Chapter 17: Fluids and Electrolytes Flashcards

1
Q

Total body water accounts approximately _ of total body weight

A

60%

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2
Q

The ECF is composed of ___ and ___, or interstitial, fluid

A

Intravascular and Extravascular

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3
Q

What are the 3 fundamental homeostatic equilibriums?

A
  1. osmotic equilibrium
  2. electric equilibrium
  3. acid-base equilibrium
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4
Q

The key point is that sodium is much more concentrated in the ECF (approximately ___ mEq/L) than in the ICF (approximately ___ mEq/L)

A

40

10

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5
Q

Why Na is equal in both compartment of ECF?

A

Because the capillary membrane is permeable to water and electrolytes

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6
Q

Why Na is increase in extracellular compared to intracellular?

A

Because the cell membrane is only permeable to water but not to electrolytes

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7
Q

Measure of solute concentration per unit mass of solvent

A

Osmolality

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8
Q

Measure of solute concentration per unit volume of solvent

A

Osmolarity

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9
Q

When two solutions are separated by a membrane that is permeable only to water, water crosses into the compartment with ___

A

the more concentrated solution to equalize the ion concentration in each.

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10
Q

Contribute the most to osmotic pressure in ECF

A

Na, HCO3 and Cl plus glucose

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11
Q

Formula to calculate effective osmolality or Tonicity

A

2 x Na + glucose / 18

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12
Q

What will happen if you add 1L of water to the ECF?

A

it will cross the cell membrane into ICF to equalized ECF osmolality. TBW will expand and decrease in osmolality

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13
Q

What will happen if you add 1L of isotonic saline to the ECF?

A

no movement of water into cells and will only produce ECF expansion

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14
Q

What will happen if you give hypertonic plasma and hypotonic plasma?

A

Hypertonic plasma will shrink the cell

Hypotonic plasma will swell the cell

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15
Q

Two types of dehydration

A
water loss (hyper-osmolality)
salt loss (hypo-osmolality)
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16
Q

Example of salt loss type of dehydration

A
vomiting
sweating
diarrhea
bleeding
CKD
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17
Q

Hyponatremia is defined as a serum Na

A

<138

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18
Q

symptoms of hyponatremia occurs if serum Na

A

=/<15

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19
Q

How many percent of heart failure patient has hyponatremia?

A

approximately 20%

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20
Q

How many percent has mild hyponatremia in hospitalized patient?

A

15-30%

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21
Q

If patient has hyponatremia what is the next step?

A

volume status and calculate plasma osmolalities
Hyperosmolar hyponatremia >295
Isoosmolar hyponatremia 275 - 295
Hypoosmolar hyponatremia >295

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22
Q

Pathophysiology of hyperosmolary hyponatremia

A

large amount of osmotically active solutes accumulate in the ECF space. example is Hyperglycemia

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23
Q

Each 100mg/dL increase of glucose it will ___

A

decrease plasma Na by 1.6mEq/L

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24
Q

administration of mannitol, glycerol and maltose will cause ___

A

osmolar gap and hyponatremia

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25
Q

Difference between measured osmolality and calculated osmolality

A

osmolar gap (NV around 10)

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26
Q

Example of isoosmolar hyponatremia

A

severe hyperproteinemia or hyperlipidemia

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27
Q

Two important hyponatremic disorders are the

A

SIADH and less common cerebral salt-wasting syndrome

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28
Q

Difference of SIADH to cerebral salt-wasting syndrome

A

SIADH may also cased by non cerebral disease and volume status is normal

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29
Q

Intoxication of this substance is uncommon but important cause of hyponatremia that may be profound

A

Methylenedioxymethamphetamine (MDMA or Ecstasy)

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30
Q

The most important symptoms of hyponatremia are due to its effects on the

A

brain

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31
Q

Moderately severe symptoms often start when a plasma [Na+] is ___

A

<130 mEq/L

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32
Q

Severe symptoms often start when a plasma [Na+] is ___

A

<120 mEq/L

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33
Q

Initially if hypoosmolar the brain will ___. After 48 hours the brain will adapt and will release

A

swell producing intracranial hypertension.

