Exam 2: Fluids Flashcards
1
Q
Six most important electrolytes are __
A
sodium, potassium, chloride, bicarbonate, calcium and phosphate
2
Q
Renal filtrate: sodium is ___ and potassium is ___ and is controlled via angiotensin II and aldosterone
A
Sodium is absorbed
Potassium is excreted
3
Q
____ is released when serum potassium levels rise, serum sodium levels fall, or blood pressure drops
A
Aldosterone
4
Q
____ produces vasoconstriction and increases filtration rates in the glomerulus, activates sodium/potassium pumps, and stimulates aldosterone synthesis
A
Angiotensin II
5
Q
___ and ___ are directly controlled by hormones (parathyroid, calcitriol, and calcitonin, each of which is released in response to serum calcium levels
A
Calcium and Phosphate
6
Q
____ released from the parathyroid gland in response to reduced levels of calcium. Acts to break down bone matrices, decrease renal excretion, and increase GI absorption of calcium
A
PTH
7
Q
___ active form of vitamin D that is required for intestinal absorption. Vitamin D is converted by PTH in the GI tract
A
calcirtriol
8
Q
____ released from the thyroid gland in the presence of elevated serum calcium. Acts to increase osteoblast activity, forming more bone matrices
A
Calcitonin
9
Q
mEq refers to the electrolyte activity and concentrations are expressed in milliequivalents (mEq) in the US
____ is an exception as it exists in the body primarily as ____, which can have multiple valences in solution, with solubility and valence changing with pH (usually mmol)
A
Phosphorous exists as phosphate
10
Q
mEq euation
A
mEq = [mass (mg) x valence] / MW
11
Q
_____ (mOsm/L) the concentration of osmotically active particles per unit VOLUME of solution (i.e., the number of milliosmoles of solute per liter of solvent)
A
Osmolarity
12
Q
_____ (mOsm/kg) the concentration of dissolved particles per unit WEIGHT of solvent (i.e., the number of milliosmoles of solute per kilogram of solvent)
A
Osmolality
13
Q
____ osmoles: solutes that cannot freely cross membranes in the body
A
Effective
14
Q
Examples of effective osmoles
A
Na+, requires transport by Na+/K+-ATPase
Determine tonicity or osmolality, which affects fluid movement
15
Q
____ osmoles: solute that freely crosses membranes and reaches equilibrium
A
BUN
16
Q
_____: effective osmotic pressure equivalent across cell membranes (effective osmoles)
A
Tonicity
Note: Not necessarily the same as osmolality
Depends on osmolality of solution and permeability of membrane
17
Q
Tonicity depends on ____ of solution and ____ of membrane
A
Osmolality of solution
Permeability of membrane
18
Q
Fluid distribution: ___% is stored intracellular and __% is extracellular
A
40% intracellular
60% extracellular
19
Q
Fluid distribution: Intravascular def
A
In the cells
20
Q
Fluid distribution: Interstitial def
A
Between blood vessels and cells (can collect and needs to be drained)
21
Q
Fluid distribution: Transcellular def
A
Fluid that fills spaces that surround epithelial cells (CSF, peritoneal, pleural)
22
Q
T/F: When isotonic fluids are administered, water does not move in or out of the cells
A
TRUE – because tonicity is EQUAL
23
Q
_____ fluids create a lower concentration of water in cells than exists in blood, causing the cells to expand due to volume expansion secondary to lower tonicity in the blood.
A
Hypotonic
24
Q
____ fluids create a higher concentration of water in the cells than exists in the blood, causing the cells to contract due to volume depletion secondary to higher tonicity in the blood
A
Hypertonic
25
Isotonic solution range
270-300 mOsm/L
26
Hypotonic solution range
<270 mOsm/L
27
Hypertonic solutions range
>300mOsm/L
28
Isotonic solution examples
```
0.9% saline (NaCl) solution (~308)
Lactated ringers (~273)
```
29
Hypotonic solution examples
0. 45% NaCl -- Half-normal saline (1/2 NS)
| 0. 225% NaCl -- Quarter-normal saline (1/4 NS)
30
Hypertonic solution examples
Parenteral nutrition
10% dextrose in water (D10W)
3% NaCl - hypertonic saline
31
Significantly _____ fluids ( ____) should NOT be administered directly to patients as this can cause cellular swelling and cell death (esp. CNS)
hypotonic <154 mOsm/L
32
If lower sodium solutions are required, use ___- or ___-containing solutions
Dextrose or potassium
33
___ should NEVER be directly infused into a patient
Sterile Water
34
If a patient requires “free water”, administer ____
5% dextrose in water
35
Body water % of body weight: Infants
Thin: 80
Avg: 70
Obese: 65
36
Body water % of body weight: Adult Male
Thin: 65
Avg: 60
Obese: 55
37
Body water % of body weight: Adult Female
Thin 55
Avg 50
Obese 45
38
____ does not impact water distribution in humans (ineffective osmole)
Urea
39
_____ is the major osmotically active electrolyte in the ECF
Sodium
40
___ and ___ substances are osmotically active at high concentrations
Glucose and Mannitol
41
___, a protein, contributes to osmotic/oncotic pressure
Albumin
42
___ Forces regulate passive fluid movements across capillary membranes
Starling
43
Net filtration is the sum of all ___ and ___forces: Pc – (Pi + Πi)
hydrostatic and oncotic
44
Plasma osmoles are mostly sodium salts, with lesser contribution from ___ and ___
Glucose and Urea
45
Osmolar gap suggests presence of other osmotically-active substances such as
```
Severe hyperglycemia
Hyperlipidemia
Azotemia/uremia
Mannitol infusion
Toxic alcohols
```
46
