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Clinical Biochemistry > Investigations of Salt & Water and Acid/Base Balance > Flashcards

Investigations of Salt & Water and Acid/Base Balance Flashcards

1
Q

How much water does our body contain?

A

Total body fluids = 60% of body weight

ECF: 20%
ICF: 40%
- Interstitial: 15%
- Intravascular: 5%
- Transcellular: 1%
- Connective tissue: <1%
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2
Q

How is Water and Na+ balance determined?

A

By input and output of both

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3
Q

What are the main intake methods of Na+ and water?

A

Water Intake: Dietary intake (Thirst)

Na+ intake: Dietary (Western diet 100-200 mmol/day)

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4
Q

What are the obligatory water losses causing water output?

A

Obligatory losses

  • Skin (sweat)
  • Lungs (breath)
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5
Q

What are the controlled water losses

A

Controlled losses depend on:

  • Renal function
  • Vasopressin/ADH (antidiuretic hormone)
  • Gut (main role of the colon)
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6
Q

What are the obligatory Na+ losses

A

Obligatory loss

- Skin (sweat)

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7
Q

Describe the controlled Na+ losses

A

Controlled losses / excretion

  • Kidneys
  • Mineralocorticosteroid Aldosterone
  • GFR
  • Gut - most sodium is reabsorbed; loss is pathological
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8
Q

How does redistribution occur in order to maintain Na+ and water balance?

A

determined by intravascular volume

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9
Q

How does aldosterone effect Na+ balance?

A

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

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10
Q

What is the role of natriuretic hormones in Na+ balance?

A

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

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11
Q

How does ADH maintain water balance?

A

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

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12
Q

What is the role of aquaporins in water balance?

A

Aquaporins (AQP1 proximal tubule and not under control of ADP) AQP2 and 3 present in collecting duct and under control of ADH

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13
Q

What hormones help maintain Na+/water balance?

A

Na+

  • Aldosterone
  • ANP/BNP

Water

  • ADH/vasopressin
  • AQP1/2/3
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14
Q

What is the effect of osmotic pressure on water movement?

A

Water moves from a high Ψ to low Ψ

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15
Q

How does osmotic potential control water movement in blood?

A

Osmotically active substances in blood may result in water redistribution to maintain osmotic balance but cause changes in other measured solutes

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16
Q

What processes occur in response to water loss

A

Water loss = inc. ECF osmolality

  1. ADH release stimulated
    = renal water retention
  2. Hypothalamic thirst centre
    = inc. water intake
  3. water redistribution from ICF
    = inc. ECF water

Restoration of ECF osmolality

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17
Q

Which members of population are more susceptible to dehydration?

A

Dehydration common in elderly and v. young babies who can’t access water themselves

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18
Q

Describe what happens to Na+ in renal tubules

A

GFR ~95-98% of Na+ filtered by glomeruli undergoes obligatory reabsorption driven by renal perfusion

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19
Q

Where in the renal tubules is Na+ mainyl reabsorbed?

A

Most Na+ reabsorbed in proximal tubule

Distal tubule reabsorption due to aldosterone

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20
Q

Where does ADH produce its reabsorption effects?

A

ADH stimulates water reabsorption from the collecting duct

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21
Q

Outline the aldosterone mechanism in hypertension / Na+ depletion

A
  1. Juxtaglomerular cells produce renin
  2. Renin = conversion of angiotensinogen → angiotensin I
  3. Angiotensin I circulates body and (in lungs) ACE (angiotensin-converting enzyme) converts into angiotensin
  4. Angiotensin stimulates adrenal cortex to produce aldosterone

Helps maintain our circulating volume

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22
Q

How can we measure the osmometry of Na+?

A

Freezing point depression

Uses colligative properties of a solution

> More solute (Salt) – lower the freezing point

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23
Q

How can we measure electrolytes such as Na+?

A
  • Indirect Ion selective electrodes (main lab analysers)

- Direct Ion selective electrodes (Blood gas analyser) - measure concentrations rather than ion activity

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24
Q

What is hypernatraemia?

A

Increased water loss and sodium gain

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25
Q

What is hyponatraemia?

A

Increased sodium loss and water gain

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26
Q

How do we assess a possible fluid / electrolyte disturbance?

A
  1. history
  2. Examination
  3. Fluid chart
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27
Q

What should a patient history determine?

A

Fluid intake / output
Vomiting/diarrhoea
Past history
Medication

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28
Q

What examination can be done on a patient with NA+/water imbalance?

