

decreased effective circulating volume as sensed by baroreceptors

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94
Q

ADH MOA?

A

H2O reabsorption
urine concentration

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95
Q

SIADH is what?

A

inappropriate levels of ADH are secreted despite absence of osmotic or volume related stimuli

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96
Q

SIADH is a dysregulation of what?

A

cells secreting ADH or in feedback mechanisms responsible for release

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97
Q

SIADH causes CNS disease

A

tumor
trauma
infection
CVA
SAH
GBS
DTs
MS

98
Q

SIADH causes pulmonary disease

A

tumor
pneumonia
COPD
PPV

99
Q

SIADH causes malignancies

A

lung
pancreas
ovarian
lymphoma

100
Q

SIADH causes meds

A

NSAIDs
narcotics
diuretics
antidepressants
haldol
!

101
Q

SIADH other causes?

A

surgery
idopathic

102
Q

SIADH labratory

A

euvolemia
hyponatremia secondary to H2O excess
Elevated urine osmolality (>200 mOsm/kg)
elevated urine Na (> 20mEq/L)
decreased serum osmolality (<280 mOsm/kg)

103
Q

Hypernatremia results from?

A

Na gain or H2O deficit

104
Q

Hypernatremia Na gain comes from?

A

NS/hypertonic saline admin
chronic mineralocorticoid excess

105
Q

Hypernatremia H2O deficit comes from?

A

diaphoresis
diarrhea
osmotic diuresis (hyperglycemia)
diabetes insipidus

106
Q

Hypernatremia Clinical Presentation is r/t?

A

magnitude & rapidity of rise in Na

107
Q

Hypernatremia Clinical Presentation results form?

A

shifting of ICF to ECF & resultant contraction of brain cells

108
Q

Hypernatremia Clinical Presentation symptoms

A

altered MS
weakness
neuromuscular irritability
focal deficits
coma
seizures occasionally
thirst
polyuria if DI

109
Q

Diabetes Insipidus results from impaired what?

A

renal H2O conservation

110
Q

Diabetes Insipidus causes an excessive loss of what?

A

urine that is near pure H2O

111
Q

Diabetes insipidus r/t ADH
Central DI is d/t?

A

impaired ADH secretion from posterior pituitary

112
Q

Diabetes insipidus r/t ADH
Central DI causes?

A

trauma
anoxic encephalopathy
surgery
meningitis
brain death
ethanol
neoplastic
idiopathic

113
Q

Diabetes insipidus r/t ADH
Nephrogenic DI is d/t?

A

defective end-organ responsiveness to ADH

114
Q

Diabetes insipidus r/t ADH
Nephrogenic DI causes?

A

ampho
lithium
dye
hypokalemia

115
Q

Diabetes insipidus hallmark is what?
urine osmolarity in central is?
urine osmolarity in nephrogenic is?

A

dilute urine
<200 mOsm/L
200-500 mOsm/L

116
Q

Diabetes insipidus causes what Na balance?

A

hypernatremia

117
Q

Diabetes insipidus serum osmolality is?

A

> 290 mOsm/kg

118
Q

Diabetes insipidus dx is confirmed by?

A

response to fluid restriction
failure of urine osmolarity to increase by >30 mOsm/L in initial hours is diagnositc

119
Q

How to distinguish central DI from nephrogenic DI?Q

A

Response to vasopressin/dDAVP (1mcg SQ or IV)

120
Q

Expected response to dDAVP if its Central DI?
Expected response to dDAVP if its Nephrogenic DI?

A

Urine osmolarity will increase by >50% & UOP will decrease after admin
unchanged

121
Q

Diagnostic Approach to Hypernatremia
Urine Output is low?

