Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiology for Anaesthetists > Renal - regulation of water and electrolyte balance > Flashcards

Renal - regulation of water and electrolyte balance Flashcards

1
Q

Summarise the distribution of total body water

A

60% of 70 kg = 42 L

ECF (14 L)

  • plasma: 3
  • Interstitium: 10
  • transcellular: 1

ICF (28 L)
- Intracellular: 28

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How can intracellular fluid, interstitial fluid and total body water be calculated?

A

Plasma

  • agent cant cross endothelial membrane
  • radio-labelled albumin

ECF

  • agent can cross endothelium but not phospholipid bilayer
  • thiosulphate

Total body water

  • agent can cross both endothelial barrier and phospholipid bilayer
  • Deuterated water (2H2O)

ICF and interstitial can be calculated from these values

The above is based on the formula:

n = C x V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does osmolarity differ from molarity

A

Osmolarity is defined as the number of osmoles per litre of solution, where osmoles denotes the number of moles of particles that are able to exert an osmotic pressure.

Molarity is the number of moles of a particular solute dissolved per litre of solution; that is, the concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the formula for serum osmolarity

A

[Plasma] = 2[Na] + 2[K] + [glucose] + [urea]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does osmolality differ from osmolarity.

A

Osmolality is the number of osmoles per kilogram of solvent
–> independent of temperature and weight of solute

Osmolarity is the number of osmoles per litre of solution
–> The volume of the solution changes with temperature and volume of solute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the osmolar gap? What does the presence of an osmolar gap indicate?

A

It is the difference between the measured osmolality and calculated osmolarity

Osmolar gap = osmolality - osmolarity

The osmolar gap indicates the presence of additional unmeasured osmotically active particles in the plasma that are NOT INCLUDED IN THE ESTIMATION OF PLASMA OSMOLARITY
E.g.
1. Alcohol intoxication
2. Hypertryglyceridaemia
3. Methanol
4. Ethylene glycol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why is 5% Dextrose infused instead of free water to rehydrate patients

A

If free water is infused, acute dop in venous blood tonicity occurs. The hypotonic solution causes red blood cells to swell and haemolyse. 5% dextrose is used instead as this solution has an osmolarity of 278 mOsmol/L which is close to plasma osmolarity of 285 - 298 mOsmol/L. Once the glucose is metabolized, free water has been infused but without the acute drop in osmolarity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is plasma osmolarity controlled

A

Feedback loop.

SENSOR:
Osmoresceptors in the hypothalamus.
- Extremely sensitive: 1% change detected

CONTROL CENTER:
Hypothalamus
- Normal set point is 285 - 298 mmol/L

EFFECTORS
Hypothalamus
1. Stimulates thirst
2. Reduce water excretion by the kidney –> ADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is ADH

A

Antidiuretic Hormone
Arginine Vasopressin

It is a nine amino acid peptide

Synthesis:
Hypothalamus PVN and SON (paraventricular and supraoptic nuclei)

Transfer:
To posterior pituitary where it is stored in granules

Secretion:
Controlled by hypothalamus in response to increased osmolarity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Apart from the insertion of aquaporins into the collecting duct, what other function does ADH have?

A

Peripheral vasoconstriction
–> normally circulating ADH has negligible influence on arteriolar tone.

However, in situations of hypovolaemic shock, the posterior lobe of the pituitary secretes large amounts of ADH. At high concentrations, ADH is a powerful vascoconstrictor and plays an important role in maintaining systemic blood pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does ADH act on the kidney

A

Basolateral membrane faces capillaries

Luminal membrane faces lumen

There are existing aquaporins 3 and 4 on the basolateral membrane so this side is already permeable to water.

Aquaporin 2 is inserted into the luminal membrane of the collecting duct cells in response to stimulation of V2 receptors by ADH. V2 –> cAMP –> aquaporin 2 insertion

Water then moves in, through the collecting duct cell, into the blood down its concentration gradient established by:

  1. High osmolarity of renal medulla (LOH countercurrent exchange mechanism)
  2. Urea cycling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is the high osmolarity of the renal medulla generated

A

THIN DESCENDING LIMB LOH:

  • permeable to water
  • impermeable to ions and urea

THIN ASCENDING LIMB LOH

  • impermeable to water
  • Permeable to ions and urea

THICK ASCENDING LIMB

  • Impermeable to water
  • Permeable to ions and urea
  • Secondary active transport: Luminal Na/K/2Cl- co transporters powered by basolateral Na/K ATPase

This establishes a high osmolarity in the renal medulla. which is maintained by the hairpin countercurrent arrangement of the associated vasa recta as the solutes are not washed away. The vasa recta descend with the ascending lop and ascend with the descending loop.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is diabetes insipidus

A

CENTRAL DIABETES INSIPIDUS (E.g. intracranial disturbance –> hypothalamic dysfunction)

