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Acid-base & electrolytes > Electrolytes > Flashcards

Electrolytes Flashcards

1
Q

What is the definition of osmolality? Osmolarity?

A

Osmolality = number of particles of solute per kg of solvent

Osmolarity = number of particles of solute per liter of solvent

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2
Q

What is the normal osmolality for dogs and cats

A

Dogs: 290-310 mOsm/kg

Cats: 290-330 mOsm/kg

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3
Q

How can serum osmolality be measured

A

Using a freezing point depression osmometer

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4
Q

What is the osmolal gap and what can cause an increased osmolal gap

A

Osmolal gap = difference between measured and calculate serum osmolality

Should be close to 0 -> any increase indicates presence of other osmole(s) in circulation:
- lactate
- ethanol
- ethylene glycol
- phosphates
- sulfates
- acetylsalicylic acid
- mannitol
- methanol
- radiographic contrast
- sorbitol (/!\ in patients having received activated charcoal with sorbitol - can falsely elevate osmolal gap)
- propylene glycol

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5
Q

What is the difference between osmolarity and tonicity

A

Osmolarity includes all the osmoles in solution whereas tonicity only refers to effective osmoses

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6
Q

What is the repartition of total body water between the different compartments

A

Water = 60% total body weight

1/3 intracellular, 2/3 extracellular (75% interstitial, 25% intravascular)

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7
Q

What are the receptors in charge of osmolality regulation? How sensitive are they?

A

Osmoreceptors in the hypothalamus.
Detect changes of 2-3 mOsm/L

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8
Q

What are the 2 triggers for ADH release and they respective receptors

A
  • Decreased effective circulating volume -> baroreceptors (aortic arch and carotid bodies)
  • always prioritized
  • Increased plasma osmolality -> osmoreceptors (hypothalamus)

Secreted by the pituitary gland

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9
Q

What are the 2 mechanisms of regulation of plasma osmolality

A
  • Antidiuretic hormone
  • Thirst
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10
Q

What does total body sodium determine

A

Hydration status (independent from natremia)

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11
Q

What are the mechanisms of cerebral adaptation to hypernatremia / hyponatremia

A
  1. Hypernatremia
    - Within minutes to hours: loss of neuronal water -> decreased interstitial hydrostatic pressure -> fluid drawn from CSF to interstitium, which brings more sodium -> water reabsorption
  • Within 24 hours (2-7 days for full compensation): neuronal accumulation of idiogenic osmoses (inositol, glutamate) -> draw water into cells
  1. Hyponatremia: the opposite (increased interstitial pressure -> fluid loss into CSF + neurone expel sodium and organic osmolytes)
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12
Q

Free water deficit formula

A

Free water deficit (L) = [(current Na / normal Na)-1] * 0.6 * body weight (kg)

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13
Q

What is the rate of Na correction in a chronically hypernatremic patient without clinical signs? With clinical signs? In acute hypernatremia?

A
  • Without signs: 0.5-1 mEq/L/h (as per Silverstein ; in other sources: 8-12 mEq/L per 24h)
  • With signs: 2 mEq/L/h until signs resolved
  • Acute: correct in <12h

(as per Silverstein - achieved by giving D5W following the total body water deficit)

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14
Q

In a hyponatremic patient, how is total body sodium likely to be:
- in a dog with CHF
- in a dog with GI losses

A
  • CHF -> increased total body Na (from RAAS activation) but ADH secretion due to decreased effective circulating volume
  • GI losses -> loss of Na and water causing hypovolemia and ADH secretion (decreased total body Na)
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15
Q

List 5 causes of hyponatremia and 5 causes of hypernatremia

A
  1. Hyponatremia
    - Decreased effective circulating volume (CHF, GI / urinary losses)
    - Hypoadrenocorticism (decreased Na reabsorption and ADH due to low effective circulating volume and low cortisol)
    - Renal tubular dysfunction (inability to dilute urine + hyperkalemia causing entry of Na into cells)
    - SIADH
    - Increased water intake (psychogenic polydipsia)
  2. Hypernatremia
    - Salt poisoning (seawater, beef jerky, salt-flour dough)
    - Restricted access to water
    - Syndrome of hypodypsic hypernatremia (Min Schnauzers)
    - Urinary, GI, 3rd space, cutaneous water losses with inadequate water intake (osmotic diuresis: DM, mannitol administration)
    - Diabetes insipidus with inadequate water intake
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16
Q