A

Urine Osmolality will be high
Was there hypotonic fluid loss?
insensible losses
GI losses
Prior Renal Losses from Diuretics

122
Q

Diagnostic Approach to Hypernatremia
Urine Output is High; Urine Osmolality is Low

A

Diabetes Insipidus
Response to DDAVP indicates Central
No Response to DDAVP indicates Neprhogenic

123
Q

Diagnostic Approach to Hypernatremia
Urine Output is High; Urine Osmolality is High

A

Osmotic Diuresis?

124
Q

Management of Diabetes Insipidus depends on?

A

Acuity of development & symptoms

125
Q

Management of Diabetes Insipidus avoid rapid correction nto prevent what?

A

seizures & permanent neuro damage

126
Q

DI H2O deficit should not be corrected more rapid than?

A

10-12 mEq/L/d
less if chronic state

127
Q

Management of Diabetes Insipidus free H2O admin should be done how?

A

calculate free H2O deficit
Correct H2O deficit over 2-3 days to reduce risk of cerebral edema

128
Q

Formula for FW deficit = ?

A

0.6 x weight(kg) x [(current Na/140) - 1]

129
Q

Management of Diabetes Insipidus if central?

A

DDAVP 2-5 u SQ q 4-6hrs

130
Q

Management of Diabetes Insipidus if neprhogenic?

A

low Na diet
thiazide diuretic

131
Q

K content in ECF (mEq/L, %)?
K content in ICF (mEq/L, %)?

A

3.5 - 5 mEq/L, 2%
150 mEq/L 98%

132
Q

How is the K gradient maintained b/t ICF and ECF?

A

Na-KATPase pumps

133
Q

Small changes in ECF K alters the ratio significantly & may result in?

A

serious or lethal consequences from tissue dysfunction

134
Q

If just 2% of ICF K leaked into ECF, plama K (Pk) would increase by how much?

A

immediately doubles

135
Q

Kidneys are almost entirely responsible for maintaining balance of output to intake, dependent on?
Increased (Pk) increased what?

A

flow/Na delivery & aldosterone
aldosterone production & renal K excretion

136
Q

Factors causing cellular K influx?

A

insulin
beta agonists

137
Q

Factors causing cellular K efflux?

A

cell ischemia
exercise
plasma hypertonicity (drag)
acidosis (hyperchloremic)

138
Q

What is the distribution of K with acute loading
excretion?
transport into cells?

A

approx. 50% in urine
approx. 90% of remainder into cells over 4-6 hrs

139
Q

Acute hyperkalemia causes (<48hrs)?

A

excessive intake
ARF (30-50% of time)
rhabdo
tumor lysis syndrome
ischemia/infarction
burns
hyperglycemia
meds - digoxin OD, succinylcholine

140
Q

Chronic Hyperkalemia causes

A

CRF
mineralocorticoid deficiency
ACEIs, ARBs
Heparin
RTA
K sparing diuretics

141
Q

What should be on your radar if hyperkalemia & hypotension occur together?
how can meds cause this?

A

mineralocorticoid deficiency
COX1 & 2 inhibitors d/t decreased renin release

142
Q

How does ACEIs and ARBs cause chronic hyperkalemia?

A

decrease aldosterone synthesis

143
Q

How does heparin cause chronic hyperkalemia?

A

inhibits aldosterone synthesis

144
Q

How does RTA cause chronic hyperkalemia?

A

defect in renal K secretion association with SS disease/trait, SLE

145
Q

How does K sparing diuretics cause chronic hyperkalemia?

A

blocks Na reabsorption in distal nephron

146
Q

Clinical Manifestations of hyperkalemia
Cardiac

A

depolarizes cell membrane, slows ventricular conduction, decreases action potential duration which leads to
peaked T waves
prolonged PR interval
widened QRS
loss of P wave
Vfib or
asystole

147
Q

Clinical Manifestations of hyperkalemia
Neuromuscular

A

paresthesias
weakness progressing to paralysis
decreased/absent reflexes

148
Q

Clinical Manifestations of hyperkalemia
Metabolic

A

mild hyperchloremic acidosis

149
Q

Evaluation of Acute Hyperkalemia includes?