With hyperglycemia, the addition of glucose to the ECF results in water movement from the ICF which falsely ___ measured serum sodium
Decreases -- give insulin to reduce glucose and help close the gap (less acidotic)
47
_____ is arterial blood volume that is effective in stimulating volume receptors to maintain intravascular volume and organ perfusion
Effective Arterial Blood Volume
48
If EABV decreases:
Kidneys are ____
____ Renin-Angiotensin-Aldosterone system
Sodium and water ____ to expand EABV, restore perfusion
Kidneys are hypoperfused
Stimulates Renin-Angiotensin-Aldosterone system
Sodium and water retention to expand EABV, restore perfusion
49
Situations where total body volume is increased but EABV is low:
“______” of fluids: ascites, peritonitis, hypoalbuminemic states such as nephrotic syndrome and cachexia
Cardiovascular conditions: shock, ____ (increased load/hydrostatic pressure)
“Third spacing” of fluids: ascites, peritonitis, hypoalbuminemic states such as nephrotic syndrome and cachexia
Cardiovascular conditions: shock, CHF (increased load/hydrostatic pressure)
50
Goal of water balance: maintain EABV, normal plasma osmolality/tonicity, maintain ____
organ perfusion
51
_____ in cardiac atria, aortic arch, carotid sinus, juxtaglomerular apparatus are stimulated by change in EABV, affect heart rate & vascular tone
Baroreceptors
52
Stimulate thirst, release of _____ with as little as 5 – 10% decrease in EABV
arginine vasopressin [also called antidiuretic hormone (ADH)]
53
_____ in hypothalamus/posterior pituitary are stimulated by as little as 1 – 2% increase in plasma osmolality, stimulate thirst and release of ADH
Osmoreceptors
54
_____is the primary control of water intake
Thirst mechanism
55
Thirst is stimulated/controlled by _____ and _____– stimulated at point of maximal endogenous water conservation
osmoreceptors and EABV
56
Antidiuretic Hormone or Arginine Vasopressin are hormones synthesized in the_______, released from the pituitary gland
hypothalamus
57
ADH or AVP Acts on the ____ of the kidneys -- increases permeability to water, regulates water reabsorption and excretion
Collecting ducts
58
Release of ______ stimulated by plasma osmolality (responds with as little as 1 – 2% change in osmolality, maximal activity at plasma osmolality > 295 mOsm/kg), EABV, baroreceptors, and some medications
ADH
59
Antidiuretic hormone binds to ____receptors on the basolateral membrane of renal tubular cells.
This leads to insertion of _____ into the apical tubular lumen surface of the cell.
Water passes through the cell into the _____, then is reabsorbed into the systemic circulation.
vasopressin 2 (V2)
water channels (aquaporin 2)
peritubular capillary space
60
Water balance is maintained by the ____ nervous system and RAAS
Sympathetic
61
Sympathetic nervous system and effects on water balance
Sympathetic Nervous System – stretch receptors on blood vessels sense change in ECF volume, leading to increased renal sympathetic tone which enhances renal salt reabsorption
62
Daily maintenance water/fluid requirements (in 24hrs) for neonate (<10kg)
100mL/kg
63
Daily maintenance water/fluid requirements (in 24hrs) for Pediatric (10-30kg)
1000mL + 50mL/each kg 10-20kg
64
Daily maintenance water/fluid requirements (in 24hrs) for Adolescent/adult (>20kg)
1500mL + 20mL/each kg >20kg
65
MINIMUM daily urine production/output of ~_____ mL/day required to excrete obligatory solute load, products of metabolism/catabolism, insensible losses
500-800mL/day
66
Acute volume depletion is usually depletion in___ and loss of ___ fluid, so osmolality typically is normal
ECF and isotonic
67
Depletion of TBW and dehydration typically due to more gradual/chronic problem, often can be due to ___ fluid loss so disorders of osmolality and Na+ more common
hypotonic
68
Volume depletion and dehydration causes -- abnormal losses examples
Vomiting, diarrhea, GI losses in surgical patients (e.g., ostomy, fistula, gastric suction)
Blood loss (e.g., trauma)
Diuretics/overdiuresis, osmotic diuresis (e.g., hyperglycemia)
Insensible losses (e.g., excessive sweating, fever)
Other drugs (lithium – diabetes insipidus, demeclocycline – inhibits ADH)
Sodium-wasting nephropathy, hypoaldosteronism
Iatrogenic (inappropriate maintenance and/or supplementation)
69
Most common volume depletion and dehydration causes
Diarrhea
70
Magnitude of dehydration: Mild
Mild ~ 3 – 5% weight loss or less, symptoms less likely (possibly thirst/dry mouth)
71
Magnitude of dehydration: Moderate
Moderate ~ 5 – 10% weight loss, symptoms may be present
72
Magnitude of dehydration: Severe
Severe > 10 – 15% weight loss, symptoms likely present
73
Classification of Diarrhea: Osmotic
Unabsorbed solute
Caused: Cathartics & laxatives (e.g. castor oil, milk of magnesia), lactase deficiency, magnesium antacids, sorbitol
74
Classification of Diarrhea: Secretory
Increased secretion of electrolytes
Causes: Escherichia coli infection, cholera, ileal resection, thyroid cancer
75
Classification of Diarrhea: Exudative
Defective colonic absorption, excretion of mucus and/or blood
Causes: Ulcerative colitis, Crohn’s disease, shigellosis, leukemia
76
Classification of Diarrhea: Motility disorder
Decreased contact time
Causes: Irritable bowel syndrome, prokinetic medications (e.g., metoclopramide)
77
Oral rehydration therapy (ORT) is used in _____ dehydration
mild
**Rapid and efficient absorption of fluid
78
Too much glucose can cause ____ diarrhea
osmotic
79
