3. U and Es Flashcards

1
Q

Which 5 concepts must be considered during an electrolyte disorder?

A
Concentrations **
Compartments
Contents
Volumes
Rates of gain and loss
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2
Q

What is the result of increased excretion on the equilibrium of fluid in the ECF and ICF?

A

Decrease solute concentration

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3
Q

What is the result of haemorrhage on the equilibrium of fluid in the ECF and ICF?

A

Loss of isotonic solutions e.g. fistula fluid
Fluid is lost from ECF
No change in the {Na]
No fluid redistribution

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4
Q

What is the result of dehydration on the equilibrium of fluid in the ECF and ICF?

A

3L Loss of hypotonic fluid e.g. insensible loss

  • ->
  • Greater loss from ICF than ECF
  • Small increase in [Na]
  • Fluid redistribution ECF and ICF
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5
Q

What is the result of gain of isotonic solutions on the equilibrium of fluid in the ECF and ICF?

A
Gain of 2L of isotonic fluid e.g. saline drip
-->
Gain is to the ECF
No change in [Na]
No fluid redistribution
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6
Q

What is the result of gain of hypotonic fluid on the equilibrium of fluid in the ECF and ICF?

A
Gain of 3L of hypotonic fluid e.g. water, dextrose
-->
Greater gain to ICF than ECF
Small decrease in [Na]
Fluid redistribution between ECF and ICF
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7
Q

Name 3 physiological and therapeutic compensatory mechanisms to electrolyte and fluid imbalances?

A

Physiological: Thirst, ADH, RAAS

Therapeutic: Intravenous therapy, diuretics, dialysis

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8
Q

What is the relation of plasma and urine osmolality in ADH status testing?

A

If urine > plasma suggests ADH is active

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9
Q

What is the relation of plasma and urine urea in ADH status testing?

A

If urine&raquo_space; plasma suggests water retention

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10
Q

Where is ADH produced?

A

The median eminence

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11
Q

Describe the activation and effects of the RAAS

A

Renin –> Angiotensin —> Aldosterone

Activated by reduced intra-vascular volume (IVV)
E.g. in Na depletion, haemorrhage

Results in renal Na retention

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12
Q

Test to ascertain R/A/A status?

A

– measure plasma & urine Na

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

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13
Q

Sodium is mainly ______, potassium is mainly ____

A
Na= Extracellular
K= Intracellular
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14
Q

2 methods of replacement of 2L loss of isotonic fluid?

A
  1. With isotonic fluid
    - No change in [Na]
    - No fluid redistribution
  2. With hypotonic fluid
    - Fall in [Na]
    - Fluid redistribution
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15
Q

2 methods of replacement of 3L loss of hypotonic fluid?

A
  1. With isotonic fluid
    - [Na] slightly increased
    - No fluid redistribution
  2. With hypotonic fluid
    - [Na] restored
    - Fluid redistribution
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16
Q

How is urea formed?

A

From protein metabolism

17
Q

Where is an elevated urea found?

A

CCF
Shock
MI
Severe burns

18
Q

What is creatinine?

A

Breakdown product of protein and muscle.

Reflects muscle mass and is higher in males

19
Q

Relevance of urea and creatinine levels in urine?

A

• Loss of renal function and results in decrease
in filtered volume
• Results in increase in plasma concentrations of urea and creatinine
• Urea and creatinine used as markers of renal dysfunction

20
Q

Factors which influence GFR?

A

Influenced by renal perfusion pressure, renal vascular resistance, glomerular damage, post-glomerular resistance.

21
Q

Normal range of GFR?

A

90-150mL/min (Approx 170 L per day)
A larger healthy person has a higher GFR
Values fall with increasing age

22
Q

What is eGFR?
Use?
Based on?

A

“e” is for ESTIMATED glomerular filtration rate

Use:

  • To aid staging of kidney disease
  • Flag up incipient Acute Kidney Injury (AKI)

Based on creatinine

23
Q

How is hyponaturaemia caused by diuretics?

U&E presentation?

