1
Q
2 main reasons for deranged electrolytes
A
- net loss
- net gain
2
Q
____ changes in frail comorbid patients can have ____ clinical consequences (big/small)
A
- small
- big
3
Q
describe net loss for electrolyte derangement
A
- losing more than gaining => electrolyte level low
4
Q
describe net gain for electrolyte derangement
A
- gaining more than losing => electrolyte level high
5
Q
individuals causes for electrolyte derangement are still relating to what
A
- one of two foundational concepts of either net loss or net gain of electrolytes
6
Q
normal range of sodium
A
135-145mmol/L
7
Q
__% of sodium is extracellular
A
95%
8
Q
normal daily requirement of sodium mmol/kg/day
A
1-2mmol/kg/day
9
Q
how is sodium concentrations maintained across plasma membrane
A
sodium-potassium ATPase pump
10
Q
exchange of sodium-potassium ATPase pump
A
- 1 Na+ in cytoplasm to outside cell
- 1 Ka+ outside cell into cytoplasm
11
Q
what does normal sodium concentration mean outside and inside cell
A
- higher sodium concentration outside cell
- lower sodium concentration inside cell
12
Q
what does normal potassium concentration mean outside and inside cell
A
- lower potassium concentration outside cell
- higher potassium concentration inside cell
13
Q
sodium-potassium ATPase pump, in short, maintains what 2 concentrations
A
- high sodium outside cell
- high potassium inside cell
14
Q
extracellular volume (ECF) is maintained by ___
A
sodium
15
Q
can the volume of water in entire body be regulated without use of sodium?
A
no
16
Q
kidneys relationship to sodium
A
- kidneys pump sodium out of urine back into blood
17
Q
which ion is the biggest transmembrane ionic osmolar contributor
A
sodium
18
Q
if sodium pumped outside cell what would happen to water
if sodium pumped into cell what would happen to water
A
- draw water out with it
- draw water into cell
19
Q
sodium concentration (electrochemical gradient) also governs x and y of initial excitable cellular depolarisation
A
- speed
- magnitude
20
Q
when cell reaches threshold -> triggers action potential -> opens voltage gated ion channels -> speed and magnitude of ionic influx into cell is governed by….
A
that electrochemical concentration gradient - sodium
21
Q
__% sodium is ____ reabsorbed in proximal convoluted tubule
A
65%
passively
22
Q
__% of sodium is _______ in thick ascending limb (of loop of henley)
A
25%
absorbed
23
Q
-% of sodium is reabsorbed under the regulation of _____ in distal convoluted tubules & collecting ducts
A
- 5-12%
- hormones
24
Q
what increases sodium resabsorption
A
aldosterone (hormone)
25
where is aldosterone released from
zona glomerulosa in adrenal gland
26
mechanism for aldosterone release
- under action of RAAS system
- reduced sodium in filtrate (and chloride)
- macula densa reduced as it samples the filtrate
- when macula densa reduced, renin is released
- renin (runs thru its cascade pathway causing) -> leads to release of aldosterone
27
how does macula densa work regarding aldosterone release
- macula densa samples sodium and chloride load of filtrate passing
- macula densa reduces with reduced sodium in filtrate
- aldosterone released when reduced macula densa
28
what does aldosterone release do
- acts to increase number and activity of Na/KATPase pumps on blood-facing face of epithelium that sits in distal convoluted tubule and collecting duct
29
what 2 things lead to potassium leak into urine
- increase number and activity of NA/KATPase pumps (from aldosterone)
- insertion of ROMK channels on luminal side
30
hyperkalaemia is a stimulus for _____ which fixes that problem
- hyperkalaemia (increased K in blood)
- aldosterone release (which decreases K in blood)
31
how is sodium conserved / retained & what happens to water
- under electrochemical gradient, sodium in kidney will leak out of urine into epithelial cells
-Na/ATPase pumps will pump that sodium into blood
=> retain sodium
- water will move with it osmotically
32
what two locations does aldosterone act in kidney
- thick ascending limb (if loop of henle)
- collecting duct
33
if you have too much sodium, you will....
which will increase....