Sports drinks versus recommended ORS often contain significantly more___ and significantly less___
glucose
| electrolytes
80
Crystalloid solutions (sodium-containing): ___ or ____used to expand the intravascular and interstitial spaces for Moderate/Severe Dehydration
Normal saline
| Lactated Ringer’s
81
Gastrointestinal Fluid Losses: Replace losses at ~ 0.5 – 1 mL per ___ mL fluid lost
1
82
Gastrointestinal Fluid Losses: Gastric losses are assumed to have equal Na+ and Cl- concentrations if pH > __
4
With lower pH, Na+ is assume to be ~ half the Cl- loss\
83
Dehydration Monitoring Parameters
Physical signs and symptoms: thirst, sweat, saliva, skin texture (dry, edematous, elasticity), orthostatic changes (blood pressure, syncope, dizziness), pulse (intensity, tachycardia)
Weight changes, urine output
Measurements of “in’s and out’s: (fluid intake and output)
Serum and/or urine electrolyte profile, plasma and urine osmolality
Lost body fluids, volume lost, and their electrolyte composition
Changes/resolution of mental status or any other symptoms
84
___is expanded extracellular fluid volume, increased volume/accumulation of plasma ultrafiltrate in the interstitial space
Edema
85
___ is pronounced generalized edema
Anasarca
86
___ edema is severe edema or anasarca that can be felt or observed when pressing the fingers on the skin of the edematous area(s)
Pitting
Arbitrarily classified as 1+, 2+, 3+, or 4+ when the dent is said number of centimeters in depth
87
Examples of common edematous disorders
Heart failure leading to ”congestion”
Liver cirrhosis
Nephrotic syndrome
88
Treatment of Edema
Fluid and Na+ restriction
Diuretic therapy
Treat underlying cause
89
Osmotic diuretics like Mannitol, urea, glycerol act within the ___ and ____ of the kidney and create osmotic gradient and increase water excretion
Extract___ water via expansion of ECF and renin release inhibition
Results in___ renal blood flow, removes NaCl and urea from the renal medulla
Decreases water extraction from the___ thin limb, diminishes passive reabsorption of NaCl in____ thin limb
proximal tubule and loop of Henle
intracellular
increased
descending
ascending
90
Carbonic Anhydrase Inhibitors like ______ acts mainly in the proximal tubule
Acetazolamide
91
Loop diuretics act in the ____ limb of the loop of Henle and causes a profound increase in urinary excretion of ____ via inhibition of ____ co-transporter
thick ascending
Na+ and Cl- (water and K+)
the Na+-K+-2Cl-
92
Loop diuretic examples
bumetanide; furosemide; torsemide
Furosemide 20 mg IV = Furosemide 40 mg PO = Torsemide 20 mg PO = Bumetanide 1 mg PO/IV
93
Furosemide (Lasix®) has ___ hour duration of action
6
| Lasix = “Lasts Six”
94
___ diuretics all contain “sulfa” group
Loop
**Ethacrynic acid does not, can be used for patients with sulfa allergy
95
Thiazide diuretics act in the ______ of the kidney and causes inhibition of NaCl (and water) reabsorption
by inhibiting the ___ transporter
DCT
| Na+/Cl-
96
Thiazide diuretics volume loss is not isotonic --> risk of ___
hyponatremia
97
Thiazide diuretic examples
Hydrochlorothiazide (HCTZ); Chlorothiazide; Chlorthalidone; Metolazone; Indapamide
98
Potassium-Sparing Diuretics act in the ___ and ___
DCT and Collecting duct
99
Potassium-Sparing Diuretics: Amiloride and triamterene MOA
Renal Na+ channel inhibitors -- Block Na+ channels causing inhibition of Na+ reabsorption
100
Potassium-Sparing Diuretics: Spironolactone and eplerenone MOA
aldosterone antagonists -- Competitively inhibit the binding of aldosterone to the mineralocorticoid receptor, inhibiting Na+ reabsorption
101
Potassium-Sparing Diuretics decrease the excretion of __ and ___
K+ and H+
102
___ activity is weak, generally used in combination with loop or thiazide diuretics to restrict K+ losses
Potassium-Sparing diuretics
103
Vasopressin (ADH) Antagonists examples
Conivaptan and tolvaptan
104
Vasopressin (ADH) Antagonists: Conivaptan MOA
V1A and V2 receptor antagonist
105
Vasopressin (ADH) Antagonists: Tolvaptan MOA
Selective V2 receptor antagonist
106
Vasopressin (ADH) Antagonists
Antagonists of vasopressin receptors, primarily___ receptors in kidney and block reabsorption of water via aquaporin channels
Antagonism of ___ >>> , can also antagonize ___ receptors on vascular smooth muscle and cause vasodilation
V2
V2 >>>>> V1
V1
107
Vasopressin (ADH) Antagonists
___ excretion of free water, ____ urine osmolality, ____ urine output, increase net fluid loss
Increases serum osmolality and serum Na+ but does not alter ____
Gets rid of water but retains ____!
Increase, decrease, increase
Na+ excretion
electrolytes
108
Complications of Diuretic Tx -- Non-electrolyte mediated:
____: primarily peak effect with loops due to damage to tight cell junctions within cochlea
Hypertriglyceridemia and increased LDL cholesterol concentrations with thiazides possibly due to liver output
Possibly hyperglycemia (primarily loop and thiazide) due to impaired insulin sensitivity
____ with spironolactone due to progesterone-like effects
Hypersensitivity reactions – caution in patients with sulfonamide allergy (loops and thiazides)
Ototoxicity
| Gynceomastia
109
A pH of 7.4 is seen with a ratio of ___:__
A pH of 7.4 is seen with a ratio of 20:1
110
Acid/base balance
Pulmonary system adjusts pH via ___ (retainment or removal)
___ system adjusts pH via HCO3- and H+
CO2
Renal
111
Acidemia: pH <____ – higher bicarb (renal system?)