Na, K, Cl, glycine and taurine

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34
Q

Symptoms is hypoosmolar hyponatremia is sever and persistent in what population?

A

SIADH
Children
Menstruating women
Hypoxia

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35
Q

Diagnostic criteria of SIADH

A
Hypotonic hyponatremia (<275)
Increase urinary osmolality (>200)
Elevated urinary Na (>20)
Clinically euvolemia
Normal other organs
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36
Q

Experts recommend that when duration is unknown, the hyponatremia should be assumed to be chronic and treated as ___ with a longer correction time.

A

chronic

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37
Q

Acute vs chronic hyponatremia

A

24-48 hours

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38
Q

If no urinary osmolality, you can compute by

A

for a specific gravity (π) of 1.005, UOSM = 05 × 35 = 175 mOsm/L.

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39
Q

As a rule, only in patients with edematous syndromes and in patients with vomiting and diarrhea will UNa+ be found to be

A

<10 mEq/L

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40
Q

The most important guides for therapy in hyponatremia is

A

symptoms (hyponatremic encephalopathy)

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41
Q

When the patient presents with severe neurologic symptoms (vomiting, seizures, reduced consciousness, cardiorespiratory arrest), the initial treatment

A

infusion of 3% hypertonic saline as recommended by European guidelines

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42
Q

Raising serum sodium by ___ is typically all that is required to see an improvement in severe neurologic symptoms.

A

5 mEq/L

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43
Q

T or F: When symp- toms are mild or moderate (nausea, confusion, headache) or in chronic hyponatremia, the [Na+] correction should be faster than for acute hyponatremia

A

False. it should be slower

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44
Q

For chronic hyponatremia [Na+], the correction rate should not exceed ___ in high-risk patients and ___ h in low-risk patients

A

6 mEq/24 hour

12 mEq/24 hour

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45
Q

Hypertonic (3%) saline can be in hyponatremia given at a low infusion rate

A

0.5 to 1 mL/kg/h

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46
Q

In addition in treatment of hyponatremia using saline we can also add what?

A

Furosemide 20mg IV

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47
Q

Osmotic demyelination syndrome is caused by rapid correction of hyponatremia

A

> 12 mEq/L/24 h

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48
Q

Treatment for overcorrection of

Na

A

5% dextrose in water at 3ml/kg/h
loop diuretics
desmopressin

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49
Q

Hypernatremia is defined as serum or plasma ___

A

[Na+] >145 mEq/L and hyperosmolality (serum osmolality >295 mOsm/L).

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50
Q

Population at risk of hypernatremia

A

Elderly patients, decompensated diabetics, infants, and hospitalized patients

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51
Q

If severe hypernatremia develops in the course of minutes to hours, such as from a massive salt overdose in a suicide attempt, a suddenly shrinking brain may prompt ___

A

intracranial hemorrhage

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52
Q

Based on volume status, hypernatremia can be classified into 3

A
  1. hypovolemic hypernatremia (decreased TBW and total body Na+ with a relatively greater decrease in TBW)
  2. hypervolemic hypernatremia (increased total body Na+ with normal or increased TBW)
  3. normovolemic hypernatre- mia (near normal total body sodium and decreased TBW)
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53
Q

FDA recommends against vasopressin antagonists in patients with ___

A

liver cirrhosis

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54
Q

Therapy for cerebral salt wasting

A

isotonic (-.9%) nacl and Fludrocortisone – nacl orally at home

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55
Q

Therapy for SIADH

A

Water restriction.
Enhanced Na+ and protein intake + furosemide. Vasopressin antagonists* can be used for [Na+] <125 mEq/L. Demeclocycline. Lithium.

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56
Q

Polyuria

A

> 3000ml of urine/24hours

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57
Q

Drug may case nephrogenic diabetes insipidus

A

Demeclocycline

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58
Q

Drug may cause interstitial nephritis

A

NSAIDs

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59
Q

Example of normovolemic hypernatremia

A
Central DI (urine osm <300)
Partial DI (urine osm 300-800)
Nephrogenic DI (urine osm <200)
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60
Q

Patient has Urine osm of more than 800 and urine Na less than 10. What is your consideration?