Where are myelinolysis (= osmotic demyelination syndrome) lesions commonly seen

A

Thalamus

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17
Q

What is the treatment recommendation for clinical acute hyponatremia? Chronic?

A
  1. Stabilization (for acute and chronic): 2 mL/kg of 3%NaCl over 20 min, repeat as needed to increase Na by 5 mmol/L
  2. If acute (<48h): infuse 3% NaCl at 0.5-2 mL/kg/h until Na reaches low-normal
  3. If chronic or unknown, goal to increase Na by no more than 10 mEq/L over first 24h and 8mEq/L over each following 24h - use sodium deficit to know how much sodium to give
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18
Q

Sodium deficit formula

A

Sodium deficit (mmol) = (target Na+ - patient Na+) * 0.6 * body weight (kg)

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19
Q

What level of hyponatremia puts patients at risk of osmotic demyelination syndrome

A

Na < 110 mmol/L

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20
Q

How do blood pH and osmolality influence K concentration

A
  • Alkalosis -> intracellular movement of K in exchange for H+ -> hypoK
  • Hyperosmolarity -> extracellular movement of water -> extracellular movement of K by solvent drag -> hyperkalemia
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21
Q

What hormones are involved in changes in K concentration

A

Catecholamines, insulin, aldosterone

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22
Q

What is the kaliuretic feedforward control

A

Changes in K concentration are sensed in the stomach and hepatic portal region and send signals to the kidneys to adjust kaliuresis based on intake

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23
Q

List causes of hypokalemia

A
  1. Disorders of internal balance:
    - Metabolic alkalosis
    - Insulin therapy
    - Beta2-agonist intoxication
    - Catecholamines
    - Refeeding syndrome
  2. Disorders of external balance
    - Prolonged inadequate intake
    - Diuretic drugs, osmotic or post-obstructive diuresis
    - Renal tubular acidosis
    - Hyperladosteronism
    - DKA
    - Severe diarrhea
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24
Q

What are the 4 categories of consequences of hypokalemia

A
  1. Metabolic -> glucose intolerance (altered insulin release)
  2. Neuromuscular -> muscle weakness (hyperpolarized myocytes)
  3. Cardiovascular -> prolongation of action potential, AV dissociation, tachyarrhythmias, Vfib (hyperpolarized cardiomyocytes)
  4. Renal -> impaired tubular function
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25
Q
A
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26
Q

List causes of hyperkalemia

A
  1. Increased intake
    - IV supplementation
    - Expired pRBC transfusion
    - Drugs
  2. Translocation from intracellular to extracellular
    - Insulin deficiency
    - Mineral acidosis
    - Tumor lysis syndrome
    - Tissue reperfusion
    - CPA
  3. Decreased urinary excretion
    - Oligoanuric AKI
    - Ureteral / urethral obstruction
    - Uroabdomen
    - Hypoadrenocorticism
    - GI disease (trichuriasis)
    - Drugs (ACE inhibitors, angiotensin receptor blockers, aldosterone inhibitor
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27
Q

ECG changes associated with hypokalemia / hyperkalemia

A
  1. Hypokalemia
    - ST segment depression
    - Increased P-wave amplitude
    - Prolonged PR interval
    - Widened QRS
  2. Hyperkalemia
    - Tented T-wave
    - Wide QRS
    - ST segment depression
    - Depressed P-wave / atrial standstill
    - Vfib
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28
Q

What is the physiologic response to hypocalcemia

A
  • Secretion of PTH by chief cells of the parathyroid gland
  • Increased bone resorption
  • Increased Ca reabsorption and decreased P reabsorption by the kidneys
  • Hydroxylation of calcidiol to calcitriol in the kidneys -> increased Ca and P intestinal absorption
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29
Q

What is the metabolism leading to calcitriol

A
  • Vitamin D (cholecalciferol) intestinal absorption
  • Hydroxylation to 25(OH)D3 (calcidiol) in liver
  • Hydroxylation to 1,25(OH)2D3 (calcitriol = 1,25-dihydroxycholecalciferol) in the kidney (proximal tubular cells) by 1α-hydroxylase
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30
Q

Where is calcitonin produced? What are its effects?