A

ECG
re-send unclotted blood sample for electrolytes, glucose, BUN, Cr, CBC
assess urine for heme to exclude rhabdo/hemolysis
review med list and diet

150
Q

Management of acute hyperkalemia
Effects are proportional to?

A

level & rate of rise

151
Q

Management of acute hyperkalemia
1st disturbance seen may be?

A

vfib

152
Q

Management of acute hyperkalemia
most exhibit ECG changes with what K level?

A

> 6.7 mEq/L

153
Q

Management of acute hyperkalemia
tx should be immediate for what K level?

A

> 6.5 mEq/L

154
Q

Management of acute hyperkalemia
tx should be immediate regardless of levels when?

A

ECG changes

155
Q

Management of acute hyperkalemia
tx should focus on?

A

membrane stabilization
redistribution of K into cells
K elimination

156
Q

Management of acute hyperkalemia
Membrane stabilization includes?

A

CaGluconate (1g IV over 10 min) onset is immediate

157
Q

Management of acute hyperkalemia
Redistribution of K into cells includes?

A

insulin (10u IVP + 1 amp D50 IV)
albuterol (20mg/4mL)
Bicarb 150 mEq/L

158
Q

Management of acute hyperkalemia
insulin admin lowers K by how much?
Onset is how long?
when to not give D50?

A

approx. 1 mEq/L
20 min
if patient is already hyperglycemic

159
Q

Management of acute hyperkalemia
albuterol lowers K by how much?
drawback of albuterol?

A

approx 1 mEq/L
some may be resistant to albuterol; use as adjunct

160
Q

Management of acute hyperkalemia
Elimination of K includes?

A

diuretics (lasix 40-80 mg IV)
kayexalate - 15-30 g/ 15-30ml or lokelma
hemodialysis

161
Q

Management of acute hyperkalemia
onset for…
diuretics
sodium bicarb
sodium polystyrene sulfonate (kayexalate)

A

15 min
1 hr
> 2 hr

162
Q

Management of acute hyperkalemia
How does sodium polystyrene sulfonate work?
what are the effects?
what adverse reaction is potential?

A

exchanges Na for K in colon
variable
intestinal necrosis

163
Q

Acute hypokalemia is almost always a result of what?

A

shift from ECF to ICF

164
Q

Causes of acute hypokalemia?

A

tx for DKA (secondary to insulin tx)
refeeding (secondary to glucose stimulated hyperinsulinemia)
meds (beta agonists, epinephrine)

165
Q

Chronic Hypokalemia causes

A

decreased intake
excessive losses (mostly renal)
meds
mineralocorticoids
Mg deficiency
hypercalcemia

166
Q

Chronic Hypokalemia causes:
excessive losses from?

A

diuretics inhibit Na & Cl reabsorption causing secondary hypoaldosteronism

167
Q

Chronic Hypokalemia causes:
what meds?

A

ampho B
PCNs d/t renal K wasting

168
Q

Chronic Hypokalemia causes:
from Mineralocorticoids

A

diuretics in secondary aldosteronism (CHF, cirrhosis) are to blame d/t increased nephron flow rate

169
Q

Chronic Hypokalemia causes:
Hypercalcemia causes what?

A

Na & H2O diuresis

170
Q

Clinical Manifestations hypokalemia
Cardiac

A

hyperpolarizes cell membrane, prolongs action potential which leads to
ST depression
decreased T wave amplitude
increased U wave amplitude
ECG can be nonspecific and less reliable than w/ hyperkalemia
may be assoc. w/ arrhythmias, conduction defects

171
Q

Clinical Manifestations hypokalemia
Neuromuscular

A

weakness
myalgias
fatigue
restless legs
paralysis w/ more severe hypokalemia
ileus
gastroparesis
rhabdo w/ profound hypokalemia

172
Q

Management of Acute Hypokalemia includes?