7.35
112
Alkalosis: pH >____
7.45
113
Arterial:___ blood in the circulatory system
oxygenated
114
Venous:____ blood from the peripheral vessels
deoxygenated
115
___fluids: exert high oncotic pressures e.g. provide volume expansion
Examples: albumin, blood (both natural), hydroxyethyl hetastarch (synthetic)
Colloid
116
___fluids: as discussed, offer balanced electrolytes and are generally isotonic
Examples: D5W, 0.9% NS, LR
Crystalloid
117
While reference range of Na is ____ mEq/L, symptoms tend not to develop until levels are above/below by 10 mEq/L
135 to 146
118
ADH___ to respond to LOW osmolality
| ADH____ to respond to HIGH osmolality
formed
blocked
119
If serum osmolality decreases, so is___ secretion, reducing free water clearance via kidneys (concentrating the urine)
ADH
120
SIADH (syndrome of inappropriate anti-diuretic hormone): Body produces excessive ADH, causing ___ of free water
retention
121
_____ is a disorder where the kidneys do not respond to ADH, causing excessive free water clearance
Diabetes insipidus
122
Glucocorticoids can____ ADH release and can stimulate production of aquaporin channels (allowing for water flow between cells)
suppress
123
Serum sodium level: < ___ mEq/L is hyponatremia
135
124
Causes of hyponatremia
Loss of sodium, gain of water, or both, can induce hyponatremia
**Can be both-- drink too much water (diluting) after a hot yoga class (sweating)
125
Hyponatremia sodium loss examples
Excess sweating, nausea/vomiting, medication (diuretics), or shifting from extra to intracellular spaces.
126
Hyponatremia: Water gain exampels
Increased intake
| SIADH (syndrome of inappropriate anti-diuretic hormone) which incr. water retention
127
Symptoms of hypnatremia
Fatigue, confusion, muscle weakness/spasms, and coma in serious cases
Migraines might be a first symptom (pressure in the brain), brain edema too
Most complain about fatigue, confusion, and headaches
128
Mild hyponatremia is typically is asymptomatic/non-specific -- range is ___
126 –135 mEq/L
129
Moderate hyponatremia (____ mEq/L): depending on onset, may range from mild to profound confusion but NO concern/presentation of seizures
120 – 125
130
Severe hyponatremia (___ mEq/L): depending on onset may include stupor/coma, or any presentation including seizures or severe neurologic changes e.g. musculoskeletal changes
<120
Even if its above 120 but they have neurologic changes – consider as severe
131
Total body water may be normal (___), increased (____), or decreased (___)
euvolemic
hypervolemic
hypovolemic
132
(Urine Na + Urine K) / Serum Na
Ratio of 1: urine output does not impact serum sodium
Ratio ____: urine does contribute to serum sodium LOWERING
Ratio ___: urine does contribute to serum sodium ELEVATION
>1
<1
133
Hypovolemic hyponatremia -- Low urine sodium: often due to ___
volume loss
134
Hypovolemic hyponatremia -- High urine sodium: often due to ___
diuretics, cerebral salt-wasting/Addison disease
135
Hypovolemic hyponatremia def
Excessive electrolyte-rich solute loss relative to TBW loss
Renal and extra (non) renal causes
Renal loses account for a larger proportion of Na loss
136
Euvolemic hyponatremia def
Slightly decreased/normal total body Na and normal/slightly elevated TBW (no fluid overload)
Most commonly seen due to SIADH (may be drug-induced), alcohol-induced, or primary polydipsia
137
Euvolemic hyponatremia def
Slightly decreased/normal total body Na and normal/slightly elevated TBW (no fluid overload)
Most commonly seen due to SIADH (may be drug-induced), alcohol-induced, or primary polydipsia
Hypothyroidism, corticosteroids, or other ADH-stimulating conditions may exacerbate this (volume depletion, anxiety, hypoxia, pregnancy)
Increased aquaporin in the collecting ducts lead to water retention and down regulation of RAAS
138
Euvolemic hyponatremia: Low urine sodium: often due to ___
polydipsia, beer potomania
139
Euvolemic hyponatremia: High urine sodium: often due to ___
physiologic abnormalities (cortisol, thyroid)
140
Hypervolemic hyponatremia def
Excessive volume overload leads to a dilutional effect in the serum
Typically patients present w/peripheral or pulmonary edema, ascites or anasarca
Progressive/rapid weight gain and shortness of breath
141
Hypervolemic hyponatremia may be exacerbated by underlying conditions:
Heart failure, renal failure, cirrhosis
**“wee for a wii – person drank gals of water and then didn’t pee it out (body couldn't regulate changes to concentrations) and died”
142
Hyponatremia treatment:
Correction may be as low as 1-2 mEq/L per hour
Typical rate maximum: __ mEq/L in 6 hours; ___mEq/L per 24 hours; ___ mEq/L in 48 hours
Chronic, w/risk factors for ODS: _____
6
12
18
4 – 6 mEq/L per 24 hours
NOTE: Too fast of correction can cause CNS toxicities – be careful !!
143
Hyponatremia:
___ is the destruction of the myelin sheath which covers nerve cells of the brainstem (pons)
Rapid changes in sodium levels can cause swelling/rupture -- It’s like putting too much water in a balloon too quickly – it’ll pop
osmotic demyelinating syndrome
144
Risk factors for ODS include:
Alcoholism; malnutrition; hypokalemia; cirrhosis; malignancy
| Severe hyponatremia <105 mEq/L
145
Treatment of hypovolemic hyponatremia
Given intravascular depletion, first goal is fluid resuscitation
Need to identify total body sodium deficit and calculate total amount of sodium required to “correct” deficiency
Identify estimated change in serum sodium caused by infusion of 1 liter of infusate
Calculate rate of repletion of chosen infusate and compare to previously discussed rates of repletion
Verify your selection will not cause too “rapid” correction, or cause overcorrection
Mild/moderate 0.9% NS or LR
Severe (or seizure) initial 3% NS 100mL up to 3 doses , maintenance with 0.9% NS or LR
146
Max dosing for hypertonic saline in hyponatremia treatment
Up to 100mL / dose
| 3 doses / day
147
Treatment of hypovolemic hyponatremia: Target increase in serum Na by ___ mEq/hour with a 6-hour limit of ___ mEq/L
1-2
6
148
Euvolemic or hypervolemic hyponatremia management principles
Volume status/symptoms differentiates from hypovolemic
Patients may present as hypervolemic, and then become euvolemic after diuresis
Similar treatment targets as hypovolemic with respect to rate change per hour/day of serum sodium
Mild/moderate:
- Initial treatment is volume restriction, 1000 to 1500 mL/day, to allow internal AVP regulation to “normalize”
- Need to evaluate potassium and magnesium, if deficient, replete accordingly
- If this fails, may consider pharmacologic agents
Severe:
- Use of bolus hypertonic saline (similar dosing as hypovolemic) should be prioritized over volume restriction in the first 12-24 hours
149
Hyponatremia tx: If fluid restriction fails, add on ____
loop diuretics
IV Furosemide 20-40 mg (or equivalent) every 6 to 12 hours
“Adequate” trial may be 48-72 hours, or until patient cannot tolerate use e.g. develops hypovolemia or symptoms, due to diuresis
150
Vasopressin receptor antagonist use for hyponatremia tx
inhibit receptors in pituitary gland that regulate release of adrenocorticotropin hormone and vasopressin receptors within collecting duct
Thus ADH cannot bind, water is eliminated without removal of solutes (aquaresis – just water)
*Not indicated for hypovolemic hyponatremia or urgent management, reserved for non-responders to fluid restriction/IV diuretics
151
Vasopressin Receptor Antagonists: which is preferred due to specificity?