A
  • Parafollicular C cells in the thyroid gland
  • Inhibits bone resorption and decreases renal tubular absorption of Ca
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31
Q

What is the effect of pH on iCa

A

Alkalosis increases binding of Ca to albumin -> decreased iCa

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32
Q

What ECG changes can be associated with hypercalcemia / hypocalcemia

A
  1. Hypercalcemia
    - Prolonged PR interval
    - Widened QRS
    - Shortened QT interval
    - Shortened ST segment
    - Widened T wave
    - Bradycardia
  2. Hypocalcemia
    - Prolonged QT interval
    - Deep, wide T waves
    - AV block
    - Bradycardia
33
Q

What calcium-phosphorus product indicates a risk of soft tissue mineralization

A

Calcium * phosphorus > 60 (in mg/dL)

4calcium * 3phosphorus > 60 (in mmol/L)

34
Q

What are treatments for hypercalcemia and their mechanisms

A
  • 0.9%NaCl diuresis: competition for tubular reabsorption with Na ions
  • Furosemide: increases urinary Ca excretion
  • Glucocorticoids: reduced bone resorption, decreased intestinal Ca absorption, increased renal Ca excretion
  • Calcitonin: decreases activity of osteoclasts
  • Sodium bicarbonate: increase Ca protein binding
  • Dialysis
  • Biphosphonates (pamidronate, zoledronate, alendronate): decrease osteoclast activity - can take up to 3 days, should not be used for crisis
35
Q

List 5 causes of hypercalcemia and 5 causes of hypocalcemia

A
  1. Hypercalcemia
    - Hyperparathyroidism
    - Hypoadrenocorticism
    - Acute or chronic renal disease
    - Idiopathic
    - Bone resorption (osteosarcoma, osteomyelitis, HOD)
    - Neoplasia (lymphoma, multiple myeloma, anal sac apocrine gland adenocarcinoma, carcinoma, etc.)
    - Hypervitaminosis D (rodenticide, psoriasis cream, granulomatous disease)
  2. Hypocalcemia
    - Eclampsia
    - CKD
    - Hypoparathyroidism (primary, iatrogenic, nutritional secondary)
    - Citrate administration (transfusion)
    - Pancreatitis
    - Ethylene glycol toxicity
    - Tumor lysis syndrome
    - Intestinal malabsorption (PLE)
36
Q

What are treatments for hypocalcemia

A
  • IV calcium (gluconate, or chloride but must be given in central line) -> bolus (0.5-1.5 mL/kg of Ca gluconate) then CRI at 5-15 mg/kg/h of elemental calcium
  • Oral calcium 25-50 mg/kg/day (divided BID)
  • Calcitriol 5-15 ng/kg/day (divided BID), loading at 20-30 ng/kg/day for 3-4 days
37
Q

List 4 functions of magnesium

A
  • Coenzyme for Na-K ATPase (effect on potassium concentration)
  • Coenzyme for calcium ATPase and proton pump (effect on calcium concentration)
  • Participation in protein and nucleic acid synthesis
  • Regulation of vascular smooth muscle tone
  • Cellular second messenger
38
Q

What hormones are in charge of magnesium regulation? What are the effector organs?

