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Clinical Pathology > Electrolytes: Na, Cl, K > Flashcards

Electrolytes: Na, Cl, K Flashcards

1
Q

What is the major ion found in the ECF? How does it get there? What influence does it have?

A

sodium

actively eliminated from cells via sodium pumps

affects osmolality of plasma

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2
Q

What are the 4 major ways sodium concentration is regulated

A
  1. adequate intake, especially in herbivores
  2. renal tubular absorption via aldosterone (RAAS)
  3. intestinal absorption
  4. osmoreceptors in hypothalamus secrete ADH and has an indirect influence - increased osmolality = ADH secretion = lower water loss
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3
Q

What are the 3 mechanisms of hyponatremia?

A
  1. INTAKE - decreased Na intake (herbivores, esp. ruminants), increased water intake
  2. REDISTRIBUTION - water shift from ICF to ECF to increase plasma osmolality not due to Na, Na shifts out of vasculature and into effusions in the edematous states like heart failure, liver failure, etc.
  3. EXCRETION - Na lost in excess of water (GI, renal, cutaneous)
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4
Q

What are 2 common causes of increased water intake that can lead to hyponatremia?

A
  1. primary PD (psychogenic water drinking)
  2. excessive administration of sodium-poor hypotonic IVF
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5
Q

What is 3rd space syndrome? What are 5 examples?

A

fluid moves from the vasculature into a “third” larger space in the body, commonly body cavities (1st space = intravascular; 2nd space = interstitial/intracellular) —> fluid sequestration, causing sodium moving from the plasma down the concentration gradient into that space

  1. peritonitis
  2. ascites
  3. uroabdomen
  4. chylothorax
  5. GI sequestration
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6
Q

What is osmotic shift? What are 2 causes?

A

increased solute concentration in the ECF causes movement of water from the ICF into the ECF, which dilutes the serum

  1. hyperglycemia - increased glucose causes hyperosmolality in the ECF and water moves from the intracellular space to the extracellular space, diluting the serum sodium level —> hyperglycemic patients are mildly hyponatrmic
  2. mannitol - diuretic
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7
Q

What 5 diseases can cause osmotic shifts from ICF to ECF?

A
  1. nephrotic syndrome
  2. hepatic cirrhosis
  3. end-stage renal failure
  4. CHF
  5. psychogenic PD
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8
Q

What is the most common cause of hyponatremia? What 3 organ systems account for this?

A

hypovolemia

  1. GIT: vomiting, diarrhea, salivation
  2. RENAL: hypoadrenocorticism (Addison’s) causing decreased aldosterone, ketonuria, glucosuria, prolonged diuresis
  3. CUTANEOUS: sweating, burns
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9
Q

What is the consequence of hyponatremia? What are the 2 main clinical manifestations?

A

if other osmotically active substances are not increased, the plasma becomes hypoosmotic, and water flows into the cells causing edema (overhydration)

  1. neurological changes - lethargy, weakness, altered mentation, obtundation, seizures, death
  2. difficulty managing rehydration therapy
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10
Q

Diagnostic pathway, hyponatremia:

A
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11
Q

What are the 2 mechanisms of hypernatremia?

A
  1. INTAKE: increased Na intake (hypertonic IVF), decreased water intake (dehydration)
  2. EXCRETION: water lost in excess of Na (GI, renal, insensible loss)
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12
Q

What is the most common cause of hypernatremia?

A

DEHYDRATION from

  • inadequate water intake
  • inadequate water supply
  • inability to drink
  • defective thirst mechanism
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13
Q

What are 2 possible causes of excess sodium intake or retention?

A
  1. ingestion or IV administration
  2. increased aldosterone (increases sodium conservation)
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14
Q

What are 2 causes of increased water excretion that can lead to hypernatremia?

A
  1. pure/insensible water loss: panting, fever, heat stress, diabetes insipidus, hyperventilation
  2. hypotonic water loss
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15
Q

Diagnostic pathway, hypernatremia:

A
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16
Q

A diabetic patient is markedly hyperglycemic. What do you expect the sodium concentration to be? What is the mechanism that drives the change in sodium?