A

extrarenal hypovolemia hypernatremia

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61
Q

Severe hypernatremia ___ yields a mortality of ___

A

Severe hypernatremia (i.e., a [Na+] >150 to 160 mEq/L) yields a mortality of 75%

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62
Q

A BUN/creatinine ratio ___ is indicative of hyperosmolar dehydration.

A

A BUN/creatinine ratio >40 is indicative of hyperosmolar dehydration.

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63
Q

Steps in treatment of hypernatremia

A
  1. isotonic 0.9% saline
  2. treat underlying cause
  3. compute for free water deficit
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64
Q

When the adaptation of brain cells is incomplete (onset over

<48 hours), the correction rate of acute hypernatremia can be performed at a rate of ___

A

1 mEq/L/h

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65
Q

If hypernatremia is chronic (onset over >48 hours), the rate of correction should be slower to avoid the risk of cerebral edema, at no more than ___

A

If hypernatremia is chronic (onset over >48 hours), the rate of correction should be slower to avoid the risk of cerebral edema, at no more than 0.5 mEq/L/h or 10 to 12 mEq/24 h.

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66
Q

A disease where the ability of the kidney to reabsorb free water is compromised.

A

Diabetes insipidus characterized as

  • polyuria
  • polydipsia
  • increased volume of hypoosmolar urine
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67
Q

2 types of diabetes insipidus

A
  1. central (also called neurogenic), due to inadequate ADH secretion
  2. renal (also called nephrogenic), when ADH secretion is normal or increased but the v2R receptors of the kidney’s collecting duct cells do not respond appro- priately to ADH.
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68
Q

The most common clinical symptoms and signs are ___

A

The most common clinical symptoms and signs are excessive thirst, polydipsia, and polyuria

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69
Q

Diabetes insipidus a spot check in the ED without water deprivation will typically reveal a UOSM of

A

<300 mOsm/L

70
Q

Central diabetes insipidus is treated with

A

the synthetic hormone desmopressin, as a nasal spray, 10 micrograms (0.1 mL) every 12 hours, or PO, 0.05 milligrams every 12 hours, as starting doses.

71
Q

Nephrogenic diabetes insipidus is treated with

A

low-salt, low-protein diet, adequate hydration, and the careful use of one to three agents that act together to concentrate urine in these patients: a thiazide diuretic, the potassium- sparing diuretic amiloride, and indomethacin.

72
Q

Hypokalemia is defined as a serum [K+] of

A

<3.5 mEq/L.

73
Q

Most frequent cause of hypokalemia

A
  1. insufficient dietary intake
  2. intracellular shift
  3. increase losses
74
Q

Hypokalemia makes the resting potential more electronegative which produces in ECG

A
  • enhancing depolarization; the reduction in [K+] conduction delays repolarization, causing prolonged QTc, flattened T waves, and the appearance of U waves in the ECG
75
Q

Symptoms of hypokalemia with start at serum ___

A

2.5 mEq/L

76
Q

Arrythmias to watch out in hypokalemia

A

atrial fibrillation
torsades de pointes
ventricular tachycardia
ventricular fibrillation

77
Q

Cause of hypokalemia that mimics thiazide diuretic use

A

gitelman;s syndrome

78
Q

Cause of hypokalemia that mimics loop diuretic use

A

bartter’s syndrome

79
Q

UNa+ value <30 mEq/L and a UOSM value less than POSM suggest

A

polyuria

80
Q

How to compute transtubular K gradient?

A

(Urinary K+ × POSM)/(UOSM × Plasma K+) with normal result of 8-9 mEq/L

81
Q

transtubular K gradient result of <5 mEq/L suggest ___ and value of <3 mEq/L suggest ___

A

values <5 mEq/L suggest hyperaldosteronism; if paralysis is present, values <3 mEq/L suggest hypokalemic periodic paralysis.

