Fluid & Electrolyte Balance Disorders

Question 1

What is the level of hyponatraemia? (mmol/L)

What level of hyponatraemia gives clinical consequences?

Answer 1

Hyponatraemia = < 135 mmol/L;

clinical consequences = < 125 mmol/L

(so is 135-145 normal and then +/- 10 either way = clinical consequences)

Question 2

What is the numerical value of hypernatraemia?

What level gives clinical consequences?

Answer 2

Hypernatraemia > 145 mmol/L;

clinical consequences > 155 mmol/L

(so is 135-145 normal and then +/- 10 either way = clinical consequences)

Question 3

What numerical value (mmol/L) is “hypokalaemia”?

Answer 3

< 3.5 mmol/L

Question 4

What numerical value = “hyperkalaemia”?

Answer 4

> 4.7 mmol/L;

[so approximate range is 3.5-4.7]

clinical consequences > 6mmol/L

>6.5 = ~life threatening ventricular tachy

Question 5

What numerical level is hypercalcaemia? (corrected)

Answer 5

> 2.6 mmol/L corrected calcium

> 3 mmol/L severe

Question 6

• 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)?

Answer 6

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

Question 7

• lethargy, thirst, weakness, irritability, fits, signs of dehydration
• mild confusion –> coma,

what electrolyte imbalance caused this & how did it occur (e.g. causes)?

Answer 7

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

Question 8

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

Answer 8

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

Question 9

What electrolyte imbalance does this indicate & what could have caused it?

• weakness of skeletal muscle,
• arrhythmias

Answer 9

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,

Question 10

Why is Ca2+ important to the resting state of Na+ channels in depolarisation?

Answer 10

Ca2+ STABILISED the resting state of Na+ channels

Ca2+ TF prevents spontaneous depolarisation

Question 11

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

Answer 11

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

Question 12

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

Answer 12

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)

Question 13

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?

Answer 13

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)

Question 14

You have a patient presenting with mild confusion to coma, lethargy, thirst, weakness, irritability, fits, signs of dehydration

What is the Rx?

Answer 14

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)

Question 15

A patient presents with muscle weakness, hypotonia, hyporeflexia, fatigue, constipation/paralytic ileus, ascending paralysis (<2mmol/L), arrhythmias.

What is the appropiate Rx?

Answer 15

Hypokalaemia (<3.5mmol/L)

potassium supplements (caution with renal impairment) oral preferably,

–> IV if <2mmol/L

Question 16

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?

Answer 16

Hypokalaemia (<3.5mmol/L)

Question 17

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?

Answer 17

Hyperkalaemia (>4.7mmol/L; clinical consequences >6mmol/L)

Question 18

A patient is experiencing weakness of skeletal muscle & arrhythmias (systole, VF) what is the rx?

Answer 18

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

Question 19

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?

Answer 19

Hypocalcaemia

–> rx =

• calcium supplements,
• calcium gluconate if urgent,
• Mg if needed (low mg –> inhibits PTH secretion = hypocalcaemia),
• vit D if needed etc.

Question 20

A patient is presenting with ECG change –> Long QT and Arrhythmias including VF and heart block.

What is the likely electrolyte abnormality?

Answer 20

hypocalcaemia

(Rx: calcium supplements, calcium gluconate if urgent, Mg if needed, vit D if needed etc)

Question 21

A patient is presenting with ecg changes - short QT but no arrythmias (they are uncommon for this)

what is the likely electrolyte abnormality?

Answer 21

Hypercalcaemia (>2.6mmol/L corrected calcium, >3mmol/L severe)

(Rx: fluids, bisphosphonates, Rx cause e.g. cancer mets etc)

Question 22

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?

Answer 22

• 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

Question 23

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?

Answer 23

• 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]

Question 24

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)?

Answer 24

5% glucose (dextrose)!

Question 25

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?

Answer 25

Colloid e.g. Volplex 5% human albumin

Question 26

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?

Answer 26

0.9% NaCl (saline)

Question 27

Water balance is very important for the body, 1. where does water intake and 2. output come from and 3. how does water redistribute?

Answer 27

1. Water intake comes from drinking water but also in food - fluid is metabolically produced from food 2. output of water = sweat, faeces, urine, evaporation 3. 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)

Question 28

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?

Answer 28

Total body water = **42L** (60% body weight in a 70kg human) ICF: **2/3rds** ECF: **1/3rd** * Of the ECF 1/3rd... * Interstitial fluid **2/3**rds * (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 **1/3**rd

Question 29

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?

Answer 29

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]

Question 30

How does ADH/vasopressin work?

Answer 30

* Acts on renal collecting ducts →↑ permeable to water (aquaporin channels): * = water absorption back into the body = conctration of urine *

Question 31

What is the secretion of ADH/vasopressin stimulated by?

Answer 31

* 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%)**

Question 32

What is the secretion of ADH/vasopresin DECREASED by?

Answer 32

ADH decreases in: * decrease in plasma osmolality (plasma dilution) - ADH not needed * increase in plasma volume * ethanol (resulting in diuresis)

Question 33

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?

Answer 33

_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

Question 34

How do you diagnose syndrome of inappropriate ADH?

Answer 34

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)

Question 35

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?

Answer 35

Fluid restriction!

Question 36

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?

Answer 36

Ineffective plasma volume --\> 1. Activation of **RAS** system--\> _Na+ retention_ 2. **Thirst**, **water** drawn from **ICF** into ECF & **ADH** secretion --\> volume overrides osmolar controls --\> excessive increaase in free water --\> _hypervolaemia hyponatraemia (dilutional)_

Question 37

Sodium balance is very important physiologically. Where does our intake of salt come from?

Answer 37

* 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)

Question 38

Sodium balance is very important physiologically. Where does our output of salt come from?