A

decreased/hyponatremic - for every 100 mg/dL increase in glucose, ~2 mEq decrease in Na

osmotic shift - water shifts from ICF to ECF, diluting the plasma

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17
Q

What is the major extracellular fluid anion? What are 2 of its major functions?

A

chloride

  1. transports electrolytes and water
  2. acid-base metabolism
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18
Q

When evaluating chloride what 2 aspects of the biochemistry results should be looked at? How are changes translated?

A

Na and TCO2

  1. changes in Na and Cl are proportional - differentials that pertain to abnormalities in Na (hypernatremia, hyponatremia)
  2. change in Cl is greater than Na - acid-base abnormalities
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19
Q

In what 2 ways is chloride concentration regulated? Where in the nephron is it reabsorbed?

A
  1. electrochemical gradients between cells and plasma
  2. active transport of Na
  • PROXIMAL TUBULE: majority or chloride reabsorption by concentration gradients and anion exchanger
  • TAL OF HENLEY: NKCC co-transporter
  • DISTAL NEPHRON: passive movement, secreted to balance H+ (electroneutrality)
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20
Q

What are 2 common substances that interfere with chloride transport? What other ion is it closely related to?

A
  1. Furosemide
  2. GI enterotoxins

usually regulated secondary to and parallels Na concentration —> losses of Na cause a decrease in Cl

21
Q

What is occurring when there is a greater chloride loss compared to sodium loss? What is the most common cause?

A

Na and Cl are usually parallel, but selective chloride loss can occur

hypochloremic metabolic alkalosis - gastric secretions (HCl) are not resorbed by the small intestine in severe vomiting (monogastrics) and abomasal disorders causing GI obstruction

22
Q

What is a common cause of excess chloride loss compared to sodium in horses?

A

sweating —> hypochloremic metabolic alkalosis

23
Q

How can the proportion of sodium and chloride loss be calculated? How is the answer translated?

A

calculate the corrected chloride = [Cl] x (normal Na/measured Na)

  • PROPORTIONAL = rule out serious conditions where chloride is lost or sequestered
  • UNPROPORTIONAL/BELOW RI = selective loss of chloride
24
Q

How does proximal GI obstruction affect chloride? What are some examples?

A

an obstruction before the duodenum does not allow the Cl- and H+ secreted from parietal cells to be absorbed —> selective Cl- loss with increased Na+ and HCO3- retention

  • tennis ball obstruction in duodenum
  • goat with trichobezoar
  • left displacement of abomasum in cows
25
Q

What cells in the distal tubule respond to pH of the blood and are responsible for regulation?

A

TYPE A INTERCALATED - stimulated by acidemia and secrete H+ and Cl-, leading to HCO3- retention

TYPE B INTERCALATED - stimulated by alkalemia or HCO3- excess to conserve Cl- and excrete HCO3-

26
Q

What 2 things are required for paradoxical aciduria? How does the kidney do this? What is the result?

A
  1. volume depletion
  2. chloride depletion

resorbs Na to correct dehydration and HCO3- instead of Cl- for electroneutrality

exacerbated alkalosis

27
Q

CASE: Bull with proximal duodenal obstruction. Based on the biochemistry values, is there selected chloride loss? Interpret the results. What acid-base abnormality typically accompanies the findings?

A

corrected Cl = [Cl] x ([normal NA]/[measured Na])
= 47 x (141 (RI mean)/130)
= 51

this is below the chloride RI, indicating selective Cl loss

metabolic alkalosis

28
Q

What does hyperchloremia commonly parallel? What are 2 possible causes?

A

increases with Na+, same causes as hypernatremia

  1. hyperchloremic metabolic acidosis from GIT loss of HCO3- and proximal/distal renal tubular acidosis
  2. alkalemia from HCO3- excreted in the distal nephron, which generates H+, which Cl- will follow into the plasma to maintain electroneutrality
29
Q

What are 4 functions of potassium?

A
  1. major intracellular cation that maintains IC osmotic pressure and fluid volume
  2. resting membrane potential
  3. carbohydrate metabolism
  4. electron transport
30
Q

What are the important clinical signs of abnormal potassium concentrations?

