Investigation of salt/water and acid/base balance Flashcards

1
Q

What percentage of body weight is body fluids?

A

Total body fluids = 60% of body weight

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2
Q

What are obligatory losses of water?

A

§ Obligatory losses
□ Skin (sweat)
□ Lungs

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3
Q

What are controlled losses of water dependent on?

A

§ Controlled losses – these depend on:
□ Renal function
□ ADH
□ Gut (main role of colon)

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4
Q

What are the intakes of sodium?

A

○ Intake

□Dietary (unless vegan and doesn’t add salt)

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5
Q

What are obligatory losses of sodium?

A

§ Obligatory loss

-Skin

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6
Q

What are controlled losses/excretion of sodium?

A

§ Controlled losses/excretion
□ Kidneys
□ Aldosterone – fine controlling of Na balance
□ GFR
□ Gut – most sodium is reabsorbed; loss is pathological

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7
Q

Where is aldosterone produced and what does it regulate?

A

Aldosterone produced in the adrenal cortex: regulates sodium and potassium homeostasis and hydrogen ion balance

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8
Q

What do natriuretic hormones promote and decrease?

A

○ Natriuretic hormones (ANP cardiac atria, BNP cardiac ventricles) promote sodium excretion and decrease blood pressure

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9
Q

Where is ADH/Vasopressin synthesised in and what does its release cause?

A

ADH/vasopressin: synthesised in hypothalamus and stored in posterior pituitary. Release causes increase in water absorption in collecting ducts

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10
Q

Where is AQP1(Aquaporin 1) located and not under the control of?

A

Located on the proximal tube

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11
Q

Where are AQP2 and 3 present and what are they under the control of?

A

AQP2 and 3 present in collecting duct and under control of ADH

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12
Q

What is the response to increased ECF osmolality due to water loss?

A

○ Stimulation of vasopressin release causing renal water retention allowing the restoration ECF osmolality
○ Stimulation of hypothalamic thirst centre which leads to increased water intake allowing restoration of ECF osmolality
○ Redistribution of water from ICF which leads to increased ECF water allowing the restoration of ECF osmolality

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13
Q

Where is 85% of Na reabsorbed in renal tubules?

A

85% Na is reabsorbed in PCT

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14
Q

What is fine tuning of Na reabsorption under the influence of?

A

Fine tuning of Na reabsorption under influence of aldosterone in exchange for hydrogen and potassium ions

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15
Q

What does the kidney sense and so what signal does it send and cause the release of what?

A

• Kidney senses reduced perfusion so sends signal from adrenal cortex to release renin

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16
Q

What does renin convert angiotensin into and what does it cause?

A

• Renin converts angiotensinogen to angiotensin I in lungs
○ This goes back to adrenal cortex to stimulate aldosterone from adrenal cortex
○ Signal to start reabsorbing more Na

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17
Q

What converts angiotensin I into angiotensin II?

A

• Angiotensin I is converted to Angiotensin II by ACE

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18
Q

What does dehydration mean?

A

Dehydration means less water perfusing the kidney

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19
Q

How is there a difference in handling of urea and creatinine in dehydration?

A

○ Creatinine is excreted
○ Urea, if perfusion rate drops, starts being reabsorbed in kidney
- Mismatch between urea and creatinine

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20
Q

What would happen to the Na, urea and creatinine levels in psychogenic polydipsia?

A

They would be low

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21
Q

BP in psychogenic polydipsia

A

Normal

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22
Q

Why is there low urine sodium in psychogenic polydipsia?

A

Low urine sodium because too much water so kidney needs to reabsorb all sodium to match the water intake

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23
Q

What happens if you drop your Na really quickly?

A

• If you drop your Na really quickly, can get violent and aggressive

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24
Q

What history do you take when assessing patients with fluid/electrolyte disturbance?

