Fluid & Electrolyte Balance Disorders Flashcards
What is the level of hyponatraemia? (mmol/L)
What level of hyponatraemia gives clinical consequences?
Hyponatraemia = < 135 mmol/L;
clinical consequences = < 125 mmol/L
(so is 135-145 normal and then +/- 10 either way = clinical consequences)
What is the numerical value of hypernatraemia?
What level gives clinical consequences?
Hypernatraemia > 145 mmol/L;
clinical consequences > 155 mmol/L
(so is 135-145 normal and then +/- 10 either way = clinical consequences)
What numerical value (mmol/L) is “hypokalaemia”?
< 3.5 mmol/L
What numerical value = “hyperkalaemia”?
> 4.7 mmol/L;
[so approximate range is 3.5-4.7]
clinical consequences > 6mmol/L
>6.5 = ~life threatening ventricular tachy
What numerical level is hypercalcaemia? (corrected)
> 2.6 mmol/L corrected calcium
> 3 mmol/L severe
- asymptomatic/ anorexia,
- nausea, malaise → headache, nausea, confusion, muscle cramps, ↓GCS & seizures
- Cerebral oedema, coma, fits
what electrolyte imbalance caused this & how did it occur (e.g. causes)?
Hyponatraemia (<135mmol/L; clinical consequences <125mmol/L)
e.g:
Excessive intake/retention water (dilution):
- DH, drugs (Ecstasy, carbamazepine, anti-depressants), CCF, cirrhosis, CKD/nephrotic syndrome, hypothyroidism, pregnancy
Renal Na loss:
- diuretics (cause Na loss),
- mineralocorticoid deficiency (normally aldosterone retains Na+),
- tubular disorders - dysfunctions of transporters and channels in renal tubular system
- SIADH (inc, aquaporins), cerebral salt wasting
Other Na loss:
- vomiting, diarrhoea, burns
Pseudo-hyponatraemia: hyperprotienaemia, hyperlipidaemia
- lethargy, thirst, weakness, irritability, fits, signs of dehydration
- mild confusion –> coma,
what electrolyte imbalance caused this & how did it occur (e.g. causes)?
Hypernatraemia (>145mmol/L; clinical consequences >155mmol/L)
Causes:
- water loss, blunted thirst with age,
- –> diabetes insipidus, DM (osmotic diuresis),
- –> diuretic use
- (NB: confusing as they also cause hyponatraemia, loop diuretics can increase water clearance giving relative hypernatraemia, just rememeber diuretics affect Na i guess!!),
- iatrogenic (excessive saline e.g. water gain),
- rarely sodium gain
What electrolyte imbalance caused this type of problem and how did it occur e.g. causes?
- muscle weakness,
- hypotonia,
- hyporeflexia,
- fatigue,
- constipation/paralytic ileus,
- ascending paralysis (<2mmol/L),
- arrhythmias
Hypokalaemia (<3.5mmol/L)
- Excessive renal loss: drugs (thiazides, loop), endocrine (aldosterone excess), inherited defects
- Magnesium deficiency (Na/K ATPase)
- Processes driving K+ into cells: acute alkalosis (e.g. low H+ = K+ into cells in exchange for intracellular H+ out into blood), insulin Rx, thyrotoxicosis
- GI losses: diarrhoea, vomiting (H+ loss causes alkalosis & K+ redistribution), low dietary potassium
What electrolyte imbalance does this indicate & what could have caused it?
- weakness of skeletal muscle,
- arrhythmias
Hyperkalaemia (>4.7mmol/L; clinical consequences >6mmol/L)
Reduced renal loss: low GFR, K-sparing diruetics, trimethoprim, RAAS inhibiting drugs - ACEI, mineralocorticoid deficiency (Addison’s), dietary excess
K+ release from cells: [e.g. weakness of skeletal muscle- if K+ is not in the cells = cant move to contract it; mg and K+ are both predominant Intracellular cations]
- acidosis (exchange for H+),
- tumour lysis,
- insulin deficiency,
- depolarising muscle paralysis,
- rhabdomyolysis,
Why is Ca2+ important to the resting state of Na+ channels in depolarisation?
Ca2+ STABILISED the resting state of Na+ channels
Ca2+ TF prevents spontaneous depolarisation
What electrolyte imbalance maybe happening with these signs and syx, what is the cause?