A

Hormones increasing Mg:
- PTH
- Calcitonin
- ADH
- Beta-adrenergic agonists
- Epidermal growth factor

Hormone decreasing Mg:
- Prostaglandin E2

Effector organs:
- GI (absorption in small intestine)
- Kidneys (glomerular filtration and reabsorption in distal convoluted tubule and loop of Henle)

39
Q

What are the 3 categories of hypomagnesemia, with examples for each of them

A
  1. Decreased intake
  2. Increased losses
    - GI -> malabsorption, chronic diarrhea
    - Renal -> tubular disorders, diuretics, DKA, hyperthyroidism, hyperparathyroidism
    - Lactation
  3. Alterations in distribution
    - Extracellular to intracellular shift -> glucose / insulin or amino-acid infusion
    - Chelation -> elevation in catecholamines (chelation to fat) or massive transfusion (chelation to citrate)
    - Sequestration -> pancreatitis (in fat necrosis)
40
Q

What are the 2 electrolytic disorders commonly associated with hypomagnesemia and why

A
  • Hypokalemia: hypoMg increases renal potassium losses
  • Hypocalcemia: hypoMg increases movement of Ca from extracellular to bone and impairs PTH secretion
41
Q

What is an adverse effect of magnesium sulfate supplementation

A

Hypocalcemia because sulfate chelates calcium

42
Q

What is the emergency treatment of hypermagnesemia

A

Calcium gluconate (calcium is an antagonist of magnesium at the neuromuscular junction)

43
Q

What are physiologic roles of phosphate

A
  • Incorporated in 2,3-DPG
  • Production of ATP
  • Organic phosphate: phospholipids, nucleic acids, etc.
  • Buffer of acidosis
  • Maintenance of bone and teeth matrix (hydroxyapatite)
44
Q

What hormones are involved in phosphate regulation? What are the effector organs?

A
  1. Hormones increasing phosphate:
    - Calcitriol
    - Growth hormone
    - Insulin
    - Thyroxine
  2. Hormones decreasing phosphate:
    - PTH
    - Calcitonin and phosphatonins
    - Glucocorticoids

Effector organs:
- GI (absorption in small intestine)
- Kidneys (glomerular filtration and tubular reabsorption in proximal convoluted tubule)
- Bones

45
Q

List causes of hypophosphatemia

A
  1. Decreased GI absorption
    - Malnutrition
    - Malabsorption
    - Diarrhea / steatorrhea
    - Phosphate binders (AlOH)
    - Vitamin D deficiency
  2. Transcellular shifts
    - Alkalosis (increases glycolysis)
    - Insulin / dextrose
    - Refeeding syndrome
    - Catecholamines
  3. Increased urinary losses
    - Increased diuresis (osmotic, diuretics, post-obstructive, etc.)
    - Hyperparathyroidism (primary or nutritional secondary)
    - Glucocorticoids
    - Hyperaldosteronism
  4. Spurious
    - Hemolysis
    - Hyperbilirubinemia
    - Mannitol
46
Q

What are consequences of hypophosphatemia

A
  • Hemolysis (due to decreased RBC ATP and 2,3-DPG)
  • Impaired coagulation
  • Muscle weakness
  • Ileus
  • Encephalopathy
47
Q

What are consequences of hypermagnesemia

A
  • Severe muscle weakness (areflexia, respiratory paralysis)
  • Hypotension due to reduced vasomotor tone
  • ECG changes and bradycardia
48
Q

What does urine Na concentration reflect

A

Effective circulating volume (< 20 mmol/L -> decreased ECV, > 40 mmol/L -> adequate ECV)

Cannot be interpreted in the presence of metabolic alkalosis

49
Q

What is the transtubular potassium gradient and how is it used

A

TTKG = (urine K * plasma osmolality) / (urine osmolality * plasma K)

Reflects reabsorption of potassium in the distal convoluted tubule (effect of aldosterone). If <6 in a patient with hyperK, indicates renal cause. If >3 in a patient with hypoK, indicates renal cause.

Cannot be used if urine osmolality is < plasma osmolality of urine Na < 25

50
Q

What does urine Cl concentration indicate

A
  • Effective circulating volume (< 25 mmol/L -> decreased ECV) ; not affected by metabolic alkalosis, unlike Na urine concentration
  • If metabolic alkalosis is chloride responsive (urine Cl < 15-25) or not (urine Cl > 15-25)
51
Q

What is the urinary free water clearance? What is it used for?