A

KCL @ infusion rate of 0.6 mEq/kg/hr (normal renal function)
KCL@ infusion rate of 0.1 mEq/kg/hr (renal failure)
maximum increases seen in @ end of infusion w/ approx. 50% lost over next 2-3 hrs
Check levels @ end of infusion & in 2-3 hrs

173
Q

Serum Postassium (mEq/L) = Potassium deficit (mEq)/ % total body K
3.0
2.5
2.0
1.5
1.0

A

175 / 5
350 / 10
470 / 15
700 / 20
875 / 25

174
Q

What is the second most abundant ICF cation?

A

Mg

175
Q

Hypermagnesia causes

A

meds
tx for preeclampsia/eclampsia
hypothyroidism
hyperparathyroidism
addison’s disease
lithium tx

176
Q

What meds can cause Hypermagnesia?

A

mg containing antacids (mg aluminum hydroxide)
laxatives (mg citrate) in setting of renal insufficiency

177
Q

Clinical manifestations of Hypermagnesia
Cardiac

A

hypotension
bradycardia
SA/AV block
asystole

178
Q

Clinical manifestations of Hypermagnesia
GI

A

N/V
ileus

179
Q

Clinical manifestations of Hypermagnesia
Neuromuscular

A

hyporeflexia
paralysis
respiratory muscle weakness
lethargy
coma

180
Q

Hypomagnesia causes

A

insufficient intake (ETOHism)
renal losses
GI losses
Redistribution

181
Q

Hypomagnesia from renal losses are caused by?

A

diuretics
abx
chemo (cisplatin)
volume expansion
osmotic diuresis
ETOH

182
Q

Hypomagnesia from GI losses are caused by?

A

diarrhea
SB disorders/resection d/t disrupted absorption

183
Q

Hypomagnesia from redistribution is caused by?

A

acute pancreatitis d/t saponification
hungry bone syndrome following parathyroidectomy d/t rapid bone uptake during remineralization

184
Q

Management of Hypermagnesia includes?

A

no tx if normal renal fxn & mild symptoms
remove exogenous sources
saline administration
diuretics
CaGluconate 1g if symptoms are severe
HD

185
Q

Management of Hypomagnesia includes?

A

MgSO4 2g IV if vfib or torsades
MgSO4 IVPB or po

186
Q

Management of Hypomagnesia
Mg level 0.9 - 1.8 requires how much IVPB?
Mg level 1.9-2.0 requires how much IVPB?

A

4g MgSO4
2g MgSO4

187
Q

Calcium balance is regulated by what?

A

parathyroid hormone and calcitriol

188
Q

PTH has what effect on serum Ca?
how?

A

increases
thru bone resorption & promoting renal conversion of vit D to calcitriol

189
Q

Serum Ca regulates PTH secretion how?

A

through a negative feedback system
low serum Ca stimulates PTH release
high serum Ca suppresses PTH release

190
Q

What is the active form of vit D?
how does it affect serum Ca?

A

calcitriol (1,25-dihyrdoxycholecalciferol, 1.25 -dihyrdoxyvitamin D3)
stimulates intestinal absorption of Ca & provides feedback to parathyroid

191
Q

What is the best measurement for assessing calcium concentrations?

A

ionized Ca or iCa

192
Q

Ionized Ca
Acid-base status & protein concentrations affect total Ca concentrations.
Acidemia has what effect on Ca?
Alkalosis has what effect on Ca?

A

acidemia displaces Ca from ablumin & results in increased iCa

alkalosis causes Ca to bind to albumin & results in decreased iCa

193
Q

Ionized Ca
Changes in plasma proteins (albumin) affect total Ca concentration.
Hypoalbuminemia results in what effect on total Ca concentration?
Hyperalbuminemia?

A

hypoalbuminemia results in reduced total Ca concentration

hyperalbuminemia results in increased total Ca concentration

194
Q

Corrected Ca formula is?

