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Nephrology > Fluids and Electrolytes > Flashcards

Fluids and Electrolytes Flashcards

1
Q

WHat percentage is our intracellular fluid?

A

Intracellular fluid: 2/3 total body fluid

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2
Q

WHat makes up our extracellular fluid? 3

A
  1. Interstitial fluid
  2. Plasma
  3. Lymphatic fluid
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3
Q

Electrolytes controlled via Na-K ATPase?

6

A

ECF: Na+, Cl-, HCO3-
ICF: K+, Mg, Phosphates

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4
Q

What are the most common ions in the extracellular fluid? 2

INtracellular fluid?2

A

Na+ and Cl-

phosphate and K+

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5
Q

Water movement from ECF to ICF regulated by?

A

Starling forces—hydrostatic pressures and osmotic pressures

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6
Q
  1. What is osmolality?
  2. What is our normal plasma osmolality?
  3. WHat is the most important plasma osmolality factor and why?
A
  1. concentration of an osmotic solution when measured in osmols of solvent
  2. Plasma: 280-295 mOsm/kg
  3. Na+ most important plasma osmolality factor (Water essentially follows sodium)‏
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7
Q

WHat kind of electrolyte replacement is preferred when tretaing dehydration?

A

oral replacement

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8
Q
  1. Intravenous solutions (IV)
    2
  2. How much can we put through a peripheral line?
  3. What do can we only put through a central line?
A
  1. -Saline equivalents: crystalloids
    (Normal Saline or Lactated Ringers)
    -Water equivalents:
    (D5W)
  2. 900 mOsm/L Max through peripheral line
  3. 3% Normal Saline (1028mOsm/L) centrally (hypertonic solution)
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9
Q
  1. Whats the osmolarity of D5W?
  2. NOrmal Saline?
  3. What are the lactated ringer ions (5) and what is the osmolarity?
  4. Parenteral colliods are which ones? 4
A
  1. D5W : 252-278 mOsm/L
  2. NS: 285-300 mOsm/L —also ½ NS available
  3. Lactated Ringer’s :
    250-273 mOsm/L
    Na+, Cl-, lactate, Ca+, K+
  4. Parenteral colloids:
    - Albumin: 290-310 mOsm/L
    - Blood products:
    - Packed RBCs
    - Fresh frozen plasma
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10
Q

Name the adverse affects of the following:

Normal Saline? 3

Lactated ringers? 3

Saline: 3%, 5%, D5W1/2NS? 4

Albumin? 2

A

Normal Saline:

  1. Fluid overload
  2. Hyperchloremic metabolic acidosis
  3. Hypernatremia

Lactated Ringer’s:

  1. Fluid overload
  2. Hyponatremia
  3. Hyperkalemia

Saline: 3%, 5%, D5W1/2NS:

  1. ICF depletion
  2. Fluid overload
  3. Hypernatremia
  4. Hyperchloremia

Albumin:

  1. Allergic reactions
  2. Possible infection transmission
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11
Q

How do we access the type of fluid loss?

3

A
  1. History
  2. Symptoms
  3. Vital signs and physical exam
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12
Q

Disorders of Water Balance:

  1. Hypervolemia is what?
  2. Etiologies? 7
  3. Volume contraction–What types of fluid can be missing? 5
A
  1. Hypervolemia:
    - Expansion of the effective arterial blood volume
  2. Etiologies?
    - kidneys arent working,
    - CHF,
    - cirrohssis,
    - ADH issues,
    - aldosterone,
    - drinking too much water.
    - diabetes insipididus.
  3. Kinds:
    - hemmorhaging,
    - GI losses,
    - dehydrated,
    - diarrhea,
    - vomiting.
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13
Q

What is edema?

