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MD3002 > Urea and Electrolytes > Flashcards

Urea and Electrolytes Flashcards

1
Q

Which are the main electrolytes which are measured ? estimated ?

A 
MEASURED
 Sodium
 Potassium
 (Chloride)
 (Bicarbonate) 
 Urea
 Creatinine

ESTIMATED
 Water

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2
Q

What are possible causes of abnormal electrolyte levels ?

A

 primary disease state
 secondary consequence of a multitude of diseases
 iatrogenic problems are very common

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3
Q

Identify clinical examples causing abnormal electrolyte imbalances.

A 
♦ Haemorrhage - accidents, surgery (lost electrolytes)
♦ Diarrhea and Vomiting 
♦ Poor intake - elderly
♦ Increased losses - pyrexia, heat 
♦ Diabetes insipidus
♦ Diabetes mellitus
♦ Diuretic therapy (may be getting rid of salts in addition to water)
♦ Endocrine disorders - ADH, aldosterone
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4
Q

Describe the body fluid distribution (water, Na+ and K+).

A

WATER

♠ Extracellular Fluid
-Vascular (plasma): 3L 
-Interstital: 16L
♠ Intracellular Fluid: 23L
♠ Total: 42L
SODIUM 
♠ Extracellular Fluid
-Vascular (plasma): 140 (mmol/L)
-Interstitial: 140 (mmol/L)
♠ Intracellular Fluid: 10 (mmol/L)
POTASSIUM 
♠ Extracellular Fluid
-Vascular (plasma): 5 (mmol/L)
-Interstitial: 5 (mmol/L)
♠ Intracellular Fluid: 150 (mmol/L)
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5
Q

Which body fluids may be affected by a loss of 2L of isotonic fluid ? Describe the main consequences of losing 2L of isotonic fluid.

A

e.g. blood, fistula fluid

  • Loss is from ECF
  • No change in [Na]
  • No fluid redistribution (hence ECF become 17L instead of 19L, and ICF remains 23L)
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6
Q

Define isotonic fluid.

A

Same concentration of salts as blood

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7
Q

What happens if, upon loss of 2L of isotonic fluid, this is replaced by isotonic fluid ? Give an example of isotonic fluid which may be given.

A

No change in [Na]
No fluid redistribution

E.g. saline

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8
Q

What happens if, upon loss of 2L of isotonic fluid, this is replaced by hypotonic fluid ?

Give an example of hypotonic fluid which may be given.

A 
Fall in [Na] in blood
Fluid redistribution (due to ^), more fluid goes into ICF from ECF because larger [Na] (since fall in [Na] in blood)

E.g. dextose

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9
Q

Give examples of situation where one may lose hypotonic fluid.
Describe the main consequences of losing 3L of hypotonic fluid.

A

Insensible losses (bleeding very fast, sweating)

  • Greater loss (of fluid) from ICF than ECF
  • Small increase in [Na] in blood
  • Fluid redistribution between ECF and ICF (initially fluid taken away from ECF but then this redistribution means more fluid is lost from ICF than from ECF)
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10
Q

What happens if, upon loss of 3L of hypotonic fluid, this is replaced by isotonic fluid ?

A

[Na] remains slightly increased

No fluid redistribution

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11
Q

What happens if, upon loss of 3L of hypotonic fluid, this is replaced by hypotonic fluid ?

A

[Na] restored

Fluid redistribution

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12
Q

Identify physiological mechanisms in place to counteract electrolyte abnormalities.

A

 Thirst
 ADH (anti-diuretic hormone) (retain water)
 Renin / Angiotensin system (retain electrolytes and protect renal blood flow by constricting vessels)

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13
Q

Identify therapeutic mechanisms in place to counteract electrolyte abnormalities.

A

 Intravenous therapy
 Diuretics
 Dialysis

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14
Q

What triggers ADH release ? What are its main effects ?

A

ADH is produced in response to a rise in osmolality (osmolarity)

 Decreases renal water loss
 Increases thirst

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15
Q

Describe tests to ascertain ADH status.

A

1) Measure plasma and urine osmolality
- urine > plasma suggests ADH is active

2) Measure plasma and urine urea
- urine&raquo_space; plasma suggests water retention

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16
Q

Briefly describe the Renin-angiotensin system.

A

♦ Renin -> Angiotensin -> Aldosterone (Aldosterone induces renal Na retention)
♦ Activated by reduced intra-vascular volume (IVV), and/or by Na+ depletion (e.g. haemorrhage)

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17
Q

Describe tests to ascertain R/A/A status.

