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

lab investigations - salt/water/acid Flashcards

(56 cards)

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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?

Study These Flashcards
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?

Study These Flashcards
A

may lead to cerebral oedema

25
if your brain expands very rapidly, what happens?
it has nowhere to go except down through the base of the skull
26
if there are labs done on paired serum and urine osmolality and electrolytes, what is measured and what do the results mean?
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
Calculated Serum osmolality
2 x Na + urea + glucose (+/- 10) | 290 = (2 x 140 = 280) + 5 + 5
28
how is blood pressure/volume sensed?
Baroreceptors | Renal perfusion pressure
29
what are actions that occur at the DCT?
Sodium reabsorption | Loss of H+/K+
30
what is an inevitable by product of ATP production?
large amounts of protons/hydrogen ions
31
why is maintenance of extracellular [H+]/pH essential?
to maintain correct protein/enzyme function
32
extracellular [H+]/pH level depend on what?
- relative balance between acid production and excretion - carbon dioxide production and excretion (respiration) - hydrogen ion production and excretion (renal)
33
H+ production and H+ excretion?
production -carbonic acid and non-carbonic acids excretion -lungs and kidneys
34
pH = ?
-log10[H+] ratio of HCO3/CO2
35
Henderson Hasselbalch equation
CO2 + H20 -> H2CO3 -> HCO3- + H+ all arrows are reversible
36
metabolic acidosis?
rate of H+ generation > excretion
37
respiratory acidosis?
rate of CO2 generation > excretion
38
how can alkalosis occur?
increased renal excretion of H+, regeneration of HCO3
39
how can acidosis occur?
increased retention of CO2
40
how does the body attempt to return acid / base status to normal?
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
how do compensation speeds vary?
Respiratory compensation for a primary metabolic disturbance can occur very rapidly Metabolic compensation for primary respiratory abnormalities take 36-72 hours to occur
42
how does respiratory compensation for a primary metabolic disturbance occur?
occurs very rapidly example: Kussmaul breathing (respiratory alkalosis) in response to DKA (diabetic ketoacidosis) -deep and labored breathing pattern
43
how does metabolic compensation for primary respiratory abnormalities occur?
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
Mechanism of renal bicarbonate regeneration
renal lumen exchanges sodium for potassium, so sodium enters the tubular cell and H+ also leaves with potassium tubular cell generates bicarbonate
45
what is ABG's
arterial blood gases
46
Pitfalls of ABG?
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
interpreting ABG's - what do we look at?
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
what are the causes of respiratory acidosis (co2 retention)?
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
Respiratory acidosis - how to fix it
Increased renal acid excretion | -Requires return of normal gas exchange
50
what are the causes of respiratory alkalosis?
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
Respiratory alkalosis - how to fix it
Increased renal bicarbonate excretion (metabolic acidosis, 36-72 hrs delay)
52
what are the causes of metabolic acidosis?
-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
metabolic acidosis - how to fix it
Compensation -hyperventilation, hence low pCO2 Correction - of cause - increased renal acid excretion Features -low pH, high [H+], low [HCO3-], low pCO2
54
what are the causes of metabolic alkalosis?
-Increased addition of HCO3- -Increased loss of H+ GI loss, Gastric aspiration, vomiting with pyloric stenosis -decreased excretion of HCO3-
55
metabolic alkalosis - how to fix it
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
what is acidosis associated with?
Hyperkalaemia Acidemia will tend to shift K+ out of cells and cause hyperkalemia

2 - Clinical Biochemistry (10 decks)

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