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%
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%
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
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
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
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
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
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
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
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
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
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
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
14
Q
Use the information from the case study below to answer the following questions:
- Is the patient euvolaemic, hypovolaemic or hypervolaemic?
- What is the underlying cause of the hyponatraemia (low sodium level)?
- 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)
- Patient is euvolaemic - has normal blood fluid volume
- Patient is drinking so much water - she has psychogenic polydipsia (excessive fluid intake)
- Serum osmolality test; urine osmolality test and a urinary sodium test
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)
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
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
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
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
20
Q
How do you calculate the serum osmolality?
A
- Calculated Serum osmolality = 2 x Na + urea + glucose
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
22
Q
What sodium levels are said to be life-threatening?
A
- <115mmol/L
- >160mmol/L
23
Q
Why is it important to maintain extracellular [H+]/pH?
A
- Because extracellular [H+]/pH is essential for maintaining protein/enzyme function
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)
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
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
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