- paraesthesia (peri-oral),
- muscle cramps,
- tetany,
- laryngeal stridor,
- Chovostek & Trousseau signs,
- abdo pain,
- seizures,
- arrhythmias
Hypocalcaemia
- alkalosis,
- hypoparathyroidism,
- renal failure,
- vit D deficiency,
- malabsorption,
- acute pancreatitis (precipitation of calcium soaps in abdominal cavity but also glucagon stimulated calcitonin release)
- rhabdomyolysis, (hyperkalaemia but hypocalcaemia)
- sepsis,
- low Mg,
- panic attacks
What electrolyte imbalance maybe happening and what is the cause?
asymptomatic or
- bones (osteoporosis),
- stones (renal, UTIs, uraemia),
- abdo groans (constipation ulceration),
- psychic moans (mental disturbance),
- slow reflexes, polyuria, thirst, anorexia, weakness, HTN
Hypercalcaemia (>2.6mmol/L corrected calcium, >3mmol/L severe)
- acidosis
- hyperparathyroidism,
- thiazide diuretics (block NaCl but that is linked to calcium transport back into blood TF vs loop diuretics = inhibit the Na-K-2Cl transporter and TF increase Ca loss)
- malignant disease (BLT PK - breast, lung, thyroid, prostate (sclerotic), kidney),
- sarcoidosis,
- thyrotoxicosis,
- vit D intoxication,
- cortisol deficiency - (normally cortisol blocks calcium absorption by bone; inc cortisol = dc bone density)
- FHH (familial hypocalciuric hypercalcaemia e.g. inherited hypercalcaemia)
A patient is found to be having
- anorexia, nausea, malaise → headache, nausea, confusion, muscle cramps, ↓GCS & seizures
- Cerebral oedema, coma, fits
(NB: can be asymptomatic)
What is the Rx?
hyponatraemia
Rx: depends on if it is hypo/eu/hypervolaemic hypernatraemia –> Rx cause
- if hypervolaemic: Fluid restriction, cautious 0.9% saline, vasopressor receptor antagonists
- *Consider hypertonic saline e.g. 1.8% in emergency (–> draws fluid out…used in hyponatraemia, volume resus and brain injury)
-
Important to correct sodium at a slow speed - no more than 10mmol/L per 24hrs Na change
- Over-rapid correction may lead to central pontine myelinolysis (dehydrated brain)
-
Important to correct sodium at a slow speed - no more than 10mmol/L per 24hrs Na change
You have a patient presenting with mild confusion to coma, lethargy, thirst, weakness, irritability, fits, signs of dehydration
What is the Rx?
Hypernatraemia (>145mmol/L; clinical consequences >155mmol/L)
Rx of hypernatraemia:
- 1) WATER
- stop water loss (anti-emetic, stop diuretic, Rx diarrhoea)
- aim to replace 1/3rd water deficit per 24hrs + replace ongoing losses
- Water orally if possible
- 2) If not, give 5% glucose 1L/6h guided by UO & bloods
- 3) Important to correct sodium at a slow speed - no more than 10mmol/L per 24hrs Na change
- NB: Over-rapid correction of hypernatraemia may lead to cerebral oedema (too much fluid added)
A patient presents with muscle weakness, hypotonia, hyporeflexia, fatigue, constipation/paralytic ileus, ascending paralysis (<2mmol/L), arrhythmias.
What is the appropiate Rx?
Hypokalaemia (<3.5mmol/L)
potassium supplements (caution with renal impairment) oral preferably,
–> IV if <2mmol/L
A patients ECG is showing ST depression, flat T waves, U wave, extra-systoles
and arrythmias including AF, SVT, VT.
What electrolyde balance dysfunction does this indicate?
Hypokalaemia (<3.5mmol/L)
A patients ECG is showing tall tented T waves, broad QRS, prolonged PR, flat P waves and arrhythmias inclusing asystole & VF.
What is the underlying electrolyte disturbance?
Hyperkalaemia (>4.7mmol/L; clinical consequences >6mmol/L)
A patient is experiencing weakness of skeletal muscle & arrhythmias (systole, VF) what is the rx?