A

1) Measure plasma and urine Na

- if urine < 10 mmol/L suggests R/A/A active

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18
Q

UREA

  • How is it produced ?
  • How does it get into urine ?
A

UREA
-Produced as a breakdown product of protein metabolism
-Normally filtered at glomerulus and major component of
urine

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19
Q

What V of plasma ultrafiltre enters tubular lumen each day ? How much of this is urea ?

A 
200 L
800 mmol (48g) of urea
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20
Q

Which electrolyte is often the first to change in dehydration ?

A

Urea

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21
Q

What pathologies may elevated urea be found in ?

A

Elevated urea often found in CCF, shock, MI, severe burns

22
Q

Which other electrolyte will often mirror urea during fluid correction ?

A

Sodium and urea concentrations will often parallel each other during fluid correction

23
Q

CREATININE

  • How is it produced ?
  • How does it get into urine ?
A

CREATININE

  • Breakdown product of protein and muscle
  • Usually filtered freely at the glomerulus
24
Q

Are there any differences in creatinine between males and females ? Why ?

A

Concentrations higher in males (plasma and urine values for creatinine typically reflect muscle mass)

25
Q

Why do we need to measure urea and creatinine (i.e. what would abnormalities show) ?

A

♠ Loss of renal function results in decrease in filtered volume
♠ This results in increase in plasma concentrations of urea and creatinine
♠ Hence, urea and creatinine used as markers of renal dysfunction

26
Q

Define GFR. Identify factors which alter it.

A

Glomerular Filtration Rate is the volume of fluid passing through the glomerulus, in a given period of time.

Influenced by renal perfusion pressure, renal vascular resistance, glomerular damage, post-glomerular resistance.
Also higher for larger healthy individuals, and values fall with increasing age.

27
Q

What is the normal GFR range ?

A

♦ “Normal Range” approx 90 - 150 mL/min (can be reported as 90 - 150 mL/min/1.73m2 since larger healthy individuals may have larger GFRs)
♦ Approx 170 L per day

28
Q

What is the best overall measure of kidney function ? Why ? What is a major con of using GFR to measure kidney function ?

A

GFR, because a decrease in GFR precedes renal failure in all forms of progressive kidney disease

CON: Measuring directly is difficult.

29
Q

Define eGFR. What is this used for ? How is this calculated ?

A
  • Estimated GFR
  • Used to aid “staging” of kidney disease
  • Calculated value based on creatinine (also takes age, sex into consideration)
30
Q

Define AKI flag. How is this calculated ?

A
  • Used to flag up incipient Acute Kidney Injury, highlights subtle changes in renal function.
  • Calculated value based on creatinine
31
Q

Define hyponatraemia. What are possible causes of this ?

A

Lower than normal Sodium concentration in blood.

  • Too little Na in ECF
  • Excess water in ECF
  • May also be pseudo hyponatraemia due to increased protein or lipid (e.g. if lipaemia, myeloma)
32
Q

What are possible causes of hypernatraemia ?

A
  • Too little water in ECF

- Too much Na in ECF

33
Q

What are possible causes of dehydration ?

A
  • Water deficiency

- Fluid (Na and water) depletion

34
Q

Describe the process of identifying the cause of Hyponatraemia.

A

STEP 1: Evaluating Extravascular Volume
1) HypoV, then:
-Measure Urine Sodium
•>20 means something interfering with kidneys’s ability to hang out to Na (Diuretics, Addisons’s, Na losing Nephritis)
•<20 means kidney hanging out to as much sodium as possible, so responding appropriately to hypoN (Diarrhea, Skin loss, Vomiting)

2) OEDEMATOUS, then:
•CCF Cirrhosis
•Nephrosis
Either way, something causing both oedema and hypoNa

3) EUOVOLEMIC, then:
-Measure plasma osmolarity
• Normal means pseudo HypoNa
• High means Hypertonic hypoNa (something else replacing osmoles normally from Na, such as chronic hyperglycemia or chronic uremia)
• Low means water overload

-If latter, then measure Urine Sodium
• >20 means drugs, or chronic renal failure
• <20 can mean stress, post-surgery (potentially leading to inappropriate ADH), or endocrine (e.g. Hypothyroid)

35
Q

Describe the electrolyte findings one may found in a dehydrated patient who is already treated for CCF, explaining each (and identifying a possible cause of this).

