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Clin med A 2 > Fluid, Electrolyte, and Acid-Base Disorders > Flashcards

Fluid, Electrolyte, and Acid-Base Disorders Flashcards

1
Q

what are common complications of AKI

A
  • abnormal volume status
  • hyperphosphatemia
  • hyperkalemia
  • hyponatremia
  • uremia
  • severe metabolic acidosis (pH<7.2)
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2
Q

what adjustments are made in the body when there is a drop in osmotic pressure or blood volume

A
  • increased SNS output
  • increased RAAS activity
  • increased ADH levels
  • Increased thirst
  • decreased atrial natriuretic peptide (ANP)
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3
Q

what are the adjustments made by the body with increase in osmotic pressure or blood volume

A
  • decreased SNS output
  • decreased RAAS activity
  • decreased ADH levels
  • decreased thirst
  • increased atrial natriuretic peptide (ANP)
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4
Q

what is the body’s net goal of controlling osmotic pressure and blood volume

A

adjust water intake, water and sodium retention by the kidney, and vasoconstriction

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5
Q

what is isotonic fluid volume deficit

A

AKA hypovolemia - volume depletion.

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6
Q

what is the etiology of isotonic fluid volume deficit

A

loss of body fluids, often accompanied by decreased fluid intake.
* decreased PO intake
* Excessive fluid loss - GI, renal, skin
* Third Spacing - edema, ascites, effusions

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7
Q

what are signs and symptoms of isotonic fluid volume deficit

A
  • General - increased thirst, fatigue, altered mental status
  • CV - low BP, high HR, weak/thready pulse, flat neck veins, cap refill >3 sec
  • Low ECF - Wt loss, dry mucous membranes, low skin turgor, sunken eyes or fontales
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8
Q

what labs are seen in isotonic fluid volume deficit

A
  • High Uosm and Urine SG
  • increased Hct (if blood loss or anemia may be low)
  • abnormal renal labs
  • if d/t renal fluid wasting may see very dilute urine
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9
Q

How do you manage volume depletion (isotonic fluid loss)

A
  • fluid loss/hypovolemia/oliguria - PO fluids or IV fluids (LR or .9% NS)
  • blood loss - PRBCs
  • Poor Cardiac output - inotropes
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10
Q

what is the cause of hyperchloremic metabolic acidosis. How do you treat this?

A

excess NS given for treatment of volume depletion

treat with bicarb solution (dextrose in H2O with HCO3)

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11
Q

how do you monitor the target physiologic endpoint of treatment for volume depletion

A

patient status
mean arterial pressure
urine output

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12
Q

what is isotonic fluid volume excess

A

hypervolemia

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13
Q

what is the etiology of isotonic fluid volume excess

A

Excess intake of water/sodium - overadmin of IV fluids, hypertonic IV fluids, dietary changes

Decreased elimination - HF, Renal failure, corticosteroids

( this is the one where jensen said people come in after holidays cuz they ate too much sodium and now theyre retaining all the water!!)

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14
Q

what are signs and symptoms of isotonic fluid volume excess

A
  • general - decreased thirst, feeling bloated/swollen
  • CV - full, bounding pulse; distended neck veins, may see increased BP
  • High ECF - ascites, pulmonary edema, extremity edema
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15
Q

what are the labs present with isotonic fluid volume excess

A
  • low Uosm and urine SG
  • decreased Hct
  • abnormal renal labs
  • if d/t inability to get rid of urine may see concentrated rine or low UO
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16
Q

what is the management for isotonic fluid volume excess

A
  • assess underlying cause
  • IV diuretics (loops preferred - furosemide)
  • dialysis ( if no response to diuretics or persistent volume overload)
  • restrict fluid and sodium intake
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17
Q

What is the cause of hyperphosphatemia

A

impaired renal excretion of phosphate

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18
Q

what are the signs and symptoms of hyperphosphatemia

A

fatigue
SOB
N/V
signs of hypocalcemia

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19
Q

what are signs of hypocalcemia

A

hyperreflexia
carpopedal spasm
+trousseau’s or Chvostek signs

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20
Q

what is the treatment for hyperphosphatemia

A

limit phosphate intake by:

  • phosphate binders w meals
  • avoid processed foods containing inorganic phosphate
  • restoration of renal function
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21
Q

what is the etiology of hypokalemia

A

Less common in AKI/CKD than hyperkalemia, but possible!