A

Assess volume status

  • Lying and standing BP
  • Pulse
  • Oedema
  • Skin turgor/Tongue
  • JVP / CVP
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29
Q

What risks should we consider before treating hyper/hyponatraemia?

A

Hyponatraemia
- Over-rapid correction may lead to central pontine myelinolysis (shrinkage)

Hypernatraemia
- Over rapid correction may lead to cerebral oedema (expansion)

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30
Q

How can we overcome the potential life damaging risks of treating Na+ imbalance?

A

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

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31
Q

What are important lab investigations for Na+/water imbalance?

A
  • Paired serum + urine osmolality and electrolytes
  • Urea/creatinine ratio = inc. Urea = dehydration
  • Serum osmolality
    = Indicates presence of other osmotically active
    substances

Urinary sodium – ignore reference interval
<20 mmol/L = conservation
>20 mmol/L = loss

Urinary osmolality - ignore reference interval
Relate to serum osmolality

Urine /serum osmolality
>1 = water conservation
< 1 = water loss

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32
Q

What is hypovolaemia?

A

Hypovolaemic - Low BP due to low circulating volume of blood, Na+ &/or water

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33
Q

What is menat byeuvolaemic?

A

Euvolemic - normal Na+ and bodily fluid stores and normal BP

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34
Q

What is hypervolaemia?

A

Hypervolemic - excess fluids (blood, water etc.)

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35
Q

What mechanisms are in place to determine Na+ balance?

A
  • Baroreceptors = Blood pressure/volume sensed
  • Renal perfusion pressure = Aldosterone produced
  • Adrenal cortex = Action at DCT
  • Sodium reabsorption = Loss of H+/K+

(reference range 133-145 mmol/L)
(Life threatening range <115 >160 mmol/L)

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36
Q

What causes build up of H+ in the body?

A

Large amounts of protons/hydrogen ions are an inevitable by-product of energy/ATP production

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37
Q

Why do we need to regulate H+ levels in the body?

A

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

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38
Q

What is H+ balance dependent upon?

A

Balance depends on relative balance between acid production and excretion

  • carbon dioxide production + excretion (respiration)
  • hydrogen ion production + excretion (renal)
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39
Q

What are the threats to normal pH?

A

Carbonic acid = from burning carbohydrates (CO₂)

Non-Carbonic acids = from metabolising amino acids

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40
Q

How is H+ balance restored?

A

Majority of CO₂ removed via lungs

H+ excreted mainly through kidneys

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41
Q

Outline the pH calcualtion

A

pH = -log10[H+] or pH = log101/[H+]

pH from 7.4-7.1
[H+] 40-80
ie [H+] doubled for pH fall of 0.3

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42
Q

What is metabolic alkalosis?

A

Rate of H+ generation > excretion

[H+] increases, pH falls - acidosis

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43
Q

How is normal pH restored from metabolic alkalosis?

A

To restore normal neutral:

  • Buffer consumption of HCO₃⁻
  • CO₂ removal (kussmaul respiration)
44
Q

What is respiratory acidosis?

A

Rate of CO₂ excretion < generation
CO₂ increase ⇒ [H+] increase
pH falls = acidosis

45
Q

How is respiratory acidosis resolved?

A

There is increased CO₂ retention which can only be converted into HCO₃⁻ via normal renal function

46
Q

Why does compensation occur?

A

Attempt to return acid / base status to normal

47
Q

What are the body’s methods of compensating?

A
  1. Buffering
  2. Compensation
  3. Treatment
48
Q

Outline how the body buffers changes in acid base balance

A
  • Bicarbonate buffer in serum, phosphate in urine (for excretion)
  • Skeleton
  • Intracellular accumulation/loss of H+ ions in exchange for K+ , proteins and phosphate act as buffers
49
Q

Outline the compnestaion techniques in the body

A
  • Diametric opposite of original abnormality
  • Never overcompensates
  • Delayed and limited
50
Q

What treatment is there for loss of acid base balance?

A

Reversal of precipitating situation

51
Q

How quickly does respiratory compensation occur?

A

Respiratory compensation for a primary metabolic disturbance can occur very rapidly

Kussmaul breathing (respiratory alkalosis) in response to DKA

52
Q

How fast is metabolic compensation?

A

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

53
Q

Why is metabolic compensation slower?

A

requires enzyme induction from increased genetic transcription and translation etc

54
Q

Why does metabolic compensation not always occur?