Examples of edema? 3

A

Too much Na+ w/ water retention in the interstitial space

  • acities in ab
  • extremities- peripheral edema
  • CHF
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14
Q
  1. For oral fluid replacement what should we avoid?
  2. What are some good options?
  3. What should we tell the pt to do?
A
  1. AVOID fluids with a high sugar concentration
  2. Water and sports drinks or in children Pediolyte
  3. Stop activities that create ongoing losses!
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15
Q
  1. Assess degree of fluid loss:
    History? 2
  2. Symtpoms? 3
  3. Clinical manifestations? 3
A
  1. History:
    - GI losses??
    - Excessive exercise—Loss from??
    - Renal losses ??

Symptoms:

  1. Easy fatigability and thirst, muscle cramps
  2. Postural dizziness (orthostatic vitals), abdominal pain, chest pain
  3. Lethargy, confusion, decreased urination

Clinical manifestations:

  1. Decreased skin turgor (may not be seen very young or obese)
  2. Tachycardia
  3. Dry mucous membranes
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16
Q
  1. Name the hyponatremia etiologies of the following:
  2. Hypovolemia? 2
  3. Normovolemia? 3
  4. Hypervolemia? 5
A
  1. Hypovolemia:
    - GI losses ??
    - Renal losses—thiazide diuretics
  2. Normovolemia:
    - Syndrome of inappropriate ADH secretion (SIADH)
    - Primary polydipsia/marathon runners
    - Low dietary solute intake

Hypervolemia:

  • CHF
  • Cirrhosis
  • hypothyroidism,
  • primary adrenal insufficiency,
  • drugs
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17
Q
  1. Whats the normal Na+ serum osmolality?
  2. What level is our “panic value”?
  3. At what level does treatment depend on symtpoms and situation?
  4. At what levels is treatment not indicated?
A
  1. lower than 135

Assess severity:

  1. = 120 meq/L panic value***
  2. 120-130—depends on symptoms and situation
  3. > 130 generally not directly treated
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18
Q
  1. What is the normal serum osmolality?

2. What is the main determinansts of plasma osmolality? 3

A
  1. 285-295 mOsm/kg

2. Na, glucose, urea

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19
Q

Hyponatremia—Clinical Manifestations:

Chronic Hyponatremia

A

Cerebral adaption

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20
Q

Cerebral adaptation as a result of Chronic Hyponatremia causes what symtpoms?
8

A
  1. Fatigue,
  2. nausea,
  3. dizziness
  4. Confusion,
  5. lethargy,
  6. muscle cramps
  7. Gait disturbances,
  8. forgetfulness
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21
Q

Hyponatremia—Clinical Manifestations:

Acute Hyponatremia

A

acute hyponatremic encephalopathy

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22
Q
  1. Pathophysiology of acute hyponatremic encephalopathy?
  2. What are usually the first symtpoms? 2
  3. Later symtpoms? 5
  4. Permanent damage? 2
A
  1. Cerebral over hydration related to degree of hyponatremia
  2. Fatigue and malaise usually first symptoms
    • HA,
    • lethargy,
    • coma,
    • seizures
    • eventually respiratory arrest
  4. Acute hyponatremic encephalopathy may cause permanent neurologic damage or death
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23
Q

Hyponatremia Classification

3

A

Hypovolemic
Normovolemic
Hypervolemic

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24
Q

What are some examples of

  1. Hyponatremic-hypovolemic? 2
  2. Hyponatremic-normovolemic? 2
  3. Hyponatremic-hypervolemic? 2
A
  1. Hypovolemic:
    - GI losses
    - renal losses (thiazides)
  2. Normovolemic:
    - SIADH;
    - low Na+ intake
  3. Hypervolemic:
    - CHF;
    - cirrhosis
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25
Q
  1. Acute hypotonic, hyponatremia: can result in symtpoms of what? 2
  2. Can cause what symptoms? 5
A
  1. Can result in symptoms of
    - neuronal cell expansion and
    - cerebral edema
    • Nausea,
    • HA,
    • seizure,
    • coma,
    • death***
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26
Q

