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Clinical pathology specialities: Clinical Biochemistry > Clinical Biochemistry: Investigation of Salt & Water and Acid/Base Balance > Flashcards

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

1
Q

What % of our body weight does our body fluids make up?

A
  • 60%
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2
Q

What are the 2 main body compartments where water is stored and what % of body weight do these compartments make up?

A
  • Extracellular fluid compartment - 20%
  • Intracellular fluid compartment - 40%
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3
Q

What is water balance determined by?

A
  • Intake
    • Dietary intake (thirst)
  • Output
    • Obligatory losses: Skin, lungs
    • Controlled losses which depend on: Renal function, Vasopression/ADH and the Gut (colon)
  • Redistribution
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4
Q

What is sodium balance determined by?

A
  • Intake
    • Dietary intake (unless vegan and doesn’t add salt)
    • Western diet contains around 100-200 mmol/day
  • Output
    • ​Obligatory loss: Skin
    • Controlled losses/excretion: Kidneys, Aldosterone, Glomerular filtration rate (GFR) and Gut - most sodium is reabsorbed; loss is pathological
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5
Q

What hormones are involved in maintianing sodium balance?

A
  • Aldosterone (produced in the adrenal cortex): Regulates sodium and potassium homeostasis
  • Natriuretic hormones (ANP cardiac atria, BNP cardiac ventricles): Promote sodium excretion and decrease blood pressure
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6
Q

What hormones are involved in maintianing water balance?

A
  • ADH/vasopressin (synthesised in hypothalamus and stored in posterior pituitary): Release causes increase in water absorption in collecting ducts of the kidney
  • Aquaporins
    • ​AQP1 present in proximal tubule and not under control of ADH
    • AQP2 and 3 present in collecting duct and under control of ADH
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7
Q

How does osmotic pressure affect water movement into and out of a cell?

A
  • If there is excess solute inside the cell then water will move from outside the cell to inside the cell to maintain balance. This causes the cell to swell (odema)
  • If there is excess soulte outside the cell the then water will move from inside the cell to outside the cell to maintian balance. This causes the cell to shrink
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8
Q

What are the body’s physiological responses to water loss?

A
  • Immediately after water loss the extracellular fluid (ECF) osmolarity increases
  • This causes vasopressin (ADH) to be released from the posterior pituitary
  • This leads to increased renal water retention
    • Increased ECF osmolarity also stimulates hypothalamic thirst centre
  • This leads to increased water intake
    • Increased ECF osmolarity also causes redistribution of water from extracellular fluid compartment to the intracellular fluid compartment
  • Increased renal water retention; Increased water intake and Increased Intracellular fluid level all lead to a restoration of the ECF osmolarity
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9
Q

Describe how sodium is reabsorbed back into the body

A
  • Most of the sodium is reabsorbed in the proximal tubule of the kidney
  • Some sodium is reabsorbed in the distal tubule under the influence of aldosterone
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10
Q

Explain how aldosterone-drive sodium reabsorption in the distal tubules is dependent on the perfusion of the kidneys

A
  • Hypotension or sodium depletion will have a positive affect on the juxtaglomerular cells of the kidney
  • These juxtaglomerular cells will then secrete renin into the bloodstream
  • Renin then converts angiotensinogen into angiotensin I
  • Angiotensin I then gets converted by angiotensin-converting enzyme (ACE) in the lungs to angiotensin II
  • Angiotensin II then stimulates the adrenal glands to produce aldosterone
  • Aldosterone will cause the reabsorption of sodium in the distal tubule of the kidney
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11
Q

How can you measure water levels in the body?

A
  • Osmometry
    • Freezing point depression: Uses colligative properties of a solution
    • The more solute there is in a liquid the lower its freezing point
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12
Q

How can you measure sodium levels in the body?

A
  • Measured via indirect ion selective electrodes (on main lab analysers) - dilution of sample goes into electrodes
  • Can also be measured by direct Ion selective electrodes (on Blood gas analyser) - measures activity of ions rather than concentrations
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13
Q

Use the information from the case study below to identify what is wrong with this patient

A
  • Patient has following symptoms:
    • High temperature (38.5°)
    • Dry tongue
    • High heart rate (90bpm)
    • Low blood pressure (100/60)
  • These all indicate clinically that this patient is dehydrated
  • The laboratory results show the patient has:
    • Elevated sodium (163mmol/L)
    • Slightly elevated potassium (3.9mmol/L)
    • Elevated urea (15.8mmol/L)
    • Elevated creatinine (140µmol/L)
    • Low eGFR, estimated glomerular filtration rate, (31 mL/min/1.73m)
  • All of these lab results also indicate the patient is dehydrated
  • Fact that increase in creatintine is lower than increase in urea especially indicates this because when a person is dehydrated some creatintine can be reabsorbed by tubules whereas this can’t occur with urea
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14
Q