Answer 38

* 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)

Question 39

How is sodium balance via alsosterone stimulated?

Answer 39

BP/volume sensed * Baroreceptors (pressure sensors) * Renal perfusion pressure Aldosterone produced * Adrenal cortex Action at DCT * Na reabsorption * Loss of H/K

Question 40

How do you assess fluid balance on clinical assessment e.g. hx, exam etc

Answer 40

* 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!

Question 41

What do anticonvulsants (carbamazepine), anti-neoplastics (cyclophosphamide), hypoglycaemics (chlorpropamide), nacrotics (morphine) all do to sodium?

Answer 41

they all increase ADH secretion --\> TF associated with hyponatraemia

Question 42

What are tricyclics, SSRis (prozac), paracetamol and indomathacin associated with?

Answer 42

They potentiate ADH action --\> associated with hyponatramia

Question 43

What other medication apart from ... ## Footnote Increase ADH secretion: anticonvulsants (carbamazepine), anti-neoplastics (cyclophosphamide), hypoglycaemics (chlorpropamide), nacrotics (morphine) Potentiate ADH action: tricyclics, SSRIs (Prozac), paracetamol, indomethacin ,,, are associated with hyponatraemia?

Answer 43

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 )

Question 44

* 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?

Answer 44

* 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

Question 45

* 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?

Answer 45

Urea/creatinine ratio is useful - **high urea** = **dehydration**

Question 46

* 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?

Answer 46

\<20mmol/L of sodium in the urine = conservation, \>20mmol/L of Na+ in the urine = loss

Question 47

If a patient on assessment is hyponatraemic but hypovolaemic and their urine Na is \<20. What does this mean?

Answer 47

\<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

Question 48

If a patient on assessment is hypovolaemic and their urine Na is **\> 20**. What does this mean?

Answer 48

\>20 in urinary Na = loss and hypovolaemia = renal salt loss * addisons diuretic Rx * Salt losing nephritis * solute diuresis * cerebral salt wasting

Question 49

If a patient on assessment is hyponatraemic but euvolaemic and their urine Na is \<20. What does this mean?

Answer 49

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)

Question 50

If a patient on assessment is hyponatraemic but euvolaemic and their urine Na is \> 20. What does this mean?

Answer 50

\>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)

Question 51

If a patient on assessment is hyponatraemic but hypervolaemic and their urine Na is \< 20. What does this mean?

Answer 51

\<20 = conserving sodium * cirrhosis * cardiac failure * nephrotic syndrome * usually + diuretic Rx

Question 52

Is acidosis associated with hyper or hypokalaemia?

Answer 52

_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_

Question 53

What effect on K+ does aldosterone have?

Answer 53

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)

Question 54

What is the effect of insulin on K+?

Answer 54

insulin casues uptake of K+ into the ICF e.g. there is loss from the ECF --\> redistribution

Question 55

In tissue damage/trauma what happens to K+ levels in blood?

Answer 55

K+ in normally intracellular (98% of K+ is intracellular) in tissue damage/trauma = high K in ECF

Question 56

What can cause increased or decreased intake of potassim?

Answer 56

increased intake = hyperkalaemia --\> usually parentera decreased intake = hypokalaemia - often alcohol or anorexia

Question 57

* What can cause increased or decreased loss of potassium?

Answer 57

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)

Question 58

What effects of redistribution on potassium does acid/alkalosis have?

Answer 58

acidosis = K+ into ECF Alkalosis = K+ intracellular (in exchange for H+)

Question 59

What effects of redistribution on potassium does high/low insulin have?

Answer 59

low insulin = less K+ uptake into ICF high insulin = more K+ uptake into ICF

Question 60

What effects on redistribution of K+ does beta agonists have?

Answer 60

causes hypokalaemia in the blood e.g. pulls K+ intracellular

Question 61

What kind of electrolyte imbalance does poor venepuncture technique (not using vacutainers, narrow needles, injection blood through narrow needles into vacutainers) cause?

Answer 61

Factitious hyperkalaemia

Question 62

What patient group is often magnesium deficient?

Answer 62

ALCOHOLICS ARE OFTEN MAGNESIUM DEFICIENT

Question 63

MODEST hypoMAGNESIA stimulates what? Whilst PROFOUND hypomagnesia stimulates what?

Answer 63

* **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

Question 64

Female collapses at home; elevated urea, creatinine, hypernatraemic, high Hb What is the cause/rx?

Answer 64

* 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?*

Question 65

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

Answer 65

* 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**

Question 66

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

Answer 66

* 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**

Question 67

What is going on with this patient? 79y/o woman; D&V; tachycardic; orthostatic hypotension * Low sodium * High urea * Serum osmolality \< urine osmolality

Answer 67

* 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

Question 68

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

Answer 68

* 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)

Question 69

What is going on with this patient? * 39y/o male; * alcoholic liver disease & cirrhosis; * ascites & bilateral pleural effusions * Low sodium & potassium

Answer 69

Dx: **hypervolaemic hyponatraemia**

Question 70

What causes sodium excess?

Answer 70

* Sodium excess is Usually iatrogenic * Often multifactorial & complicated * (usually hypernatraemia is from lack of thirst, DM, dehydration)

Question 71

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

Answer 71

Dx: * Na from increased intake due to treatment (antibiotics); * kidneys concentrating ability often impaired in sick pts & so pt is experiencing polyuria

Question 72

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

Answer 72

* 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)

Question 73

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

Answer 73

* 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**

Question 74

What is going on with this patient? * 78y/o woman; * HTN; * new BP medication * U&E: * Low potassium * High urea + creatinine (creatinine \> urea)

Answer 74

**_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]*

Question 75

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

Answer 75

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)*

Question 76

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

Answer 76

* 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)