The two ADH etiologies of hyponatremia:
Inability to suppress ADH:
Causes? 3

Appropriate suppression of ADH secretion:
Causes? 3

A
  1. True volume depletion (GI or renal losses—thiazide diuretics)
  2. Decreased tissue perfusion (reduced cardiac output or systemic vasodilation in cirrhosis for instance)
  3. Syndrome of inappropriate ADH secretion (SIADH)
  4. Primary polydipsia*
  5. Low dietary solute intake
  6. Advanced renal failure (elevated BUN/Cr)
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27
Q

Hypovolemic Hyponatremia
Causes? 2

How do we treat? 4

A
  1. Such as with GI or renal losses
  2. If serum Na+ has not dropped critically low quickly
  3. Usually just volume replacement orally or IV if more severe
  4. Normal saline/isotonic saline
  5. Depending on patient status may do slow bolus
  6. Then maintenance depending on ongoing losses**
28
Q

Hypervolemic Hyponatremia
examples? 3

Treatment? 3

A
  1. CHF
  2. Cirrhosis
  3. Renal failure
  4. Restrict fluids: 1000-1200 ml/day
  5. Restrict sodium: 1000-1200 mg/day
  6. Utilize loop diuretics to remove excess fluid
29
Q
  1. What kind of hyponatremic presentation is SIADH?
  2. Can be induced by drugs such as? 4
  3. Can be induced by diseases such as? 4
  4. Treatment? 4
A
  1. Eu/hypervolemic hypotonic hyponatremia presentation
  2. Drug-induced:
    - Carbamazepine,
    - SSRIs,
    - haloperidol,
    - thorazine
  3. Disease-induced:
    - Malignancies,
    - CNS disorders,
    - post-surgery,
    - pulmonary infections
  4. Treatment:
    - Treat underlying cause
    - Fluid restriction mainstay**
    - May use oral salt tablets
    - Loop diuretics
30
Q

Therapy for Severe Hyponatremia:

  1. What is the pt at risk for?
  2. Treatment?
  3. WHat is our goal?
  4. How often should we measure the serum Na+?
  5. What else should we measure?
A
  1. Severe hyponatremia patient at risk for brain herniation!
  2. Tx—3% hypertonic saline:
  3. Goal to increase Na+ by 4-6 meq/L in 24 hr. period
  4. Measure serum Na+ every hour
  5. Measure urine output
31
Q

Risk if we correct Severe Hyponatremia too rapidly?

What are the high risk populations for this? 3

A

Develop osmotic demyelination

  1. Women and children acute postop period
  2. Patients w/ hyperacute hyponatremia –psychosis, marathons, ecstasy
  3. Those w/ intracranial pathology
32
Q

Hypernatremia Etiologies?

7

A

Unreplaced water loss

  1. INsensible and sweat losses
  2. GI losses
  3. Central or nephrogenic diabetes insipidus
  4. Osmotic diuresis
  5. Hypothalamic lesions impairing thirst or osmoreceptor function

Water loss into cells
6. Severe exercise or seizures

Sodium overload
7. Intake or administration of hypertonic sodium solutions

33
Q

Acute Hypernatremia Manifestations:

3

A

Rapid decrease in brain volume can rupture cerebral veins leading to

  1. focal intracerebral or
  2. subarachnoid hemorrhage
  3. Demyelinating brain lesions as seen with overly rapid correction of chronic hyopnatremia
34
Q
  1. Chronic Hypernatremia Pathophysiology?

2. Why is assessment difficult for this?

A
  1. Brain adapts (within a day!) by pulling water from the CSF and increasing the uptake of solutes by the cells which also increases the amount of water in the cells
  2. Assessment is difficult because most affected adults already have neurologic disease diminishing the thirst response
35
Q
  1. Hypernatremia is considered to be a concentraion at what?
  2. Etiology? 3
  3. Treatment?
    4
A

more then 145

Etiology:

  1. **Loss of water
  2. Addition of hypertonic solution
  3. Sodium overload

Treatment:

  1. Replace free water with D5W
  2. Add normal saline solution if hypovolemic—use a second IV!!
  3. If replacing ongoing electrolyte losses (use 0.45% NS possibly w/ added K+)
  4. Calculate total body water replacement plus on going losses and needs and give fluid over extended time period-monitoring serum Na+/K+ closely
36
Q

If its fast onset Hypernatremia?