A

Urinary free water clearance = Urine volume * [1-(urine Na + urine K) / serum Na]

It is used to assess the role of kidneys in dysnatremias:
- in patient with hypoNa, should be positive (if negative, indicates renal cause)
- in patient with hyperNa, should be negative

52
Q

What are possible mechanisms leading to hypercalcemia in hypoadrenocorticism

A
  • Hemoconcentration
  • Decreased GFR
  • Metabolic acidosis
  • Increased vitamin D activity
  • Increased parathyroid activity
53
Q

What is a simplified relationship between USG and urine osmolality

A

Multiplying the last 2 digits of USG by 36 gives an estimate of urine osmolality.
Not true if there are some high-molecular-weight solutes in the urine (eg. synthetic colloids)

54
Q

How do the volume and solute concentration change in the extra-cellular fluid and intra-cellular fluid following:
- pure water loss
- hypotonic fluid loss
- isotonic fluid loss
- hypertonic fluid loss
- isotonic fluid loss with pure water replacement

A

See picture

55
Q

What hormones are involved in the regulation of natremia

A
  • Angiotensin II (increases tubular reabsorption)
  • Aldosterone (increases tubular reabsorption)
  • Catecholamines (increases tubular reabsorption)
  • Vasopressin (increases free water diuresis)
  • ANP (decreases tubular reabsorption and increases GFR)
56
Q

What are the possible volume statuses of a hypernatremic patient?

A
  • Hypervolemic -> solute gain (salt poisoning)
  • Normovolemic -> free water deficit
  • Hypovolemic -> hypotonic loss (renal or extra renal)
57
Q

What is the treatment for a salt poisoning

A

D5W potentially combined with a diuretic (furosemide) since the patient is already hypervolemic

58
Q

What are 2 causes of spurious hyponatremia

A

Hyperlipidemia and hyperproteinemia (because sodium is only present in the aqueous phase of the serum)
Patient’s measured osmolality will be normal

59
Q

How can the osmolality be in a patient with hyponatremia

A
  • Increased (hyperglycemia, mannitol causing movement of water from intracellular to extracellular)
  • Decreased (decrease in Na without addition of other osmoles)
  • Normal (pseudohyponatremia)
60
Q

Give causes of hypochloremia and hyperchloremia

A

Hypochloremia:
- GI loss (vomiting of stomach contents)
- Renal loss (loop diuretics)
- Chronic respiratory acidosis
- Hyperadrenocorticism, glucocorticoid administration

Hyperchloremia:
- GI loss of sodium relative to chloride (“loss of HCO3): diarrhea
- Renal chloride retention: RTA, hypoadrenocorticism, chronic respiratory alkalosis
- Therapy with chloride salts, TPN, NaCl fluids

61
Q

What is the effect of hyperkalemia / hypokalemia on resting membrane potential

A
  • Hypokalemia “increases” the resting potential = makes it more negative
  • Hyperkalemia “decreases” the resting potential = makes it less negative
62
Q

What is the benefit of calcium administration in hyperkalemia

A
  • Calcium decreases the threshold of depolarization (makes it less negative), re-establishing the difference between the resting membrane potential (decreased by hyperkalemia) and the threshold
  • Calcium speeds impulse propagation in SA and AV nodes
    => returns excitability to normal
63
Q

What is the mechanism of secondary hyperparathyroidism? What is a consequence?

A

Parathyroid gland becomes hyperplastic with increased secretion of PTH in patients with renal disease or vitamin D deficiency or a low Ca / high P diet.

