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RUSVM Clin Path > Electrolytes > Flashcards

Electrolytes Flashcards

1
Q

Plasma [Na+]

A

Major extracellular fluid (ECF) ion

Actively eliminated from cells via sodium pump

Major influence on osmolality

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2
Q

T/F Osmoreceptors that secrete ALDOSTERONE indirectly influence serum Na+ concentration

A

False: its ADH

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3
Q

Renal tubular absorption of Na is regulated via

A

Aldosterone

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4
Q

T/F Na is absorbed through the GI

A

true: intestinal absorption

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5
Q

what 3 things effect plasma volume of Na

A

Urine, gastrointestinal tract (GIT), sweat (horses)

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6
Q

Sodium balance – 2 related & interdependent systems:

A

osmoregulation & volume regulation

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7
Q

osmoreceptors in hypothalamus

A

sense increased osmolality & secrete ADH

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8
Q

stretch receptors

A

sense volume changes

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9
Q

How does ADH regulate Na

A

Responds to:
- ↑ osmolality
- ↓↓↓ plasma volume
Acts on collecting ducts; maximizes water reabsorption

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10
Q

what is the main regulator of Na balance

A

Renin-angiotensin-aldosterone system (Na resorbed in distal tubule)

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11
Q

aldosterone is secreted in response to

A
  • Angiotensin
  • Hyperkalemia
  • ACTH
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12
Q

aldosterone

A

conserves Na+

Secretes K+

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13
Q

causes of hyponatremia

A

loss of Na+ (GIT, renal, cutaneous)

Shifts (diabetes)

↑ extracellular H2O (CHF)

↓ intake (herbivores)

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14
Q

most common cause of hyponatremia

A

hypovolemia

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15
Q

causes of hypovolemia

A

GIT: vomiting, diarrhea, saliva

Renal loss:

  • Hypoadrenocorticism (Addison’s): ↓ aldosterone
  • Ketonuria
  • Prolonged diuresis

Cutaneous: sweating, burns

3rd space: sequestration of fluid

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16
Q

examples of 3rd space syndromes (causing hyponatremia)

A

Peritonitis

Ascites

Uroabdomen

Chylothorax

GI sequestration

This effectively “dilutes” plasma Na+

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17
Q

2 causes of osmotic shifts (causing hyponatrmia)

A

hyperglycemia

mannitol administration

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18
Q

2 causes of increased extracellular water leading to hyponatremia

A

primary polydipsia (psychogenic water drinking)

excessive administration of Na+ poor IVF

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19
Q

consequences of hyponatremia if other osmotically active substances are NOT increased

A

hypoosmolality

cellular edema (cellular overhydration)

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20
Q

what is hypernatremia usually due to

A

dehydration

  • inadequate water intake
  • pure water loss (panting, fever, diabetes insipidus)
21
Q

hypernatremia is less commonly due to

A

excessive Na+ intake or retention

22
Q

Chloride

A

Major extracellular fluid (ECF) anion

Important in transport of electrolytes and water

Anion involved in acid base metabolism

23
Q

who is chloride’s BFF

A

Na

24
Q

if changes in Cl- and Na+ are proportional:

A

consider differentials that pertain to abnormalities in Na+ (Cl- is following Na+)

25
Q

if the changes in Cl- are greater than Na+

A

consider acid-base abnormalities

26
Q

how is chloride regulated

A

Controlled by electrochemical gradients

Corresponds to the active transport of sodium

27
Q

what interferes with Cl transport

A

furosemide

GI enterotoxins

28
Q

T/F Cl is usually regulated secondary to Na

A

true: usually parallels [Na]

29
Q

T/F All causes of ↓Na+ are causes of ↓Cl-

A

true

30
Q

most common cause of Cl- loss being greater than Na+ loss

A

hypochloremia metabolic alkalosis

  • severe vomiting
  • abomasal disorders, high GI obstructions
31
Q

what can selective chloride loss lead to

A

Hypochloremic metabolic alkalosis +/- Paradoxical aciduria

32
Q

when should selective chloride loss be suspected

A

corrected Cl- is below the reference interval

33
Q

what 2 things does paradoxical aciduria require

A

volume depletion

chloride depletion

34
Q

mechanism of paradoxical aciduria

A

Kidney:
• Resorbs Na+ to correct dehydration
• Resorbs HCO3- instead of Cl- (electoneutrality)

Result: exacerbated alkalosis (more HCO3-)

35
Q

causes of hyperchloremia

A

Generally parallels increases with Na+

Hyperchloremic metabolic acidosis
− GIT loss of HCO3-

Alkalemia / HCO3- excess

36
Q

functions of potassium

A

Major intracellular (IC) cation- IC osmotic pressure and fluid volume

Resting cell membrane potential

Carbohydrate metabolism

Electron transport

37
Q

clinical signs of abnormal serum K+

A

cardiac dysfunction

skeletal muscle dysfunction

38
Q

regulation of potassium

A

adequate intake

renal excretion

sweat

GI loss

39
Q

causes of hyperkalemia

A

Failure of renal Excretion: most common

Redistribution

↑ intake: Parenteral administration of K+

40
Q

examples of redistribution leading to hyperkalemia

A
  • Inorganic acidosis
  • Insulin deficiency
  • Muscle trauma: rhabdomyolysis, seizures
  • Massive hemolysis
41
Q

hyperkalemia: examples of failure of renal excretion

A

Oliguria/ Anuria

Urethral obstruction

Ruptured urinary bladder

Hypoadrenocorticism (Addison’s): ↓ aldosterone

Drugs that decrease K+ excretion
• “Potassium Sparing Diuretics”

42
Q

T/F redistribution is a major mechanism of hyperkalemia

A

true

43
Q

T/F H+ & K+ balance maintains electroneutrality between ICF and ECF

A

true

44
Q

pseudohyperkalemia

A

Generally in vitro, not in vivo

Marked thrombocytosis: leakage of intracellular K+

Hemolysis: K+ released from RBCs

EDTA CONTAMINATION!!

45
Q

hypokalemia

A

Usually indicates marked depletion of cellular K+

46
Q

causes of hypokalemia

A

Decreased intake or low K+ IV fluids

Loss

  • Alimentary: vomiting, diarrhea, abomasal disorders
  • Renal
  • Horse sweat

Redistribution

  • Alkalemia
  • INSULIN injection (or glucose bolus)
47
Q

consequences of hypokalemia

A
  • Weakness
  • Neurologic signs
  • EKG abnormalities
48
Q

potassium in diarrhea

A

loss of bicarb and K+

  • leads to an acidosis
  • H+ entersinto the cells and K+ leaves cells
  • may mask total body K+ deficit
49
Q

T/F With diarrhea, potassium supplementation may be indicated despite normal serum K+

A

true

RUSVM Clin Path (11 decks)

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