If insideous?

A
  1. Fast onset ( 24 hrs): decrease serum Na+ by no more then 10 mEq/24 hrs
37
Q

Why do we need fluid replacements with NS and not just water?

A

plasma volume is concentrated so you also have to give them Na+ and not just free water because other wise it will cause brain injury. hyponatremic too quickly

38
Q

What is the pathology behind Central DI?

How should we treat? 3

A
  1. Not enough ADH production
  2. Tx central DI:
    - Desmopressin 10 mcg/day: ADH like activity
    - Titrate to 10 mcg/bid intranasally
    - Also restrict fluid intake
39
Q

What is the pathology behind Nephrogenic DI?

How should we treat? 2

A

Kidney resistant to ADH

Tx nephrogenic DI:

  1. Thiazide diuretic to decrease ECF and Na+
  2. Sodium restriction (2000 mg/day)‏
40
Q

Hypernatremia Tx
For hypernatremia from unreplaced water loss: Steps 3

What could overly rapid correction lead to?

A
  1. Need to estimate water deficit
  2. Need to replace ongoing losses***:
  3. Determine safe rate plasma Na+ can be normalized:

Overly rapid correction can lead to cerebral edema

41
Q

Hypernatremia Tx:
We Need to replace ongoing losses. What would these be from?
4

Determine safe rate plasma Na+ can be normalized:
Usually?

A 
Any ongoing 
1. GI losses and 
2. urine losses
Obligatory losses: 
3. sweat & 
4. stool
  1. Usually less than 0.5 mEq/L/hr or about 10 mEq/day
  2. Usually use 0.45% NS with K+
  3. Monitor lytes closely*** (every 4 hours usually)
42
Q
  1. How much of calcium is bound to albumin?
  2. Each 1g/dL drop albumin below 4.5g/dL, decreases serum calcium by ___mg/dL
  3. Whats the calculation for corrected calcium?
  4. What space is calcium found mostly?
  5. Whats the normal serum range?
A
  1. 46% bound primarily to albumin
  2. 0.8
  3. [(4.5 - serum albumin) x 0.8] + measured Ca = Corrected Ca
  4. Extracellular electrolyte**
    Unbound/free fraction active form
  5. Normal serum range (free): 8.5-10.5 mg/dL
43
Q
  1. At what level is a pt hypercalcemic? 2
  2. What are the primary causes of hypercalcemia?
  3. What drugs cause hypercacemia? 3
  4. Symtpoms of hypercalcemia? 4
  5. Untreated manifestations?3
A
  1. Hypercalcemia: >10.5
  2. Cancer and primary hyperparathyroidism*** primary causes (benign adenoma, hypertrophy, cancer of the parathyroid gland)
  3. Drugs:
    - thiazide diuretics,
    - calcium supplements,
    - lithium
    • EKG changes
    • N/V, anorexia, constipation
    • Polyuria/-dypsia
    • Neuro/psych symptoms
    • metastatic calcification
    • nephrolithiasis,
    • renal failure
44
Q

Outcome of hypercalcemic crisis? 4

Treatment? 4

A
  1. Oliguric renal failure,
  2. coma,
  3. v-arrhythmias,
  4. death
  5. Saline and loop diuretics: 2-3 mg/dL drop in 24-48 hours
  6. Bisphosphonates:
    Zoledronic acid: 4mg IV over 15 min
  7. Osteoclast inhibitors: calcitonin
  8. Dialysis
45
Q

Why do we give biphosphates for hypercalcemia crisis?