A

4.2 - albumin level + total Ca level

195
Q

Hypercalcemia causes

A

primary hyperparathyroidism
malignancy
rhabdo
immobility
meds

196
Q

Most common cause of Hypercalcemia?
most common cause of this problem?

A

primary hyperparathyroidism
benign adenoma (80-90% of cases)

197
Q

Hypercalcemia causes
malignancy causes?

A

secondary to PTH r/t peptide secretion by malignant cells
increased 1,25-dihyroxycholecalciferol production by malignant cells in lymphoma
osteolytic bone lesions

198
Q

Hypercalcemia causes
from meds?

A

lithium (induces hyperparathyroidsim)
thiazides (increased reabsorption)
vit D supplementation

199
Q

Clinical Manifestations of Hypercalcemia depend on?

A

rate of increase & level

200
Q

Clinical Manifestations of Hypercalcemia
Neuro?

A

weakness
fatigue
depression
altered MS

201
Q

Clinical Manifestations of Hypercalcemia
Cardiovascular

A

increased rate of repolarization
shortened QT interval
arrhythmias

202
Q

Clinical Manifestations of Hypercalcemia
GI

A

anorexia
N/V
Constipation

203
Q

Management of Hypercalcemia
assess what?

A

is PTH intact
vit D metabolites

204
Q

Management of Hypercalcemia
mild hypercalcemia (total Ca < 12 mg/dL) is usually d/t?

A

primary hyperparathyroidism
thiazides
supplementation
lithium
immobility

205
Q

Management of Hypercalcemia
mild hypercalcemia (total Ca < 12 mg/dL) txs?

A

remove offending agent
mobilize
hydrate

206
Q

Management of Hypercalcemia
moderate hypercalcemia (total Ca 12-14 mg/dL) usually d/t?

A

primary hyperparathyroidism
thiazides
supplementation
lithium
immobility

207
Q

Management of Hypercalcemia
moderate hypercalcemia (total Ca 12-14 mg/dL) txs?

A

remove offending agent
hydrate
diuresis to increase excretion, but avoid volume depletion

208
Q

Management of Hypercalcemia
severe hypercalcemia (total Ca > 14mg/dL) txs

A

volume expansion with NS
loop diuretics after resuscitation for increased renal excretion
HD
bisphosphonates (pamidronate, zoledronic acid-inhibit osteoclast function & number & inhibit bone turnover

209
Q

Hypocalcemia causes

A

Hypoparathyroidsm
Vit D deficiency

210
Q

Vit D deficiency causes?

A

decreased intake
inadequate sunlight
impaired synthesis (requires hydroxylation in liver & kidneys to be converted to active form; if dysfunction, impaired vit D synthesis)

211
Q

Hypocalcemia causes
Redistribution

A

chelation of Ca by citrate from massive blood transfusions
elevated phospohorus levels - binds to Ca
rhabdo (d/t Ca deposition in injured muscle, ARF/decreased synthesis of vit D)
acute pancreatitis (unclear; may be secondary to accumulation in pancreas, liver, skeletal muscle, high levels of endotoxin)

212
Q

Hypocalcemia causes
meds

A

cisplatin
biphosphonates

213
Q

Hypocalcemia causes
sepsis

A

sequestration
PTH resistance
vit D deficiency

214
Q

Clinical manifestations of hypocalcemia
neuro

A

paresthesias (perioral)
hyperactive reflexes
tetany (Chvostek sign - ipsilateral muscle twitching w/ facial nerve tapping, Trousseau sign - carpal smasm w/ occlusion of brachial artery)
seizures

215
Q

Clinical manifestations of hypocalcemia
Cardiovascular

A

prolonged QT interval
bradycardia
hypotension
heart block/cardiac arrest

216
Q

Management of hypocalcemia
iCa < 3.2 mg/dL w/ serious CV or neuo signs requires?