  • ADH secretion failure
  • large volume dilute urine
  • hypernatraema
  • elevated serum osmolarity
  • low urine osmolarity

NEPHROGENIC DIABETES INSIPIDUS

  • E.g. Lithium
  • Collecting ducts fail to respond to ADH
  • same clinical findings as above
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is SIADH

A

Syndrome of inappropriate ADH secretion
- excessive ADH from posterior pituitary or from an ectopic source (e.g. small cell lung carcinoma)

–> HYPONATRAEMA (and low plasma osmolarity)
Headache, nausea, confusion, seizures, coma
Sometimes with fluid overload

–> Inappropriately high urine osmolarity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe how urea is handled through the nephron

A

PCT
50% of filtered urea is reabsorbed

LOH
60% urea is secreted into the tubular lumen

110% of filtered urea is now present within the lumen at the DCT

Collecting duct (Inner medullary)
70% urea reabsorbed

Urine contains about 40% of filtered urea.

so essentially urea is reabsorbed (PCT), the secreted (LOH), then transported in the lumen to the inner medullary collecting duct where it is reabsorbed. The reabsorption of urea here contributes to the high inner medullary osmolarity necessary for water reabsorption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Apart from aquaporin 2 insertion into the CD luminal membrane and vascoconstriction during shock, what other function does ADH have

A

It increases the insertion of Urea Transporter A1 (UT-A1) into the luminal membrane of the inner medullary collecting duct

17
Q

Classify the mechanisms of control of sodium excretion

A
  1. Changes to GFR
    - high plasma volume –> high GFR –> increases Na excretion
    - low plasma volume –> low GFR –> reduced Na excretion
  2. Changes to tubular Na reabsorption
18
Q

Discuss the reabsorption of Na in the various regions of the nephron

A

PCT - 60%

  • Basolateral Na/K ATPase
  • ->
    1. Passive diffusion Na (low intracellular Na)
    2. Co-transport: SGLT
    3. Counter-transport: Na+/H+

LOH (thick ascending) - 30%
- Na/K/2Cl co-transporter

DCT and collecting duct

  • Aldosterone mediated Na reabsorption
    1. Early DCT Na/Cl co-transporter (5%)
    2. Late DCT and collecting duct (2%)
  • —–> PRINCIPLE cells: Na/K counter-transporter
  • —–> INTERCALATED cells: Na/H counter-transporter
19
Q

Summarise the physiological response to low plasma volume

A

ANP and BNP reduced (atrial stretch receptors)
‘Hypovolaemia hormones’ secreted

  1. Noradrenalin
    - -> afferent and efferent VC –> reduced GFR –> reduced Na excretion
  2. ADH increase
    - -> Increased reabsorption H2O from collecting duct
  3. Renin increase
    - -> ANG II: PCT –> increases Na reabsorption
    - -> Aldosterone: DCT –> increased Na reabsorption

Overall: Conservation of fluid through reduction of GFR and reduction in sodium excretion

20
Q

What is the maximum possible concentration of urine. And what is the minimum daily urine output and why?
What is the volume of insensible fluid losses per day?

Therefore, what is the minimum daily intake of fluid required?

A

1200 mmol/L and equals the concentration of the interstitium in the inner renal medulla.

The kidney must excrete osmotically active waste products accounting for about 600 mOsmol/day

So, minimum daily urine out: V = n/c

600 mOsmol
____________

1200 mOsmol/L

= 500 mL/day

Insensible losses ± 500 ml/day

Minimum daily fluid intake is therefore 1000 mL

21
Q

Classify diuretics and summarise their mechanism of action

A

Osmotic diretics e.g. mannitol
- Freely filtered into lumen with no reabsorption –> increase osmolarity of the filtrate –> reduced water reabsorption –> increased urine volume

CA inhibitors (acetazolamide)
- Reduced HCO3- reabsorption --> increased HCO3- excretion in the urine

Loop diuretics (furosemide and bumetanide)

  • Inhibit Na/K/2Cl co-transporter in thick ascending LOH
  • reduced Na/K/Cl reabsorption PLUS disruption of counter-current mechanisms. Very effective and known as high-ceiling diuretics

Thiazide (HCTZ, bedroflumethiazide)
- Block Na/Cl co-transporter in the early DCT

Potassium sparing diuretics (spironolactone, amiloride, trimaterene)

  • Spironolactone blocks aldosterone receptors in DCT / CD. Increased Na excretion and H+/K+ retention
  • Amiloride blocks Na channels in the DCT and collecting duct (similar effects to spironolactone)
22
Q

ADH is involved in regulating osmolarity and plasma volume. Which takes priority?

