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Renal system > Control, volume and composition of ECF > Flashcards

Control, volume and composition of ECF Flashcards

1
Q

what is osmolarity?

A

when particles dissolve in solution they exert osmotic force that attracts water water

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2
Q

what determines osmotic pressure?

A

the number of active particles per unit of volume, not their size, all particles exert 1 unit of osmolarity

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3
Q

what is osmolality?

A

the number of particles of solute per kg of solvent

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4
Q

interstitial fluid

A

no protein
same as plasma otherwise
high sodium
low potassium

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5
Q

plasma

A

proteins - higher than interstitial but less than intracellular
otherwise same as interstitial fluid
high sodium
low potassium

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6
Q

intracellular fluid

A 
high potassium
low sodium 
no calcium 
lower carbonate
higher phosphate
highest protein
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7
Q

what do proteins contribute to?

A

oncotic pressure

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8
Q

osmolarity

A

starting osmotic pressure with all solutes

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9
Q

what is tonicity?

A

glucose taken up by cells and so this is the final osmotic pressure after any solute is removed

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10
Q

what is oncotic pressure?

A

the pressure generated by proteins, makes a major contribution to fluid movement between plasma and interstitial fluid, as it is the difference between the 2

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11
Q

IV fluids

A

usually approximately isosmolar but not all is isotonic

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12
Q

fluid distribution

A

2/3 body weight is liquid
1/3 is solid
of the 2/3 liquid 2/3 is intracellular and 1/3 extracellular
of the extracellular fluid 1/3 intravascular and 2/3 interstitial

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13
Q

composition of intravascular fluid

A

40% cells

60% plasma

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14
Q

water movement

A

moves between all compartments

movement sped by aquaporins

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15
Q

glucose movement

A

move into and out of cells through endothelium via glucose transporters
gaps in endothelium enhance movement

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16
Q

electrocyte movement

A

electrolytes pass through endothelial gaps easily but not through cell membranes as they need special channels/ pumps

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17
Q

protein movement

A

minimal movement of proteins between compartments as they are large and need movement by pinocytosis

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18
Q

osmoregulation

A

regulated by alterations in water content of urine or changing degree of thirst
ADH is the main regulating hormone

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19
Q

ADH

A

peptide
controlled by osmoreceptors
aka vasopressin

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20
Q

urine output

A

varies from 300mL/day to 10L/ day

very concentrated to very dilute

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21
Q

normal osmolality

A

290mosm/L

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22
Q

what happens if osmolality increases?

A

increased ECF osmolality
hypothalamic osmoreceptors stimulated
paraventricular and supra-optic nuclei make and control release of ADH
ADH release from posterior pituitary
ADH inserts aquaporins into collecting duct, increasing permeability
water retention by kidney
lateral preoptic area in hypothalamus causes thirst
drink water
osmolarity brought back to normal

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23
Q

what causes increased osmolality?

A

water deprivation
salt ingestion
diarrhoea

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24
Q

what happens if there is a decrease in osmolality?

A
  • decreased ECF osmolality
  • hypothalamic osmoreceptors are inhibited
  • lateral preoptic area supresses thirst
  • paraventricular and supra-optic nuclei cause ADH release to be suppressed
  • the collecting duct becomes more water impermeable
  • water excretion increased by kidney
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25
Q

what causes decreased osmolality?

A

excessive fluid ingestion

decreased ECF osmolality

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26
Q

how is ADH made?

A
  • made as pre-pro-hormone from 166 amino acid residues
  • successive cleavage during passage down neural transport system from hypothalamus to posterior pituitary
  • final form is a 9-peptide
  • stored in secretory granules
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27
Q

what stimulates ADH release?

A

osmoreceptors
RAAS - part of shock response system
sympathetic NS and angiotensin II

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28
Q

where are osmoreceptors?

A

vascular organ of lamina terminalis

outside BBB

29
Q

how do osmoreceptors work?

A

contain aquaporins
when plasma osmolarity rises water leaves the cells causing shrinkage
triggers mechanically regulated ion channels to create an action potential
causes ADH synthesis and release

30
Q

how does ADH work?

A

loop of henle has created a hypertonic environment around medullary collecting ducts
insertion of aquaporins allowing reabsorption of water via osmotic gradient
ADH binds to ADH V2 receptors causing aquaporin insertion on luminal side due to activation of conversion of ATP to cAMP via GPCR
extreme osmotic gradient between interstitial fluid and ECF so water pulled in

31
Q

what else effects ADH release?

A

stimulated by nicotine
inhibited by ANP
inhibited by alcohol

32
Q

damage to posterior pituitary

A

ADH production will cease
causing diabetes insipidus (low ADH)
large volumes of dilute urine excreted

33
Q

volume regulation

A

osmolarity of ECF is tightly controlled
volume of ECF is determined by total quantity of solute - mainly NaCl
regulation of ECF volume is about sodium balance

34
Q

what controls sodium balance?