82
Q

A calcium/phosphate ratio ___ on a spot urine is 100% sensitive and 96% specific for thyrotoxic hypokalemic periodic paralysis.

A

A calcium/phosphate ratio >1.7 on a spot urine is 100% sensitive and 96% specific for thyrotoxic hypokalemic periodic paralysis.

83
Q

Level of mild, moderate and severe hypokalemia

A
mild = >3 mEq/L
moderate = 2.5 - 3 mEq/L
severe = <2.5 mEq/L
84
Q

In tintinally, fluid correction of hypokalemia is ___

A

500 mL of a saline solution is 40 mEq, to be infused in 4 to 6 hours in a peripheral line

85
Q

In most cases, hypokalemic patients are also hypomagnesemic.

A

Thus, magnesium (20 to 60 mEq/24 h) may be added to the infusion both to optimize tubular reuptake of potassium and to contrast proar- rhythmic effect of hypokalemia.

86
Q

Hyperkalemia is defined as measured serum [K+] of ___

A

> 5.5 mEq/L

87
Q

The most common cause is factitious hyperkalemia due to

A

release of intracellular potassium caused by hemolysis during phlebotomy.

88
Q

What is the role of Calcium in hyperkalemia?

A

calcium antagonizes the effects of hyperkalemia at the level of the cell membrane, raising the threshold potential

89
Q

Death from hyperkalemia is usually the result of ___

A

diastolic arrest or ventricular fibrillation

90
Q

In hyperkalemia, elevated spot urine K (>20mEq/L) suggest ___

A

extra renal cause

91
Q

In hyperkalemia, low urine K+ output (<10 mEq/L) suggests ___

A

oliguric kidney failure or drug effect, such as angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers.

92
Q

Treatment modalities for hyperkalemia

A
  1. membrane stabilization
  2. intracellular shift of K
  3. removal/excretion of K
93
Q

This study does not recommend the routine administration of sodium bicarbonate for hyperkalemia unless there is concomitant metabolic acidosis.

A

Cochrane review of 2015

94
Q

Causes of hyperkalemia

A
  1. pseudohyperkalemia
  2. intracellular shift to extracellualr
  3. potassium load
  4. decrease potassium excretion
95
Q

This oral was previously used to excrete potassium but noted with intestinal necrosis

A

sodium polystyrene sulfonate

96
Q

2 oral K binding agents can be use in ED

A

patiromer

sodium zirconium cyclosilicate

97
Q

___ enhances the toxic cardiac effects of digitalis.

A

hypercalcemia enhances the toxic cardiac effects of digitalis.

98
Q

The total body content of magnesium (Mg2+) is ___

A

24 grams, or 2000 mEq,

99
Q

____ of which is fixed in bone and only slowly exchange- able.

A

50% to 70%

100
Q

Most of the remaining Mg2+ is found in the ICF space, with a concentration of approximately ___

A

40 mEq/L

101
Q

Circulating Mg2+ is ___ to ___ bound to proteins (mainly albumin), ___ to ___ complexed, and ___ to ___ ionized,

A

Circulating Mg2+ is 25% to 35% bound to proteins (mainly albumin), 10% to 15% complexed, and 50% to 60% ionized

102
Q

How many percent of circulating Mg2+ is active form?

A

50% - 60% inonized

103
Q

The normal dietary intake of Mg2+ is approximately ___ and is found in vegetables such as dry beans and leafy greens, meat, and cereals.

A

The normal dietary intake of Mg2+ is approximately 240 to 336 milligrams/d and is found in vegetables such as dry beans and leafy greens, meat, and cereals.

104
Q

Hyperkalemia 12LECG changes levels
Prolonged PR interval, tall peaked T waves, short QT interval
Flattening of the P wave, QRS widening
QRS complex degradation into a sinusoidal pattern

A

6.5–7.5 = Prolonged PR interval, tall peaked T waves, short QT interval
7.5–8.0 = Flattening of the P wave, QRS widening
10–12 = QRS complex degradation into a sinusoidal pattern

105
Q

Membrane stabilization used for hyperkalemia

A
calcium chloride (5-10ml IV) 1-3 ml
calcium glutinate (10-20ml IV) 1-3 ml
106
Q

T or F: Renal reabsorption of Mg2+ is carried out with sodium and water and is unidi- rectional

A

True

107
Q

___ enhances neuromuscular activity (thus provoking tremors and cramps) by
rapidly decreasing ionized [Mg2+] and [Ca2+] at the same time.