A

Low plasma Na (hypoNa) and high plasma urea
High urine Na and high urine urea

Because patient probably given diuretics for CCF, which then reduces Na reabsorption and increases renal loss of Sodium (increased Na diuresis) (greater than loss of water), so increased urine sodium and reduced IVV.

Reduced IVV means reduced GFR, which then leads to increased plasma creatinine and urea.

Reduced IVV also triggers ADH which stimulates thirst and water retention by kidney (so increased urine urea). Water intake (due to thirst), further decreases plasma Sodium concentration.

36
Q

Describe the electrolyte findings one may found in a thirsty but well hydrated patient, explaining each (and identifying a possible cause of this).

A

Plasma Na, urea, and osmolality low.
Slightly increased urea in urine relative to plasma, and greatly increased urine osmolality relative to plasma. Also slightly increased urine Sodium relative to normal.

Increased urine urea and osmolality suggest ADH is switched on. Hence, this is because of SIADH. Pituitary produces too much ADH, which leads to decreased urine V (water retention) and therefore increased urine Na.

Increased ADH also results in increased renal water reabsorption which leads to increased urine osmolality. Increased renal water reabsorption also leads to increased IVV.

Increased IVV leads to haemodilution, which results in low plasma Na, urea/creatinine, and osmolality.

Increased IVV also leads to decreased renal Na reabsorption, so also contributes to increased urine Na.

37
Q

Describe the electrolyte findings one may found in a dehydrated with difficulty swallowing patient, explaining each (and identifying a possible cause of this).

A

High plasma Na and urea
High urine urea relative to plasma urea (suggests ADH is switched on)

Difficulty swallowing leads to decreased water intake, which leads to haemoconcentration, increased plasma Na, increased plasma osmolality, increased ADH (appropriately this time, since patient needs to conserve water), and therefore increased urine osmolality and decreased urine V.

Decreased water intake also leads to reduced IVV which leads to decreased renal blood flow, decreased GFR, and therefore decreased increased plasma urea/creatinine and increased urine osmolality/decreased urine V.

Reduced IVV due to decreased water intake also leads to activation of R/A/A system, which increases Na renal reabsorption, which leads to decreased urine Na.

38
Q

Describe the electrolyte findings one may found in a dehydrated and thirsty patient, explaining each (and identifying a possible cause of this).

A

Increased plasma Na, urea, and glucose
High urine urea relative to plasma urea (suggests ADH is switched on)

Hypernatremia (and uremia) due to osmotic diuresis. Increased plasma glucose (due to undiagnosed or poorly managed diabetes) leads to osmotic diuresis (kidney cannot reabsorb that amount of glucose, so excrete some, taking lot of water with it). This leads to increased renal loss of water, and sodium. This leads to increased urine Sodium.

Increased renal loss of water and sodium also leads to reduced IVV, then reduced GFR, so raised plasma urea and creatinine.

Increased renal loss of water and sodium finally leads to haemoconcentration, which leads to increased plasma sodium on the one hand, and increased plasma osmolality on the other. This plasma osmolality triggers ADH production, which leads to increased urine osmolality.

Increased plasma glucose also directly increases plasma osmolality, leading to ADH production and increased urine osmolality.

Patient attempting to keep up through thirst and resulting water intake, but insufficient to compensate for this dehydration.

39
Q

Describe the electrolyte findings one may found in a hypertensive patient, explaining each (and identifying a possible cause of this).

A

Increased plasma Na, normal urea.
Low urine Na, relatively normal urine urea relative to plasma urea (not excessively increased c.f. plasma urea, suggests ADH not active)

Hypernatremia likely caused by hyperaldosteronism (a cause of hypertension). This leads to increased urine Na reabsorption (due to R/A/A system) which leads to decreased renal loss of sodium and water (losing more water than sodium), which leads to decreased urine Na concentration.

This decreased renal loss of sodium and water also results in increased plasma Na concentration.

Finally, this decreased renal loss of sodium and water leads to increased IVV, resulting in increased GFR and decreased plasma urea and creatinine.
Increased IVV (resulting from decreased renal loss of sodium and water) also leads to decreased ADH production, leading to water loss and once again, increased plasma Na concentration.
40
Q

Identify normal ranges for urine urea.

A

Urine Urea: No real ones because they are very variable, need to look at this relative to plasma urea (but normally more concentrated than in plasma)

41
Q

State normal ranges for plasma potassium. Which values should we worry at ?