A

aldosterone

35
Q

aldosterone

A

main mineralocorticoid

steroid hormone

36
Q

where is aldosterone made?

A

zona glomerulosa of adrenal cortex

37
Q

what does aldosterone target?

A

principal cell - ENaC in

distal convoluted tubule

38
Q

how does aldosterone work?

A

alters gene expression
stimulates epithelial sodium channel - increases Na+ reabsorption and K+ secretion
stimulates Na+/K+ pump to keep intracellular Na+ low

39
Q

what stimulates release of aldosterone?

A

angiotensin II - RAAS
increased plasma K+ - reabsorbing Na+ causes K+ loss, so if K+ increases it needs to be lost
ACTH has some but little impact

40
Q

what inhibits aldosterone release?

A

ANP

41
Q

what causes ANP release?

A

elevated ECF volumes
stretch receptors
released from atrial wall

42
Q

how does ANP work?

A 
dilutes sodium 
increases GFR
aldosterone secretion is inhibited 
renin and ADH release inhibited
increases Na+ excretion in urine
43
Q

how is osmolarity regulated?

A

altering water

44
Q

how is volume regulated?

A

altering Na+

45
Q

addison’s disease

A

causes deficiency of aldosterone

46
Q

Aldosterone drugs

A 
agonist = fludrocortisone
antagonist = spironolactone
47
Q

ADH drugs

A

agonists = terlipressin/ desmopressin
antagonist = tolvaptan
vasopressors - raise low BP

48
Q

ANP drugs

A

agonists = anartide

not in clinical use

49
Q

spironolactone

A

given with loop diuretic
diuretic on its own
reduces effect of aldosterone
causes loss of Na+

50
Q

daily requirements

A

2.5-3L of water (drink just over 2L)

1mmol/kg/day of Na+ and K+

51
Q

what are the IV solution options?

A

0.9% saline
Hartmann’s saline
5% dextrose
4% dextrose and 0.18% saline

52
Q

0.9% saline

A

physiological saline
osmolarity close to plasma
slightly higher conc of Na+
use being reduced due to concern over too much Cl-

53
Q

Hartmann’s solution

A

contains lactate and calcium as well as sodium, potassium, chloride and glucose
closer to plasma

54
Q

5% dextrose solution

A

close osmolarity to plasma
gives water due to metabolism of glucose
only contains dextrose

55
Q

dextrose 4% and 0.18% saline

A

toxic as causes hyponatraemia

sick patients need more Na+ due to hormonal response to stress, surgery, illness which produces Na+ and water retention

56
Q

24hr IV fluid plan

A

1L 0.9% saline or Hartmann’s
2L 5% dextrose
60mmol K+

57
Q

high K+ concentrations

A

cause death

58
Q

hyponatraemia

A

<130mmol/L

caused by water retention which dilutes sodium or Na+ loss

59
Q

what causes water retention?

A

heart failure
inappropriate ADH - secretion
excess intake - oral/ IV

60
Q

what causes Na+ loss?

A

diuretics
vomiting
diarrhoea
adrenal failure - Addison’s disease

61
Q

what is the danger of hyponatraemia?

A

water will move to equalise
water into brain cells by osmosis causing cerebral oedema, coma and death
greater risk in children

62
Q

what is SIADH?

A

syndrome of inappropriate ADH secretion

oversecretion of ADH

63
Q

causes of SIADH

A

tumours - small cell lung cancer
infections - pneumonia
drugs - SSRIs
hypothyroidism

64
Q

irrigation fluid for endoscopic resections

A

has to be non-conductive and heat stable (no glucose) due to diathermy so glycine (amino acid solution) used

65
Q

problem with glycine

A

no sodium
resection exposes open blood vessels and so irrigation fluid is absorbed straight into blood vessels
causes hyponatraemia
due to fluid overload

66
Q

how to treat hyponatraemia?

A

water restriction/ no more IV saline
can use hypertonic aline in a crisis
over-rapid correction risks neuronal damage - demyelination

67
Q

sweat

A

normal sodium content = 40mmol/L - lower than plasma concentration
relative to ECF more water than sodium is lost in sweat
hyperosmolar because sodium concentration rises with more loss of water
increases thirst

68
Q

rehydration after exercise

A

with just water restores volume but causes hyponatraemia as lowers ECF sodium concentration
causes a fall in osmolarity
inhibits ADH - excretion of water

69
Q

what does alcohol do?

A

inhibits ADH
water diuresis
sodium concentration increases
increased thirst

Renal system (17 decks)

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