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

Investigation of Salt/Water and Acid/Base Balance Flashcards

1
Q
  1. How many litres is the total fluid in the body?
A

50 L

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2
Q
  1. We can break down the total body weight into extracellular and intracellular fluid.
    What % does intracellular fluid make up of total body weight
A

40%

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3
Q
  1. What % of total body weight does extracellular fluid make up?
A

20%

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4
Q 
4. Extracellular fluid makes up 20% of body weight
Break that down into how much % for:
-Interstitial
-Intravascular
-Transcellular
-H20 in connective tissue
A
  • Interstitial = 15%
  • Intravascular = 5%
  • Transcellular = 1%
  • H20 in connective tissue = <1%
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5
Q
  1. What is our ‘intake’ of water? how do we get water?
A

Dietary intake by thirst mechanism

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6
Q
  1. What is our ‘intake’ of sodium? how do we get sodium?
A

Western diet has 100-200 mmol/day so our diet

unless vegan or no salt added to food

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7
Q
  1. What is our output of water and sodium that is obligatory( just happens, we cant control it)?
A

Water loss through skin and lungs

Sodium loss through skin

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8
Q
  1. What is our output of water that is controlled?
A
  • Renal Function
  • Vasopressin/ADH
  • Gut (Most water gets reabsorbed)
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9
Q
  1. What is the redistribution of sodium determined by?
A

Intravascular volume

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10
Q
  1. Which hormones are involved in 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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11
Q
  1. Which hormones are involved in water balance?
A

• ADH/vasopressin (synthesised in hypothalamus and stored in posterior pituitary) causes increase in water absorption in collecting ducts
•Aquaporins:
- AQP1 proximal tubule and not under control of ADP.
- AQP2 and 3 present in collecting duct and under control of ADH

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12
Q
  1. What does a presence of osmotically active substances in the blood result in?
A

water redistribution to maintain osmotic balance but cause changes in other measured solutes.

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13
Q
  1. What does excess solute cause?
A

oExcess solute (hyperosmolarity) cause cells to shrink due to dehydration

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14
Q
  1. What does excess water cause?
A

hypoosmolality (excess water) causes cells to swell causing oedema.

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15
Q
  1. Fill in the blank:

Water will move from areas of **to ******areas.

A

Water will move from areas of hyporosmolarity to hyperosmotic areas.

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16
Q
  1. What is the physiological response to water loss?
A

Water loss increases osmolarity which triggers vasopressin release, water redistribution and stimulation of the thirst response to restore osmolarity.

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17
Q
  1. How does the stimulation of vasopressin release result in the restoration of ECF osmolarity?
A

Renal water retention

less water loss in kidneys

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18
Q
  1. How does the redistribution of water from the ICF ,result is the restoration of ECF osmolarity?
A

It causes increased ECF water

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19
Q
  1. How does the stimulation of the hypothalamic thirst centre result in the restoration of ECF osmolarity?
A

We take in more water- increased water intake

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20
Q
  1. Approx. what % of Na is filtered by the glomeruli (obligatory reabsorption by renal perfusion)
A

95-98%

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21
Q
  1. Where is the most of Na reabsorbed in?
A

PCT

proximal convoluted tubule

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22
Q
  1. What does the DCT to?
A

Fine tuning using aldosterone

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23
Q
  1. What is aldosterone produced by
A

Angiotensin II

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24
Q
  1. The Juxtaglomerular apparatus (JGA) produces renin, what is the result of this?
A

oJGA produces renin (hypo-osmolarity) which coverts angiotensinogen to angiotensin I (this is converted into II by ACE from the lungs).

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25
Q
  1. What is the difference between hypo-osmolarity and hyperosmolarity?
A 
Hypo-osmolarity = Sodium is LOWER than normal (keeps water in) 
Hyper-osmolarity= Sodium HIGHER than normal (draws water out)
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26
Q
  1. What is the name for the device that measures osmotic strength?
A

Osmometry

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27
Q
  1. The osmometry can use a concept of freezing point depression and be called a freezing point depression osmometer. How do these work?
A

okay so your freezing point is the temp is which a liquid solidifies
So this osmometer using colligative properties (which means properties because of how much solute is in the sample) to determine osmolarity
More solute = LOWER the freezing point

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28
Q
  1. How would you measure sodium?
A

you can measure :
DIRECTLY or INDIRECTLY

Indirect Ion selective electrodes (main lab analysers)

Direct Ion selective electrodes (Blood gas analyser)

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29
Q 
29. An 80yr old women comes in a drowsy/confused state, no previous history, tongue markedly dry, febrile (38.5 0C), BP 100/60 and pulse rate 90b/m
Her results are shown below:
o	Sodium		163 mmol/L		(133-146)
Potassium		3.9 mmol/L		(3.5-5.3)
Urea		15.8 mmol/L		(2.5-7.8)
Creatinine		140 µmol/L		(60-110)
eGFR		31 mL/min/1.73m            (>90)

What can you diagnose her with?