absorb water from urine
-> which increases total circulating blood volume
34
what will an increase total circulating blood volume lead to in heart
- increase preload into right atria
35
mechanism that occurs from an increased preload into right atria, which occurs due to excess sodium
- increases right atrial stretch
- stretch-stimulated ion channels depolarise
- causing secondary messenger cascade for release of brain natriuretic peptide (BNP)
- antagonises effects of aldosterone (so trying to get sodium thus also water out of blood)
- by stimulating excretion sodium into urine
- thus takes water with it, reducing blood volume, reducing sodium load
36
simply, what does aldosterone aim to do
ie/ increase sodium reabsorption
- increase amount of sodium in bloodstream
(hence increase amount potassium in urine)
- thus also causes more water retain in blood -> incr blood volume (due to osmotic gradient)
37
hyponatremia definition
- sodium <135mmol/L
38
when have hyponatremia (low sodium in blood), pathophysiology is mainly which
- less osmotic pull on intracellular water
- increase water movement into cell
- cellular swelling and functional disruption
- reduced action potential frequency and magnitude
39
explain sodium if there is less osmotic pull on intracellular water
- normal high concentration of sodium outside of cell, due to its osmotic force
- tendency to pull water from inside cell to outside cell
thus
- have less sodium outside such that the osmotic pull contributed to by sodium is less
- therefore there may shift the balance to increase water movement into cell
40
what happens in cells when there is increased water movement into cell
- cells compensate
41
can cells compensate if there is rapid changes in sodium outside cell and rapid changes of osmotic force generated in isolation by sodium (ie/ rapid sodium osmotic water changes)
- no because compensation takes time
- cannot generate idiogenic osmoles at fast enough rate
42
what happens to cell if cannot compensate for rapid sodium change outside cell
- net movement of water into cell
- cell begins to swell / increase in volume
43
describe cause of cellular functional disruption in regard to hyponatremia
- cell swelling / increasing in volume within a fixed space
44
what would happen if cells in brain swell within skull
- raised ICP
- disrupt usual architectural parenchyma of neurons -> functional dysfunction in overall cellular communications
45
two triggers for aldosterone release
- reduced macula densa sodium load
- hyperkalaemia
goal: sodium reabsorption
46
reduced sodium conc outside of cell also reduces _____ gradient by which sodium is forced into cell ie/ reduced AP _____ and _____
- electrochemical gradient
- action potential frequency and magnitude
47
why does reduced sodium conc outside of cell reduce AP frequency and magnitude
- causes sodium move into cell slower, as gradient is reduced
48
hyponatremia history risk factors
- aged
- frail
- comorbid - renal, cardiac failure
- medications - diuretics, antidepressants
49
why is spironolactone (diuretic medication) RF for hyponatremia
- preserves K, wastes Na
50
which diuretic medications can lead to hyponatremia
- spironolactone
- thiazide
51
why is thiazide (diuretic medication) RF for hyponatremia
- cause wasting of Na in the urine
52
how can antidepressants lead to hyponatremia
- cause syndrome of inappropriate diuretic hormone release
53
history of sodium derangement - timing: why is it important to delineate onset of sodium derangement
- determine speed of correction
54
2 foundational causes of hyponatremia
- losing too quickly
- not getting enough
55
describe cause 'exposure' for hyponatremia
- outside in sun sweating
- replacing sweat with water
56
2 sweat consistencies
- high volume, low concentration (electrolytes)
- small volume, high concentration (electrolytes)
57
when is a time that you would have small volume, high concentration (electrolytes) of sweat
- early summer before acclimatise to heat
58
why is sweat more amenable to replacement with water further on in the summertime
- as become more acclimatised to weather, you sweat greater volume but overall electrolyte loss is lower
- sweat is more dilute => more amenable to replacement with water
59
non-foundational causes of hyponatremia
- exposure
- poor oral intake
- fluid excess / restriction (esp use of diuretics)
- precipitating illness
60
why is hyponatremia due to poor oral intake less likely
examples of what could lead to restricted intake
- western diet
----
- mental health issue
- cognitive decline
- isolated
- strange dieting habits
61
symptoms of hyponatremia
(primarily neurological)
- confusion
- irritability
- somnolence (excess sleepiness)
- coma (severe)
- seizures (severe)
- muscle weakness
- cerebral oedema / swelling in brain (symptoms -> headaches, nausea, vomiting; esp if sudden drop)
62
what is swelling in brain
- abnormal accumulation of water within the brain
63
clinical signs of hyponatremia
- altered mental state
- somnolence
- agitation
- seizure
- coma
- often not much to find on neurological exam
- CT head: cerebral oedema (esp if occurred rapidly)
64
diagnostic algorithm - hyponatraemia
- determine serum osmolality
- check urine sodium and urine osmolality; takes time (do before treatment for accuracy)
65
serum osmolality calculation
> measured sodium sent off to lab; more time consuming; most accurate
> bedside calculation = 2x [measured sodium] + glucose + urea (all available on blood test)
-> should be within 10mosm of each other; if greater, than there is unseen component that is altering patient's osmolarity - osmolic gap
- normal serum: 275-295 mosm