A

For malignant etiologies

46
Q
  1. At what level is a pt hypocalcemic?
  2. Etiologies? 4
  3. What do we have to correct the levels for?
  4. What might be associated with refractory severe hypocalcemia?
  5. Symtpoms? 4
    (which two are the hallmark signs?)
A
  1. Hypocalcemia: less than 8.5
  2. Etiologies: Hypoparathyroidism, Vitamin D deficiency, loop diuretics, phosphates
  3. Correct level for hypoalbuminemia!
  4. Hypomagnesemia associated with refractory severe hypocalcemia***
  5. Symptoms:
    tetany, paresthesias around mouth—hallmark symptoms
    ECG changes: QT prolongation
    Decreased myocardial contractility
47
Q

TX: Acute Symptomatic HypoCa++

5 steps

A

IV administration of calcium salts:
1. 100-300 mg elemental calcium IV over 5-10 minutes (chloride for peripheral administration
Less irritation
5. Magnesium if hypomagnesaemia present

48
Q

Chronic Hypocalcemia
Tx?

If they arent responding what should we add?

A

1-3 grams oral elemental calcium/day

If not responding add Vitamin D: 1000 IU/day

49
Q

What are the side effects from oral calcium? 2

What are the different kinds and what are their benefits?

A
  1. Constipation
  2. GI upset
  3. Carbonate less $$ than Gluconate/Citrate
  4. Citrate better absorption
50
Q
  1. Phosphorus Homeostasis
    normal serum level?
  2. What could hyperphosphatemia be caused by? 3
  3. What are the symptoms of hyperphosphatemia used for?
  4. What imbalance results with chronic Hyperphosphatemia?
  5. Treatment?
A
  1. Normal serum level: 2.0-4.5 mg/dL
    • Decreased excretion due to low GFR
    • Chemotherapy and
    • rhabdomyalysis
  3. Symptoms due to Ca-Phosphate interaction
  4. Hypocalcemia
  5. Treatment: GI binders…..IV calcium salts
51
Q

Hyperphosphatemia Treatment:
Emergency treatment seldom necessary but if you need to what should you do? 1

Usually occurs in renal failure. How would we treat this? 4

A
  1. Can be done w/ dialysis
  2. Diet restriction
  3. Phosphate-binding gel: Selvelamer (decreases mortality)
  4. Calcium supplements
  5. Avoid alluminum-containing antacids—can cause bone disease
52
Q
  1. Hypophosphatemia is at what level?
  2. Symptoms are rare until what levels?
  3. Long term symptoms? 2
  4. Severe or symptomatic hypophosphatemia treatment? 3
  5. Mild to moderate treatment?
A
  1. less than 2.0
  2. Symptoms rare until level less than 1.0 mg/dL
  3. Long term:
    - proximal muscle weakness &
    - osteomalacia
  4. Severe or symptomatic hypophosphatemia:
    - IV phosphorus: Give slowly
    - Sodium PO4 (4mEq/mL Na)‏
    - Potassium PO4 (4.4mEq/mL K)‏
  5. Oral phosphate replacement for mild to moderate:
    - Neutra-Phos (7meq/ml Na and K)‏
    - Neutra-Phos K (14.25 mEq/mL K)‏
    * 250 mg phosphate
53
Q

What is the major side effect of oral phosphate replacement?

A

*GI upset

54
Q

Causes of hypomagnesia?

3

A
  1. Reduced intake- dieting, unbalanced diet, depleted foods
  2. Impaired absorption- GI diseases
  3. Increased excretion- Alcoholism, laxative abuse, treatment with diuretics or dig
55
Q

Hypomagnesemia:

  1. Occurs in what percent of hospitalized pts?
  2. Clinical manifestations? 3
  3. Drugs that cause it? 5
A
  1. Occurs in nearly 12% of hospitalized patients
  2. Clinical manifestations:
    - Neuromuscular: muscle cramps, tetany, seizures, coma
    - Abnormalities of calcium metabolism–hypocalcemia
    - Cardiovascular: widened QRS, a fib, ventricular arrhythmias
  3. Drugs that cause it:
    - diuretics,
    - aminoglycosides,
    - cisplatin,
    - cyclosporine and
    - alcohol
56
Q
  1. Hypomagnesemia occurs at what level?
  2. When should we treat?
  3. Severe/symptomatic treatment?
  4. Mild to moderate treatment?
A
  1. less than 1.4 mEq/L
  2. Treat if less than 1.0 mEq/mL or symptomatic
  3. IV MgSO4 if symptomatic/severe:
    - Bolus: can cause flushing, sweating
  4. Oral replacement if mild-moderate:
    - Sustained release preparations preferred
    - Otherwise usual dosing 800-1600mg a day in divided dosing
57
Q

IV MgSO4: A large amount is secreted in the urine so what is needed after the bolus to raise the magnesium level?