Hyperkalaemia (>4.7mmol/L; clinical consequences >6mmol/L)
Rx:
- K+ restriction (including K+ sparing drugs); if >6.3mmol/L:
- IV calcium gluconate (10ml 10%) if abnormal ECG to stabilise
- Measures to reduce serum K+
- 10U insulin + dextrose 50mL of 50%
- Salbutamol 10-20mg nebs
- If acidaemia & hypovolaemic - 1.4% sodium bicarbonate
- If resistant may need dialysis or hemofiltration
a patient is showing symptoms of - paraesthesia (peri-oral), muscle cramps, tetany, laryngeal stridor, Chovostek & Trousseau signs, abdo pain, seizures, arrhythmias.
What is the Rx?
Hypocalcaemia
–> rx =
- calcium supplements,
- calcium gluconate if urgent,
- Mg if needed (low mg –> inhibits PTH secretion = hypocalcaemia),
- vit D if needed etc.
A patient is presenting with ECG change –> Long QT and Arrhythmias including VF and heart block.
What is the likely electrolyte abnormality?
hypocalcaemia
(Rx: calcium supplements, calcium gluconate if urgent, Mg if needed, vit D if needed etc)
A patient is presenting with ecg changes - short QT but no arrythmias (they are uncommon for this)
what is the likely electrolyte abnormality?
Hypercalcaemia (>2.6mmol/L corrected calcium, >3mmol/L severe)
(Rx: fluids, bisphosphonates, Rx cause e.g. cancer mets etc)
How do you investigate for hypercalcaemia e.g. pt with
asymptomatic or bones (osteoporosis), stones (renal, UTIs, uraemia), abdo groans (constipation ulceration), psychic moans (mental disturbance), slow reflexes, polyuria, thirst, anorexia, weakness, HTN?
- Ca,
- PTH,
- phosphate,
- ALP,
- 24hr urinary Ca,
- TFTs,
- vit D,
- XR,
- DEXA,
- sestamibi (nuclear medicine used to look at heart, breast and PTH!)
Rx: fluids, bisphosphonates, Rx cause
How do you Rx for hypercalcaemia
e.g. pt with (asymptomatic) or bones (osteoporosis), stones (renal, UTIs, uraemia), abdo groans (constipation ulceration), psychic moans (mental disturbance), slow reflexes, polyuria, thirst, anorexia, weakness, HTN?
- fluids, bisphosphonates, Rx cause
[hyperparathyroidism, thiazide diuretics, malignant disease (BLT PK - breast, lung, thyroid, prostate (sclerotic), kidney), sarcoidosis, thyrotoxicosis, vit D intoxication, cortisol deficiency, FHH, acidosis]
Fluid replacement can be 5% glucose (dextrose), 0.9% NaCl (saline) or colloid e.g. volplex - 5% human albumin
Which fluid replacement is given the way you give IV water, but not bulk blood volume - as Only 5% of this fluid stays in the intravascular space (the rest Intracellular aka the same distribution as for water)?
5% glucose (dextrose)!
Fluid replacement can be 5% glucose (dextrose), 0.9% NaCl (saline) or colloid e.g. volplex - 5% human albumin
Which fluid replacement is best for resuscitating blood volume in very haemodyamically compromised patient - where initally most of it stays in the intravascular space?
Colloid e.g. Volplex 5% human albumin
Fluid replacement can be 5% glucose (dextrose), 0.9% NaCl (saline) or colloid e.g. volplex - 5% human albumin
Which fluid replacement is better for resuscitating blood volume with 33% staying in the intravascular space and distribution as for ECF?
0.9% NaCl (saline)
Water balance is very important for the body,
- where does water intake and
- output come from and
- how does water redistribute?
- Water intake comes from drinking water but also in food - fluid is metabolically produced from food
- output of water = sweat, faeces, urine, evaporation
- redistribution of water occurs when osmotically active substances are in the blood and may result in water distribution to maintain osmotic balance but cause changes in other measured solutes
- Excess solute in ECF = hyperosmolality –> cells shrink (dehydrate)
- excess water in ECF (hypoosmolality) –> cells swell (oedema)
Water balance is very important in the body and exists in different fluid compartments: ICF, ECF and as total body water. What are the levels of these?
Total body water = 42L (60% body weight in a 70kg human)
ICF: 2/3rds
ECF: 1/3rd
- Of the ECF 1/3rd…
- Interstitial fluid 2/3rds
- (comes from substances that link out of blood capillaries & so is fluid found in the spaces around cells - helps bring oxygen and nutrients to cells to remove waste products from them)
- Plasma + lymph 1/3rd
- Interstitial fluid 2/3rds
What are stimulation of vasopressin release. stimulation of hypothalamic thirst centre and redistribution of water from ICF all triggered by and then all work towards?