Use the information from the case study below to answer the following questions:

  1. Is the patient euvolaemic, hypovolaemic or hypervolaemic?
  2. What is the underlying cause of the hyponatraemia (low sodium level)?
  3. What other laboratory tests might help you interpret the data and come to a conclusion?
A
  • Laboratory results show this patient has the following symptoms:
    • Very low sodium (106 mmol/L)
    • Low urea (3.2 mmol/L)
  1. Patient is euvolaemic - has normal blood fluid volume
  2. Patient is drinking so much water - she has psychogenic polydipsia (excessive fluid intake)
  3. Serum osmolality test; urine osmolality test and a urinary sodium test
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15
Q

Explain how the balance between sodium intake ans water intake affect sodium levels within the body

A
  • If you gain sodium and gain water then sodium levels will remain normal
  • If you lose both sodium and water then sodium levels will remain normal
  • If you lose sodium and gain water then sodium levels will decrease (hyponatraemia)
  • If you gain sodium and lose water then sodium levels will increase (hypernatraemia)
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16
Q

Describe how you could assess a patient with possible fluid/electrolyte disturbance

A
  • History
    • Fluid intake / output
    • Vomiting/diarrhoea
    • Past history
    • Medication
  • Examination - Assess volume status
    • ​Lying down and standing blood pressure
    • Pulse
    • Oedema
    • Skin turgor/Tongue
    • JVP (jugular venous pressure) / CVP (central venous pressure)
  • Fluid chart
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17
Q

Why is it important to manage fluid/electrolyte problems over the correct period of time - not too slow/too quickly?

A
  • Because over-rapid correction of hyponatraemia may lead to central pontine myelinolysis
  • Also, over-rapid correction of hypernatraemia may lead to cerebral oedema
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18
Q

For correction of both hypo/hypernatraemia it is important to correct sodium at the same speed, what is that speed?

A
  • No more than 10mmol/L per 24 hours sodium change
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19
Q

What are some useful laborartory investigations that are used to investigate sodium and water balanace?

A
  • Urea/creatinine ratio - used to diagnose dehydration, large urea increase = dehydration
  • Urinary sodium - <20 mmol/L = conservation, >20 mmol/L = loss
  • Urinary osmolality - Ignore the reference interval, relates to the serum osmolality
  • Serum osmolality - Indicates if other osmotically active substances are present e.g. glucose or ethanol
  • Urine /serum osmolality - >1 = water conservation, < 1 = water loss
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20
Q

How do you calculate the serum osmolality?

A
  • Calculated Serum osmolality = 2 x Na + urea + glucose
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21
Q

Explain how to investigate the cause of a patient’s hyponatraemia

A
  • Patient could have one of 3 types of hyponatraemia:
    • Hypertonic hyponatraemia - increased glucose
    • Hypotonic hyponatraemia - Volume status
    • Pseudohyponatraemia - increased triglyceride/protein level
  • If the patient is hypovolaemic (low blood fluid level) then the urinary sodium needs to be looked at
  • If urinary sodium ​of hypovolaemic patient is < 20mM then person is conserving sodium in their kideneys and sodium loss is occuring elsewhere such as:
    • GI loss - Vomiting, Diarrhoea
    • Skin loss - Burns, Sweating
    • Haemorrhage
  • ​If urinary sodium is of hypovolaemic patient is >20 mM then person is losing salt from the kidneys which may be due to:
    • Addison’s disease
    • Diuretic use
    • Cerebral Salt wasting
  • ​If patient is Euvolaemic you also look at urinary sodium
  • If urinary sodium ​of euvolaemic patient is < 20mM then again person is conserving sodium in kidneys which occurs because of Acute H20 overload.
  • Person may have Acute H20 overload due to:
    • Psychogenic polydipsia
    • Beer potomania
    • Iatrogenic​
  • If urinary sodium ​of euvolaemic patient is >20mM then patient is losing sodium from kidneys which occurs because of Chronic H20 overload as well as Impaired excretion
  • These occur because of:
    • SIADH (Syndrome of inappropriate antidiuretic hormone)
    • Hypothyroidism
    • Glucocorticoid deficiency
  • ​​If patient is Hypervolaemic you also look at urinary sodium
  • Urinary sodium of hypovolaemic can only really be <20mM so they are conserving sodium in their kidneys
  • This occurs because patient will usually have odema which may be because of:
    • Liver Cirrhosis
    • Cardiac failure
    • Nephrotic syndrome
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22
Q

What sodium levels are said to be life-threatening?

A
  • <115mmol/L
  • >160mmol/L
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23
Q

Why is it important to maintain extracellular [H+]/pH?

A
  • Because extracellular [H+]/pH is essential for maintaining protein/enzyme function
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24
Q

What does the maintainence of acid-base balance depend on?