  • renal - intrinsic potassium wasting, or d/t diuretic SE
  • GI - poor intake (nutrition/NPO)
  • other - insulin, beta-agonists, loops, alkalosis
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22
Q

What are the signs and symptoms of hypokalemia

A

often effects smooth, skeletal and cardiac muscle!

MSK - weak, fatigue, cramps, tenderness
GI - abdominal cramps, constipation
Cardiac - hypotension, palps, dysrhythmias
ECG - flattened T waves -> prolonged QT -> U wave -> ST depression

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23
Q

what is the general management of hypokalemia?

A

correction of underlying cause

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24
Q

what is the management of acute severe hypokalemia

A

potassium replacement:
* oral or IV K chloride or K gluconate
* IV - 10-20mEq/hr max
* oral - 10-40 QD - QID

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25
Q

how do you treat chronic recurrent hypokalemia

A
  • increase potassium rich foods in diet
  • K replacement (K chloride or K gluconate)
  • adjust meds (isulin, beta agonists, loops)
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26
Q

what are the possible contributing factors of hypokalemia

A

hypomagnesemia
metabolic alkalosis
medications

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27
Q

what should be monitored with hypokalemia

A

renal function
electrolytes
general symptoms

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28
Q

What are the possible etiologies of hyperkalemia

A

VERY common complication of AKI and CKD

causes include:
* Renal - inadequate excretion, metabolic acidosis
* Adrenal insufficiency
* Cellular breakdown - traumatic stick, hemolysis, crush injury
* Release from ICF - cell damage, excessive/severe muscle contraction
* Other causes - ACEI/ARB, beta-blockers, excess intake (usually IV)

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29
Q

What are the signs and symptoms of hyperkalemia

A

Often affects muscles

  • MSK - weakness, cramps (including abdominal)
  • GI - abdominal cramps, diarrhea, vomiting
  • Cardiac - hypotension, palpitations, dysrhythmias, cardiac arrest
  • ECG - peaked T waves → loss of P waves → widened QRS → sine wave
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30
Q

when should hyperkalemia be treated

A

immediate treatment if very high levels, ECG changes or neuromuscular symptoms

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31
Q

what are the three steps to managing hyperkalemia

A
  1. immediate clocking of cardiac effects
  2. rapid reduction in plasma K+
  3. removal of potassium
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32
Q

How do you antagonize cardiac effects in hyperkalemia

A
  • IV calcium - reduced cardiac excitability
  • 10mL of 10% calcium gluconate IV over 2-3 minutes w monitoring
  • repeat if ECG changes do not improve or recur in 1-3 minutes
  • may not be needed if there are no cardiac s/s or arrhythmias present

Note: Caution - potentiates cardiac toxicity of digoxin; consider
slower infusion of calcium if it must be used
(im not sure what this means)

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33
Q

how do you rapidly reduce plasma K+ in hyperkalemia

A
  • IV insulin - 10 units regular insulin followed by 40 mL of 50% dextrose
  • albuterol and insulin + glucose (caution in CHF pts, ESRD patients do not respond to this)

cannot use albuterol by itself, must combine with insulin

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34
Q

how do you remove potassium in hyperkalemic patients

A

GI cation exchangers
Loop diuretics
thiazide diuretics
Hemodialysis

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35
Q

what are the GI cation exchangers

A
  • sodium polystyrene sulfonate (aka SPS or Kayexelate)
  • zirconium cyclosilicate (lokelma)
  • patiromer (veltassa)
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36
Q

what is the MOA of GI cation exchangers

A

exchanges Na+ for K+ in GI tract which increases fecal excretion of K+

37
Q

what is the onset of action for the GI cation exchangers

A
  • SPS - 2-24 hours
  • Zirconium cyclosilicate - 1 hour
  • Patiromer - 7 hours
38
Q

what are the SE of GI cation exchangers

A
  • GI - intestinal necrosis, GI upset, constipation, fecal impaction
  • Endocrine - ↑ Na; ↓ Mg, K, Ca
39
Q

What are major DD interactions of GI cation exchangers

A
  • sorbitol (increased risk intestinal necrosis)
  • digitalis
  • antacids or laxatives w Al or Mg
  • Lithium
  • LT4
  • metformin
40
Q

what are contraindications/cautions for GI cation Exchangers

A

avoid with:
* hx of bowel obstruction
* post op pts
* slow intestinal transit
* hx ischemic bowel disease
* hx renal transplant

41
Q

when are loop or thiazide diuretics used for removal of potassium

A

in volume replete or hypervolemic pts with enough renal function for diuretic response

be sure to monitor for other electrolyte imbalances!