A

Her creatinine level is too high and her eGFR is too low

Indicates water deficiency - dehydration

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30
Q 
20.  A 38 year old female, confused, known psychiatric history, can’t remember eating, drank lots of water. 
oResults: 
•	Na 106mmol/L (high)
•	K 4.8 mmol/L
•	Urea 3.2 mmol/L
•	Creatinine 71 umol/L
•	Glucose 5.6 mmol/L
•	Serum Osmolality 245 mosm/Kg (low)
•	Urine Osmolality 227 mosm/Kg
•	Urine Na	<20 mmol/L
Whats you diagnoses
A

Sodium and serum osmolarity is LOW
indicates a lot of water so water excess
As patient has psychiatric history we call this psychogenic polydipsia, is a form of polydipsia characterised by excessive fluid intake in the absence of physiological stimuli to drink.
or caused by medication such as Prozac

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31
Q
  1. What is the difference between Euvolemic, hypovolemic or hypervolemic Hyponatremia
A

Hypovolemic hyponatremia: decrease in total body water with greater decrease in total body sodium.

Euvolemic hyponatremia: normal body sodium with increase in total body water.

Hypervolemic hyponatremia: increase in total body sodium with greater increase in total body water.

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32
Q
  1. What does osmolality mean? In a practical sense what is high osmolality and what is low?
A

“Osmolality” refers to the concentration of dissolved particles of chemicals and minerals – such as sodium and other electrolytes – in your serum. Higher osmolality means more particles in your serum. Lower osmolality means they’re more diluted.

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33
Q
  1. Does prozac increase or decrease Na?
A

decrease

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34
Q
  1. How would you assess a patient who has possible fluid/electrolyte disturbances?
A

oFluid chart (input and output measured hourly): usually not done very well.

oHistory: Fluid intake / output, Vomiting/diarrhoea, Past history, Medication (Prozac reduces Na).

oExamination - Assess volume status
•Lying and standing BP, Pulse, Oedema, Skin turgor/Tongue
•Jugular and Central Venous Pressures.

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35
Q
  1. If a patient has Hyponatraemia , what can rapid over correction lead to?
A

may lead to central pontine myelinolysis (myelin destruction).

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36
Q
  1. If a patient has Hypernatremia , what can over rapid correction result in?
A

cerebral oedema

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37
Q
  1. Its important to correct sodium at the same speed, what speed would this be?
A
  • no more than 10mmol/L per 24 hours sodium change.
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38
Q
  1. Why is the urea/creatinine ratio useful?
A

Urea increase shows dehydration

39
Q
  1. What does serum osmolality indicate?
A

Indicates if other osmotically active substances are present

40
Q
  1. What does urinary sodium tell us?
A

<20 mmol/L = conservation and >20 mmol/L = loss

41
Q
  1. What does urine/serum osmolality tell us?
A

> 1 = water conservation and < 1 = water loss.

42
Q
  1. What is the serum osmolality calculation and when is it useful?
A

(only useful if you think something else is present)

•2 x Na + urea + glucose (+/- 10) 290 = (2 x 140 = 280) + 5 + 5

43
Q
  1. What is meant by “overriding control is intravascular volume”?
A

salt + water in ‘wrong place’, intravascularly volume deplete, this activates renin-angiotensin-aldosterone (RAAS ) to promote Na +H20 retention.