A
  1. Decrease in urine Na reabsorption –> Na diuresis
  2. Increase in renal loss of sodium > water.
    - -> Increase in urine [Na]
    - -> Decrease in plasma [Na]
    - -> Decrease Intravenous volume.
    - Decrease in GFR hence increase in plasma [creatinine] and [urea]
    - Increase ADH release so increased water intake, hence decrease plasma [Na]

U&E:

  • Low plasma [Na]
  • High plasma [urea]
  • High urine [Na]
24
Q

How is hyponatraemia caused by SIADH?
U&E presentation?

SIADH= Sydrome of inappropriate ADH secretion

A
  1. Increase in ADH hormone release
  2. Increased renal water reabsorption
    - -> Increase IVV
    - Haemodilution (Decrease in plasma [Na] and [creat]/[urea]
    - Decrease in renal [Na] absorption
    - -> Increase in urine osmolality
  3. Decrease in urine volume
    - -> Increase urine [Na]

U&E:

  • Low plasma [Na], [Urea] and osmolality.
  • High urine [Na]
25
How does decreased water intake cause hypernatraemia? | U&E presentation?
1. Decrease in water intake 2. Haemoconcentration --> Increase in plasma Na --> Increase in plasma osmolarity --> Increase in ADH 2. Decrease IVV --> Decrease RBF --> Decrease GFR --> Increase in urine osmolality, decrease in urine volume (Decrease IVV also results in RAAS, so reduces urine [Na] U&E presentation: - HIgh plasma [urea] and [Na] - Low urine output - Low urine [Na]
26
How does osmotic diuresis cause hypernatraemia? | U&E presentation?
Increase in plasma glucose 1. Osmotic diuresis - -> Increase in renal loss of water and Na. - --> Increase in urine Na, decrease IVV (so higher plasma [creat]/[urea], Haemoconcentration (leads to increase plasma [Na], increase is plasma osmolality) 1. Increase in plasma osmolality - -> Increase ADH - -> Increase urine osmolality U&E: - Increase plasma [Na} - Increase plasma [urea] - High plasma [glucose]
27
Potassium reference range?
3.6 to 5.0 mmol/L
28
Low or high potassium values can cause?
Cardiac conduction defects | Abnormal neuromuscular excitability
29
How is plasma K effected by exchange of plasma between the ICF and ECF?
Acid-base status Insulin/glucose therapy Adrenaline Rapid cellular incorporation- TPN, leukaemia
30
Where is most of the potassium in the body?
In the intracellular fluid
31
Relationship of potassium to hydrogen ions?
• K+ and H+ exchange across cell membrane • Both bind to negatively charged proteins (eg Hb) • 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
32
Causes of hyperkalaemia?
• Artefactual – Delay in sample analysis – Haemolysis – Drugtherapy-Excessintake • Renal – Acute Renal Failure – ChronicRenalFailure • Acidosis (intracellular exchange) • Mineralocorticoid Dysfunction – Adrenocorticalfailure – Mineralocorticoid resistance - eg spironolactone • Cell Death – Cytoxic therapy
33
Treatment of hyperkalaemia
• Correct acidosis if this is cause • Stop unnecessary supplements / intake • Give Glucose & insulin (Drives potassium into cells) • Ion exchange resins (GIT potassium binding) • Dialysis – short and long-term
34
Causes of potassium depletion?
Low intake Increase urine loss – diuretics / osmotic diuresis – tubular dysfunction – mineralocorticoid excess GIT losses – vomiting – diarrhoea / laxatives – fistulae Hypokalaemia without depletion – alkalosis – insulin/glucosetherapy.
35
Effects of potassium depletion?
Acute changes to ICF/ECF ratios: -Neuromuscular effects: Lethargy, muscle weakness, heart arryhythmias Chronic losses from the ICF: - Neuromuscular effects: Lethargy, muscle weakness, heart arryhythmias - Kidney: Polyuria, alkalosis - Vascular - Gut
36
Detection of potassium depletion?
HISTORY: – diarrhoea, vomiting, drugs (diuretics, digoxin) – symptoms of lethargy / weakness – cardiac arrythmias ELECTROLYTES INVESTIGATION: – hypokalaemia – alkalosis-raised HCO3
37
Treatment of potassium depletion?
Prevention: Adequate supplementation Replacement of deficit via oral and IV route Monitor plasma potassium regularly especially during: - Diuretic therapy - Digoxin use - Compromised renal function - In support of IV resuscitation