42
Q

What is the most effective/reliable method of potassium removal

A

hemodialysis!

may be used in combo with other meds

43
Q

What are the types of hyponatremia

A

isotonic hyponatremia
hypertonic hyponatremia

44
Q

what is isotonic hyponatreamia

A

low Na with normal serum osmolality.

(caused by extra molecules in the blood like proteins and lipids)

PAY ATTENTION CUZ I DONT GET THIS

45
Q

what is hypertonic hyponatremia

A

low Na with high serum osmolality

other molecules are present such as glucose, radiocontrast, mannitol

PAY ATTENTION CUZ WHAT

46
Q

What is hypovolemic hyponatremia

A

inappropriate salt loss in the presence of decreased blood volume (from google)

47
Q

what are the etiologies of hypovolemic hyponatremia

A
  • GI loss (N/V)
  • burns
  • dehydration
  • ACEi
  • diuretics
  • mineralocorticoid deficiency
  • intrinsic renal salt wasting
48
Q

what is hypervolemic hyponatremia

A

sodium is retained but water retention is disproportionately larger than Na retention

(too much water, normal amount of sodium = hypervolemic hyponatremia)

49
Q

what are the etiologies of hypervolemic hyponatremia

A
  • intrinsic renal fluid retention
  • nephrotic syndrome
  • heart failure
  • liver disease
50
Q

what is euvolemic hyponatremia

A

having normal H2O retention and blood volume but having too little Na

(google)

51
Q

what are the etiologies of euvolemic hyponatremia

A
  • SIADH
  • Hypothyroidism
  • psychogenic polydipsia
  • beer potomania
52
Q

what is evaluated to assess ADH activity

A

UNa+ and Uosm

53
Q

what are the signs and symptoms of hyponatremia

A

primarily neurologic s/s d/t cerebral edema:

  • Early - N/V, HA, confusion, lethargy
  • Late - seizure, brainstem herniation, coma, death
  • Others - May see muscle cramps or weakness, third spacing of fluid
  • If chronic hyponatremia (>48 h), less likely to have severe s/s
54
Q

How do you manage non severe hypovolemic hyponatremia

A

IV rehydration with isotonic 0.9% NS

55
Q

how do you manage severe hyponatremia

A
  • achieve 4-6mEq/L increase in sodium ASAP
  • repeat 1-2x at 10 min intervals if serum Na or s/s do not improve
  • monitor tx by measuring Na every 2 hours
  • may co admin a loop to avoid volume overload and/or desmopressin to avoid osmotic demyelination syndrome
56
Q

how do you treat nonemergent hyponatremia

A

hypertonic saline
salt tablets
fluid restriction
vasopressin receptor antagonists

57
Q

what are the vasopressin receptor antagonists

A

conivaptan (vaprisol) IV
tolvaptan (samsca) Oral

58
Q

what is CI for vasopressin receptor antagonists

A

Fluid restriction CI while on a vasopressin receptor antagonist

59
Q

what is the major concerning SE of vasopressin receptor antagonists

A

Hepatotoxicity. max recommended use of 30 days d/t this.

60
Q

what should you monitor when administering a vasopressin receptor antagonist

A

LFTs
Renal function
electrolytes

61
Q

what is the etiology of hypernatremia

A

loss of body water of inability to retain water appropriately, and/or excessive sodium intake

62
Q

what is the etiology of hypernatremia with normal urine osmolality

A

excessive water loss through renal or non renal sources

63
Q

what is the etiology of hypernatremia with low urine osmolality

A

diabetes insipidus (neurogenic or nephrogenic)

64
Q

what are the signs and symptoms of hypernatremia

A

Neuro - Increased thirst, HA, agitation, delirium, seizures, coma, death

CV - low BP, high HR, weak/thready pulse, dry mucous membranes, low skin turgor

65
Q

what are the labs associated with hypernatremia

A
  • increased Hct (decreased if accompanied with blood loss)
  • abnormal Uosm and Urine SG
  • abnormal renal labs
  • if d/t renal fluid wasting - dilute urine
66
Q

what is the treatment for hypernatremia that has been present for less than 48 hours

