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Clinical Pathology > Electrolytes I & II > Flashcards

Electrolytes I & II Flashcards

1
Q

Where is Na+ and K+ more concentrated?

A

Na+: outside the cell

K+: inside the cell

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2
Q

With significant cell lysis, what electrolyte concentrations typically ↑ in the blood?

A

PO4
K+

higher in cell, so lysis causes increase in the blood

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3
Q

What is electroneutrality?

A

total body cations and anions must be balanced

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4
Q

Which ions like to exchange?

A

K+, Na+, H+

Cl- and HCO3-

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5
Q

What is the response to hypovolemia?

A

the RAAS system

Na+ reabsorption in the proximal tubules

Aldosterone secretion (adrenal)

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6
Q

What is the response to hypervolemia?

A

mechanoreceptors in cardiac atria (sense atrial distention)
stimulate release of atrial natriuretic peptide (ANP)

  • inhibits renin
  • inhibits aldosterone
  • inhibits ADH release
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7
Q

What is the result to the response to hypervolemia?

A

sodium and water excretion “pressure natriuresis” - to decrease circulating blood volume and decrease pressure

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8
Q

What is the response to hyperosmolality - ADH and thirst?

A

stimulate ADH response
stimulate thirst response

(hold on to water to dilute osmolality)

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9
Q

What is the response to hypoosmolality - ADH and thirst?

A

inhibit ADH response
inhibit thirst response

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10
Q

What ion contributes the most to serum osmolality?

A

Na+

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11
Q

Why are urea and K+ considered ineffective osmoses?

A

cell membranes are permeable to urea and K+

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12
Q

What is the order the body tries to deal with regarding overall fluid/electrolytes regulation?

A
  1. hypovolemia response
  2. hyperosmolality response
  3. hypervolemia response
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13
Q

What if a patient is hypovolemic and hyperosmolar (diabetes insipidus)?

A

RAAS will still be activates

low circulating volume is always corrected first, then hyperosmolality if need be

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14
Q

What if a patient is hyperosmolar and hypervolemic (primary hyperalfosteronism)?

A

ADH will still be released - even if it makes things worse

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15
Q

What happens with hypernatremia?

A

water deficit (low total body H2O)

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16
Q

Does water or sodium leave the body faster?

A

water

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17
Q

What are examples of pathology - increased water loss, when H2O loss > Na loss?

A
  • renal (e.g. diabetes insipidus, osmotic diuresis
  • GI - osmotic diarrhea, grain overload, paintball toxicosis)
  • respiratory
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18
Q

What are examples of Na+ excess (↑ total body Na+)

A

salt poisoning - play dough, seawater ingestion - also has chloride

administration of sodium bicarbonate (baking soda) - no Cl=

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19
Q

Explain a water deficit in the context of hypernatremia

A
  • decreased intake
  • increased water loss when H2O loss > Na+ loss
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20
Q

What are clinical signs of hypernatremia?

A

neurologic signs associated with Na+ values - water moves out of Brian cells
- decreased brain volume —> rupture of cerebral vessels —> hemorrhage

then sudden dehydration with hypotonic water —> water influx —> cerebral swelling

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21
Q

What are main causes of hyponatremia?

A
  • Na+ deficit (net Na+ loss > H2O loss)
  • H2O excess
  • Shifting of water from ICF to ECF
  • pseudo-hyponatremia
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22
Q

Explain some causes of having a Na+ deficit- hyponatremia

A
  • GI loss
  • renal loss
  • third space loss
  • cutaneous loss
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23
Q

Elaborate on H2O excess regarding hyponatremia

A

edematous disorders (congestive heart failure, cirrhosis, nephrotic syndrome)

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24
Q

Elaborate on shifting of H2O from ICF to ECF regarding hyponatremia

A

water being pulled out of cells which dilutes Na+
- hyperglycemia

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25
Q

Elaborate on pseudo-hyponatremia (and pseudo-hypochloremia) regarding hyponatremia

A

lipemia (indirect potentiometry)

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26
Q

What do you always interpret with Na+? Why?

A

chloride - they move together

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27
Q

What happens when Na+ and Cl- don’t move together?

A

represents an acid-base normality

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28
Q

What happens with high and low potassium?

A

high K+: bradycardia, atria standstill, systole, death

low K+: extreme muscle weakness, inability to breathe (respiratory muscle weakness), death

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29
Q

List some reasons of hyperkalemia

A
  • increased total body K+ (decreased renal excretion)
  • redistribution (intracellular —> extracellular)
  • pseudo-hyperkalemia (artifacts)
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30
Q

Elaborate on increased total body K+ regarding hyperkalemia

A

decreased renal excretion - kidneys not getting rid of K+

urinary disease, urethral obstruction, ruptured urinary bladder, hypoadrenocorticism

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31
Q

Elaborate on redistribution (intracellular —> extracellular) regarding hyperkalemia

A

metabolic acidosis
insulin deficiency
severe tissue/muscle damage

32
Q

Elaborate onpseudo-hyperkalemia regarding hyperkalemia

A

extreme thrombocytosis due to delayed processing

hemolysis (if high K+ in RBCs)

EDTA contamination

33
Q

List some reasons of hypokalemia

A
  • decreased total body K+
  • redistribution (extracellular —> intracellular)
  • renal losses
  • GI losses
34
Q

Elaborate on decreased total body K+ regarding hypokalemia

A
  • decreased intake (or K+ poor fluids)
  • renal loss
  • GI loss
  • skin loss (sweating in horses)
35
Q