Tolvapatan
152
For hypovolemia hyponatremia; start with an isotonic solution
- NS or LR at a rate of 0.5 to 1 mL/kg/hr
For euvolemic or hypervolemic hyponatremia: start with fluid restriction
- Typically no more than ___liters of fluid/day or ___ mL less than urine output/day
- IV diuresis for up to ___hours, consideration of VRA
1.5, 500
72
153
Hypernatremia Serum sodium level:___ mEq/L
145 or greater
154
Hypernatremia is usually due to ___ loss, but also ___ gain
water
sodium
**TBW is typically decreased secondary to reduced intake and/or GI / GU losses
155
Hypernatremia: Hypovolemic due to
excessive urine output
156
Hypernatremia: Hypervolemic due to __
mineralocorticoid or hypertonic solution administration
157
Hypernatremia: Euvolemic due to___
diabetes insipidus (insufficient ADH secretion, decreased ADH responsiveness in kidney) leads to dilute urine
158
Hypernatremia pt presentation
Intense thirst may seen, along with varying levels of lethargy, weakness, and consciousness
If hyperreflexia, myoclonus, tremor, or asterixis is present, constitutes “severe” symptoms as these may progress to seizure, coma, mortality
Urine sodium, osmolality, and overall volume are key monitoring parameters, in addition to serum electrolytes
Osmotic shifting from intra to extracellular space may lead to brain shrinkage, which can induce rupture and hemorrhage
159
Hypernatremia treatment: Calculate total free water deficit with a plan to replace ___ within 12 – 24 hours, and remaining ___24 hours after
Avoid reducing serum Na by no more than ___mEq/L in 24 hours (0.5 mEq/L per hour)
50%
10
160
Hypernatremia tx: Use of ____ sodium content solutions are preferred
If unable to take PO, use of______ should be used unless severe hypovolemia exists (isotonic)
oral, low/no
D5W IV (or other hypotonic fluids)
161
Chronic hypernatremia is not as severe as acute hypernatremia due to ___
brain adaptations (less CNS toxicity)
162
Hypernatremia: Hypovolemia: isotonic solution over ___ at a low rate
2-4 days
163
Hypernatremia: Hypervolemia: ___ eliminates excess fluid and sodium
loop diuresis
164
Hypernatremia: Nephrogenic diabetes insipidus:___ intranasal
desmopressin
*Acts as a vasopressin analog, enhancing antidiuresis
165
Chloride General reference range: __
96 – 106 mEq/L
166
Chloride is primarily absorbed via ___, secreted to aid in protein digestion, and regulated via ___
intestine (GI tract)
renal tubules
167
Chlroide has an inverse relationship with _____
Bicarbonate HCO3-
168
Dysfunction in chloride channels can also produce myriad disease states:
cystic fibrosis, bronchiectasis, and epilepsy among others
169
Hypochloremia Serum chloride level: ___
97 mEq/L or less
170
Hypochloremia: Given primary absorption points, most common cause is ____ secondary to vomiting or prolonged/excessive diuresis and/or renal failure
In response, bicarbonate reabsorption is stimulated, producing in a metabolic___
GI loss
alkalosis
171
Hypochloremia: Urine chloride concentration aids in evaluation: <___mEq/L is considered responsive
10
172
Chloride responsive metabolic___: commonly seen in diuresis or vomiting outpatient, excessive bicarbonate administration inpatient
Kidneys attempt to resorb chloride, sodium, and potassium resulting in low urine concentration (dilute)
alkalosis
173
Chloride responsive hypochloremia tx:
Discontinue or reduce causative agent (diuretic, acid suppression) and replete chloride
Typically replacement with oral agents (sodium chloride tablets) or IV rehydration with NS
600 mg oral tablet = 10 mEq of sodium/chloride
1 Liter of NS = 154 mEq of sodium/chloride
174
Hypochloremia non-reponsive hpyochloremia tx
Typically seen as excessive aldosteronism (e.g use ACEI, ARB, or AA diuretic) or mineralocorticoid state (hyperaldosteronism, tumors)
Manage underlying condition(s),
AVOID use of chloride-containing products as these will increase extracellular volume, treat with potassium supplementation (see next section)
175
Hyperchloremia serum chloride level: ____
108 mEq/L or greater
176
Hyperchloremia: Common causes are agents that induce a non-anion gap metabolic acidosis (opposite of hypochloremia)
Use/ingestion of corticosteroids, diuretics that promote chloride resorption (acetazolamide/triamterene) or strong acids (outpatient), rapid administration of sodium chloride (inpatient)
May also be seen with bowel, pancreatic, or biliary fistulas
177
Hyperchloremia: Given development of metabolic acidosis, common symptoms include ___
arrhythmia, hypotension, and immunosuppression
178
Hyperchloremia Assessed via monitoring of ___ and ___
serum and urinary electrolytes
179
Hyperchloremia: Treatment principles
Discontinue or reduce causative agent (diuretic, acid suppression) and replete bicarbonate, if deficit
Clinical controversy remains over appropriate “balanced” crystalloid for hospitalized patients
Recent literature supports use of LR over NS to prevent development of hyperchloremia, among other outcomes during hospitalization
Rates of renal replacement therapy, 30-day mortality and length of hospital stay favored LR
180
Potassium General reference range: ___
3.5 – 5 mEq/L
181
Potassium is orimarily regulated by___ and regulated via ___ with up to 90% being reabsorbed via ___
kidneys
excretion
tubules
182
Potassium most concerning adverse effects include