44
Q
  1. We can break down hyponatraemia into :
    -Hypertonic
    -Hypotonic
    -Pseudo
    What do all of these mean?
A
  • Hypotonic is when there is low plasma osmolality- (too much water, not enough solutes).
  • Hypertonic is when there is increased glucose (too concentrated) and so increased reabsorption of water
  • Pseudo is when it seems sodium levels are low when in fact they are not, because of an increase in serum proteins and lipids , there is less water content (so seems less sodium) but actually sodium is the same!
45
Q
  1. What does hypovolaemic hyponatraemia result in?
A
  • Cirrhosis (liver does not function properly)
  • Cardiac Failure
  • Nephrotic Syndrome (kidneys usually + diuretic (pills that make you release more water) prescription
46
Q
  1. What does Euvolemic hyponatremia mean?
A

SIADH (too much ADH released)
Hypothyroidism
Glucocorticoid deficiency (low cortisol)

47
Q
  1. What is psychogenic beer potomania? What can it result in
A

excessive intake of alcohol, particularly beer, together with poor dietary solute

48
Q
  1. what is meant by “Iatrogenic medication”, what can it cause?
A

sometimes adverse effects of a medical treatment are iatrogenic.
Can result in Euvolaemic hyponatraemia

49
Q
  1. What can cause hypovolaemic hyponatraemia?
A

GI LOSS ( replacement with hypotonic fluid) through vomiting or diarrhoea
SKIN LOSS through burns and sweating
Lastly HAEMORRHAGE

50
Q
  1. What can Hypovolaemic hyponatraemia result in?
A
  • Addisions
  • Diuretic Rx
  • Salt losing nephritis
  • Solute Diuresis
  • Cerebral Salt wasting
51
Q
  1. What is the reference range for sodium?
A

133- 145 mmol/L

52
Q
  1. What is the low and high life threatening level for sodium?
A

<115

>160

53
Q
  1. What is blood pressure/volume sensed by?
A

Baroreceptors

Renal perfusion pressure

54
Q
  1. What is aldosterone produced by?what cause it cause?
A

oAldosterone is produced by the adrenal cortex- causes sodium reabsorption and the loss of H+/K+ at the DCT.

55
Q
  1. Whats an inevitable by-product of ATP production
A

large amounts of protons and hydrogens

56
Q
  1. Why is it important to maintain extracellular pH / {H+} ?
A

to maintain protein/enzyme function as it depends on balance between acid production and excretion

57
Q
  1. Through what biological process is carbon dioxide produced/excreted?
A

Respiration

58
Q
  1. Through which physiological compartment is H+ ions produced and excreted?
A

Renal

59
Q
  1. Fill in the blanks
    “H+ can be carbonic (carbohydrate burning) or non-carbonic (amino acid metabolism), most of it is removed by the* and the rest is closely regulated by the*.
A

Lungs

Kindney

60
Q
  1. What two equations can you use to find pH using H+ conc?
A

pH = -log(10)[H+]
or
pH = log(10)1/[H+]
(10) is small right hand side

61
Q
  1. On a pH/{H+} graph, what is the range for pH and {H+}?
A

pH ranges from 7.4-7.1 and [H+] ranges from 40-80 so when [H+] is doubled, the pH falls by 0.3.

62
Q
  1. What is pH proportional to and inversely proportional to?
A

pH is proportional to HCO3- and inversely proportional to the partial pressure of CO2

63
Q
  1. What is the henderson Hasselbalch equation?
A

pH =pKa + log 10 ( A- / H+)

64
Q
  1. Using henderson Hasselbalch equation, what would it be for when
    CO2 + H2 —> (K hydration) H2CO3 —-> (K dissociation) (H+) + HCO3
A

pH = pK + log10 [HCO3] / {pC02)

65
Q
  1. How does the body respond to metabolic acidosis?
A

compensated for by the removal of CO2 (Kussmaul respiration: deep, laboured breathing) and the buffering action of HCO3- (increased consumption).

66
Q
  1. How does the body compensate for respiratory acidosis?
A

increased renal H+ excretion and increased HCO3- regeneration.

67
Q
  1. Explain the three steps of trying to return acid / base status to normal
    ?
A
  • Buffering
  • Compensation
  • Treatment
68
Q
  1. Explain the buffering step?
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

69
Q
  1. Explain the step compensation?
A

Diametric opposite of original abnormality
Never overcompensates
Delayed and limited

70
Q
  1. Explain the step Treatment
A

By reversal of precipitating situation

71
Q
  1. Compare the speed of compensation for respiratory and metabolic disturbances?
A

Respiratory compensation for a primary metabolic disturbance can occur very rapidly.
• Kussmaul breathing (respiratory alkalosis) in response to DKA.

Metabolic compensation for primary respiratory abnormalities take 36-72 hours to occur.
• Limited because it requires enzyme induction (needs increased genetic transcription and translation etc).
• No compensation seen in acute respiratory acidosis such as asthma.
• Requires more chronic scenario to include compensation mechanism.

