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PATH 406 > Lecture 2: Electrolyte Abnormalities > Flashcards

Lecture 2: Electrolyte Abnormalities Flashcards

1
Q

What is osmolality?

A

Concentration of all chemical particles found in the fluid part of the blood.

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2
Q

What is the difference between osmolality and osmolarity?

A

Osmolality is the number of solute particles per 1 kg solute.

Osmolarity is the number of solute particles per 1 L of solute.

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3
Q

What are colligative properties?

A

Properties of solutions that depend on the ratio of the number of solute particles to the number of solvent particles in a solution.

For ex. vapour pressure, boiling point, freezing point

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4
Q

How do we measure body fluid osmolality in the clinical lab?

A

Osmometer

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5
Q

What are the two types of osmometers?

A
  1. Freezing point osmometers
  2. Vapour pressure osmometers
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6
Q

Plasma/serum osmolality is regulated between?

A

280 and 295 mmol/kg

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7
Q

What are the major organs involved in water and electrolyte homeostasis? And what are their regulatory systems?

A

Brain - Thirst centre
Brain and Kidney - ADH
Kidney - RAAS
Kidney and Heart - Atrial natriuretic peptide (ANP), B-type natriuretic peptide

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8
Q

What part of the body responds to an increase in osmotic pressure?

A

Osmoreceptors in hypothalamus

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9
Q

When is ADH released?

A

When the hypothalamus osmoreceptors sense high osmolality (>280 mmol/kg)

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10
Q

In absence of ADH urine volume is?

A

> 15 L/day

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11
Q

In presence of ADH urine volume is?

A

0.5 L/day

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12
Q

What is the function of ADH?

A
  1. Increased vessel tone (V1 receptors)
  2. Water re-absorption (V2 receptors and aquaporin 2, AQ2, channels)
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13
Q

What is the function of RAAS?

A
  1. Modulates blood volume and vascular tone
  2. Maintain water and electrolyte homeostasis
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14
Q

How do natriuretic peptides maintain water and electrolyte homeostasis?

A
  1. Stretch of the atrial myocardium or ventricles causes release of ANP and BNP
  2. ANP and BNP decrease sodium reabsorption from the kidney (DCT and CT)
  3. They also directly inhibit aldosterone release by the adrenal.
  4. Both effects result in decrease of plasma volume and sodium
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15
Q

What is the formula for water excess?

A

([Na] - 140)/140 x TBW

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16
Q

What is the most common electrolyte disorder?

A

Hyponatremia

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17
Q

How does the body react when it detects hyponatremia?

A
  1. Suppress ADH
  2. Excrete dilute urine
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18
Q

Why is the rapid correction of chronic hyponatremia contraindicated?

A

The correction must happen slowly to ensure that the extracellular and the intracellular osmolality is similar. This prevents the brain from shrinking.

Rapid correction will result in a higher amount of ions on the intracellular side. This will allow the fluid from the brain to enter the intracellular side, shrinking the brain.

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19
Q

What are the three categories of hyponatremia and what are these categories based on?

A
  1. Hypovolemia
  2. Hypervolemia
  3. Euvolemia

Volume

20
Q

Hypovolemia can be broken down into 2 subcategories. What are they and how do you distinguish between the two?

A
  1. Renal loss
  2. Non-renal loss

If urine sodium > 20, focus on renal loss

21
Q

Hypervolemia can be broken down into 2 subcategories. What are they?

A
  1. End stage kidney disease
  2. Congestive heart failure, cirrhosis, nephrotic syndrome
22
Q

How does congestive heart failure cause hypervolemia hyponatremia?

A

Congestive heart failure is a condition in which the heart cannot pump enough blood to meet the body’s needs.

When the heart’s blood pumping ability decreases, the kidneys cannot work as they should, which leads to an excess of fluid in the body.

23
Q

Euvolemia hyponatremia is caused by?

A

Syndrome of Inappropriate ADH (SIADH) - excess ADH

24
Q

What are the causes of SIADH?

A
  1. CNS disturbance
  2. Small cell carcinoma of the lung
  3. Drugs
  4. Exogenous hormone
25
Q

What is pseudohyponatremia caused by?

A
  1. Hyperglycemia
  2. Hyperlipdemia/Hyperproteinemia
26
Q

How do we measure sodium in clinical labs?

A

Ion selective electrodes (ISE)

27
Q

What is the difference between direct and indirect ISE?

