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SEM 4: Clinical Biochemistry > Investigation of Salt & Water and Acid/Base Balance > Flashcards

Investigation of Salt & Water and Acid/Base Balance Flashcards

1
Q

Total body fluids weight?

  • Extracellular fluid compartment
    - Interstitial
    - Intravascular
    - Transcellular
    - H2O in connective tissue
  • Intracellular fluid compartment
A

60% of body weight

  • 20%
    • 15%
    • 5%
    • 1%
    • <1%
  • 40%
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2
Q

What determines the water and sodium balance?

A
  • Intakes and Output of Water and Sodium

- Redistribution of water

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3
Q

Water intake

A

Dietary intake (Thirst)

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4
Q

Water output

A

Obligatory losses
- Skin
- Lungs - lose water when cold
Controlled losses - these depend on:
- Renal function
- Vasopressin/ADH - controls loss of water from kidneys
- Gut - the main role of the colon: lots of water secreted into gut then reabsorbed.

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5
Q

Sodium intake

A
  • Dietary (unless vegan and doesn’t add salt)
  • Western diet 100-200 mmol/day
    Encouraged to take less salt a day
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6
Q

Sodium output

A

Obligatory loss
- Skin: lose water during the day due to sweat
Controlled losses/excretion:
- Kidneys
- Aldosterone (mineralocorticoid)
- GFR
- Gut: most sodium is reabsorbed; unless lost pathologically.

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7
Q

Hormones that are involved in the balance of sodium (with water)

A
  • Aldosterone: produced in the adrenal cortex; regulates sodium and potassium homeostasis; if there is a disorder, it will have profound effects and the sodium levels of the body are affected.
  • Natriuretic hormones (ANP and BNP): promote sodium excretion and decrease blood pressure
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8
Q

Hormones that are involved in the balance of water (with sodium)

A
  • ADH/vasopressin: synthesized in the hypothalamus and stored in the posterior pituitary. release causes an increase in water absorption in collecting ducts
  • Aquaporins (AQP1 proximal tubule and not under the control of ADP) AQP2 and 3 in the collecting duct and under control of ADH
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9
Q

Osmotic pressure and water movement

A

Water moves across a semi-permeable membrane from a low osmolality to a high osmolality down a concentration gradient.
Osmotically active substances in the blood may result in water redistribution to maintain osmotic balance but cause changes in other measured solutes.

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10
Q

3 Physiological responses to water loss

A
  1. a) Low water triggers the release of vasopressin
    b) There is an increase in osmolality which triggers the brain
    c) This increases water intake
  2. ADH increases water absorption: most is reabsorbed in the kidneys and is dependent on the filtering rate of the kidneys
  3. Aldosterone mechanism that is dependent on the perfusion rate of the kidney
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11
Q

Where is most sodium reabsorbed?

A

In the kidney

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12
Q

The mechanism for a person with hypertension

A
  1. Positive action on the juxtaglomerular cells in the kidney.
  2. Renin is activated and converts angiotensinogen into angiotensin I then ACE converts into angiotensin 2 in the lungs
  3. Then this increases the release of aldosterone which affects the sodium levels.
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13
Q

Osmometry

A
  • Used to see if someone has taken alcohol
  • Freezing point depression is measured
    • > If more salt = lower freezing point
    • > Also vapor pressure ones, however, cannot be used to measure volatile substances
    • > Uses colligative properties of a solution
    • > More solute - lower the freezing point
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14
Q

What types of electrodes can be used to measure Sodium levels?

A
  • Indirect ion-selective electrodes (main lab analyzers): dilution of the sample that enters the electrode and gets a result coming out
  • Direct ion-selective electrodes (blood gas analyzers): measures activity of ions rather than concentration
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15
Q

Hypernatraemia

A

More water loss, more sodium gain

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16
Q

Hyponatraemia

A

More water gain, more sodium loss

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17
Q

Normal sodium

A

Water loss and Sodium Loss; Water gain and Sodium gain

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18
Q

How to assess a patient with possible fluid/electrolyte disturbance?

A
  • History of: fluid intake/output; vomiting/diarrhoea; past history; medication
  • Examination - Assess volume status: lying and standing BP; pulse; oedema; Skin turgor/Tongue; JVP/CVP
  • Fluid chart
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19
Q

What can over-rapid correction of hyponatremia cause?

A

Over-rapid correction may lead to central pontine myelinolysis (brain shrinks)

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20
Q

What can over-rapid correction of hypernatraemia cause?

A

Over-rapid correction may lead to cerebral oedema

- Limited scope, therefore, if it expands rapidly it could cause a lot of damage.

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21
Q

Why is it important to correct sodium at the same speed?

A

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

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22
Q

What investigations are used to look at serum and urine osmolality and electrolytes?

A
  • Urea/creatinine ratio is useful
  • Serum osmolality: indicates if other osmotically active substances are present
  • Urinary sodium: < 20 mmol/L and > 20 mmol/L -> switch off sodium excretion to conserve
  • Urinary osmolality: relates to serum osmolality -> concentrated urine -> water conservation
  • Urine/serum osmolaltiy: >1 = water conservation and < 1 = water loss -> indicates if other osmotically active substances are present.
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23
Q

When is calculated serum osmolality used?