A

correction with fluid replacement within 24 hours to avoid CNS damage

67
Q

what is the treatment for hypernatremia that has been present for more than 48 hours

A

correction with fluid replacement gradually at 6-12 mEq/L per 24 hours

68
Q

what are the three etiologic categories of metabolic alkalosis

A

increased acid loss
excess bicarbonate/alkali
abnormal renal excretion/absorption

69
Q

what are etiologies of increased acid loss

A
  • GI - vomiting, gastric suction
  • Hypokalemia
70
Q

what are etiologies of excess bicarbonate/alkali

A
  • Bicarbonate administration
  • Hypochloremia
  • Administration of alkaline solutions
71
Q

what are the etiologies of abnormal renal excretion leading to metabolic alkalosis

A
  • Diuretics→volume depletion
  • The combination of hypovolemia, hypochloremia, hypokalemia, and reduced GFR create the perfect setting for metabolic alkalosis
72
Q

what are signs and symptoms of metabolic alkalosis

A
  • neuro - Increased neuronal excitability leading to dizziness, panic, lightheadedness, seizures.
  • CV - dysrhythmias
  • GI - may have hx of abdominal pain, N/V, GI suctioning
73
Q

how do you treat metabolic alkalosis

A
  • usually directed at underlying cause
  • antiemetics and dc GI suctioning
  • decrease bicarb admin
  • fluid/electrolyte supplements
  • tx of adrenal dz if present
74
Q

what are the major etiologic categories of metabolic acidosis

A

increased acid generation
loss of bicarbonate
deceased renal acid excretion

75
Q

what are the etiologies of inceased acid generation

A

lactic acidosis
ketoacidosis
ingestion (methanol, ethylene glycol, aspirin poisoning, chronic APAP, tolulene)

76
Q

What are the etiologies of loss of bicarbonate

A

severe diarrhea
urine exposure to GI mucosa
Proximal renal tubular acidosis

77
Q

what are the etiologies of decreased renal acid excretion

A

Decreased GFR
distal renal tubular acidosis

78
Q

what are the signs and symptoms of metabolic acidosis

A

Neuro - decreased neuronal excitability - confusion, weakness, drowsiness
CV - vasodilation (flushing), dysrhythmias
GI - Abdominal pain, NVD, constipation
pulm - increased depth and rate of respiration
bone - decreased density with chronic

79
Q

what during metabolic acidosis can lead to functional hypercalcemia? what are the s/s of this?

A

decreased protein binding to calcium d/t decreased neuronal excitability.

s/s include muscle weakness, increased thirst, nephrolithiasis (if chronic)

80
Q

what is considered severe metabolic acidosis

A

pH<7.2

81
Q

how do you treat severe metabolic acidosis

A

remember severe is pH<7.2

treat underlying problem
+
treat w IV HCO3 to get pH to >7.2

82
Q

how do you treat non-severe metabolic acidosis

A

correct underlying problem which will allow body to return to normal pH

83
Q

how do you treat chronic metabolic acidosis

A

HCO3 replacement.
decreased animal content (esp proteins) in diet

84
Q

what is chronic metabolic acidosis usually due to

A

GI loss
CKD
Renal tubular acidosis

85
Q

how does AKI create metabolic acidosis

A

a lower GFR hinders the kidneys ability to excrete HCO3 and reabsorb H+

86
Q

how do you treat metabolic acidosis in the context of AKI

A

dialysis
HCO3

87
Q

when would you use bicarbonate as treatment for metabolic acidosis in AKI

A

if acidosis is severe (pH<7.2) AND:
* non-anion gap acidosis d/t diarrhea
* waiting for dialysis
* readily reversible AKI cause
* rhabdomyolysis w/o other dialysis indications or hypervolemia

88
Q

when is dialysis indicated for treating metabolic acidosis in AKI

A
  • severe oliguric or anuric AKI with volume overload and severe metabolic acidosis
  • AKI and organic acidosis and pH <7.1 especially if oliguric/anuric
89
Q

what are other indications for dialysis use in AKI

A
  • azotemia
  • uremia (the worse the symptoms, the greater the indication for dialysis)
  • severe or life threatening electrolyte disturbances
  • Volume overload
  • Metabolic Acidosis (<7.1)
  • uremia
  • pateints with prolonged AKI even without meeting the above criteria

Clin med A 2 (30 decks)

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