A

No compensation seen in acute respiratory acidosis such as asthma
Requires more chronic scenario to include compensation mechanism

55
Q

Where is bicarbonate produced in the kidneys?

A

Bicarbonate produced in 2 places:

  • renal lumen
  • renal tubular cells
56
Q

How does renal lumen restore acid base balance?

A

Renal lumen exchanges Na+/K+

K+ excreted in urine

57
Q

How do tubular cells regenerate bicarbonate?

A

Tubular cell undergoes buffer mechanism
H₂O + CO₂ H₂CO₃

Water & carbon dioxide form carbonic acid which breaks down into hydrogen ions and bicarbonate
H₂CO₃ ⇆ HCO₃⁻ + H+

58
Q

How is bicarbonate regenerated in kidneys?

A

In the proximal renal lumen bicarbonate is reclaimed, and in the distal tubular cells, bicarbonate is regenerated and H+ ions are removed

59
Q

Why is H+ and K+ unable to be excreted at the same time?

A

H+ and K+ removal can’t occur simultaneously due to electrochemical imbalance - only occurs one at a time

60
Q

What are the pitfalls of using 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
61
Q

How do errors in ABG analysis arise?

A

Errors in blood gas analysis are dependent more on the clinician than on the analyser

62
Q

How do we interpret ABG results?

A

pO2 remember to check FiO2

pH – Normal or does it show an acidosis or alkalosis

pCO2 – primary respiratory or compensatory response

HCO3 – metabolic component (calculated using Henderson-Hasselbach)

63
Q

What causes respiratory acidosis?

A

Retention of Carbon dioxide may be due to:

  • Airway obstruction
  • Respiratory centre depression
  • Extrapulmonary thoracic disease: flail chest
  • Pulmonary disease
  • Neuromuscular disease
64
Q

What airway obstructions lead to respiratory acidosis?

A

Airway obstructions include:

  • Bronchospasm (Acute)
  • COPD (Chronic)
  • Aspiration
  • Strangulation
65
Q

What causes respiratory centre depression leading to respiratory acidosis?

A
  • Anaesthetics
  • Sedatives
  • Cerebral trauma
  • Tumours
66
Q

What neuro-muscular diseases lead to respiratory acidosis?

A

Guillain-Barre Syndrome

Motor Neurone Disease

67
Q

What aspects of pulmonary disease can lead to acidosis?

A
  • Pulmonary fibrosis
  • Respiratory Distress Syndrome
  • Pneumonia
68
Q

Describe respiratory acidosis compensation

A

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

Correction - Requires return of normal gas exchange

69
Q

Describe features of acute and chronic resp. acidosis

A

Acute:
🡻pH (🡹[H+]),
🡹pCO2,
🡺[HCO3-],– ie. no compensation

Chronic:
🡻pH (🡹[H+]),
🡹pCO2,
🡹[HCO3-],– ie. compensation

70
Q

Outline the condition of the following patient:
21 y/o male

RTA (road traffic accident) flail chest
Low pO2 - pt can’t oxygenate properly
Low pH = acidic and raised CO2
Normal HCO3 - not compensating

A

Uncompensated acute respiratory acidosis +impaired oxygenation

71
Q

What is a flail chest?

A

Flail chest - broken ribs front & back

72
Q

How does the body compensate for respiratory alkalosis?

A

Compensation - Increased renal bicarbonate excretion (metabolic acidosis, 36-72 hrs delay)
Correction - Of cause

73
Q

Outline acute and chronic resp. alkalosis

A

Acute:
high pH
low [H+], n[HCO3-]
low pCO2 – no compensation

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

74
Q

What causes respiratory alkalosis?

A

Low pCO2 – excess removal of carbon dioxide

75
Q

What conditions lead to resp alkalosis?

A
  • Hypoxia
  • Pulmonary disease
  • Mechanical overventilation
  • Increased respiratory drive
76
Q

What may cause an increased respiratory drive?

A 
Respiratory stimulants > eg. salicylates
Cerebral disturbance > eg. trauma, infection and tumours
Hepatic failure
G-ve septicaemia
Primary hyperventilation syndrome
Voluntary hyperventilation
77
Q

What causes hypoxia?

A
  • High altitude
  • Severe anaemia
  • Pulmonary disease
78
Q

What causes pulmonary disease?

A

Pulmonary oedema

Pulmonary embolism

79
Q

A Student volunteered to have arterial blood sample taken, but became increasingly anxious and had tingling in fingers and toes
Patient began hyperventilating ⇒ excessive CO2 removal
High pH = alkalotic
Normal HCO3 - not compensating

What condition has the following patient developed?