66
urine sodium is low if x (same number)
40mmol
67
urine osmolality low if x (_____ urine) same no
- 100mosm
- dilute
- concentrated
68
3 different types of hyponatraemia
- serum hypo osmolar
- serum iso osmolar
- serum hyper osmolar
69
serum iso osmolar cause DDx (3)
- TURP syndrome
- hyperlipidaemia
- hyperproteinaemia
70
serum iso osmolar - hyponatraemia: serum osmolarity is _____, sodium conc is ___, conc of other solutes is ____
- normal
- low
- normal
71
serum hyper osmolar cause DDx (2)
- mannitol
- hyperglycaemia
72
what is mannitol & what does it do
- large sugar that acts as a diuretic
- shrink the brain (so can do surgery)
73
serum hyper osmolar - hyponatraemia: serum osmolarity is _____, sodium conc is ___, conc of other solutes is ____
elevated
- sodium conc low
- but conc other solutes is high
74
explain how hyperglycaemia leads to serum hyper osmolar hyponatraemia
- high glucose (in blood) osmotically sucks water out of cells
-> diluting sodium in blood sample
- fake-ish hyponatraemia
- correct serum sodium for your glucose (0.3 x glucose) + Na
- sodium not as low as you think - less hyponatraemic
75
keep hyperglycaemia which 2 patients in back of mind
- dka
- HHS (hyper osmolar hyperglycaemic patients) - most sim to dka in type II diabetics
76
(4) types of hyponatraemia serum hypo osmolar based on urine osmolality and urinary sodium
- high urine osmolality (>100mosm) & high urinary sodium (>40mmol)
- high urine osmolality (>100mosm) & low urine sodium (<40mmol)
- low urine osmolality (<100mosm) & high urinary sodium (>40mmol)
- low urine osmolality (<100mosm) & low urinary sodium (<40mmol)
77
what does low urine osmolality and high urine sodium translate to in serum hypo osmolar hyponatraemia
sodium ___ and water ____
- making dilute urine w/ lots of sodium in it
sodium wasting and water wasting
- producing vast amounts of both
78
what does high urine osmolality and high urine sodium translate to in serum hypo osmolar hyponatraemia
sodium ___ and water ____
- making concentrated (low volume) urine w/ lots of sodium in it
- sodium waste and water retention
79
what does high urine osmolality and low urine sodium translate to in serum hypo osmolar hyponatraemia
sodium ___ and water ____
- making concentrated urine (low volume) w/ low amount of sodium in it
- sodium retention & water retention
80
what does low urine osmolality and low urine sodium translate to in serum hypo osmolar hyponatraemia
sodium ___ and water ____
- dilute urine w/ low amounts of sodium in it
- sodium retention & water wasting
81
serum hypo osmolar hyponatraemia, high urine osmolality, high urinary sodium, cause DDx
- SIADH (syndrome of inappropriate anti-diuretic hormone excretion / vasopressin excretion)
- cerebral salt wasting
- chronic renal failure
- thiazide
- hypothyroidism
82
what do diuretics do
- draw more water into urine (via moving sodium causing osmotic pressure for water follow)
- increase pee
- reduce fluid build up in body
- help kidneys remove salt and water thru urine
- decr bp as result
83
____volemia and ____ urine output would you expect from examination of a SIADH patient
- normovolemia or hypervolemia patient
- w/ low urine output
- high conc of Na in urine
84
what does volemia refer too
amount of fluid in the blood
85
mechasnism for SIADH (hypo osmolar hyponatraemia)
- patients pituitary gland is releasing too much ADH / vasopressin
-> draw too much water out of urine
=> producing small amounts of concentrated salty urine
> patient is normovolemic or hypervolemic
86
____volemia and ____ urine output would you expect from examination of a cerebral salt wasting patient (high urine osmolality and high urinary sodium)
& why
- hypovolemia (low amount fluid in blood)
- w/ high urine output
- highly concentrated Na in urine
- their kidneys incapable thru unknown mechanism of holding onto salt
- so producing high quantities of concentrated salty urine
- peeing themselves dry
87
what is cerebral salt wasting associated with?
brain injuries
88
what patients (4) would have sodium and water retention ie/ high urine osmolality & low urinary sodium
- true hypovolemia (low fluid in blood; body trying to compensate)
- heart failure (even tho hypervolemic, their low blood flow to kidneys due to poor CO -> trick kidneys into thinking have low volume, so begin to compensate)
- cirrhosis
- nephrotic syndrome
89
what patients (4) would have sodium and water wasting (low urine osmolality & high urinary sodium)
- renal sodium loss
- post obstructive diuresis (obstruction eg/ tumour or stone causes build-up of back pressure -> kidneys shut down as need pressure gradient to filter -> relieve obstruction -> sudden drop in pressure gradient => kidney starts producing large quantities of dilute urine) (produces diuresis w sodium for a short time)
- post ATN diuresis (acute tubular necrosis - following bad infection, sepsis, heart attack, cardiogenic shock; kidneys weren't doing job and now switching back on, produce diuresis w sodium)
- acute renal failure
90
what patients (3) would have sodium retention and water wasting (low urine osmolality & low urinary sodium)
- polydipsia
- water administration [overshooting] - IV, enteral (consider patients who cannot control their own water intake; borderline water toxicity - too diluted)
- beer potomania (chronic alcoholics; alcohol contains low amounts sodium, drinking themselves into hyponatraemia & kidneys trying to retain sodium => allowing large quantities dilute urine to be produced)
91
why would body retain sodium
if perceives to not have enough in body
92
Electrolyte Imbalance
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