Due to:
- Increased phosphorus (eg. from decreased phosphorus excretion in renal disease)
- Decreased secretion of calcitriol from vitamin D deficiency or due to diseased kidneys (-> no inhibition of PTH by calcitriol + lower Ca stimulates PTH)
- Lower Ca due to renal losses or low intake

Consequence: bone resorption

64
Q

What is a cause of hypocalcemia in renal failure

A

Decreased calcitriol production (decreased activity of 1alpha-hydroxylase in renal tubules)

65
Q

What are possible causes of hypocalcemia of critical illness

A
  • Decreased PTH secretion
  • Hypovitaminosis D
  • Hypercalcitonism
  • Altered calcium binding to proteins
  • Calcium forming complexes with lactate
  • Hypomagnesemia (decreases PTH)
    (- Underlying disease
  • Drugs, transfusions)
66
Q

Where does vitamin D come from in cats and dogs

A

Diet (intestinal absorption) mostly

67
Q

Why does hyperphosphatemia lead to hypocalcemia

A

Mass-law effects: formation of calcium-phosphate salts

68
Q

Why does bicarbonate administration lead to hypocalcemia

A
  • Alkalosis increases calcium binding to albumin
  • Calcium can form complexes with bicarbonates
69
Q

What is the Adrogue-Madias formula

A

Gives the expected change in Na after infusion of fluids or the volume of fluid needed to reach a target change in Na

change in serum Na = [(infusate Na + infusate K) - serum Na]*V / (total body water + V)

or

V = (change in Na * total body water) / (infusate Na + infusate K - target Na)

(where V is the volume of fluid administered)

70
Q

What are the main intracellular / extracellular anions / cations

A
  • Intracellular cations: K+, Mg2+
  • Intracellular anions: proteins, phosphates
  • Extracellular cations: Na+, Ca2+
  • Extracellular anions: Cl-, HCO3-
71
Q

What is the emergency dose of magnesium sulfate in case of arrhythmias

A

0.15-0.3 mEq/kg Mg = 0.075-0.15 mmol/kg Mg = 18.75-37.5 mg/kg MgSO4

72
Q

An animal presents with acute onset of profuse vomiting. The patient is tachycardic, mildly hypotensive, has a decreased ventilation rate and pale MM. Blood gas analysis shows a metabolic alkalosis, hypochloremia, hypokalemia. Explain the pathophysiology behind each abnormality.

A

+ CV signs:

Decreased blood volume and arterial pressure from vomiting –> activates the baroreceptor reflex –> increased sympathetic outflow to the heart and blood vessels –> tachycardia and vasoconstriction (pale MM)

73
Q

What are the 3 forms of circulating calcium?

A
  • Ionized (free)
  • Protein bound
  • Complexed (bound to phosphate, bicarbonate, lactate, citrate, oxalate)
74
Q

True or false: FGF-23 enhances calcitriol synthesis, while PTH inhibits the synthesis of calcitriol

A

False! The opposite

75
Q

What is the cutoff ionized calcium value for hypercalcemia and hypocalcemia in dogs and cats?

A

Hyper:
Dogs: 1.5 mmol/L
Cats: 1.4 mmol/L

Hypo:
Dogs: 1.25 mmol/L
Cats: 1.1 mmol/L

76
Q

What is NaCl 0.9% the fluid of choice for hypercalcemia (2 reasons)?

A

1- Na+ competes with Ca2+ in the renal tubule resulting in calciuresis

2 - NaCl is a calcium free fluid

77
Q

Ddx for hypocalcemia in the face of hyperphosphatemia?

A
  • Renal dysfunction
  • Pancreatitis
  • Excessive phosphorus intake
  • Primary hypoparathyroidism
78
Q

In 2018, a prospective multicenter study was done looking at NaHCO3 therapy for patients with severe metabolic academia. What were the outcomes of this study?

A
  • RRT was started earlier in the control groupe vs NaHCO3 group (for AKI patients)
  • NaHCO3 therapy was associated with less hyperkalemia
  • Number of days free from vasopressors was higher in th NaHCO3 group
  • Length of ICU stay did not differ
  • NaHCO3 was associated with metabolic alkalosis, hypernatremia, hypocalcemia (not life-threatening)

Acid-base & electrolytes (3 decks)

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