A

respiratory alkalosis

108
Q

Drug that causes hypomagnesemia

A

proton pump inhibitor

diuretic therapy

109
Q

Hypomagnesemia is common in acute illness; it has been found in ___ of hospitalized patients and in up to ___ of medical intensive care patients.

A

Hypomagnesemia is common in acute illness; it has been found in 12% of hospitalized patients and in up to 65% of medical intensive care patients.

110
Q

Hypo- calcemia does not develop until [Mg2+] falls below ___

A

Hypo- calcemia does not develop until [Mg2+] falls below 1.2 milligrams/dL

111
Q

Treatment principles for hypomagnesemia

A
  1. treat or stop cause of hypomagnesemia
  2. asymptomatic patient may use supplementation
  3. for severe and symptomatic hypomagnesemia, urgent IV replacement is mandatory
  4. chronic Mg2+ def may require >50 meds of oral Mg (6 grams of MgSO4 per day)
  5. spironolactone - reducing incidence of arrhythmias in congestive heart failure
112
Q

In life-threatening conditions hypomagnesemia (torsades de pointes, eclampsia) treatment is

A

1 to 4 grams or 8 to 32 mEq diluted in at least 100 mL of 5% dextrose or normal saline (0.9%) solution can be administered in 10 to 60 minutes under continuous monitoring

113
Q

Hypermagnesemia is more commonly seen in the ___

A

Hypermagnesemia is more commonly seen in the perinatal setting secondary to the treatment of preeclampsia or eclampsia

114
Q

The possibility of hypermagnesemia should be considered in patients with ___

A

hyperkalemia or hypercalcemia

115
Q

Severe symptomatic hypermagnesemia can be treated with ___

A

Severe symptomatic hypermag- nesemia can be treated with 10 mL of 10% calcium chloride IV over 2 to 3 minutes

116
Q

Signs and symptoms of hypermagnesemia and magnesium level

A
  1. 0–3.0 = Nausea
  2. 0–4.0 = Somnolence
  3. 0–8.0 = Loss of deep tendon reflexes
  4. 0–12.0 = Respiratory depression
  5. 0–15.0 = Hypotension, heart block, cardiac arrest
117
Q

___ is the most abundant mineral in the body.

A

Calcium (Ca2+)

118
Q

Total body Ca is?

A

15grams/kg of body weight or about 1kg in an average-sized adult

119
Q

Ca2+ is ___ bound in bone as phosphate and carbonate

A

99%

120
Q

The normal daily intake of Ca2+ is ___ milligrams

A

The normal daily intake of Ca2+ is 800 to 3000 milligrams

121
Q

Excretion of Ca2+ is primarily via the ___

A

stool

122
Q

Plasma [Ca2+] is between

A

Plasma [Ca2+] is between 8.5 and 10.5 milligrams/dL (4.3 to 5.3 mEq/L or 2.2 to 2.7 mmol/L)

1 mEq/L = 2 milligrams/dL = 0.5 mmol/L

123
Q

3 forms of calcium

A

50% ionized which is active
40% protein bound which is inactive
10 % bound to anions which are phosphate, carbonate and citrate

124
Q

Total serum Ca is equal to?

A

Ionized [Ca2+] plus the product of 0.8 and total protein.

125
Q

T or F: Alkalosis produces a decrease in ionized fraction with no change in the total serum [Ca2+]

A

True

126
Q

T or F: Each 0.1 rise in pH lowers ionized [Ca2+] by about 3% to 8%.