A

Only useful if you think something else is present
= 2 x Na + urea + glucose (+/- 10)
290 = (2 x 140 = 280) + 5 + 5

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24
Q

Hypertonic hyponatremia

A

High glucose

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25
Q

Pseudohyponatraemia

A

High triglycerides and high protein

- Looks like cream and lots of protein if someone has a myeloma

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26
Q

Hypotonic hyponatremia

A

Volume status

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27
Q

Hypovolaemic

A
  • Low circulating volume = low BP
28
Q

What happens if salt is below 20mM?

A

Look at urine sodium and if salt is below 20mM then there is extra-renal salt loss - can be through GI loss - vomiting, diarrhea, skin loss burns, sweating and haemorrhage

29
Q

Euvolemic

A

Normal circulating volume + normal BP

  • Below 20 mM: - acute water overload, excess intake; due to psychogenic polydipsia, a beer that is weak, polomania and ketogenic
  • Above 20 mM: - due to chronic water overload - impaired excretion; no water loss - SIADH when producing vasopressin/ADH is appropriate, can also have hypothyroid and glucocorticoid deficiency
30
Q

What happens if sodium levels are above 20mM?

A
  • Then there is a renal salt loss.

- Addison’s disease: where you cannot produce cortisol, aldosterone and taking diuretics

31
Q

What senses blood pressure/volume?

A
  • Baroreceptors and renal perfusion pressure
32
Q

What produces aldosterone?

A

Adrenal cortex

33
Q

Action at DCT

A

Sodium reabsorption

Loss of H+/K+

34
Q

What is a byproduct of energy/ATP production?

A

Large amounts of protons/hydrogen ions are an inevitable by-product. The body controls our blood levels at nanomolar amounts however, we produce millimolar amounts protons.

35
Q

What is needed to maintain protein/enzyme function?

A

Maintained by extracellular [H+]/pH

  • depends on the relative balance between acid production and excretion.
  • dependent on how much acid you produce and how much acid you are able to excrete.
    • > Carbon dioxide production and excretion (respiration)
    • > Hydrogen ion production and excretion (renal)
36
Q

What are some threats to the normal pH level?

A

H+ production:

  • Carbonic acid (volatile) 15,000 mmol/Day
  • Non-carbonic acids (non-volatile) 80 mmol/Day

H+ excretion:

  • 15,000 mmol/Day from the lungs
  • 80 mmol/Day from the kidneys

Make sure the extracellular fluid is 40 nmol/L and the pH is 7.4

37
Q

pH and [H+]

A

The higer the pH; the lower the hydrogen ion concentration.
- pH is proportional to the carbonic acid
pH =-log10[H+]

38
Q

Henderson Hasselbalch equation

A

Say it - google it

39
Q

Metabolic acidosis

A
  • Rate of H+ generation is more than excretion
  • Buffering - consumption of HCO3 should be reduced
  • Removal of CO2
40
Q

Respiratory acidosis

A
  • Rate of CO2 excretion is less than the generation
  • Increased retention of CO2
  • Increased renal excretion of H+ and regenerate HCO3
41
Q

What is compensation?

A

Attempt to return acid/base status to normal

42
Q

Buffering

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
  • Someone who has renal failure will take up H+ into the skeleton
43
Q

Compensation

A
  • Diametric opposite of original abnormality
  • Never overcompensates
  • Delayed and limited -> takes time as you need to replenish proteins through transcription and translation
44
Q

Treatment

A
  • By reversal of the precipitating situation

- If you have metabolic acidosis, compensate by developing respiratory alkalosis

45
Q

Respiratory compensation

A

For a primary metabolic disturbance can occur very rapidly

- Kussmaul breathing (respiratory alkalosis) in response to DKA

46
Q

Metabolic compensation

A

For primary respiratory abnormalities takes 36-72 hours to occur

  • Requires enzyme induction from increased genetic transcription and translation etc
  • No compensation see in acute respiratory acidosis such as asthma
  • Requires more chronic scenario to include compensation mechanism
47
Q

Mechanism of renal bicarbonate regeneration

A
  1. Takes place at the renal lumen - exchanges sodium for potassium
  2. The potassium is switched off into the urine.
  3. The buffer system - water and CO2 produces carbonic acid which will break down to hydrogen ions and bicarbonate.
  4. Depending on which part of the kidney:
    • > proximal tubule - reclaiming part of the bicarbonate
    • > distal tubule - regenerate bicarbonate
  5. The H+ is removed from the kidneys:
    • > When removing H+, you can’t remove potassium as well.
    • > Need electrical neutrality across the membrane; therefore either lose hydrogen or potassium.
  6. There is a reuptake of sodium and hydrogen is then lost.
48
Q

How long does a blood gas machine run for and what is it used for?

A

Used for ABG readings and can run for 2 hours on a battery pack

49
Q

Modulator of the blood gas machine

A

Blood gas components can measure sodium, potassium, creatinine, glucose, and iron etc.

50
Q

How to carry out a blood gas reading?

