Sodium Flashcards
2 main reasons for deranged electrolytes
- net loss
- net gain
____ changes in frail comorbid patients can have ____ clinical consequences (big/small)
- small
- big
describe net loss for electrolyte derangement
- losing more than gaining => electrolyte level low
describe net gain for electrolyte derangement
- gaining more than losing => electrolyte level high
individuals causes for electrolyte derangement are still relating to what
- one of two foundational concepts of either net loss or net gain of electrolytes
normal range of sodium
135-145mmol/L
__% of sodium is extracellular
95%
normal daily requirement of sodium mmol/kg/day
1-2mmol/kg/day
how is sodium concentrations maintained across plasma membrane
sodium-potassium ATPase pump
exchange of sodium-potassium ATPase pump
- 1 Na+ in cytoplasm to outside cell
- 1 Ka+ outside cell into cytoplasm
what does normal sodium concentration mean outside and inside cell
- higher sodium concentration outside cell
- lower sodium concentration inside cell
what does normal potassium concentration mean outside and inside cell
- lower potassium concentration outside cell
- higher potassium concentration inside cell
sodium-potassium ATPase pump, in short, maintains what 2 concentrations
- high sodium outside cell
- high potassium inside cell
extracellular volume (ECF) is maintained by ___
sodium
can the volume of water in entire body be regulated without use of sodium?
no
kidneys relationship to sodium
- kidneys pump sodium out of urine back into blood
which ion is the biggest transmembrane ionic osmolar contributor
sodium
if sodium pumped outside cell what would happen to water
if sodium pumped into cell what would happen to water
- draw water out with it
- draw water into cell
sodium concentration (electrochemical gradient) also governs x and y of initial excitable cellular depolarisation
- speed
- magnitude
when cell reaches threshold -> triggers action potential -> opens voltage gated ion channels -> speed and magnitude of ionic influx into cell is governed by….
that electrochemical concentration gradient - sodium
__% sodium is ____ reabsorbed in proximal convoluted tubule
65%
passively
__% of sodium is _______ in thick ascending limb (of loop of henley)
25%
absorbed
-% of sodium is reabsorbed under the regulation of _____ in distal convoluted tubules & collecting ducts
- 5-12%
- hormones
what increases sodium resabsorption
aldosterone (hormone)
where is aldosterone released from
zona glomerulosa in adrenal gland
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
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
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
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
hyperkalaemia is a stimulus for _____ which fixes that problem
- hyperkalaemia (increased K in blood)
- aldosterone release (which decreases K in blood)
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
what two locations does aldosterone act in kidney
- thick ascending limb (if loop of henle)
- collecting duct
if you have too much sodium, you will….
which will increase….
absorb water from urine
-> which increases total circulating blood volume
what will an increase total circulating blood volume lead to in heart
- increase preload into right atria
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
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)
hyponatremia definition
- sodium <135mmol/L
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
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
what happens in cells when there is increased water movement into cell
- cells compensate
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
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
describe cause of cellular functional disruption in regard to hyponatremia
- cell swelling / increasing in volume within a fixed space
what would happen if cells in brain swell within skull
- raised ICP
- disrupt usual architectural parenchyma of neurons -> functional dysfunction in overall cellular communications
two triggers for aldosterone release
- reduced macula densa sodium load
- hyperkalaemia
goal: sodium reabsorption
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
why does reduced sodium conc outside of cell reduce AP frequency and magnitude
- causes sodium move into cell slower, as gradient is reduced
hyponatremia history risk factors
- aged
- frail
- comorbid - renal, cardiac failure
- medications - diuretics, antidepressants
why is spironolactone (diuretic medication) RF for hyponatremia
- preserves K, wastes Na
which diuretic medications can lead to hyponatremia
- spironolactone
- thiazide
why is thiazide (diuretic medication) RF for hyponatremia
- cause wasting of Na in the urine
how can antidepressants lead to hyponatremia
- cause syndrome of inappropriate diuretic hormone release
history of sodium derangement - timing: why is it important to delineate onset of sodium derangement
- determine speed of correction
2 foundational causes of hyponatremia
- losing too quickly
- not getting enough
describe cause ‘exposure’ for hyponatremia
- outside in sun sweating
- replacing sweat with water
2 sweat consistencies
- high volume, low concentration (electrolytes)
- small volume, high concentration (electrolytes)
when is a time that you would have small volume, high concentration (electrolytes) of sweat
- early summer before acclimatise to heat
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
non-foundational causes of hyponatremia
- exposure
- poor oral intake
- fluid excess / restriction (esp use of diuretics)
- precipitating illness
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
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)
what is swelling in brain
- abnormal accumulation of water within the brain
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)
diagnostic algorithm - hyponatraemia
- determine serum osmolality
- check urine sodium and urine osmolality; takes time (do before treatment for accuracy)
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
urine sodium is low if <x, high if >x (same number)
40mmol
urine osmolality low if <x (____ urine), high if >x (_____ urine) same no
- 100mosm
- dilute
- concentrated
3 different types of hyponatraemia
- serum hypo osmolar
- serum iso osmolar
- serum hyper osmolar
serum iso osmolar cause DDx (3)
- TURP syndrome
- hyperlipidaemia
- hyperproteinaemia
serum iso osmolar - hyponatraemia: serum osmolarity is _____, sodium conc is ___, conc of other solutes is ____
- normal
- low
- normal
serum hyper osmolar cause DDx (2)
- mannitol
- hyperglycaemia
what is mannitol & what does it do
- large sugar that acts as a diuretic
- shrink the brain (so can do surgery)
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
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
keep hyperglycaemia which 2 patients in back of mind
- dka
- HHS (hyper osmolar hyperglycaemic patients) - most sim to dka in type II diabetics
(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)
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
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
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
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
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
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
____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
what does volemia refer too
amount of fluid in the blood
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
____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
what is cerebral salt wasting associated with?
brain injuries
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
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
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)
why would body retain sodium
if perceives to not have enough in body