A

Uncompensated acute respiratory alkalosis

Tingling sensation due to low [H]+ ions (alkalotic) - albumin proteins buffer a lot of H+ ions

Albumin also has bound Ca2+
⇒ H+ ions come off albumin, and more Ca2+ is bound, so to compensate Ca2+ is dropped from albumin causing tingling

80
Q

What are the causes of metabolic acidosis?

A

Increased addition of acid

  • Increased H+ formation
  • Acid ingestion

Decreased H+ excretion

  • decreased H+ excretion
  • loss of bicarbonate
81
Q

How do we get increased H+ forming?

A
  • Ketoacidosis
  • Lactic acidosis
  • Poisoning – methanol, ethanol, ethylene glycol, salicylate
  • Inherited organic acidosis
82
Q

How can acid ingetsion occur?

A

Acid poisoning

XS parenteral administration of amino acids eg arginine

83
Q

What causes decreased H+ excretion?

A
  • Renal tubular acidosis
  • Renal failure
  • Carbonic dehydratase inhibitors
84
Q

What conditions lead to a loss of bicarbonate?

A

Diarrhoea

Pancreatic, intestinal or biliary fistulae/drainage

85
Q

How is metabolic acidosis comepnsated for

A

Compensation - hyperventilation, hence low pCO2

Correction - of cause, increased renal acid excretion

86
Q

Outline the features of metabolic acidosis

A

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

87
Q

Diagnose the following:

17 year old male – Type 1 diabetes – not taken insulin for 24 hours

Low pH = acidotic
Low HCO3

A

Uncompensated acute metabolic acidosis

88
Q

What are the common causes of metabolic alkalosis?

A
  • Increased addition of base
  • Increased loss of acid
  • Decreased elimination of base
89
Q

How does base addition increase to a pathological level?

A

Inappropriate Rx of acidotic states

Chronic alkali ingestion

90
Q

Describe the causes of acid loss through GI

A

Gastric aspiration

Vomiting with pyloric stenosis

91
Q

How is acid lost through the kidneys?

A
  • Diuretic Rx (not-K+sparing)
  • Potassium depletion
  • Mineralocorticoid excess- Cushing’s, Conn’s
  • Drugs with mineralocorticoid activity – carbenoxolon
92
Q

Describe the compensation mechanism for metabolic alkalosis

A

Compensation - hypoventilation with CO2 retention (respiratory acidosis)

Correction - increased renal bicarbonate excretion, reduce renal proton loss

93
Q

Outline the features of metabolic alkalosis

A

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

94
Q

What condition does a 56 year old female – vomiting last 48 hours with High pH = alkalotic and High HCO3 - not compensating have?

A

Uncompensated acute metabolic alkalosis

95
Q

How can metabolic alkalosis arise due to hypovolemia?

A

Hypovolaemia from persistent vomiting

  • Loss of HCl
  • Loss of potassium
  • Loss of fluid
96
Q

How do diuretics lead to metabolic alkalosis?

A

Chronic K+ depletion

97
Q

How does the body respond to fluid loss?

A

Response to fluid loss is aldosterone activation

Reabsorb NaCl/H2O at distal convoluted tubule in kidney in exchange for K+ /H+

98
Q

Summarise resp acidosis

A

CO2 retention

Compensation is metabolic alkalosis

99
Q

Summarise respiratory alkalosis

A

increased CO2 loss

Compensation is metabolic acidosis

100
Q

Summarise metabolic alkalosis

A

Very difficult primary disturbance to produce and maintain in proton producers!

(Very specific factors required) - need to switch off RAAS via antiemetics and fluids to replace ciruclating volume

Compensation – respiratory acidosis

101
Q

Summarise metabolic acidosis

A

Acid ingestion
Increases acid production
Reduced acid excretion
Compensation respiratory alkalosis

102
Q

How does hyperkalaemia arise?

A

Acidosis usually associated with hyperkalemia as more significant to remove H+ than K+ ⇒ K+ build up

103
Q

What is hypokalaemia?

A

excess k+ loss associated with alkalosis

104
Q

Describe regular K+ redistribution in the body

A

K+ redistributes between ICF and ECF very rapidly

105
Q

When does artifactual hyperkalaemia occur?

A

Artifactual hyperkalemia usually when patients take K+ into wrong tube or contaminated with K+ EDTA

Clinical Biochemistry (7 decks)

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