Water loss –> INCREASE ECF OSMOLALITY
- stimulates vasopressin release –> renal water retention
- stimulation of hypothalamic thirst centre –> increased water intake
- redistribution of water from ICF –> increased ECF water
–> restoration of ECF osmolality
[ECF = interstitial fluid and plasma + lymph]
How does ADH/vasopressin work?
- Acts on renal collecting ducts →↑ permeable to water (aquaporin channels):
- = water absorption back into the body = conctration of urine
*
What is the secretion of ADH/vasopressin stimulated by?
- Increase in plasma osmolality (v. sensitive 1 -2% change) - e.g. ADH wants to dilute it
- Pain, stress, nausea, drugs, lung and CNS lesions, ectopic - post-operative accumulation of water
- Decrease in plasma volume (>5-8%)
What is the secretion of ADH/vasopresin DECREASED by?
ADH decreases in:
- decrease in plasma osmolality (plasma dilution) - ADH not needed
- increase in plasma volume
- ethanol (resulting in diuresis)
ADH secretion or not depends on plasma osmolality and plasma volume as well as some other diseases/factors e.g. stress/ethanol
between plasma osmolality and plasma volume which one would win if plasma osmolality was low (stopping ADH) but ECF/intravascular was low too?
FOR ADH: ECF/INTRAVASCULAR VOLUME OVERRIDES OSMOLAR CONTROLS
This is a key message;
- if salt & water in the wrong place you get RAAS activation! –> promotes Na & water retention
How do you diagnose syndrome of inappropriate ADH?
it is a diagnosis of exclusion although SIADH can be due to small cell carcinoma of the lung, post brain trauma (SAH)
–> look for
- Euvolaemia ie. no evidence of volume depletion or oedema (that would stimulate ADH)
- Hyponatraemia and hypo-osmolality
- Inappropriately high urine osmolality & excessive renal excretion of Na –> shows ADH is being used to concentrate uring
- Normal renal, adrenal, pituitary, thyroid
- pt Not on any drugs (diuretics, antidiuretics)
once excluded all other causes of ADH like physiological, drugs, renal, adrenal, pit and thyroid and the urine is concentrated to diagnose SIADH via exclusion - what is the Rx for SIADH?
Fluid restriction!
Low oncotic pressure e.g. from low albumin
diuretics
splanchnic vasodilation
all lead to ineffective plasma volume, how does the body make up for this?
Ineffective plasma volume –>
- Activation of RAS system–> Na+ retention
- Thirst, water drawn from ICF into ECF & ADH secretion –> volume overrides osmolar controls –> excessive increaase in free water –> hypervolaemia hyponatraemia (dilutional)
Sodium balance is very important physiologically.
Where does our intake of salt come from?
- Dietary (unless vegan don’t need to add salt)
- Western diet 100-200 mmol/day
- Iatrogenic -
- antibiotics,
- fluid resuscitation
- (0.9% saline has more Na & Cl than normal plasma - Hartmann’s is more physiological)
Sodium balance is very important physiologically.
Where does our output of salt come from?
- Obligatory loss - Skin (NB Na+ loss in burns!)
- Controlled excretion (determined by intravascular volume)
-
Kidneys -
- 95-98% Na reabsorbed by PCT driven by renal perfusion; fine tuning occurs later in tubule
- Aldosterone (of RAAS)
- GFR (see kindeys section)
-
Gut - most sodium is reabsorbed;
- –> loss is pathological - when gut integrity is disturbed e.g. cholera ! (aka loss of Na in diarrhoea, vomiting, burns)
-
Kidneys -
How is sodium balance via alsosterone stimulated?
BP/volume sensed
- Baroreceptors (pressure sensors)
- Renal perfusion pressure
Aldosterone produced
- Adrenal cortex
Action at DCT
- Na reabsorption
- Loss of H/K
How do you assess fluid balance on clinical assessment e.g. hx, exam etc
- History:
- fluid intake/output,
- D&V,
- PMH,
- *medication
- Exam (volume status):
- lying & standing BP,
- pulse,
- oedema,
- skin turgor,
- JVP/CVP
- Fluid chart: not always accurate!
What do anticonvulsants (carbamazepine), anti-neoplastics (cyclophosphamide), hypoglycaemics (chlorpropamide), nacrotics (morphine) all do to sodium?
they all increase ADH secretion –> TF associated with hyponatraemia
What are tricyclics, SSRis (prozac), paracetamol and indomathacin associated with?