A

Potassium reference range - 3.6 to 5.0 mmol/L

Values < 3.0 or > 6.0 are potentially dangerous

42
Q

Why are abnormal Potassium concentrations dangerous ?

A

Can result in:

  • Cardiac conduction defects
  • Abnormal neuromuscular excitability
43
Q

What are the main causes of Potassium abnormalities ?

A

Many are iatrogenic (and therefore avoidable)

44
Q

Is most Potassium inside or outside cells ?

A

Majority of Potassium inside cells (ICF rather than ECF)

45
Q

Identify examples of ICF - ECF exchange which may affect plasma potassium.

A

1) Acid-base status (K+ H+ exchanges during acidosis, with K+ rushing out and H+ into cells)
2) Insulin/glucose therapy (causing K+ to rush in cell)
3) Adrenaline
4) Rapid cellular incorporation (TPN (if too high a rate to start with, can cause K+ to rush into cell), leukaemia)

46
Q

State the normal dietary intake of Potassium in a day.

A

Dietary intake 60-200 mmol/day

47
Q

Describe the relationship of Potassium and Hydrogen ions.

A

K+ and H+ exchange can occur across cell membrane

Changes in pH cause shifts in the equilibrium:

  • acidosis - potassium moves out of cells -> hyperkalaemia
  • alkalosis - potassium moves into cells -> hypokalaemia

Conversely Potassium depletion and excess can affect acid- base status

48
Q

Identify the main causes of HyperK+.

A

1) Artefactual Issues
- Delay in sample analysis (causes slower pumps unable to keep potassium inside. Keeping sample in the fridge does the same)
- Haemolysis (in the process of vena puncture due to inadequate technique)
- Drug therapy - Excess intake
- Contaminate sample with potassium

2) Renal
- Acute Renal Failure
- Chronic Renal Failure

3) Acidosis (intracellular exchange)

4) Mineralocorticoid Dysfunction
- Adrenocortical failure
- Mineralocorticoid resistance - eg spironolactone (interferes with adrenal action)

5) Cell Death
- Cytoxic therapy

49
Q

Identify the main causes of Potassium depletion.

A

1) Low intake
- anorexia

2) Increased urine loss
- diuretics / osmotic diuresis
- tubular dysfunction
- mineralocorticoid excess

3) Gastrointenstinal losses
- vomiting
- diarrhoea / laxatives
- Fistulae

4) Hypokalaemia without depletion (still in body, just not in the right place)
- alkalosis (K+ rushes into cell)
- insulin / glucose therapy (K+ rushes into cell)

50
Q

What value is defined as Potassium depletion ? What are the effects of Potassium depletion ?

A

Potassium depletion = plasma concentration < 2.5 mmol/L

1) Acute changes in ICF/ECF ratios
• Neuromuscular:
- lethargy, muscle weakness, heart arrhythmias

2) Chronic losses from the ICF 
• Neuromuscular:
- lethargy, muscle weakness, heart arrhythmias 
• Kidney:
- polyuria
- alkalosis - increase renal HCO3 production 
• Vascular
• Gut
51
Q

How can we detect/diagnose Potassium depletion ?

A

1) History:
- diarrhoea, vomiting, drugs (diuretics, digoxin)
- symptoms of lethargy / weakness
- cardiac arrythmias

2) Electrolytes investigation:
- hypokalaemia
- alkalosis - raised HCO3

A high index of clinical suspicion is needed

52
Q

Describe the main findings of the following scenario. How is this treated ?

A 16 year old admitted in coma with a history of severe weight loss, thirst and polyuria over the previous 4 weeks.

Initial tests
Glucose 35.0  (3.5 - 5.5 mmol/L)
pH 7.01  (7.38 - 7.42)
[H+] 100 (35 - 45 nmol/L)
Sodium 130  (135-145 mmol/L) 
Potassium 6.7 (3.5 - 5.0 mmol/L)
Urine ketones +++
A 
High glucose
Acidotic
High potassium 
Mild hypoNa
Lots of ketones

Diabetic Ketoacidosis. Treated with insulin and glucose (since insulin will push things into the cell, so don’t want her to turn hypoglycaemic). Problem is Potassium will drop suddenly (because first comes out of cell giving high measured K+, and then excreted by kidneys). Furthermore, insulin will cause what’s in ECF to rush into ICF, so leaves ECF depleted of K+.
As a result, also give Potassium infusion but only when K+ levels drop (not whilst hyperK+).

MD3002 (95 decks)

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