A

Small changes in osmolarity may lead to catastrophic brain swelling in the closed compartment of the cranium.
–> ADH response triggered with 2 - 3 % change in osmolarity

In contrast small changes in plasma volume are relatively well tolerated owing to the high compliance of the venous circulation, which acts as a blood reservoir
–> ADH response triggered with 7- 10% change in blood volume

HOWEVER, with large volume losses > 10% –> volume regulation takes priority owing to the possibility for tissue ischaemia.

23
Q

What happens to ADH secretion when hypertonic saline is administered. What does this illustrate

A

Hypertonic saline will increase osmolarity (should increase ADH) and increase volume (should reduce ADH)

The response is an increase in ADH showing that ADH is regulation is more sensitive to osmolarity than volume.

24
Q

Summarise the physiological response to a high plasma volume

A
  1. Stretch receptors: atria and pulmonary vessels –> respond to hypervolaemia by reducing their afferent output to the medulla –> reduced: noradrenalin, ADH and renin –> increased Na excreted in urine
  2. Dilution of plasma proteins and hence lower plasma oncotic pressure –> increased filtration fraction (Starling)
  3. ANP (atria) and BNP (ventricles)
    - —-> 1. Afferent arteriolar vasodilatation with efferent arteriolar vasoconstriction –> increase GFR and hence Na excretion
    - —-> 2. Relax glomerular mesangial cells –> increases surface area for filtration
    - —-> 3. Block Na channels in DCT and CD
    - —-> 4. Inhibits renin secretion by granular cells
    - —-> 5. Inhibits aldosterone secretion from adrenal cortex
25
Q

Summarise the effects of ANP and BNP

A
  1. Afferent VD + Efferent VC –> increased GFR and Na loss
  2. Mesangial cell relaxation –> increased SA for filtration –> increased GFR –> Na loss
  3. Block Na channels DCT + CD
  4. Inhibit renin release (granular cells)
  5. Inhibit aldosterone release (renal cortex)
26
Q

Which substance is responsible for most of the intracellular osmotic pressure. Discuss proportions of this substance in the ECF and ICF

A

Potassium

98% in the ICF (150 mmol/L)

2 % in the ECF (3.5 - 5.5 mmol/L)

27
Q

Why is it important that a concentration gradient of potassium from the ICF to the ECF is maintained

A

This gradient is responsible for maintaining the resting membrane potential of cells.

28
Q

What is the minimum RDA water and electrolytes:

H2O –
Na+ – 
K+ – 
Ca2+ – 
Mg2+ – 
PO4 –
A 
H2O – 30 mL/kg
Na+ – 2mmol/kg
K+ – 1mmol/kg
Ca2+ – 0.1 mmol/kg
Mg2+ – 0.1 mmol/kg
PO4 – 0.1 mmolkg

LITFL

29
Q

How does the body deal with excessive potassium ingestion in the diet

A

Insulin stimulates basolateral Na/K ATPase whcih increases cellular K uptake reducing plasma levels

30
Q

What are the mechanisms for potassium shifts

A
  1. Insulin –> Stimulates basolateral Na/K ATPase
  2. Alpha adrenoreceptor –> triggers K release from cells (ECF K triggers glycogenolysis + vasodilation in active muscle)
  3. Beta adrenoreceptor –> Stimulates basolateral Na/K ATPase
  4. Extracellular pH –> Excess H+ (acidosis) buffered by uptake into cells
    - electroneutrality maintained by pushing K out
    - or intracellular acidosis impaire Na/K ATPase less K moved in.
    Reverse occurs in alkalosis.
31
Q

Describe renal handling of potassium

A

Filtration: Freely filtered

PCT and LOH:

  • Almost all K is reabsorbed in PCT and LOH (Na/K/2Cl)
  • this occurs irrespective of whether body K is high or low

DCT and CD

  • When plasma K is low:
  • —–> Additional K is absorbed in the DCT (H+/K+ ATPase). 99% reabsorbed.
  • When K + is high
  • —-> Adrenal cortex directly stimulated to release aldosterone

Overall:
In low K –> 99% of K can be reabsorbed
In high K –> 80% of filtered potassium can be excreted

32
Q

What is the mechanism of membrane stabilization when Calcium is given during hyperkalaemia

A

High K outside cell –> Less gradient for movement of K+ leaking out –> More positive charge remains in cell (vs outside cell) –> More depolarized membrane which is closer to membrane potential) –> cells are more excitable –> dysrhythmogenic.

Reverse is true for hypokalaemia

Ca+ ions bind to the outer surface of the membrane. This creates a local high density of positive charge outside the cell, hence creating a relatively more negative intracellular voltage.

33
Q

What are the classical ECG findings in hypokalaemia

A

Think hyperpolarization of RMP
Think reduced excitability

Prolonged PR
ST depression
Inverted/flattened T waves
U waves

Physiology for Anaesthetists (61 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions