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Clinical biochemistry > Investigation of salt/water and acid/base balance > Flashcards

Investigation of salt/water and acid/base balance Flashcards

1
Q

What percentage of body weight is body fluids?

A

Total body fluids = 60% of body weight

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2
Q

What are obligatory losses of water?

A

§ Obligatory losses
□ Skin (sweat)
□ Lungs

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3
Q

What are controlled losses of water dependent on?

A

§ Controlled losses – these depend on:
□ Renal function
□ ADH
□ Gut (main role of colon)

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4
Q

What are the intakes of sodium?

A

○ Intake

□Dietary (unless vegan and doesn’t add salt)

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5
Q

What are obligatory losses of sodium?

A

§ Obligatory loss

-Skin

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6
Q

What are controlled losses/excretion of sodium?

A

§ Controlled losses/excretion
□ Kidneys
□ Aldosterone – fine controlling of Na balance
□ GFR
□ Gut – most sodium is reabsorbed; loss is pathological

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7
Q

Where is aldosterone produced and what does it regulate?

A

Aldosterone produced in the adrenal cortex: regulates sodium and potassium homeostasis and hydrogen ion balance

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8
Q

What do natriuretic hormones promote and decrease?

A

○ Natriuretic hormones (ANP cardiac atria, BNP cardiac ventricles) promote sodium excretion and decrease blood pressure

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9
Q

Where is ADH/Vasopressin synthesised in and what does its release cause?

A

ADH/vasopressin: synthesised in hypothalamus and stored in posterior pituitary. Release causes increase in water absorption in collecting ducts

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10
Q

Where is AQP1(Aquaporin 1) located and not under the control of?

A

Located on the proximal tube

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11
Q

Where are AQP2 and 3 present and what are they under the control of?

A

AQP2 and 3 present in collecting duct and under control of ADH

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12
Q

What is the response to increased ECF osmolality due to water loss?

A

○ Stimulation of vasopressin release causing renal water retention allowing the restoration ECF osmolality
○ Stimulation of hypothalamic thirst centre which leads to increased water intake allowing restoration of ECF osmolality
○ Redistribution of water from ICF which leads to increased ECF water allowing the restoration of ECF osmolality

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13
Q

Where is 85% of Na reabsorbed in renal tubules?

A

85% Na is reabsorbed in PCT

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14
Q

What is fine tuning of Na reabsorption under the influence of?

A

Fine tuning of Na reabsorption under influence of aldosterone in exchange for hydrogen and potassium ions

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15
Q

What does the kidney sense and so what signal does it send and cause the release of what?

A

• Kidney senses reduced perfusion so sends signal from adrenal cortex to release renin

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16
Q

What does renin convert angiotensin into and what does it cause?

A

• Renin converts angiotensinogen to angiotensin I in lungs
○ This goes back to adrenal cortex to stimulate aldosterone from adrenal cortex
○ Signal to start reabsorbing more Na

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17
Q

What converts angiotensin I into angiotensin II?

A

• Angiotensin I is converted to Angiotensin II by ACE

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18
Q

What does dehydration mean?

A

Dehydration means less water perfusing the kidney

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19
Q

How is there a difference in handling of urea and creatinine in dehydration?

A

○ Creatinine is excreted
○ Urea, if perfusion rate drops, starts being reabsorbed in kidney
- Mismatch between urea and creatinine

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20
Q

What would happen to the Na, urea and creatinine levels in psychogenic polydipsia?

A

They would be low

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21
Q

BP in psychogenic polydipsia

A

Normal

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22
Q

Why is there low urine sodium in psychogenic polydipsia?

A

Low urine sodium because too much water so kidney needs to reabsorb all sodium to match the water intake

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23
Q

What happens if you drop your Na really quickly?

A

• If you drop your Na really quickly, can get violent and aggressive

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24
Q

What history do you take when assessing patients with fluid/electrolyte disturbance?

A 
○ Fluid intake/output
○ Vomiting/diarrhoea
○ Past history
○ Medication
     -Drugs that may predispose them to imbalances in Na
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25
Q

What examinations do you take when assessing patients with fluid/electrolyte disturbance?

A 
○ Lying and standing BP
○ Pulse
○ Oedema
○ Skin turgor/tongue dryness
○ JVP/CVP
      -BP monitors
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26
Q

What can over rapid correction in hyponatremia lead to?

A

○ Over rapid correction may lead to central pontine myelinolysis

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27
Q

What can over rapid correction in hypernatremia lead to?

A

○ Over rapid correction may lead to cerebral oedema

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28
Q

What speed is it important to correct sodium at?

A

Important to correct sodium at the same speed no more than 10mmol/L per 24 hours of sodium change

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29
Q

What does it mean if urea is significantly higher than creatinine?

A

○ Urea significantly higher than creatinine = dehydration

30
Q

What does a urinary sodium of <20mmol/L mean?

A

Conservation

31
Q

What does a urinary sodium of >20mmol/L mean?

32
Q

What does urine osmolality >1 mean?

A

Water conservation

33
Q

What does urine osmolality of <1 mean?

A

Water loss

34
Q

What are the common causes of hypernatraemia?

A

Dehydration, drugs containing Na

35
Q

What does hypertonic hyponatremia occur due to?

A

Occurs due to increased glucose

36
Q

What happens to levels in pseudohypoNa?

A

○ High TGs

○ High protein

37
Q

What layer is present on top of blood in pseudohypoNa?

A

○ Creamy layer on top of blood

38
Q

What do we measure if someone is hypovolemic in hypotonic hyponatraemia?

A

measure Na in urine
§ If conserving Na, Na is being lost somewhere else e.g. GI loss (vomiting, diarrhoea), skin loss, haemorrhage
§ High urine Na: loss through kidney

39
Q

What happens if urine Na is <20mM and the patient is euvolemic in hypotonic hyponatremia?