A

Direct - does not dilute before measuring with ISE

Indirect - dilutes before measuring with ISE

28
Q

What are the cons of using indirect ISE to measure electrolytes?

A

Affected by electrolyte exclusion effect hence, not ideal for patients with severe hyperlipidemia or hyperproteinemia

29
Q

Why would measuring with indirect ISE lead to pseudohyponatremia? Why does this not happen with direct ISE?

A

ISE measure Na ion activity, which is directly proportional to Na ion concentration in the water fraction of plasma.

Direct:
ISE w/o dilution therefore measures what the body regulates: Na activity

Indirect:
Would also work if the water fraction of a plasma sample is equal to the average ~93%, as this is what reference intervals are based on

When solutes are much higher, water fraction is lower and this assumption no longer holds. Results produce low Na level that does not correlate with Na activity in plasma. This may present with pseudohyponatremia when patient is in fact hypernatremic.

30
Q

What is hypernatremia caused by and why?

A

Dehydration. Because patients forget or cannot drink (ex. coma, anesthesia, dementia)

31
Q

What are the three categories of hypernatremia and what is it based on?

A
  1. Hypovolemia
  2. Hypervolemia
  3. Euvolemia

Volume

32
Q

Hypernatremia is always associated with?

A

High plasma osmolality

33
Q

What is euvolemia hypernatremia caused by? Why?

A

Diabetes Insipidus

  1. Absent/insufficient ADH production (central)
  2. Absent/insufficient ADH action (nephrogenic)
34
Q

We cannot measure ADH because it is analytically challenging and overlaps in results between health and disease. What do we measure instead?

A

Copeptin

35
Q

What is copeptin?

A

C-terminal part of ADH’s prohormone. It is secreted 1:1 and is more stable in vivo and ex vivo.

36
Q

The availability of epithelial sodium channel (ENaC) is controlled by?

A

Aldosterone

37
Q

Why is alkalosis associated with hypokalemia?

A

Excess sodium absorption will leave a negatively charged lumen, which will augment potassium trapping in the lumen as well as protons leading to hypokalemia and metabolic alkalosis.

38
Q

How does K homeostasis work?

A

Cells act as buffer
K is constantly diffusing out of cells so Na-K ATPase pumps K in to maintain high intracellular

Shift into cells: Insulin, beta adrenergics
Shift outside cells: lack of insulin, acidosis (except lactic), beta adrenergic antagonists

39
Q

What are the causes of hypokalemia?

A
  1. Increased loss
  2. Decreased intake (rare)
  3. Redistribution
40
Q

What is the treatment for hypokalemia?

A
  1. Potassium replacement
  2. If IV replacement: no more than 20 mmol/h
  3. Long term managment in generally dietary, and oral K if necessary
41
Q

What are the clinical features of hyperkalemia?

A

Slowing of electrical conduction
- ECG changes may be seen at values >6 mmol/L

Final event: ventricular asystole or cardiac arrest
- Arrest with ventricular fibrillation is first sign of hyperkalemia in a patient

42
Q

What are the causes of hyperkalemia?

A
  1. Excessive intake
  2. Decreased loss
  3. Redistribution
43
Q

How does decreased loss lead to hyperkalemia?

A
  1. K sparing diuretics are aldosterone antagonists or ENaC blockers
  2. ACE inhibitor block angiotensin II which prevents secretion of aldosterone

(Aldosterone causes Na to be absorbed and K to be excreted into the lumen by principal cells)

44
Q

What are the causes of pseudohyperkalemia?

A
  1. Hemolysis
  2. Delay in processing blood samples
  3. Inappropriate storage temp of blood tubes
  4. IV contmaintation
  5. Severe leukocytosis
  6. Thrombocytosis
45
Q

What are the treatments used for hyperkalemia and why?

A

In acute settings where risk of cardiac conduction abnormality:
1. Calcium gluconate because it stablizes myocardium
2. Insulin because it shifts K into cells by stimulating the activity of Na-H antiporter on cell membrane, promoting the entry of Na into cells, which leads to activation of Na-K ATPase causing an electrogenic influx of K
3. Dextrose stimulates insulin secretion causing shift of extracellular K into cells by activating cell membrane Na-K ATPase pump
4. Bicarbonate raises blood pH and shifts extracellular K into cells

PATH 406 (24 decks)

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