A
  • Expel air
  • Mix sample
  • Analyse ASAP
  • Plastic syringes OK at room temp for 30 mins
  • Ice is not required
  • Ensure no clot in syringe tip
51
Q

Pitfalls of ABG

A

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

52
Q

How to interpret ABG readings?

A
  • PO2 remember to check F1O2 -> influence the partial pressure concentration
  • pH - Normal or does it show an acidosis or alkalosis
  • PCO2 - primary respiratory or compensatory response
  • HCO3 - metabolic component: calculated by using the H-H equation
53
Q

Causes of respiratory acidosis through CO2 retention

A

Airway obstruction:

  • Bronchospasm (Acute)
  • COPD (chronic)
  • Aspiration
  • Strangulation

Respiratory centre depression:

  • Anaesthetics
  • Sedatives
  • Cerebral trauma
  • Tumours

Neuromuscular disease:

  • Guillain-Bare syndrome
  • Motor neurone disease

Pulmonary disease:

  • Pulmonary fibrosis
  • Respiratory distress syndrome
  • Pneumonia

Extrapulmonary thoracic disease
- Flail chest

54
Q

Compensation, Correction, and Features of Respiratory acidosis

A

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

Correction:
- Requires return of normal gas exchange

Features:
- Acute: decrease in pH (increase in [H+]), increase in pCO2, no change [HCO3-], i.e. no compensation
- Chronic: decrease in pH (increase in [H+]), increase in pCO2, increase in [HCO3-], i.e. compensation
There is only an increase in bicarbonate when you have compensation

55
Q

Causes of respiratory alkalosis: low pCO2 removing carbon dioxide

A

Hypoxia:

  • High altitude
  • Severe anaemia
  • Pulmonary disease

Pulmonary disease:

  • Pulmonary oedema
  • Pulmonary embolism

Mechanical overventilation

Increased respiratory drive:

  • Respiratory stimulants e.g. salicylates
  • Cerebral disturbance e.g. trauma, infection and tumours
  • Hepatic failure
  • G -ve septicaemia
  • Primary hyperventilation syndrome
  • Voluntary hyperventilation
56
Q

Compensation, correction, and features of Respiratory alkalosis

A

Compensation:
- Increased renal bicarbonate excretion (metabolic acidosis, 36-72 hrs delay)

Correction:
- Of cause

Features:

  • Acute: high pH, low [H+], n[HCO3-], low pCO2 - no compensation
  • Chronic: high pH, low [H+], low [HCO3-], low pCO2 - compensation
57
Q

Causes of metabolic acidosis: increased addition of acid

A

Increased H+ formation:

  • Ketoacidosis
  • Lactic acidosis
  • Poisoning - methanol, ethanol, ethylene glycol, salicylate
  • Inherited organic acidosis

Acid ingestion:

  • Acid poisoning
  • XS parenteral administration of amino acids e.g. arginine
58
Q

Causes of metabolic acidosis: Decreased H+ excretion through the loss of bicarbonate

A
  • Renal tubular acidosis
  • Renal failure
  • Carbonic dehydratase inhibitors
  • Diarrhoea
  • Pancreatic, intestinal or biliary fistulae/drainage
59
Q

Compensation, Correction, and Features of Metabolic acidosis

A

Compensation:
- Hyperventilation, hence low pCO2

Correction:

  • Of cause
  • Increased renal acid excretion

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

60
Q

Causes of metabolic alkalosis

A

Increased addition of base:

  • Inappropriate Rx of acidotic states
  • Chronic alkali ingestion

Decreased elimination of base

Increased loss of acid:

  • GI loss
    • > Gastric aspiration
    • > Vomiting with pyloric stenosis: a lot can cause damage to the oesophagus and dissolve teeth

Renal:

  • Diuretic Rx (not K+ sparing)
  • Potassium depletion
  • Mineralocorticoid excess-Cushing’s, Conn’s
  • Drugs with mineralocorticoid activity - carbenoxolone
61
Q

Compensation, Correction, and Features of Metabolic alkalosis

A

Compensation:
- Hypoventilation with Co2 retention (respiratory acidosis)
Correction:
- Increased renal bicarbonate excretion
- Reduce renal proton loss
Features:
- high pH, low [H+], high [HCO3-], N/high pCO2

62
Q

Hypovolaemia from persistent vomiting - Metabolic alkalosis

A

Metabolic alkalosis

  • Loss of HCl
  • Loss of potassium
  • Loss of fluid stimulates the RAAS system
  • Try to reabsorb Na+ and water in exchange for potassium and H+ ions
63
Q

Diuretics - Metabolic alkalosis

A

Chronic K+ depletion

64
Q

Response to fluid loss is aldosterone activation - Metabolic alkalosis

A

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

65
Q

Why is it important to get rid of the hydrogen ions instead of the potassium ions?

A

To have:

  • Redistribution: the potassium will redistribute between the intracellular and the extracellular fluid rapidly - will cause acidosis.
  • This will cause artefactual hyperkalaemia.
66
Q

Artefactual hyperkalaemia

A

False hyperkalaemia

SEM 4: Clinical Biochemistry (7 decks)

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