arrhythmias and/or seizure development
183
Hypokalemia: Serum potassium level:
3.4 mEq/L or lower
184
Hypokalemia often arises due to
intracellular shifting, urinary loss (drug-induced diuretics), or volume loss (GI loss)
185
Hypokalemia: Intracellular shifting exmaples
β2 agonists/catecholamines, insulin, hypomagnesemia
186
Hypokalemia: Urinary alteration/excretion examples
diuretics, aminoglycosides, amphotericin
187
Hypokalemia: Removal examples
sodium polystyrene sulfonate, patiromer
188
Hypokalemia can present as generalized weakness due to ___
respiratory muscle paralysis or breakdown, and arrhythmia
189
Hypokalemia treatment principles
If possible, discontinuation/reduction of offending agent
Check potassium deficiency (recheck 2-4 hours after repletion)
Mild (3.0 – 3.4): 20 mEq orally x 1
Moderate (2.5 – 2.9): 40 mEq orally x 1
Severe (2.4 or lower) asymptomatic: 80 mEq orally (40 mEq x 2)
Severe and symptomatic (ECG changes): 80 mEq orally (40 mEq x 2) plus 20 to 40 mEq IV
190
Hypokalemia Mild range and treatment
Mild (3.0 – 3.4): 20 mEq orally x 1
191
Hypokalemia Moderate range and treatment
Moderate (2.5 – 2.9): 40 mEq orally x 1
192
Hypokalemia Severe range and treatment
Severe (2.4 or lower) asymptomatic: 80 mEq orally (40 mEq x 2)
193
Hypokalemia Severe and symptomatic (ECG changes) range and treatment
Severe and symptomatic (ECG changes): 80 mEq orally (40 mEq x 2) plus 20 to 40 mEq IV
(ORAL and then IV)
194
Hypokalemia goal
Goal: somewhere 3.5 - 5
195
Hypokalemia
IV administration can either be added into fluids if indicated, or slow IV and preferably via central line due to phlebitis/vesicant
Rate typically capped at ___mEq/hour without cardiac monitoring
Generally no more than ___mEq administered via peripheral line; ___ mEq via central line
10
80
120
196
Hypokalemia If patient has impaired renal function (Crcl <30 mL/min) reduce dose by___
50%
197
Hypokalemia: Oral replacement is preferred but may induce gastritis in doses >___
40 mEq
198
Hyperkalemia Serum potassium level: ___
5 mEq/L or lower
199
Hyperkalemia Often arises due to ___
extracellular shifting, urinary impairment (drug-induced), or increased ingestion/administration
Extracellular shifting: metabolic acidosis
Urinary alteration/retention: acute kidney injury, rhabdomyolysis, adrenal insufficiency
200
Hyperkalemia: Arrhythmia, including ventricular fibrillation and asystole are of greatest concern (more common w/ potassium levels of ___mEq)
6 or greater
201
Hyperkalemia treatment principles
If possible, discontinuation/reduction of offending agent
If symptomatic/ECG changes:
- Calcium gluconate (over chloride) administration: 1-2 grams IV push
- Stabilizes cardiac cell membranes and prevents arrhythmia
- (Provides calcium that will help kick out potassium in the heart to stabilize – THEN figure out potassium)
Monitor serum potassium levels every 2-4 hours after treatment approach
202
Hyperkalemia if symptomatic/ECG changes: Treatment
```
Calcium gluconate (over chloride) administration: 1-2 grams IV push
Stabilizes cardiac cell membranes and prevents arrhythmia
```
203
Hyperkalemia tx: Calcium gluconate admin dosgin
1-2g IV push
204
Hyperkalemia calcium gluconate rationale
Stabilizes cardiac cell membranes and prevents arrhythmia
| Provides calcium that will help kick out potassium in the heart to stabilize – THEN figure out potassium
205
Hyperkalemia: Monitor serum potassium levels every ___ hours after treatment approach
2-4 h
206
Hyperkalemia acute treatmnet: intracellular SHIFTING of potassium
Regular insulin: 10 units plus dextrose 50 mL x 1 (avoid hypoglycemia)
Sodium bicarbonate: 50 mEq x 1
Albuterol: 20 mg (16 puffs) x 1, responsiveness is less predictable than above
207
Hyperkalemia acute treatment: Removal (fecally)
Sodium polystyrene sulfonate (Kayexalate): cation exchange resin
- 15 to 30 grams PO or PR x 1 or 2 doses as needed
Hemodialysis: if patient remains hyperkalemic/non-responsive to other modalities and life-threatening symptoms develop, acute dialysis can be considered
208
Hyperkalemia simplified treatment (my words)
First give calcium gluconate
Then given then either of these (insulin)
ECG changes still occur, then consider removal (Kayexalate)
Hemodialysis (last line therapy)
209
Hyperkalemia chronic treatment
Patiromer (Veltassa) and sodium zirconium cyclosilicate (Lokelma) -- have delayed onset
210
Hyperkalemia acute vs chronic treatment
Know kayexalate is for ACUTE vs Veltassa and Lokelma is for CHRONIC
211
Phosphorus General reference range: ___
2.7 – 4.5 mg/dL
212
Phosphorus is predominately found within ___ and___; main component of lipid membranes
bones
| soft tissue
213
Phosphorous facilitates ___ and ___
| Also a co-factor for ____ by providing ___
Nerve conduction and muscle function
Cellular activity by providing ATP
214
Significant proportion of phosphorus is reabsorbed via ____
proximal/distal tubules
Diuresis enhances loss
Regulated via calcitonin, parathyroid hormone
215
Hypophosphatemia Serum phosphate level: ___
2.6 mg/dL or lower
216
Hypophosphatemia -- Increased excretion can commonly be seen with:
Vitamin D deficiency, hyperparathyroidism, use of loop diuretics or corticosteroids
217
Hypophosphatemia: Loss from the system can be seen with:___
vomiting/diarrhea
218
Hypophosphatemia Redistribution can be commonly seen with:
