Investigation of Salt/Water and Acid/Base Balance Flashcards
1
Q
- How many litres is the total fluid in the body?
A
50 L
2
Q
- 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%
3
Q
- What % of total body weight does extracellular fluid make up?
A
20%
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%
5
Q
- What is our ‘intake’ of water? how do we get water?
A
Dietary intake by thirst mechanism
6
Q
- 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
7
Q
- 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
8
Q
- What is our output of water that is controlled?
A
- Renal Function
- Vasopressin/ADH
- Gut (Most water gets reabsorbed)
9
Q
- What is the redistribution of sodium determined by?
A
Intravascular volume
10
Q
- 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.
11
Q
- 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
12
Q
- 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.
13
Q
- What does excess solute cause?
A
oExcess solute (hyperosmolarity) cause cells to shrink due to dehydration
14
Q
- What does excess water cause?
A
hypoosmolality (excess water) causes cells to swell causing oedema.
15
Q
- Fill in the blank:
Water will move from areas of **to ******areas.
A
Water will move from areas of hyporosmolarity to hyperosmotic areas.
16
Q
- 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.
17
Q
- How does the stimulation of vasopressin release result in the restoration of ECF osmolarity?
A
Renal water retention
less water loss in kidneys
18
Q
- How does the redistribution of water from the ICF ,result is the restoration of ECF osmolarity?
A
It causes increased ECF water
19
Q
- 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
20
Q
- Approx. what % of Na is filtered by the glomeruli (obligatory reabsorption by renal perfusion)
A
95-98%
21
Q
- Where is the most of Na reabsorbed in?
A
PCT
proximal convoluted tubule
22
Q
- What does the DCT to?
A
Fine tuning using aldosterone
23
Q
- What is aldosterone produced by
A
Angiotensin II
24
Q
- 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).
25
25. What is the difference between hypo-osmolarity and hyperosmolarity?
```
Hypo-osmolarity = Sodium is LOWER than normal (keeps water in)
Hyper-osmolarity= Sodium HIGHER than normal (draws water out)
```
26
26. What is the name for the device that measures osmotic strength?
Osmometry
27
27. The osmometry can use a concept of freezing point depression and be called a freezing point depression osmometer. How do these work?
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
28
28. How would you measure sodium?
you can measure :
DIRECTLY or INDIRECTLY
Indirect Ion selective electrodes (main lab analysers)
Direct Ion selective electrodes (Blood gas analyser)
29
```
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?
Her creatinine level is too high and her eGFR is too low
| Indicates water deficiency - dehydration
30
```
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
```
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
31
31. What is the difference between Euvolemic, hypovolemic or hypervolemic Hyponatremia
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.
32
32. What does osmolality mean? In a practical sense what is high osmolality and what is low?
“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.
33
33. Does prozac increase or decrease Na?
decrease
34
34. How would you assess a patient who has possible fluid/electrolyte disturbances?
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.
35
35. If a patient has Hyponatraemia , what can rapid over correction lead to?
may lead to central pontine myelinolysis (myelin destruction).
36
36. If a patient has Hypernatremia , what can over rapid correction result in?
cerebral oedema
37
37. Its important to correct sodium at the same speed, what speed would this be?
- no more than 10mmol/L per 24 hours sodium change.
38
38. Why is the urea/creatinine ratio useful?
Urea increase shows dehydration
39
39. What does serum osmolality indicate?
Indicates if other osmotically active substances are present
40
40. What does urinary sodium tell us?
<20 mmol/L = conservation and >20 mmol/L = loss
41
41. What does urine/serum osmolality tell us?
>1 = water conservation and < 1 = water loss.
42
42. What is the serum osmolality calculation and when is it useful?
(only useful if you think something else is present)
•2 x Na + urea + glucose (+/- 10) 290 = (2 x 140 = 280) + 5 + 5
43
43. What is meant by "overriding control is intravascular volume"?
salt + water in ‘wrong place’, intravascularly volume deplete, this activates renin-angiotensin-aldosterone (RAAS ) to promote Na +H20 retention.
44
44. We can break down hyponatraemia into :
-Hypertonic
-Hypotonic
-Pseudo
What do all of these mean?
- 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
45. What does hypovolaemic hyponatraemia result in?
- Cirrhosis (liver does not function properly)
- Cardiac Failure
- Nephrotic Syndrome (kidneys usually + diuretic (pills that make you release more water) prescription
46
46. What does Euvolemic hyponatremia mean?
SIADH (too much ADH released)
Hypothyroidism
Glucocorticoid deficiency (low cortisol)
47
47. What is psychogenic beer potomania? What can it result in
excessive intake of alcohol, particularly beer, together with poor dietary solute
48
48. what is meant by "Iatrogenic medication", what can it cause?
sometimes adverse effects of a medical treatment are iatrogenic.