A
○ Fluid intake/output
○ Vomiting/diarrhoea
○ Past history
○ Medication
     -Drugs that may predispose them to imbalances in Na
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25
What examinations do you take when assessing patients with fluid/electrolyte disturbance?
``` ○ Lying and standing BP ○ Pulse ○ Oedema ○ Skin turgor/tongue dryness  ○ JVP/CVP -BP monitors  ```
26
What can over rapid correction in hyponatremia lead to?
○ Over rapid correction may lead to central pontine myelinolysis
27
What can over rapid correction in hypernatremia lead to?
○ Over rapid correction may lead to cerebral oedema
28
What speed is it important to correct sodium at?
Important to correct sodium at the same speed no more than 10mmol/L per 24 hours of sodium change
29
What does it mean if urea is significantly higher than creatinine?
○ Urea significantly higher than creatinine = dehydration 
30
What does a urinary sodium of <20mmol/L mean?
Conservation
31
What does a urinary sodium of >20mmol/L mean?
Loss
32
What does urine osmolality >1 mean?
Water conservation
33
What does urine osmolality of <1 mean?
Water loss
34
What are the common causes of hypernatraemia?
Dehydration, drugs containing Na
35
What does hypertonic hyponatremia occur due to?
Occurs due to increased glucose
36
What happens to levels in pseudohypoNa?
○ High TGs | ○ High protein 
37
What layer is present on top of blood in pseudohypoNa?
○ Creamy layer on top of blood 
38
What do we measure if someone is hypovolemic in hypotonic hyponatraemia?
measure Na in urine  § If conserving Na, Na is being lost somewhere else e.g. GI loss (vomiting, diarrhoea), skin loss, haemorrhage  § High urine Na: loss through kidney 
39
What happens if urine Na is <20mM and the patient is euvolemic in hypotonic hyponatremia?
§ Urine Na: <20mM □ Acute water overload □ Psychogenic polydipsia 
40
What happens if urine Na is >20mM and the patient is euvolemic?
□ Chronic water overload  □ Impaired excretion  □ Hypothyroidism 
41
What happens if urine Na is <20mM and the patient is hypervolaemic?
□ Oedema  □ Cirrhosis  □ Cardiac failure  □ Nephrotic failure 
42
Why is maintenance of extracellular [H+]/pH essential?
Maintenance of extracellular [H+]/pH is essential to maintain protein/enzyme function
43
What systems are involved in the maintenance of extracellular [H+]/pH?
○ Overall pH on the relative balance between acid production and excretion ○ Carbon dioxide production and excretion (respiration) ○ Hydrogen ion production and excretion (renal)
44
Henderson Hasselbalch equation
Just derive and look at ppt slide
45
What is metabolic acidosis?
Rate of H+ generation > excretion 
46
What is the compensation for metabolic acidosis?
○ Compensation is respiratory  § Consumption of HCO3 § Removal of CO2 
47
What is respiratory acidosis?
Rate of CO2 excretion < generation
48
What is the compensation for respiratory acidosis?
○ Metabolic compensation § Increased renal excretion of H+ § Regeneration of HCO3
49
What is compensation?
• Attempt to return acid / base status to normal
50
When can respiratory compensation for a primary metabolic disturbance occur?
Respiratory compensation for a primary metabolic disturbance can occur very rapidly
51
How long does it take for metabolic compensation for primary respiratory abnormalities?
Metabolic compensation for primary respiratory abnormalities take 36-72 hours to occur
52
What is the mechanism of renal bicarbonate regeneration?
* HCO3 is reabsorbed in DCT  * Na is taken up into cell in exchange for K  * Lose hydrogen in preference to K because H is more toxic 
53
What are the pitfalls of ABG?
* Expel air * Mix sample * Analyse ASAP * Plastic syringes OK at room temp for  ̴ 30mins * Ice not required * Ensure no clot in syringe tip
54
Interpretation of ABG
* pO2 - remember to check FiO2 * pH – Normal or does it show an acidosis/alkalosis * pCO2 – primary respiratory or compensatory response * HCO3 – metabolic component
55
How do we obtain the HCO3 value?
Not measured, is calculated using Hendersson Hasselbalch 
56
Causes of respiratory acidosis
``` • Airway obstruction ○ Bronchospasm (Acute) ○ COPD (Chronic) ○ Aspiration ○ Strangulation • Respiratory centre depression ○ Anaesthetics ○ Sedatives ○ Cerebral trauma ○ Tumours • Neuromuscular disease ○ Guillain-Barre Syndrome ○ Motor Neurone Disease • Pulmonary disease ○ Pulmonary fibrosis ○ Respiratory Distress Syndrome ○ Pneumonia • Extrapulmonary thoracic disease ○ Flail chest  ```
57
How do you compensate for respiratory acidosis?
Increased renal acid excretion (metabolic alkalosis, 36-72 hrs delay)
58
What does correction of respiratory acidosis require?
○ Requires return of normal gas exchange
59
What are the features of acute respiratory acidosis?
acute: increased pH (increased[H+]), increasedpCO2, -->[HCO3-],– ie. no compensation
60
What are the features of chronic respiratory acidosis?
Decreased pH(Increased[H+]), Increased pCO2, increased[HCO3-], ie. compensation
61
What are the causes of respiratory alkaolosis?
- Hypoxia - Mechanical overventilation - Increased respiratory drive
62
How do you compensate for respiratory alkalosis?
Increased renal bicarbonate excretion
63
What are the features of acute respiratory alkalosis?
high pH, low [H+], n[HCO3-], low pCO2
64
What are the features of chronic respiratory alkalosis?
high pH, low [H+], low [HCO3-], low pCO2
65
How do you compensate metabolic acidosis?
hyperventilation, hence low pCO2
66
How is there correction of metabolic acidosis?
• Correction ○ of cause ○ increased renal acid excretion
67
What are the features of metabolic acidosis?
○ Low pH, high [H+], low [HCO3-], low pCO2
68
What are the causes of metabolic alkalosis?
- Increased addition of base - Decreased elimination of base - Increased loss of acid - GI loss - Renal
69
How do you compensate for metabolic alkalosis?
• Compensation  | -Hypoventilation with CO2 retention (respiratory acidosis)
70
How is there correction of metabolic alkalosis?
○ Increased renal bicarbonate excretion  | ○ Reduce renal proton loss
71
What are the features of metabolic alkalosis?
High pH, low [H+], high [HCO3-], N/highpCO2
72
Clinical scenarios of metabolic alkaolosis
``` • Hypovolaemia from persistent vomiting ○ Loss of HCl ○ Loss of potassium ○ Loss of fluid • Diuretics ○ Chronic K+ depletion • Response to fluid loss is aldosterone activation ○ Reabsorb NaCl/H2O at distal convoluted tubule in kidney in exchange for K+ /H+ ```