DKA, malnutrition, alkalosis, hormonal alterations (cortisol, glucagon, insulin)
219
Hypophosphatemia: Most severe presentations can include: ___
respiratory failure, decreased cardiac contractility, paralysis, seizure, death
220
Hypophosphatemia Identified via ___
serum and urinary electrolytes, parathyroid and vitamin D concentrations
221
Hypophsophatemia: Mild to moderate - range and treatment
Mild (2 – 2.5) to moderate (1 – 1.9):
| If functioning GI tract and asymptomatic, oral supplementation
222
Hypophosphatemia severe or symptomatic: range and treatment
Severe (<1) or symptomatic:
| IV phosphate replacement is required, avoid potassium-based products if serum K >4
223
Hypophosphatemia safety
Reminder: must check ___ levels
potassium levels
Avoid / minimize potassium-based products replacement if >4
Both PO and IV forms exist
224
Hypophosphatemia: IV doses
IV doses typically infused over 4-6 hours due to risk of ____
IV doses >30 mmol are administered via central line, capped at __mmol/day
Diluted into 250 mL of NS or D5W; avoid concomitant ___ (precipitation)
phlebitis
45
calcium
225
Hyperphosphatemia: Serum phosphate level: ___
4.5 mg/dL or greater
226
Hyperphosphatemia is most commonly seen with ___
CKD
Can also be seen w/parenteral/enteral feeding, vitamin D toxicity, hypoparathyroidism
227
Hyperphosphatemia Most severe presentations can include:____
respiratory failure, decreased cardiac contractility, paralysis, seizure, death
228
Hyperphosphatemia is identified via____
serum and urinary electrolytes, parathyroid and vitamin D concentrations
229
Hyperphosphatemia may present with ___
osteopenia/osteomalacia/fracture, heart failure/arrhythmia
230
Hyperphosphatemia Treatment Principles
Treat any underlying conditions e.g. vitamin D, PTH disorders
Avoidance of high-phosphorus-containing foods: dairy, meat, nuts
231
Hyperphosphatemis: Treatment:
Most patients with CKD, or chronic elevations, require oral ___
Depending on calcium levels, may use calcium or non-calcium containing agents
Older guidelines recommended monitoring of Calcium x Phosphorus levels with a target of <55;
KDIGO currently recommends monitoring trends (no threshold but see trends instead)
Dosing is guided by phosphate levels, and not a specific ratio
phosphate binders
232
Phosphate Binder examples
```
Calcium carbonate
Lanthanum carbonate
Calcium acetate
Sevelamer HCl
Sevelamer carbonate
```
233
Phosphate binder most effective
Most effective is calcium acetate for binding capacity but we might have to watch out for levels of calcium [consider hypercalcemia for calcium carbonate and calcium acetate]
234
Non-calcium phosphate binders
Sevelamer HCl
| Sevelamer carbonate
235
Phosphate binders all work via ___ and calcium containing products should be administered with ___
reducing absorption of dietary phosphorus within GI tract
Food (so it works on phosphate binding, not acid suppression -- empty stomach will cause acid binding, less phosphate binding)
236
Calcium containing phosphate binders may exceed ___ tabs/day
16
237
Non-calcium containing phosphate binders may alter _____ and may still require ___ doses per day
fat soluble vitamin absorption
6-8
238
Calcium Serum reference range:
8.5 – 10.2 mg/dL
239
Ionized calcium range
1.1 – 1.35 mg/dL
240
Ionized calcium is ___
the "free" calcium and most active form
241
Serum calcium is regulated by ___
PTH
Vitamin
Calcitonin
242
Calcium is predominately stored within ____ and almost 50% is bound to ____
bones
Serum proteins (albumin)
243
serum calcium may need to be corrected for ____
hypoalbuminemia (<4)
244
If calcium levels in the blood INCREASES, ____ is released
Calcitonin
245
If calcium levels FALL, ___ is released
PTH
246
Hypocalcemia: Serum calcium range
8.5 mg/dL or lower
247
Hypocalcemia: ionized calcium range
<1.1 mmol/L
248
Hypocalcemia: Increased excretion of calcium can be commonly be seen with
Vitamin D deficiency, hyperparathyroidism, use of loop diuretics or corticosteroids
Drug-induced: corticosteroids, alcohol, phenytoin/phenobarbital/carbamazepine
249
Hypocalcemia: Acute presentation can include
neuromuscular excitability (twitching/spasm), QT prolongation leading to seizure/arrhythmia
250
Hypocalcemia: Acute treatmnet
Serum calcium <7.5 ; ionized calcium <0.9:
3 grams of IV calcium gluconate (or 1 gram of calcium chloride)
Calcium gluconate usually preferred over calcium chloride due to toxicities
Serum calcium 7.6– 8.4; ionized calcium 1.1:
1-2 grams of calcium gluconate plus initiation of oral maintenance calcium therapy after normalization
251
Hypocalcemia: Chronic treatment principles
Oral maintenance calcium therapy to prevent hypocalcemia, and management of hypoparathyroidism if present
Oral calcium: dosed at 1-2 grams of elemental calcium in divided doses
Hypoparathyroidism: 0.5 to 2 mcg of calcitriol/day
252
Hypocalcemia caution when selecting IV calcium replacement products: ____ is more potent but produces higher rates of____
Calcium chloride
Tissue nescrosis
**why calcium gluconate is preferred
253
Hypocalcemia: Caution of precipitation with ____products
Phosphorus
254
Hypocalcemia: Serum levels should be re-checked after___ hours for acute and over the course of days/weeks in chronic
4-6
255
Hypercalcemia Serum calcium range
10.2 mg/dL or higher
256