72
Q
  1. What is the mechanism of renal bicarbonate regeneration?
A

o H2O and CO2 produce carbonic acid which dissociates into H+ and HCO3-.
o The HCO3- is reabsorbed in exchanged for Cl- ions. PCT reclaims bicarbonate and DCT regenerates bicarbonate.
o The H+ ions are excreted by an Na/H exchanger. When H+ is being excreted, K+ can’t be excreted simultaneously.

73
Q
  1. How does an ABG work? What are some pitfalls? What are errors due to?
A

o Errors in blood gas analysis are dependent more on the clinician than on the analyser.
o All air has to be expelled and the sample mixed well - analyse ASAP
o Plastic syringes are OK at room temp for for 30mins, ensure there is no clot in the syringe tip.
o Ice is not required

74
Q
  1. How do we interpret the results of an ABG?
A

o pO2 remember to check FiO2 (fraction of inspired oxygen – oxygen concentration inhaled).
o pH – is it normal or does it show an acidosis or alkalosis
o pCO2 – primary respiratory or compensatory response
o HCO3 – metabolic component

75
Q
  1. What are some causes of respiratory acidosis (co2 retention)
A

Airway obstruction
•Bronchospasm (Acute), COPD (Chronic), Aspiration (breathing)/Strangulation (circulation cut off by constriction).

Respiratory centre depression
•Anaesthetics, Sedatives, Cerebral trauma, Tumours

Neuromuscular disease (respiratory muscle weakness- shallow breathing). 
•Guillain-Barre Syndrome, Motor Neurone Disease

Pulmonary disease
•Pulmonary fibrosis, Respiratory Distress Syndrome, Pneumonia (inflamed lungs filled with pus).

Extrapulmonary thoracic disease
•Flail chest (trauma breaks part of rib cage – rib detached from the rest of the chest wall).

76
Q 
76. What is the :
compensation
correction
and features
of RESPIRATORY ACIDOSIS?
A

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

oCorrection: Requires return of normal gas exchange

Features

acute: low pH (Increase[H+]), increased pCO2, ->[HCO3-],– i.e. no compensation.
chronic: low pH (increased[H+]), increased pCO2, increased [HCO3-],– i.e. Compensation.

77
Q 
77. Case study:
21 yr old male with RTA flail chest:
pO2	     8.0 kPa	Low
pH	     7.24	        Acidotic
pCO2   8.0 kPa	High
HCO3   25	        Normal
Diagnosis?
A

oUncompensated acute respiratory acidosis + impaired oxygenation.
oHCO3 is normal: uncompensated.

78
Q
  1. What are the causes of respiratory alkalosis (low pCO2- C02 removal)
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 or G-ve septicaemia
•Primary hyperventilation syndrome or Voluntary hyperventilation

79
Q
  1. What is the :
    -Compensation
    -Correction
    -Features
    of RESPIRATORY ALKALOSIS?
A

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

o Correction: Of cause

Features
•acute: high pH, low [H+], normal [HCO3-], low pCO2 – no compensation
•chronic: high pH, low [H+], low [HCO3-], low pCO2

80
Q
  1. Case study:
    : Anxious student with tingling in fingers/toes who is giving a blood sample.

pO2 12.8 kPa Normal
pH 7.52 Alkalotic
pCO2 3.5 kPa Low (due to hyperventilation)
HCO3 23 Normal

Diagnosis?

A

o Uncompensated acute respiratory alkalosis.

81
Q
  1. What are some causes of metabolic acidosis?
A

1.Increased acid addition:
o Increased H+ formation: Ketoacidosis, Lactic acidosis, Poisoning (methanol, ethanol, ethylene glycol, salicylate), Inherited organic acidosis.
o Acid ingestion: Acid poisoning or XS parenteral administration of amino acids e.g. arginine.

2.Reduced H+ excretion:
o Renal tubular acidosis or failure
o Carbonic dehydratase inhibitors

3.Loss of bicarbonates:
o Diarrhoea
o Pancreatic, intestinal or biliary fistulae/drainage

82
Q
  1. What is the:
    -Compensation
    -Correction
    -Features
    of METABOLIC ACIDOSIS?
A

o Compensation: hyperventilation, hence low pCO2
o Correction of cause and increased renal acid excretion
o Features: low pH, high [H+], low [HCO3-], low pCO2

83
Q
  1. Case study:
    : 7 year old Type 1 diabetic who hasn’t taken insulin for 24 hours – build-up of acidic ketone bodies.

pO2 12 kPa Normal
pH 7.20 Acidotic
pCO2 5.0 kPa Normal
HCO3 15 Low

Diagnosis?