A

§ Urine Na: <20mM
□ Acute water overload
□ Psychogenic polydipsia

40
Q

What happens if urine Na is >20mM and the patient is euvolemic?

A

□ Chronic water overload
□ Impaired excretion
□ Hypothyroidism

41
Q

What happens if urine Na is <20mM and the patient is hypervolaemic?

A

□ Oedema
□ Cirrhosis
□ Cardiac failure
□ Nephrotic failure

42
Q

Why is maintenance of extracellular [H+]/pH essential?

A

Maintenance of extracellular [H+]/pH is essential to maintain protein/enzyme function

43
Q

What systems are involved in the maintenance of extracellular [H+]/pH?

A

○ Overall pH on the relative balance between acid production and excretion
○ Carbon dioxide production and excretion (respiration)
○ Hydrogen ion production and excretion (renal)

44
Q

Henderson Hasselbalch equation

A

Just derive and look at ppt slide

45
Q

What is metabolic acidosis?

A

Rate of H+ generation > excretion

46
Q

What is the compensation for metabolic acidosis?

A

○ Compensation is respiratory
§ Consumption of HCO3
§ Removal of CO2

47
Q

What is respiratory acidosis?

A

Rate of CO2 excretion < generation

48
Q

What is the compensation for respiratory acidosis?

A

○ Metabolic compensation
§ Increased renal excretion of H+
§ Regeneration of HCO3

49
Q

What is compensation?

A

• Attempt to return acid / base status to normal

50
Q

When can respiratory compensation for a primary metabolic disturbance occur?

A

Respiratory compensation for a primary metabolic disturbance can occur very rapidly

51
Q

How long does it take for metabolic compensation for primary respiratory abnormalities?

A

Metabolic compensation for primary respiratory abnormalities take 36-72 hours to occur

52
Q

What is the mechanism of renal bicarbonate regeneration?

A
  • HCO3 is reabsorbed in DCT
  • Na is taken up into cell in exchange for K
  • Lose hydrogen in preference to K because H is more toxic
53
Q

What are the pitfalls of ABG?

A
  • Expel air
  • Mix sample
  • Analyse ASAP
  • Plastic syringes OK at room temp for ̴ 30mins
  • Ice not required
  • Ensure no clot in syringe tip
54
Q

Interpretation of ABG

A
  • pO2 - remember to check FiO2
  • pH – Normal or does it show an acidosis/alkalosis
  • pCO2 – primary respiratory or compensatory response
  • HCO3 – metabolic component
55
Q

How do we obtain the HCO3 value?

A

Not measured, is calculated using Hendersson Hasselbalch

56
Q

Causes of respiratory acidosis

A 
• Airway obstruction
	○ Bronchospasm (Acute)
	○ COPD (Chronic)
	○ Aspiration
	○ Strangulation
• Respiratory centre depression
	○ Anaesthetics
	○ Sedatives
	○ Cerebral trauma
	○ Tumours 
• Neuromuscular disease
	○ Guillain-Barre Syndrome
	○ Motor Neurone Disease
• Pulmonary disease
	○ Pulmonary fibrosis
	○ Respiratory Distress Syndrome
	○ Pneumonia
• Extrapulmonary thoracic disease
        ○ Flail chest
57
Q

How do you compensate for respiratory acidosis?

A

Increased renal acid excretion (metabolic alkalosis, 36-72 hrs delay)

58
Q

What does correction of respiratory acidosis require?

A

○ Requires return of normal gas exchange

59
Q

What are the features of acute respiratory acidosis?

A

acute: increased pH (increased[H+]), increasedpCO2, –>[HCO3-],– ie. no compensation

60
Q

What are the features of chronic respiratory acidosis?

A

Decreased pH(Increased[H+]), Increased pCO2, increased[HCO3-], ie. compensation

61
Q

What are the causes of respiratory alkaolosis?

A
  • Hypoxia
  • Mechanical overventilation
  • Increased respiratory drive
62
Q

How do you compensate for respiratory alkalosis?

A

Increased renal bicarbonate excretion

63
Q

What are the features of acute respiratory alkalosis?

A

high pH, low [H+], n[HCO3-], low pCO2

64
Q

What are the features of chronic respiratory alkalosis?

A

high pH, low [H+], low [HCO3-], low pCO2

65
Q

How do you compensate metabolic acidosis?

A

hyperventilation, hence low pCO2

66
Q

How is there correction of metabolic acidosis?

A

• Correction
○ of cause
○ increased renal acid excretion

67
Q

What are the features of metabolic acidosis?

A

○ Low pH, high [H+], low [HCO3-], low pCO2

68
Q

What are the causes of metabolic alkalosis?

A
  • Increased addition of base
  • Decreased elimination of base
  • Increased loss of acid
  • GI loss
  • Renal
69
Q

How do you compensate for metabolic alkalosis?

A

• Compensation

-Hypoventilation with CO2 retention (respiratory acidosis)

70
Q

How is there correction of metabolic alkalosis?

A

○ Increased renal bicarbonate excretion

○ Reduce renal proton loss

71
Q

What are the features of metabolic alkalosis?

A

High pH, low [H+], high [HCO3-], N/highpCO2

72
Q

Clinical scenarios of metabolic alkaolosis

A 
• Hypovolaemia from persistent vomiting
	○ Loss of HCl
	○ Loss of potassium
	○ Loss of fluid
• Diuretics
	○ Chronic K+ depletion
• Response to fluid loss is aldosterone activation
	○ Reabsorb NaCl/H2O at distal convoluted tubule in kidney in exchange for K+ /H+

Clinical biochemistry (6 decks)

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