A

True

127
Q

When Ca is increase our body will release ___ and if Ca is decrease our body will release __

A
Calcitonin = resorption
PTH = demineralization
128
Q

Ca2+-sensing receptor58,59 is mainly present on plasma membranes of ___

A

parathyroids
kidney
bones
thyroid

129
Q

Physiology that increases urinary secretion of Ca

A
  • hypercalcemia
  • metabolic acidosis
  • hypervolemia
  • loop diuretics
130
Q

Cause of hypocalcemia that decrease production of 25(OH)D3?

A

liver failure

131
Q

Cause of hypocalcemia that decrease synthesis of 1,25(OH2)D3

A

renal failure and hyperphospathemia

132
Q

Hypocalcemia is defined by an ionized [Ca2+] level ___

A

<2.0 mEq/L (<4 milligrams/dL or <1.1 mmol/L).

133
Q

Example drugs that causes hypocalcemia

A
  • Phosphates (e.g., enemas, laxatives)
  • Phenytoin, phenobarbital
  • Gentamicin, tobramycin, dactinomycin, foscarnet
  • Cisplatin
  • Citrate
  • Loop diuretics
  • Glucocorticoids
  • Magnesium sulfate
  • Bisphosphonates, calcitonin, denosumab
  • Cinacalcet
134
Q

If serum Ca falls the neuronal membranes becomes ___

A

permeable to sodium which enhancing excitation and cause contraction

135
Q

The most characteristic ECG finding in hypocalcemia is a ___

A

prolonged QTc interval

136
Q

Serum level of Ca that can produce T wave mimics ischemia

A

<6.0mg/dL

137
Q

T or F: Chvostek and Trousseau signs only seen in hypocalcemia?

A

False. can also seen in hypomagnesemia and respiratory alkalosis

138
Q

1 mEq of elemental Ca2+ is equal to ___

A

20 milligrams of elemental Ca2

139
Q

Regimen of correction of hypocalcemia

A

Regimens can be 500 to 3000 milligrams of elemental Ca2+ by mouth daily, in one dose or up to three divided doses. The dose must be individualized for each patient, according to the cause and severity of hypocalcemia

140
Q

IV Ca2+ is only recommended is cases of?

A

symptomatic or severe hypocalcemia (ionized [Ca2+] <1.9 mEq/L or <0.95 mmol/L)

141
Q

T or F: IV Ca2+ gluconate is preferred over IV calcium chloride (CaCl2) in nonemergency settings due to the dangers of extravasation with CaCl2 (calcinosis cutis)

A

True

142
Q

T or F: With severe acute hypocalcemia, 10 mL of 10% CaCl2 (or 10 to 30 mL of 10% Ca2+ gluconate) may be given IV over 10 to 20 minutes and repeated every 60 minutes until symptoms resolve or followed by a continuous IV infusion of 10% CaCl2 at 0.02 to 0.08 mL/kg/h (1.4 to 5.6 mL/h in a 70-kg patient)

A

True

143
Q

T or F: IV Ca2+ should be used with caution in patients taking digitalis because hypocalcemia can potentiate digitalis toxicity.

A

False. hypercalcemia

144
Q

When to give Calcium chloride in massive transfusion?

A

During massive transfusions, if the blood is being given faster than 1 unit every 5 minutes, 10 mL of 10% CaCl2 can be given after every 4 to 6 units

145
Q

Hypercalcemia is defined as

A

A total [Ca2+] >10.5 milligrams/dL or an ionized [Ca2+] level >2.7 mEq/L

146
Q

What is the level of Calcium in mild, moderate and severe hypercalcemia?

A

mild hypercalcemia = 10.5 to 11.9 milligrams/dL
moderate = 12 to 13.9 milligrams/dL
severe = >14 milligrams/dL

147
Q

What is the most frequent renal effect of hypercalcemia?

A

loss of concentrating ability

148
Q

A mnemonic sometimes used for the signs and symp- toms of hypercalcemia

A

stones (renal calculi)
bones (osteolysis)
moans (psychiatric disorders) groans (peptic ulcer disease, pancreatitis, and constipation).