Can result in Euvolaemic hyponatraemia
49
49. What can cause hypovolaemic hyponatraemia?
GI LOSS ( replacement with hypotonic fluid) through vomiting or diarrhoea
SKIN LOSS through burns and sweating
Lastly HAEMORRHAGE
50
50. What can Hypovolaemic hyponatraemia result in?
- Addisions
- Diuretic Rx
- Salt losing nephritis
- Solute Diuresis
- Cerebral Salt wasting
51
51. What is the reference range for sodium?
133- 145 mmol/L
52
52. What is the low and high life threatening level for sodium?
<115
| >160
53
53. What is blood pressure/volume sensed by?
Baroreceptors
| Renal perfusion pressure
54
54. What is aldosterone produced by?what cause it cause?
oAldosterone is produced by the adrenal cortex- causes sodium reabsorption and the loss of H+/K+ at the DCT.
55
55. Whats an inevitable by-product of ATP production
large amounts of protons and hydrogens
56
56. Why is it important to maintain extracellular pH / {H+} ?
to maintain protein/enzyme function as it depends on balance between acid production and excretion
57
57. Through what biological process is carbon dioxide produced/excreted?
Respiration
58
58. Through which physiological compartment is H+ ions produced and excreted?
Renal
59
59. 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*****.
Lungs
| Kindney
60
60. What two equations can you use to find pH using H+ conc?
pH = -log(10)[H+]
or
pH = log(10)1/[H+]
(10) is small right hand side
61
61. On a pH/{H+} graph, what is the range for pH and {H+}?
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
62. What is pH proportional to and inversely proportional to?
pH is proportional to HCO3- and inversely proportional to the partial pressure of CO2
63
63. What is the henderson Hasselbalch equation?
pH =pKa + log 10 ( A- / H+)
64
64. Using henderson Hasselbalch equation, what would it be for when
CO2 + H2 ---> (K hydration) H2CO3 ----> (K dissociation) (H+) + HCO3
pH = pK + log10 [HCO3] / {pC02)
65
65. How does the body respond to metabolic acidosis?
compensated for by the removal of CO2 (Kussmaul respiration: deep, laboured breathing) and the buffering action of HCO3- (increased consumption).
66
66. How does the body compensate for respiratory acidosis?
increased renal H+ excretion and increased HCO3- regeneration.
67
67. Explain the three steps of trying to return acid / base status to normal
?
- Buffering
- Compensation
- Treatment
68
68. Explain the buffering step?
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
69. Explain the step compensation?
Diametric opposite of original abnormality
Never overcompensates
Delayed and limited
70
70. Explain the step Treatment
By reversal of precipitating situation
71
71. Compare the speed of compensation for respiratory and metabolic disturbances?
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
72. What is the mechanism of renal bicarbonate regeneration?
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
73. How does an ABG work? What are some pitfalls? What are errors due to?
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
74. How do we interpret the results of an ABG?
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
75. What are some causes of respiratory acidosis (co2 retention)
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
```
76. What is the :
compensation
correction
and features
of RESPIRATORY ACIDOSIS?
```
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
```
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?
```
oUncompensated acute respiratory acidosis + impaired oxygenation.
oHCO3 is normal: uncompensated.
78
78. What are the causes of respiratory alkalosis (low pCO2- C02 removal)
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
79. What is the :
-Compensation
-Correction
-Features
of RESPIRATORY ALKALOSIS?
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
80. 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?
o Uncompensated acute respiratory alkalosis.
81
81. What are some causes of metabolic acidosis?
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
82. What is the:
-Compensation
-Correction
-Features
of METABOLIC ACIDOSIS?
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
83. 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?
o Uncompensated acute metabolic acidosis.
84
84. Metabolic Alkalosis causes?
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
85. What is the ;
-Compensation
-Correction
-Features
of metabolic alkalosis?
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
86. 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
o Uncompensated acute metabolic alkalosis.
87
87. What are some clinical scenarios of Metabolic Alkalosis?
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
88. Summarise the clinical scenarios of :
- Respiratory Acidosis
- Respiratory Alkalosis
- Metabolic Acidosis
- Metabolic Alkalosis
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
89. Acidosis causes hyperkalaemia, how?
* 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
90. Alkalosis causes hypokalaemia, how?
* 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
91. 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
```
```
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
```
92. Case Study:
23y female nurse, several A&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
```
o Mild hypokalaemic alkalosis given oral potassium supplements.
o Renal potassium loss - Diuretic abuse.
93
93. Hypokalaemia is either due to increased loss or decreased intake - give examples of how each would occur?
Increased Loss:
Gut (diarrhoea, laxatives)
Kidney (diuretics, magnesium deficiency, mineralocorticoid XS, renal tubular abnormalities)
Decreased Intake:
- Alcholol
- Anorexia
94
94.Hyperkalaemia is either due to increased intake or decreased loss - give examples of how each would occur?
Decreased loss:
- Reduced GFR
- Reduced tubular loss (potassium sparing diuretics anti-inflammatories, ACEIs, mineralocorticoid deficiency)
Increased Intake:
Usually parenteral
