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2 - Clinical Biochemistry > lab investigations - salt/water/acid > Flashcards

lab investigations - salt/water/acid Flashcards

1
Q

body fluids make up how much of our body weight?

A

60%

40% = Intracellular Fluid Compartment
20% = Extracellular Fluid Compartment
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2
Q

20% of our fluid is in the Extracellular Fluid Compartment - what is this made up of?

A

Interstitial
Intravascular
Transcellular
H2O in connective tissue

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3
Q

water and sodium balance are determined by what?

A

input

output (obligatory and controlled losses)

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4
Q

obligatory and controlled losses of water?

A

Obligatory losses

  • Skin
  • Lungs

Controlled losses – these depend on:

  • Renal function
  • Vasopressin/ADH (anti-diuretic hormone)
  • Gut (main role of the colon)
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5
Q

obligatory and controlled losses of sodium?

A

Obligatory loss
-Skin

Controlled losses / excretion

  • Kidneys
  • Aldosterone
  • GFR
  • Gut - most sodium is reabsorbed; loss is pathological
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6
Q

what do controlled losses depend on?

A

depend on renal function

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7
Q

where does the majority of water get reabsorbed?

A

in the gut (colon)

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8
Q

where is majority of sodium lost?

A

kidney

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9
Q

hormones involved in sodium balance?

A

aldosterone

  • produced in the adrenal cortex
  • regulates sodium and potassium homeostasis

natriuretic hormones

  • ANP cardiac atria, BNP cardiac ventricles
  • promotes sodium excretion and decreases blood pressure
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10
Q

hormones involved in water balance?

A

ADH/vasopressin

  • synthesised in hypothalamus
  • stored in posterior pituitary
  • release causes increase in water absorption in collecting ducts

Aquaporins

  • AQP1 - proximal tubule, not under control of ADh
  • AQP2 and 3 - collecting duct, under control of ADH
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11
Q

how does water move?

A
  • moves across a semi-permeable membrane
  • moves from a more diluted area to a more concentrated area, in order to maintain an osmotic balance across the membrane
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12
Q

what effect do osmotically active substances have?

A

osmotically active substances in the blood will result in water redistribution to maintain osmotic balance

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13
Q

water loss causes an increase in ECF osmolality - what happens as a result?

A
  1. stimulation of VP release
  2. stimulation of hypothalamic thirst centre
  3. redistribution of water from ICF
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14
Q

sodium reabsorption in the renal tubules

A
  • majority of Na reabsorbed in PCT
  • fine tuning in DCT, under the influence of aldosterone
  • ADH acts in collecting duct to stimulate water reabsorption
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15
Q

sodium depletion will have what effect?

A
  • will have a positive effect on JGC’s within the kidney
  • JGC’s will produce renin
  • Renin converts angiotensinogen to angiotensin I
  • Angiotensin I stimulates the adrenal cortex to produce aldosterone
  • ACE in the lungs converts angiotensin I to angiotensin II
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16
Q

what converts Ang I to Ang II?

A

ACE in the lungs

angiotensin converting enzyme

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17
Q

what is osmometry?

A

measuring the osmotic strength of a solution

Freezing point depression

  • Uses colligative properties of a solution
  • More solute – lower the freezing point
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18
Q

how is sodium measured in the body?

A

Indirect Ion selective electrodes (main lab analysers)

Direct Ion selective electrodes (Blood gas analyser)

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19
Q

increased water gain (and sodium loss), will cause what?

A

hyponatraemia

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20
Q

increased sodium gain can cause what?

A

hypernatraemia

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21
Q

how do you assess a patient with possible fluid/electrolyte disturbance?

A

History

  • 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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22
Q

explain the importance of managing fluid/electrolyte problems?

A

important to not do over rapid correction

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

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23
Q

over rapid correction of hyponatraemia can cause what?

A

central pontine myelinolysis

-rapid rise in sodium concentration is accompanied by the movement of small molecules and pulls water from brain cells

24
Q

over rapid correction of hypernatraemia can cause what?

A

may lead to cerebral oedema

25
Q

if your brain expands very rapidly, what happens?

A

it has nowhere to go except down through the base of the skull

26
Q

if there are labs done on paired serum and urine osmolality and electrolytes, what is measured and what do the results mean?

A

Urea/creatinine ratio is useful
-Urea up a lot = dehydration

Serum osmolality
-Indicates if other osmotically active substances are present

Urinary sodium

Urinary osmolality

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

27
Q

Calculated Serum osmolality

A

2 x Na + urea + glucose (+/- 10)

290 = (2 x 140 = 280) + 5 + 5

28
Q

how is blood pressure/volume sensed?

A

Baroreceptors

Renal perfusion pressure

29
Q

what are actions that occur at the DCT?