A

urgent tx
CaGluc 10%/10 ml (90mg) IV over 5-10 min followed by 500-1000mg/500 ml over 6 hrs
CaCl 10/10 ml (272mg)
freq iCa levels

217
Q

Management of hypocalcemia
iCa > 3.2 mg/dL manifestations?

A

may have few or none

218
Q

Management of hypocalcemia
PO supplementation for chronic conditions which are?
dose?

A

vit D deficiency, hypoparathyroidism
1-4gm/d + vit D in divided doses

219
Q

Management of hypocalcemia
correct hyperphosphatemia (in renal failure) with?

A

binders & hypocalcemia will often correct

220
Q

Management of hypocalcemia
correct what other electrolyte abnormality?

A

Mg deficits

221
Q

Phosphorus balance is determined by?

A

PTH regulates bone stores, decreases reabsorption & increases excretion
phosphate conc regulates reabsorption
insulin shifts into cells
calcitriol increases intestinal absorption

222
Q

Phos normal level?

A

2.5-4.5 mg/dL

223
Q

Hyperphosphatemia (plasma level > 5 mg/dL) causes?

A

redistribution
increased intake
decreased renal excretion

224
Q

Hyperphosphatemia (plasma level > 5 mg/dL) causes
redistribution from?

A

tumor lysis syndrome
rhabdo
pancreatitis
resp acidosis

225
Q

Hyperphosphatemia (plasma level > 5 mg/dL) causes
decreased renal excretion from?

A

hypoparathyroidism

226
Q

Clinical manifestations of hyperphosphatemia?

A

Similar to hypocalcemia d/t binding

227
Q

Management of hyperphosphatemia?

A

reduce intake
phosphate binders
volume expansion to increase excretion

228
Q

Hypophosphatemia (plasma level < 2.5 mg/dL) causes?

A

redistribution
increased renal excretion
decreased intestinal absorption

229
Q

Hypophosphatemia (plasma level < 2.5 mg/dL) causes
redistribution from?

A

acute resp alkalosis
refeeding syndrome
DKA

230
Q

Hypophosphatemia (plasma level < 2.5 mg/dL) causes
increased renal excretion from?

A

primary hyperparathyroidism causing phosphaturia
vit D deficiency causes decreased absorption
volume expansion
post-obstructive diuresis
diuretics

231
Q

Hypophosphatemia (plasma level < 2.5 mg/dL) causes
decreased intestinal absorption

A

malnutrition
phosphate binders
chronic diarrhea
chronic ETOH

232
Q

Clinical manifestations of hypophosphatemia
patients are usually asymptomatic until?

A

level < 1.5 mg/dL

233
Q

Clinical manifestations of hypophosphatemia
skeletal

A

weakness
rhabdo

234
Q

Clinical manifestations of hypophosphatemia
cardiac

A

decreased CO

235
Q

Clinical manifestations of hypophosphatemia
hematologic

A

decreased 2,3-DPG (decreased O2 delivery)
impaired leukocyte & platelet fxn

236
Q

Clinical manifestations of hypophosphatemia
neuro

A

irritability
confusion
paresthesias

237
Q

Clinical manifestations of hypophosphatemia
endocrine

A

insulin resistance

238
Q

Management of Hypophosphatemia includes?

A

anticipate hypophosphatemia
Supplementation is weight based

239
Q

Phos supplementation for patients weighing 40-60kg
phos level <1mg?
phos level 1-1.7mg?
phos level 1.8-2.2mg?

A

30mmol
20mmol
10mmol

240
Q

Phos supplementation for patients weighing 61-80kg
phos level <1mg?
phos level 1-1.7mg?
phos level 1.8-2.2mg?

A

40mmol
30mmol
15mmol

241
Q

Phos supplementation for patients weighing 81-120kg
phos level <1mg?
phos level 1-1.7mg?
phos level 1.8-2.2mg?

A

50mmol
40mmol
20mmol

Acute Care I (15 decks)

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