A
  • Depends on the relative balance between acid production and excretion
    • Carbon dioxide production and excretion (respiration)
    • Hydrogen ion production and excretion (renal)
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25
Q

How is H+ produced within our bodies?

A
  • Carbonic acid (volatile) - produced from the burning of carbohydrates
  • Non-carbonic acids (non-volatile) - produced from the metabolism of amino acids
26
Q

How is H+ excreted from our bodies?

A
  • H+ excreted from a our bodies as a part of CO2 removal in the lungs
  • H+ also excreted from the kidneys
27
Q

Explain the relationship between pH and [H+]

A
  • There’s a reciprocal logarrithmic association between pH and [H+]
  • This means the higher the pH the lower the [H+]
  • [H+] is doubled for every fall in pH of 0.3
28
Q

What is the Henderson Hasselbalch equation?

A
  • pH = pK + log10 [HCO3]/pCO2
  • This equation means that: pH α [HCO3]/pCO2
  • Where:
    • α = proportional to
    • pCO2 = partial pressure of CO2
29
Q

When does metabolic acidosis occur?

A
  • Occurs when rate of H+ generation exceeds rate of H+ excretion
30
Q

How does the body respond to metabolic acidosis?

A
  • Buffering – consumption of HCO3
  • Removal of CO2 via Kussmaul respiration
31
Q

When does respiratory acidosis occur?

A
  • Occurs when the rate of CO2 generation exceeds CO2 excretion
32
Q

How does the body respond to respiratory acidosis?

A
  • Increased renal excretion of H+ & regeneration of HCO3
  • Increased retention of CO2 - will eventually form H2CO3 when it reacts with H20
33
Q

How does the body compensate when acid/base balance is disrupted?

A
  • It attempts to return acid / base status to normal via:
  • Buffering
    • Bicarbonate buffer in serum, phosphate buffer in urine (for excretion)
    • Skeleton - takes up H+ ions
    • Intracellular accumulation/loss of H+ ions in exchange for K+ , proteins and phosphate act as buffers
  • Compensation
    • ​Diametric opposite of original abnormality
    • Never overcompensates
    • Delayed and limited
  • Treatment
    • ​By reversal of precipitating situation
34
Q

How long does compensation for acid/base disturbances take?

A
  • Respiratory compensation for a primary metabolic disturbance can occur very rapidly e.g. Kussmaul breathing
  • Metabolic compensation for primary respiratory abnormalities take 36-72 hours to occur
    • This is because it requires enzyme induction from increased genetic transcription and translation etc
  • NOTE: Metabolic compensation only occurs in more chronic scenarios
35
Q

Describe the process of renal bicarbonate regeneration

A
  • Na+/K+ co-transporter within tubular cell membrane transports Na+ into tubular cell and K+ out into tubular lumen
  • H20 and CO2 in tubular cells react with each other to produce H2CO3
  • H2CO3 is then broken down into HCO3- (bicarbonate) and H+
  • If HCO3- is formed in proximal tubule it’s reclaimed but if it’s formed in distal tubule HCO3- is regenerated
  • H+ is co-transported out of Tubular cell with Na+ which is transported in
  • Co-transporter can only transport either H+ or K+ out of tubular cell so you either lose H+ or K+ ions
36
Q

What are some of the problems with the arterial blood gas (ABG) test?

A
  • Errors in blood gas analysis are dependent more on the clinician than on the analyser
  • Need to expel air from sample
  • Needs to mix sample well
  • Samples need to be analysed ASAP
  • Ice not required
  • Ensure no clot in syringe tip
37
Q

How can results from the an ABG test be interpreted?

A
  • pO2 - Check FiO2 (Fraction of inspired oxygen) as it’ll influlence result
  • pH - Is it normal or does it show an acidosis or alkalosis
  • pCO2 - Does it show a primary respiratory or compensatory response
  • HCO3 - metabolic component (calculated using Henderson Hasselbach equation)
38
Q

What are some of the causes of respiratory acidosis (high retention of CO2)?

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
39
Q

How does the body compensate for respiratory acidosis?

A
  • Increased renal acid excretion (metabolic alkalosis, 36-72 hrs delay)
40
Q

How is respiratory acidosis corrected?

A
  • Requires return of normal gas exchange
41
Q

What are some of the features of respiratory acidosis?

A
  • Acute: Decreased pH (Increased [H+]), Increased pCO2, Normal [HCO3-],– no compensation
  • Chronic: Decreased pH (Increased [H+]), Increased pCO2, Increased [HCO3-] - due to compensation
42
Q

What are some of the causes of respiratory alkalosis (Low pCO2, high excretion of CO2)?

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-negative septicaemia
    • Primary hyperventilation syndrome
    • Voluntary hyperventilation
43
Q

How does the body compensate for respiratory alkalosis?