149
Q

On ECG, hypercalcemia may be associated with ___

A
  • depressed ST segments
  • widened T waves
  • shortened ST segments
  • QT intervals.
150
Q

Levels of [Ca2+] above ___ may cause cardiac arrest.

A

20 milligrams/dL

151
Q

corrected Ca2+ (milligrams/dL) equation?

A

corrected Ca2+ (milligrams/dL) = measured total Ca2+ (milli- grams/dL) + 0.8 (4.0 – serum albumin [grams/dL])

corrected Ca2+ (mmol/L) = measured total Ca2+ (mmol/L) + 0.02 (40 – serum albumin [grams/L])

152
Q

Treatment for hypercalcemia

A

if patient is symptomatic or >14mg/dL even without symptoms administer 0.9% normal saline at 500 to 1000ml/hr for 2 - 4 hours.

furosemide of 20 -40mg

corticosteroids (prednisone 1to 2 mg/kg PO or hydrocortisone 200 to 300mg tiv)

153
Q

It decreases mobilization of Ca from bone through reduction of osteoclastic activity

A

Corticosteroids

154
Q

Hypercalcemia associated malignancy can give

A

IV bisphosphonates are now considered first-line therapy

155
Q

T or F: Zoledronic acid is recommended; for a corrected [Ca2+] level of 12 milligrams/dL or higher, 4 milligrams as a single dose can be given IV over 15 minutes. Calcitonin works more rapidly than bisphos- phonates and can be given at a dose of 4 units/kg SC or IM.

A

True

156
Q

Phosphorus mainly exist as?

A

hydroxyapatite (85%)

157
Q

How many percent of phosphorus is found at ECF?

A

1%

158
Q

Serum phosphorus in newborns and adults?

A

Serum [PO43–] decreases with age from a range of 4.0 to 7.0 milligrams/dL in newborns to 2.5 to 5.0 milligrams/dL in adults.

159
Q

What is the total phosphorus store in a man?

A

700 grams (10 - 15grams/kg)

160
Q

Gut absorption of phosphorus is localized in 2 different sites which are?

A

1st part of duodenum and jejunum and ileum

161
Q

Increase absorption of phosphorus in proximal tubule is?

A
  • hypoparathyroidism
  • volume depletion
  • hypocalcemia
  • presence of growth hormone.
162
Q

Hypophosphatemia is defined as serum [PO 3–]?

A

Hypophosphatemia is defined as serum [PO 3–] <2.5 milligrams/dL

163
Q

Severe symptoms of phosphorus may occur at what level?

A

<1mg/dL

164
Q

What drug may cause pseudohypophosphatemia?

A

mannitol

165
Q

The symptoms of hypophophatemia is due to?

A

depletion of adenosine triphosphate and reduction of erythrocyte 2,3-diphosphoglycerate

166
Q

In asymptomatic or mildly symptomatic patients, hypophosphatemia may be treated orally with?

A

ith skim milk ([PO43–] 1 gram/L) or oral prepa- rations such as Neutra-Phos®, one to two tabs PO four times daily, or K-Phos®, one tab PO four times daily, which contain 150 to 250 mil- ligrams per tablet (PO43–: 1 mmol/L = 3.1 milligrams/dL)

167
Q

Hyperphosphatemia is defined as serum [PO43–]?

A

Hyperphosphatemia is defined as serum [PO43–] >4.5 milligrams/dL

168
Q

Causes of hypophophatemia

A
  • shift of phosphate into cells
  • increased renal excretion
  • decreased GI absorption
169
Q

Cause of hyperphophatemia

A
  • decrease in renal excretion of PO43–
  • addition or movement of PO43– from ICF to ECF
  • drugs
170
Q

In clinical practice, the most important cause of hyperphosphatemia is ___

A

acute or chronic renal failure

171
Q

Ir reduced survival and function of platelets and red and white blood cells and impaired macrophage function

A

hypophosphatemia

172
Q

Phosphate correction

A

<1 mEq/L = 0.6 with duration of 6–72
1–1.7 mEq/L = 0.3–0.4 with duration of 6–72
1.8–2.2 mEq/L = 0.15–0.2 with duration of 6–72