They potentiate ADH action –> associated with hyponatramia
What other medication apart from …
Increase ADH secretion: anticonvulsants (carbamazepine), anti-neoplastics (cyclophosphamide), hypoglycaemics (chlorpropamide), nacrotics (morphine)
Potentiate ADH action: tricyclics, SSRIs (Prozac), paracetamol, indomethacin
,,, are associated with hyponatraemia?
Diuretics! –> thiazides, frusemide, K+ sparing (amiloride, spironolactone)
all are assosicated with hyponatramia
(asymptomatic/ anorexia, nausea, malaise → headache, nausea, confusion, muscle cramps, ↓GCS & seizures, Cerebral oedema, coma, fits )
- Paired serum & urine osmolality & electrolytes–>which includes serum osmolality, urine osmolality and urine:serum ratio
- urea/creatinine ratio
- urinary sodium
- & calculated serum osmolality
are all key lab investigations for hyponatraemia.
What do the paired serum & urine osmolality & electrolytes represent?
- Paired serum & urine osmolality & electrolytes
- Serum osmolality: indicates if other osmotically active substances are present
- Urinary osmolality: ignore the reference interval, relate to serum osmolality
- Urine/serum: >1 water conservation, <1 water loss
- Paired serum & urine osmolality & electrolytes–>which includes serum osmolality, urine osmolality and urine:serum ratio
- urea/creatinine ratio
- urinary sodium
- & calculated serum osmolality
are all key lab investigations for hyponatraemia.
What does the urea/creatinine ratio represent?
Urea/creatinine ratio is useful -
high urea = dehydration
- Paired serum & urine osmolality & electrolytes–>which includes serum osmolality, urine osmolality and urine:serum ratio
- urea/creatinine ratio
- urinary sodium
- & calculated serum osmolality (2Na+urea+glucose +/-10)
are all key lab investigations for hyponatraemia.
What does the urinary sodium & its levels represent?
<20mmol/L of sodium in the urine = conservation,
>20mmol/L of Na+ in the urine = loss
If a patient on assessment is hyponatraemic but hypovolaemic and their urine Na is <20. What does this mean?
<20mmol/L = consevation yet the patient is euvolaemic (so normal physiological)
–> extra-renal salt loss
- gi loss –> replacement with hypotonic fluid e.g. water/dex
- vomiting
- diarrhoea
- skin loss
- burns
- sweating
- haemorrhage
If a patient on assessment is hypovolaemic and their urine Na is > 20. What does this mean?
>20 in urinary Na = loss and hypovolaemia
= renal salt loss
- addisons diuretic Rx
- Salt losing nephritis
- solute diuresis
- cerebral salt wasting
If a patient on assessment is hyponatraemic but euvolaemic and their urine Na is <20. What does this mean?
acute H20 overload - excess intake of fluid…
as body is conserving self (<20mmol/L in urine) but euvolaemic
- psychogenic
- beer
- potomania [condition where Na dc due to excessive beer consumption poto=alc + mania]
- iatrogenic (IV fluids etc)
If a patient on assessment is hyponatraemic but euvolaemic and their urine Na is > 20. What does this mean?
>20mmol/L = loss of Na –>
- Chronic H2O overload
- impaired excretion
e.g. SIADH, hypothyroid, glucocorticoid deficiency (as in cushings = Na retain, K+ and H+ loss, and if deficient e.g. addisons then is opposite so na loss, K+ and H+ retain)
If a patient on assessment is hyponatraemic but hypervolaemic and their urine Na is < 20. What does this mean?
<20 = conserving sodium
- cirrhosis
- cardiac failure
- nephrotic syndrome
- usually + diuretic Rx
Is acidosis associated with hyper or hypokalaemia?
Acidosis is associated with hyperkalaemia
- K+ (and Mg2+) are the most predominant Intracellular ions
- in excess H+ in ECM –> taken intracellularly at K+ expense
[insulin drives K+ into the cell for Na out, beta and alpha catecholamines switch K= in and out and osmollaity allows passive leakage of K= from cells)
TF alkalosis is assoc w/ hypokalaemia
What effect on K+ does aldosterone have?