A
  • Increased renal bicarbonate excretion (metabolic acidosis, 36-72 hrs delay)
44
Q

How is respiratory alkalosis corrected?

A
  • Correction based on cause of respiratoty alkalosis
45
Q

What are some features of respiratoty alkalosis?

A
  • Acute: Increased pH, Decreased [H+], Normal [HCO3-], Decreased pCO2 – no compensation
  • Chronic: Increased pH, Decreased [H+], Decreased [HCO3-], Decreased pCO2 - compensation
46
Q

What are some causes of metabolic acidosis?

A
  • Increased H+ formation
    • Ketoacidosis
    • Lactic acidosis
    • Poisoning – methanol, ethanol, ethylene glycol, salicylate
    • Inherited organic acidosis
  • Acid ingestion
    • ​Acid poisoning
    • Excess parenteral administration of amino acids e.g. arginine
  • Decreased H+ excretion
    • ​Renal tubular acidosis
    • Renal failure
    • Carbonic dehydratase inhibitors
  • Loss of bicarbonate (HCO3-)
    • ​Diarrhoea
    • Pancreatic, intestinal or biliary fistulae/drainage
47
Q

How does the body compensate for metabolic acidosis?

A
  • Hyperventilation, hence low pCO2
48
Q

How is metabolic acidosis corrected?

A
  • Increased renal acid excretion
49
Q

What are some of the features of metabolic acidosis?

A
  • Decreased pH, Increased [H+], Decreased [HCO3-], Decreased pCO2
50
Q

What are some causes of metabolic alkalosis?

A
  • Increased addition of base
    • Inappropriate taking of acidotic states
    • Chronic alkali ingestion
  • Decreased elimination of base
  • Increased loss of acid
    • GI loss - Gastric aspiration, Vomiting with pyloric stenosis
  • Renal
    • ​Taking of Diuretics (not-K+ sparing)
    • Potassium depletion
    • Mineralocorticoid excess - Cushing’s, Conn’s syndrome
    • Drugs with mineralocorticoid activity – carbenoxolone
51
Q

How does the body compensate for metabolic alkalosis?

A
  • Hypoventilation with CO2 retention (respiratory acidosis)
52
Q

How is metabolic alkalosis corrected?

A
  • Increased renal bicarbonate excretion
  • Reduced renal proton loss
53
Q

What are some of the features of metabolic alkalosis?

A
  • Increased pH, Deceased [H+], Increased [HCO3-], Normal/Increased pCO2
54
Q

Describe a clinical scenario in which a person has metabolic alkalosis

A
  • Metabolic alkalosis leads to hypovolaemia due to persistant vomiting
  • Hypovolaemia results in:
    • Loss of HCL
    • Loss of potassium
    • Loss of fluid
  • Metabolic alkalosis may also be caused by diruetics which cause:
    • Chronic K+ depletion
  • ​In response to fluid loss as a result of hypovolaemia there’s increased aldosterone activation
  • This leads to reabsorbtion of NaCl/H2O at distal convoluted tubule in kidney in exchange for K+ /H+
55
Q

Is acidosis associated with hyperkalaemia or hypokalaemia? Why is this?

A
  • Acidosis associated with hyperkalaemia (High blood [K+]
  • This is because when renal bicarbonate regeneration occurs, to compensate for acidosis, H+ produced is transported out of tubular cell instead of K+ leading to increased K+ levels
56
Q

Is alkalosis associated with hyperkalaemia or hypokalaemia?

A
  • Alkalosis associated with hypokalaemia (low blood [K+])
57
Q

What are some of the causes of hyperkalaemia?

A
  • Increased intake of K+
    • Usually parenteral (intake of K+ occurs somewhere other than the mouth)
  • Decreased loss of K+
    • Reduced GFR
    • Reduced tubular loss (potassium sparing diuretics, anti-inflammatories, ACEIs, mineralocorticoid deficiency)
58
Q

What are some causes of hypokalaemia?

A
  • Increased loss of K+
    • Gut (diarrhoea, laxatives)
    • Kidney (diuretics, magnesium deficiency, mineralocorticoids, renal tubular abnormalities)
  • Decreased intake of K+
    • Often alcohol
    • Anorexia
59
Q

How is K+ redistributed by the cell as a result of hypokalaemia?

A
  • Redistribution of K+ into the intracellular fluid
  • This redistribution can be caused by:
    • Alkalosis
    • Insulin
    • B agonists
60
Q

How is K+ redistributed by the cell as a result of hyperkalaemia?

A
  • Redistribution of K+ into extracellular fluid
  • This redistribution can be caused by:
    • Acidosis
    • Decreased insulin
    • Tissue damage

Clinical pathology specialities: Clinical Biochemistry (7 decks)

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