What does oral mag often cause?

A

a continuous infusion is needed after the bolus to raise the magnesium level

Often causes diarrhea

58
Q

Hypermag symptoms:

  1. Mg 3-5 meq/L? 2
  2. Mg 4-7? 3
  3. Mg 5-10? 3
  4. Mg 10-15? 3
A
  1. Nausea, vomiting
  2. sedation, weakness, decreased reflexes
  3. hypotension, bradycardia, quadriplegia
  4. no reflexes, resp. paralysis, cardiac arrest
59
Q
  1. Hypermagnesemia occurs at what levels?
  2. Treatment? (why do we do this?)
  3. What do we need to add if they have renal failure?
  4. What do we add if they have normal kidney function?
  5. How would a pregnant woman become hypermag?
A
  1. > 2mEq/L
  2. IV calcium (100-200 mg elemental Ca++) to antagonize neuromuscular and cardiovascular effects of magnesium

Treatment:

  1. Renal failure: hemodialysis
  2. Normal renal function: forced diuresis w/ fluid and loop diuretics
  3. preg woman can get hypermag because of their treatment for preeclampsia (which is mag sulfate)
60
Q
  1. Hypokalemia occurs at what level?
  2. Drugs that could cause this? 4
  3. Medical causes of hypokalemia? 3
  4. Cardiac symtpoms? 3
A
  1. less than 3.5mEq/L
    • Beta2-agonists
    • Loop diuretics, ACE inhibitors, thiazides
    • High-dose penicillin’s, amphotericin B
    • Insulin
    • metabolic acidosis,
    • vomiting,
    • diarrhea
    • EKG changes: “u” wave
    • Cardiac arrhythmias
    • Danger in persons on digoxin!!!
61
Q

Hypokalemia Treatment
Loop or thiazide induced deficit: 3

Severe or symptomatic:
3

A
  1. 40-100 mEq potassium supplementation (BID or TID)
  2. Oral therapy is preferred: KCL (given in mEq NOT mg!)
  3. With food to avoid GI upset
  4. IV potassium in saline bag
    dextrose stimulates insulin to further shift K (dont give dextrose)
  5. 10-20 mEq KCl in 100 mL 0.9% saline over one hour
  6. > 10 meq/hour monitor ECG
62
Q

Why do we have to limit 40-60 mEq/L to the peripheral line?

A

phlebitis

63
Q
  1. Hyperkalemia occurs at what level?
  2. Etiologies? 4
  3. Clincial manifestations? 2
  4. Cardiac effects? 2
A
  1. > 5.5mEq/L

2.

  • Increased K+ intake
  • Decreased excretion
  • Aldosterone resistance
  • Shift to ECF
    • Ascending muscle weakness
    • Usually does NOT affect respiratory muscles
    • EKG changes: initially peaked T waves and shortened QT interval
    • Progresses to prolonged QRS and QT interval and P waves may disappear, can then lead to dysrhythmias
64
Q

Hyperkalemia
treatment?
3

A
  1. Abnormal ECG: calcium gluconate IV
  2. Give D5W to create a hyperglycemic state then insulin
  3. Consider bicarbonate if acidotic:
    - -H+ exchanged for K+ in ICF to compensate for acidosis: bicarbonate reverses this
65
Q

Hyperkalemia: If the pt is in renal failure?

2

A
  1. Dialysis

2. Potassium binders: Sodium polystyrene sulfonate (Kayexelate)‏: exchanges Na for K in gut: constipation

66
Q

When can we give loop diuretics in hyperkalemia?

A

if they arent volume depleated then you can give it.

Nephrology (15 decks)

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