Aldosterone causes K+ loss into the urine as in exchange for retaining Na+ it loses K+ and H+
e.g. glucocorticoids do this too because at high concentrations cortisol can exhibit mineralocorticoid activity (e.g. aldosterone)
What is the effect of insulin on K+?
insulin casues uptake of K+ into the ICF e.g. there is loss from the ECF –> redistribution
In tissue damage/trauma what happens to K+ levels in blood?
K+ in normally intracellular (98% of K+ is intracellular)
in tissue damage/trauma = high K in ECF
What can cause increased or decreased intake of potassim?
increased intake = hyperkalaemia –> usually parentera
decreased intake = hypokalaemia - often alcohol or anorexia
- What can cause increased or decreased loss of potassium?
Decreased loss - hyperkalaemia
- Reduced GFR (diet contains excess K, we spend our lives getting rid of it)
- Reduced tubular loss (K+ sparing diuretics, anti-inflammatories, ACEIs, mineralocorticoid deficiency)
INCREASED LOSS - hypokalaemia
- Gut (diarrhoea, laxatives)
- Kidneys (diuretics, magnesium deficiency, mineralocorticoid excess, renal tubular abnormalities)
What effects of redistribution on potassium does acid/alkalosis have?
acidosis = K+ into ECF
Alkalosis = K+ intracellular (in exchange for H+)
What effects of redistribution on potassium does high/low insulin have?
low insulin = less K+ uptake into ICF
high insulin = more K+ uptake into ICF
What effects on redistribution of K+ does beta agonists have?
causes hypokalaemia in the blood e.g. pulls K+ intracellular
What kind of electrolyte imbalance does poor venepuncture technique (not using vacutainers, narrow needles, injection blood through narrow needles into vacutainers) cause?
Factitious hyperkalaemia
What patient group is often magnesium deficient?
ALCOHOLICS ARE OFTEN MAGNESIUM DEFICIENT
MODEST hypoMAGNESIA stimulates what?
Whilst PROFOUND hypomagnesia stimulates what?
- modest hypomagnesaemia stimulates PTH secretion (hypercalcaemia, bone resorption?)
-
Profound hypomagnesaemia inhibits PTH secretion → hypocalcaemia
- Some evidence that Mg deficiency may impair renal 1a-hydroxylation of vitamin D (TF cant absorb calcium and promote bone growth)
- Severe hypomagnesia also causes K+ to be lost from cells (as mg normally aids the ATPase pumping K+ intracellularly) into ECF and then K+ is lost from urine (ROMK channels are inhibited by Mg to excrete K+ into renal tubules) ==> HYPOKALAEMIA w/ hypomagnesia
Female collapses at home; elevated urea, creatinine, hypernatraemic, high Hb
What is the cause/rx?
- Causes: almost always H2O loss > Na+ gain
- Rx: aim to replace 1/3rd of the water deficit in addition to usual fluid maintenance in 1st 24hrs
- Fluid replacement of Water orally or via NG is the best way - its how we are designed!
NB:
- Don’t want to give fluid/ lower Na too quickly -(fall of >8mmol/L in 24hrs is risky) risk of cerebral oedema
- Neurons exposed to high external Na concentration, they build up their own Na concentration
- Don’t want to raise Na too quickly either - risk central pontine myolinolysis?
What is going on with this pt:
- 80y/o woman;
- drowsy
- confused;
- febrile;
- dry mucous membranes;
- hypotensive
- & tachycardic;
- High sodium
- High urea (disproportional to raised creatinine)
- High creatinine
- Low eGFR
- High sodium - indicative of dehydration
- High urea (disproportional to raised creatinine) - useful for PRE-RENAL blood loss/dehydration
- High creatinine
- Low eGFR - AKI
Dx: dehydration due to fever
What is going on with this patient?
38y/o woman; psychiatric hx; not eaten but drunk lots of water
- Low sodium
- Normal potassium
- Serum osmolality > urine osmolality
- Low sodium - volume overload, dilution
- Normal potassium - K mostly intracellular, not affected by ECF change
- Serum osmolality > urine osmolality - dilute urine, trying to get rid of water (ADH) & keep Na+ (RAAS)
Dx: volume overload
What is going on with this patient?
79y/o woman; D&V; tachycardic; orthostatic hypotension
- Low sodium
- High urea
- Serum osmolality < urine osmolality
- Low sodium
- High urea
- Serum osmolality < urine osmolality - concentrated urine, trying to conserve water & salt
Dx: dehydration due to D&V
NB: Serum osmolality = 2Na + urea + glucose
What is going on with this patient?