A

Sodium reabsorption

Loss of H+/K+

30
Q

what is an inevitable by product of ATP production?

A

large amounts of protons/hydrogen ions

31
Q

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

A

to maintain correct protein/enzyme function

32
Q

extracellular [H+]/pH level depend on what?

A
  • relative balance between acid production and excretion
  • carbon dioxide production and excretion (respiration)
  • hydrogen ion production and excretion (renal)
33
Q

H+ production and H+ excretion?

A

production
-carbonic acid and non-carbonic acids

excretion
-lungs and kidneys

34
Q

pH = ?

A

-log10[H+]

ratio of HCO3/CO2

35
Q

Henderson Hasselbalch equation

A

CO2 + H20 -> H2CO3 -> HCO3- + H+

all arrows are reversible

36
Q

metabolic acidosis?

A

rate of H+ generation > excretion

37
Q

respiratory acidosis?

A

rate of CO2 generation > excretion

38
Q

how can alkalosis occur?

A

increased renal excretion of H+, regeneration of HCO3

39
Q

how can acidosis occur?

A

increased retention of CO2

40
Q

how does the body attempt to return acid / base status to normal?

A
  1. Buffering
    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
  2. Compensation
    Diametric opposite of original abnormality
    Never overcompensates
    Delayed and limited
  3. Treatment
    By reversal of precipitating situation
41
Q

how do compensation speeds vary?

A

Respiratory compensation for a primary metabolic disturbance can occur very rapidly

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

42
Q

how does respiratory compensation for a primary metabolic disturbance occur?

A

occurs very rapidly

example:
Kussmaul breathing (respiratory alkalosis) in response to DKA (diabetic ketoacidosis)
-deep and laboredbreathingpattern

43
Q

how does metabolic compensation for primary respiratory abnormalities occur?

A

36-72 hours

requires enzyme induction from increased genetic transcription and translation

no compensation seen in acute respiratory acidosis such as asthma

requires more chronic scenario to include compensation mechanism

44
Q

Mechanism of renal bicarbonate regeneration

A

renal lumen exchanges sodium for potassium, so sodium enters the tubular cell and H+ also leaves with potassium

tubular cell generates bicarbonate

45
Q

what is ABG’s

A

arterial blood gases

46
Q

Pitfalls of ABG?

A

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

  • Expel air
  • Mix sample
  • Analyse ASAP
  • Plastic syringes are ok at room temp for 30 mins
  • Ice not required
  • Ensure no clot in syringe tip
47
Q

interpreting ABG’s - what do we look at?

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

48
Q

what are the causes of respiratory acidosis (co2 retention)?

A

airway obstruction
-Bronchospasm (Acute), COPD (Chronic), Aspiration, Strangulation

respiratory centre depression
-anaesthetics, sedatives, tumours

neuromuscular disease
-Motor Neurone Disease

pulmonary disease
-Pulmonary fibrosis, pneumonia, Respiratory Distress Syndrome

extrapulmonary thoracic disease
-Flail chest

49
Q

Respiratory acidosis - how to fix it

A

Increased renal acid excretion

-Requires return of normal gas exchange

50
Q

what are the causes of respiratory alkalosis?

A

Hypoxia
-High altitude, Severe anaemia, Pulmonary disease

Pulmonary disease
-Pulmonary oedema, Pulmonary embolism

Mechanical overventilation

Increased respiratory drive

  • Respiratory stimulants eg salicylates
  • Cerebral disturbance eg trauma, infection and tumours
  • Hepatic failure
51
Q

Respiratory alkalosis - how to fix it

A

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

52
Q

what are the causes of metabolic acidosis?

A

-Increased H+ formation
Ketoacidosis
Lactic acidosis

-Acid ingestion
Acid poisoning (methanol, ethanol)
XS parenteral administration of amino acids e.g. arginine

Decreased H+ excretion

  • Renal tubular acidosis
  • Renal failure
  • Carbonic dehydratase inhibitors

Loss of bicarbonate

  • Diarrhoea
  • Pancreatic, intestinal or biliary fistulae/drainage
53
Q

metabolic acidosis - how to fix it

A

Compensation
-hyperventilation, hence low pCO2

Correction

  • of cause
  • increased renal acid excretion

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

54
Q

what are the causes of metabolic alkalosis?

A

-Increased addition of HCO3-

-Increased loss of H+
GI loss, Gastric aspiration, vomiting with pyloric stenosis

-decreased excretion of HCO3-

55
Q

metabolic alkalosis - how to fix it

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/highpCO2

56
Q

what is acidosis associated with?

A

Hyperkalaemia

Acidemia will tend to shift K+ out of cells and cause hyperkalemia

2 - Clinical Biochemistry (10 decks)

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