A

o Uncompensated acute metabolic acidosis.

84
Q
  1. Metabolic Alkalosis causes?
A

o Increased addition of base: Inappropriate Rx of acidotic states and Chronic alkali ingestion
o Decreased elimination of base
o Increased loss of acid
1. GI loss:
• Gastric aspiration (technique for collecting gut contents) or Vomiting with pyloric stenosis (increased HCL loss).
2. Renal:
• Diuretic Rx (not K+ sparing)
• Potassium depletion
• Mineralocorticoid excess (stimulate ENaC and H+ ATPase) e.g. in Cushing’s or Conn’s.
• Drugs with mineralocorticoid activity – carbenoxolone

85
Q
  1. What is the ;
    -Compensation
    -Correction
    -Features
    of metabolic alkalosis?
A

oCompensation: hypoventilation with CO2 retention (respiratory acidosis)
oCorrection: increased renal bicarbonate excretion and reduce renal proton loss.
oFeatures: high pH, low [H+], high [HCO3-], N/high pCO2.

86
Q
  1. Case study:
    56 year old female who has been vomiting for the last 48 hours.

pO2 13 kPa Normal
pH 7.48 Alkalotic
pCO2 5.8 kPa Normal
HCO3 33 High

A

o Uncompensated acute metabolic alkalosis.

87
Q
  1. What are some clinical scenarios of Metabolic Alkalosis?
A

o Hypovolaemia from persistent vomiting: Loss of HCl, Loss of potassium, Loss of fluid
o Diuretics: Chronic K+ depletion
o Response to fluid loss is aldosterone activation:
• Reabsorb NaCl/H2O at distal convoluted tubule in kidney in exchange for K+ /H+

88
Q
  1. Summarise the clinical scenarios of :
    - Respiratory Acidosis
    - Respiratory Alkalosis
    - Metabolic Acidosis
    - Metabolic Alkalosis
A

o Respiratory acidosis (CO2 retention): Compensation is metabolic alkalosis
o Respiratory alkalosis (increased CO2 loss): Compensation is metabolic acidosis
o Metabolic acidosis (Acid ingestion, Increases acid production, Reduced acid excretion):
• Compensation respiratory alkalosis
o Metabolic alkalosis: compensation is respiratory acidosis.
• very difficult primary disturbance to produce and maintain in proton producers! (Very specific factors required)

89
Q
  1. Acidosis causes hyperkalaemia, how?
A
  • Causes K+ movement to the plasma for exchange on H+ ions.

* Insulin corrects hyperkalaemia as it causes a reduction in serum K+ levels by causing influx into cells.

90
Q
  1. Alkalosis causes hypokalaemia, how?
A
  • Causes K+ movement out of the plasma into the tubules in exchange for H+.
  • Catecholamines increase cellular uptake of K+ so reduces plasma concentration
91
Q
  1. Case study:
    76 year old male with a long history of prostatism and 24 hour anuria (failure of urine production).
o	Results: 
•	Na		137 	mmol/L
•	K		6.7 	mmol/L
•	HCO3      10 	mmol/L
•	Urea 	 59  mmol/L
•	Creat     	470 µmol/L
•	eGFR       	<5
A 
o	Hyperkalaemia (reduced loss as kidneys aren’t working) - AKI leading to failure of K excretion. 
o	Redistribution across the cells (effect of acidosis).
92
Q 
92. Case Study:
23y female nurse, several A&amp;E visits due to malaise, generalised muscle weakness etc. 
Results: 
•	Na 		137 mmol/L
•	K 		2.6 mmol/L
•	HCO3      36 mmol/L
•	Urea         6.5 mmol/L
•	Creat       100 µmol/L
A

o Mild hypokalaemic alkalosis given oral potassium supplements.
o Renal potassium loss - Diuretic abuse.

93
Q
  1. Hypokalaemia is either due to increased loss or decreased intake - give examples of how each would occur?
A

Increased Loss:
Gut (diarrhoea, laxatives)
Kidney (diuretics, magnesium deficiency, mineralocorticoid XS, renal tubular abnormalities)

Decreased Intake:

  • Alcholol
  • Anorexia
94
Q

94.Hyperkalaemia is either due to increased intake or decreased loss - give examples of how each would occur?

A

Decreased loss:

  • Reduced GFR
  • Reduced tubular loss (potassium sparing diuretics anti-inflammatories, ACEIs, mineralocorticoid deficiency)

Increased Intake:
Usually parenteral

Clinical Biochemistry (7 decks)

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