Hypercalcemia: ionized calcium:
>1.35 mmol/L
257
Mild to moderate hyper calcemia
10. 2 mg/dL – 12.9 mg/dl
| 2. 61 – 3
258
Severe hypercalcemia
13 mg/dL
>3
Symptomatic
259
Hypercalcemia: common causes include
hyperactive parathyroid gland; malignancy/tumor of the bone, toxic calcium/vitamin D ingestion
260
Hypercalcemia: Acute presentation can include:
mental status changes (fatigue to encephalopathy), neuromuscular changes (hyperreflexia,), cardiac (bradycardia, arrhythmias)
261
Hypercalcemia: Chronic presentation can include:
nephrolithiasis, renal failure, calcifications
262
Hypercalcemia: Acute treatment 1st step
HYDRATION THERAPY -- 1st step regardless of severity
Mild/moderate: 100 – 150 mL/hour of NS for 1 – 2 liters
Severe: 200 – 300 mL/hour of NS for 2 – 6 liters
Not a couple sips, it’s cups until you reach 2-6L
Hydration to have you pee it all out
263
Hypercalcemia acute treatment: bisphosphonate thearpy rationale
inhibits bone resorption, stimulates calcium excretion
264
Hypercalcemia: Bisphosphonate therapy examples
Zoledronic acid
| Pamidronate
265
Bisphosphonate thearpy renal adj
Zoledronic acid: AVOID w CrCl <30
Pamidronate use 60mg w CrCl <30
266
Hypercalcemia: RANK ligand inhibitor rationale
Blocks osteoclast maturation and function, reducing bone resorption
267
RANK ligand inhibitor example
Denosumab 120mg x1
Reserved for bisphosphonate-refractory
268
Hypercalcemia: Acute Treatment options
1st step: Hydration
Bisphosphonate therapy (zoledronic acid, pamidronate)
RANK ligand inhibitor (denosumab)
Calcitonin
Dialysis
269
Hypercalcemia chronic treatment principles
Management of underlying disease is required e.g. malignancy
Primary hyperparathyroidism:
Cincalcet: calicimimetic that downregulates PTH via calcium sensing receptors
30 mg/day twice daily to start, up to 90 mg four times/daily
Bisphosphonates: (a little slower acting, useful for longer half-ilfe longer therapy)
Zoledronic acid: 4 mg 7 days apart, may repeat every 1 – 3 months
Pamidronate: 60 – 90 mg every 2 weeks
Denosumab: 120 mg on days 0, 8, 15 and then monthly thereafter
270
Hypercalcemia: Hyperparathyroidism treatment options
Cincalcet (calcimimetic that downregulates PTH via calcium sensing receptors)
Bisphosphonates
Denosumab
271
Hypercalcemia: hyperparathyroidism: Cincalcet MOA
calicimimetic that downregulates PTH via calcium sensing receptors
272
Hypercalcemia safety notes:
Caution with IV bisphosphonates: Increased risk of___ of the jaw, especially with creatinine clearance <30 mL/min
Repeat dosing in chronic hypercalcemia is not clearly outlined, follows oncology literature
No role for___ calcitonin (indicated for osteoporosis)
Serum levels should be re-checked after ___hours for acute and over the course of days/weeks in chronic
osteonecrosis
intranasal
4-6
273
Magnesium Serum reference range:
1.5 – 2.5 mg/dL
274
Magnesium predominately stored within ___
bones, soft tissue and muscles
275
___ maintains sodium, potassium, and calcium homeostasis
Magnesium
276
Magnesium is reabsorbed primarily through___ and regulated by ___
small intestines
| kidneys
277
Hypomagnesemia Serum magnesium:
1.5 mg/dL or lower
278
Hypomagnesemia primary cause
Excessive gastric or renal loss
- Celiac, Crohn's IBS, diuretics
Also noted with sepsis/infections, burns, malnutrition and/or alcoholism
279
Hypomagnesemia may exacerbate concomitant ___ and __
Hypokalemia and hypocalcemia
280
Hypomagnesemia presentation is similar to ___
hypocalcemia
281
Severe <1 hypomagnesemia make produce ___ and ___
ECG changes and arrhythmia
282
Mild/moderate hypomagnesemia range
1-1.5
283
Mild/moderate treatment principles
8-32 mEq
Can be achieved with oral agents
284
Severe hypomagnesemia range
<1
285
Severe hypomagnesemia treatment principles
requires IV agents (reduce dose by 20-50% if CrCl <30)
286
1 gram of magnesium sulfate contains ___ mEq = __mg of elemental mg
8mEq = 98.6mg of elemental mg
287
Hypomagnesemia safety notes
Caution with oral magnesium:
Often included as part of laxation for its ability to exert osmotic effects in ____
Doses often capped at ___ per day
```
GI tract (GI Distress)
800 mg
```
288
Hypomagnesemia safety notes
IV magnesium: required to be diluted to 20% or less, and administered at a maximum rate of ___
Thus, for patients requiring 2-4 grams (16 – 32 mEq) dose is administered over several hours
If symptomatic, doses up to ___ grams can be administered rapidly via IV push
8 mEq/hour
| 4
289
Hypomagnesemia Safety notes
Monitoring
Cardiac monitoring is required, due to risk of arrhythmia
290
Hypermagnesemia: Serum magnesium range
2.4 mg/dL or greater
291
Hypermagnesemia is extremely rare, often seen with ___ but may be seen with DKA, adrenal insufficiency, or hyperparathyroidism
acute kidney injury
292
Hypermagnesemia presentation may include
nausea/vomiting, parasthesias, dysarthria, seizure, and/or respiratory paralysis
293
Hypermagnesemia treatment principles
If patient is on hemodialysis, repeat dialysis sessions may be indicated
IV calcium: reverse cardio or neuromuscular defects
Calcium chloride: 500 – 1000 mg IV over 10 minutes
If no central line, calcium gluconate 1 – 2 grams can be substituted
As previously discussed, caution should be used with calcium products due to vesicant status
294
___ is usually reserved for hypermagnesemia NOT hypocalcemia
Calcium chloride