Elaborate on redistribution (extracellular —> intracellular) regarding hypokalemia

A
  • metabolic alkalosis
  • increased insulin
  • endotoxemia
36
Q

Elaborate on renal losses regarding hypokalemia

A
  • chronic kidney disease
  • post-obstructive diuresis
  • diuretics
  • diabetic ketoacidosis
  • distal RTA
37
Q

Elaborate on GI losses regarding hypokalemia

A

gastric vomiting

small intestinal diarrhea

38
Q

Metabolic acidosis is associated with [hyper/hypo]kalemia

A

hyperkalemia

39
Q

Metabolic alkalosis is associated with [hyper/hypo]kalemia

A

hypokalemia

40
Q

Addison’s disease is [hyper/hypo]natremia and [hyper/hypo]kalemia

A

hyponatremia
hyperkalemia

41
Q

Explain how hypokalemia is related to metabolic alkalosis

A

potassium is low in the blood, so more from the cells move into the blood = LOW serum K+

this positive charge in the cell is increasing, so positive H+ moves out of the blood and into the cells

= metabolic alkalosis (assesses pH via blood so more alkaline here)

42
Q

What if you see ↓ or WRI K+ with an acidemia?

A

suggests low total body K+

43
Q

What if you see ↑ or WRI K+ with an alkalemia?

A

suggests high total body K+

44
Q

What does EDTA contamination look like on a chemistry?

A

hypocalcemia (chelates calcium)
hyperkalemia - released into the blood from the inside content of cells

45
Q

What does a decreased Na:K ratio suggest?

A

RAGU

R - renal disease
A - Addison’s
G - gastroenteritis
U - uroabdomen

46
Q

What are the values that are suspicious for Addison’s disease or highly associated?

A

< 27 - suspicious
< 19

47
Q

How do you assess metabolic acidosis and metabolic alkalosis?

A

chemistry or blood gas

48
Q

How do you assess respiratory acidosis and respiratory alkalosis?

A

blood gas

49
Q

How do you assess acid/base on chemistry?

A

bicarbonate (HCO3 or TCO2)

chloride

anion gap

50
Q

What abnormalities regarding acid/base can you detect via chemistry?

A

metabolic acidosis - titration or secretion

metabolic alkalosis

51
Q

What is bicarbonate also called?

A

TCO2

52
Q

If there is low HCO3-, we have a _______

A

metabolic acidosis

53
Q

What are the types of metabolic acidosis?

A

titrational - causes listed with increased anion gap

sectional causes listed with increased chloride

54
Q

Secretional metabolic acidosis are causes listed with ______

A

increased chloride

55
Q

Metabolic acidosis is due to [increased/decreased] HCO3 and [increased/decreased] Cl-

A

decreased HCO3
decreased Cl-

56
Q

What is the corrected chloride equation?

A

Cl- (corrected) = Cl- (measured) [Na+ normal avg. / Na+ measured]

57
Q

Calculate the corrected chloride

A
58
Q

If we have a corrected chloride of 117 (RI = 107-115), what is this called?

A

sectional metabolic acidosis

59
Q

Look at this flow chart for corrected chloride

A
60
Q

What is selective hyperchloremia?

A

secretional metabolic acidosis

61
Q

What are some causes of secretions metabolic acidosis?

A
  • GI loss of HCO3 - “secretory diarrhea” with calf scours
  • Renal loss of HCO3 (renal tubular acidosis, RTA)
  • compensation for chronic respiratory alkalosis
62
Q

What can potassium bromide cause?

A

pseudo-hyperchloremia

63
Q

What are causes of selective hyochloremia?

A
  • VOMITING - gastric
  • upper GI sequestration - displaced abomasum, pyloric obstruction, hemorrhagic bowel syndrom ein cows, proximal enteritis in horses
  • diuretics (e.g. furosemide)
  • bovine renal failure
  • excessive gastric reflux in horses
64
Q

What is lost from gastric contents vs duodenal contents?

A

gastric: HCl
base: HCO3

65
Q

How do you calculate the anion gap?

A

AG = (Na+ + K+) - (Cl- + HCO3-)

66
Q

What does an increased anion gap mean?

A

titration metabolic acidosis
- ketones
- lactic acidosis
- renal disease (uremic acids)
- toxins (ethylene glycol)

67
Q

What is KLUE - what does it stand for and what context?

A

increased anion gap = titration metabolic acidosis

Ketones
Lactic acid
Uremic acids (renal disease)
Ethylene glycol (toxins)

“gap acidosis”

68
Q

What can cause a negative anion gap?

A

potassium bromide therapy

69
Q

What does a decreased anion gap mean?

A

hypoalbuminemia
potassium bromide

an increase in unmeasured cations

70
Q

Look at this table

A
71
Q

How does urine pH interact with acid/base abnormalities?

A

H+ in urine: make it acidic

H+ in urine: make it basic if too much HCO3 in blood

72
Q

What is paradoxical aciduria?

A

pH should be alkaline because should reflect blood but it is inappropriately acidic urine

73
Q

Look at this aciduria example

A
74
Q

When is there paradoxical aciduria?

A
  1. hypovolemia
  2. hypochloremia
  3. hypokalemia

displaced abomasum

75
Q

Interpret this case of a 5 day-old Holstein calf

A
76
Q

Interpret this case: 4 month old female intact Labrador presented lethargic and whimpering. Earlier today, a neighbor found and returned the puppy after she had apparently gotten out. Prior to this, she had been a normal energetic puppy, according to the owner

A

Clinical Pathology (28 decks)

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