78y/o male; persistent chest infection symptoms for 2 months
- Low sodium
- Low chloride
- High bicarbonate
- Low creatinine
- Serum osmolality < urine osmolality
- Low sodium
- Low chloride
- High bicarbonate
- Low creatinine
- Serum osmolality < urine osmolality - conserving water but this is INAPPRORPIATE
Dx: volume overload (all electrolytes are diluted), due to SIADH - likely due to small cell carcinoma of lung (SIADH can also be from SAH)
What is going on with this patient?
- 39y/o male;
- alcoholic liver disease & cirrhosis;
- ascites & bilateral pleural effusions
- Low sodium & potassium
Dx: hypervolaemic hyponatraemia
What causes sodium excess?
- Sodium excess is Usually iatrogenic
- Often multifactorial & complicated
- (usually hypernatraemia is from lack of thirst, DM, dehydration)
What is going on with this patient?
73y/o male;
- ITU following bowel perforation;
- septic;
- fluid resuscitated;
- cef + met;
- polyuric
- Test results:
- High sodium
- High urea + creatinine (creatinine > urea) - no evidence of dehydration
Dx:
- Na from increased intake due to treatment (antibiotics);
- kidneys concentrating ability often impaired in sick pts & so pt is experiencing polyuria
What is going on in this patient?
76y/o male, hx prostatism, 24hrs anuria
- High potassium
- High urea + creatinine (creatinine > urea)
- Very low eGFR
- Low HCO3 - acidosis
- Hyperkalaemia due to AKI
- (e.g. rise in creatinine 1.5x from baseline and/or decreased urine output (0.5mL/kg for >6hrs)
- & failure of K excretion
- (also redistribution due to acidosis)
What is going on with this patient?
- 16y/o woman;
- T1DM with poor control;
- vomiting & drowsy
- U&E’s
- Low sodium
- High potassium
- High urea + creatinine (creatinine > urea)
- Low HCO3
- V high osmolality
- Low sodium - water moving into ECF due to osmotic force of high glucose
- High potassium - acidosis, H into cell, K out cells
- High urea + creatinine (creatinine > urea) - not dehydration
- Low HCO3 - acidotic
- V high osmolality - DIABETES & glucose
Dx: redistribution hyperkalaemia due to insulin deficiency & acidosis
What is going on with this patient?
- 78y/o woman;
- HTN;
- new BP medication
- U&E:
- Low potassium
- High urea + creatinine (creatinine > urea)
Diuretic induced hypokalaemia –> give potassium supplements with diuretics!
[diuretics preventing sodium ion reabsorption from the nephron –> increased delivery of sodium to the distal tubule whre it can be exchanged for K+ increases urinaty K+ losses –> hypokalaemia]
What is going on with this patient?
45y/o male; alcoholic; presented after a binge
- Low potassium
- Low adjusted calcium
- High creatinine (urea fine)
- Low magnesium
Low Mg= alcoholics! Magnesium needed for N/K ATPase & PTH secretion?
Dx: hypokalaemia due to decreased intake + renal loss (2o to low magnesium)
NB: severe hypomagnesaemia often coexist with hypokakaemia as mg is needed for ATPase of K Intracellulerly and then Mg is used to STOP ROMK channels in renal apical tubular membrane so with low Mg = K+ lost from urine. (profound hypomagnesia inhibits PTH = hypocalcaemia)
What is going on with this patient?
- 21y/o woman;
- collapse 7d post-appendectomy;
- weight loss,
- tired & lethargic;
- hypotensive;
- tachycardic but afebrile
- U&Es
- Low sodium
- High potassium
- High urea + creatinine (creatinine > urea)
- Serum osmolality < urine osmolalityE
- Low sodium - NOT BEING RESORBED
- High potassium - WOULD BE NORMAL/LOW IF ADH PROBLEM! K NOT BEING EXCRETED…
- THINK ALDOSTERONE…
- High urea + creatinine (creatinine > urea)
- Low sodium - loss of glucocorticoid control
- Serum osmolality < urine osmolality - conserving water but this is INAPRORPRIATE
diagnosis: Addison’s disease - primary ADRENAL INSUFFICIENCY = low cortisol/glucocorticoid and mineralocorticoids e.g. aldosterone causing
(addisons = low na, high K+ and H+ … see pic attached)