A
  1. cardiac dysfunction
  2. skeletal muscle dysfunction
31
Q

What 4 regulation systems are responsible for maintaining potassium concentrations?

A
  1. adequate intake
  2. renal excretion promoted by aldosterone where K is exchanged for Na
  3. GI loss
  4. sweat
32
Q

What is the most common cause of hyperkalemia? What are 2 other causes?

A

failure of renal excretion

  1. redistribution by inorganic acidosis, insulin deficiency, muscle trauma (rhabdomyolysis), massive hemolysis
  2. increased intake from parenteral fluids
33
Q

What are 4 causes of rhabdomyolysis?

A
  1. strenuous exercise
  2. serizures
  3. vitamin E/selenium deficiency
  4. equine hyperkalemic periodic paralysis (massive cellular lysis)
34
Q

What are the most common causes of hyperkalemia due to decreased renal excretion?

A
  • oliguria/anuria
  • urethral obstruction
  • ruptured bladder
  • hypoadrenocorticism (Addison’s) - decreased aldosterone
  • drugs that decreased K excretion: potassium-sparing diuretics, like Spironolactone
35
Q

How can anemia cause hyperkalemia?

A

animals with RBCs rich in K+ and hemolytic anemia causes redistribution of the K+ into the plasma

36
Q

What is the concentration of H+ and K+ normally like in ICF and ECF? What happens during inorganic acidosis?

A

K+ and H+ normally are electroneutrally balanced by themselves

to preserve vascular pH, H+ moves into the ICF and K+ moves into the ECF to maintain electroneutrality —> hyperkalemia

37
Q

How does insulin deficiency cause redistribution hyperkalemia?

A

increased glucose in the vasculature pulls water out of the cell and into the ECF, causing the cell to shrink which increases ICF K concentration and is leaked into the vasculature

38
Q

How does cellular lysis cause redistribution hyperkalemia?

A

(rhabdomyolysis, acute tumor lysis syndrome)

during cellular lysis, K+ is released from the cell and into the vasculature

39
Q

What is a common iatrogenic cause of hyperkalemia?

A

administration of high [K+] IV fluids

40
Q

What causes pseudohyperkalemia? What are 2 indications?

A

in vitro, NOT IN VIVO —> EDTA contamination

  1. marked thrombocytosis due to leakage of intracellular K+
  2. hemolysis where K+ is released from RBCs
41
Q

What 5 animals have RBCs rich in potassium?

A
  1. horses
  2. pigs
  3. cattle (some sheep)
  4. Akitas and other Japanese dog breeds
  5. mice, rats, monkeys

(separate serum quickly!)

42
Q

Diagnostic pathway, hyperkalemia:

A
43
Q

What is considered hypokalemic? What are the 3 most common clinical signs?

A

[K+] < 2.5 mmol/L

  1. weakness
  2. neurological signs
  3. EKG abnormalities: flattened T-waves indicative of decreased ventricular repolarisation
44
Q

What are the 3 major causes of hypokalemia?

A
  1. LOSS: vomiting, diarrhea, abomasal disorders, diuresis, hyperaldosteronism (Cushing’s), renal failure in cats, sweating in horses
  2. REDISTRIBUTION: alkalemia, insulin injection, glucose bolus
  3. INTAKE: decreased intake, low K+ IV fluids
45
Q

How does diarrhea cause redistribution hypokalemia? What is a common treatment?

A

diarrhea is electrolyte and bicarbonate rich —> loss of K+, HCO3-, Na+, and Cl- resulting in metbolic acidosis (which tends to mask this condition) and movement of H+ intreacellularly and K+ extracellularly

potassium supplementation

46
Q

How does alkalemia cause redistribution hypokalemia?

A

to preserve vascular pH, H+ moves into the ECF and K+ moves into the ICF to maintain electroneutrality

47
Q

What are common causes of insulin spikes? How does this cause redistribution hypokalemia?

A

glucose bolus, excitement

insulin upregulates the Na/K ATPase that moves K+ into the cell and H+ moves into the ECF to maintain electroneutrality

48
Q

Diagnostic pathway, hypokalemia:

A

Clinical Pathology (33 decks)

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