Chem Flashcards
SUMMARY CARD:
All relevant equations in Chem Path:
1. Osmolarity
2. Osmolar gap
3. Anion gap
- Osmolarity =
2(Na + K) + urea + glucose
- Osmolar gap =
osmolality (measured) - osmolarity (calculated)
(if < 10, then normal) - Anion gap =
(Na + K) - (Cl + HCO3)
(normal range = 14-18)
SUMMARY CARD:
- Where is fluid found in the body?
- What is osmolality vs osmolarity?
- BONUS: which ion is the largest contributor to osmolality?
- 60-40-20 rule = 60% of total body weight is water (40% is intracellular, 20% extra cellular)
-
Osmolality = total number of particles in a solution measured with an osmometer; units are mmol/kg (AKA the
mass
of a solvent); normal range for serum osmolality is 275-279 mmol/kg -
Osmola
R
ity = the volume in litR
es of the solvement; units are mOsm/L
Omolality is more accurate, but osmolarity is easier to calculate!
NOTE: osmolality is more accurate because it uses mass of the solvent, which always stay the same, whereas volume expands with increasing temperatures
-
BONUS:
Na+
is the biggest contributor to plasma osmolality
SUMMARY CARD:
Fluid balance equations:
1. Osmolarity equation
2. Osmolar gap equation
3. What does it mean to have a raised osmolar gap?
- Osmolarity = 2(Na + K) + urea + glucose
-
Osmolality - osmolarity =
< 10
(NORMAL)
If the osmolar gap is > 10
, then there are other unmeasured ions in the sample –> SKALP
:
-
S
ugar: mannitol, sorbitol -
K
etones -
A
lcohol: methanol, ethanol -
L
ipids (↑ triglycerides) /L
actate -
P
roteins: ↑ gammaglobulinaemia
SUMMARY CARD:
- What is the normal range for plasma [Na+]?
- How is Na+ regulated?
135-145 mmol/L
TWO
ways to regulate Na+:
1. Blood volume
: ↑ blood volume = atrial stretch = ANP (atrial natriuretic peptide) release = ↓ aldosterone release + ADH + renin = ↓ [Na+] in blood
2. Blood osmolality
: ↑ blood osmolality = ↑ thirst + ADH release = ↓ [Na+] in blood
SUMMARY CARD:
- What is mild vs severe hyponatraemia?
- What are the Sx of hyponatraemia?
- How do you define true vs pseudohyponatraemia and what are possible causes of each?
- Mild hyponatraemia = 130-135 mmol/L; severe = < 125 mmol/L
- Sx = N&V, confusion, muscle weakness/cramps, seizures, coma
- Mx with
IV 0.9% NaCl
ONLY if symptomatic (orv. severe
) hyponatraemia
Use OSMOLALITY to determine true vs pseudohyponatraemia
If LOW
plasma osmolality, then TRUE
hyponatraemia:
- Assess volume status w/ clinical exam (e.g. BP, HR, oedema, cap refill) AND check urinary Na+ for cause
-
Hypovolaemic + urinary Na+ < 20 mmol/L =
extra-renal
causes e.g. D&V, burns, TURP syndrome (hypotonic irrigation absorbed through damaged prostate) -
Hypovolaemic + urinary Na+ > 20 mmol/L =
renal
loss e.g. AKI/CKD, diuretics, Addison’s (can also be eu) -
Euvolaemic = psychogenic polydipsia,
SIADH
, Addison’s (can also be hypo) -
Hypervolaemic + urinary Na+ < 20 mmol/L =
extra-renal
e.g. HF, cirrhosis, nephrotic syndrome -
Hypervolaemic + urinary Na+ > 20 mmol/L =
renal
failure
If NORMAL
or HIGH
plasma osmolality, then PSEUDO
hyponatraemia:
- May be caused by the sample coming from an arm with a
drip
in it OR due to otherunmeasured ions
e.g. mannitol, glucose (HHS) ORpost-surgery
(e.g. over hydration w/ IV fluids, or ↑ ADH release due to stress of the surgery)
SUMMARY CARD:
What are the steps to assessing the cause of hyponatraemia?
-
Step 1: assess
plasma osmolality
(true vs pseudo) -
Step 2: assess
volume status
-
Step 3: measure
urinary sodium
(extra-renal vs renal causes)
SUMMARY CARD:
What is the management for each of these?
- If
HYPO
voloaemic hyponatraemia: regardless of renal or extra-renal cause, Mx withIV 0.9% NaCl
if symptomatic (orv. severe
) hyponatraemia
If EUVO
laemic hyponatraemia:
-
Psychogenic polydipsia: if
acute
+ symptomatic hyponatraemia = IV 0.9% saline; ifchronic
= fluid restriction + CBT (can consider furosemide) - Chronic hypothyroidism =
levothyroxine
-
Addison’s (AKA adrenal insufficiency) =
Hydrocortisone
(glucocorticoid) +/-fludrocortisone
(mineralocorticoid) -
SIADH =
demecocycline
(check renal function first as it can cause NDI) ORtolvaptan
- If
HYPER
volaemic hyponatraemia:fluid restrict
+/- diuresis (unless due to cirrhosis, then requires specialist input)
SUMMARY CARD:
For SIADH, what is / are the:
- Diagnostic criteria?
- Causes?
- Mx?
1. Diagnostic criteria = diagnosis of exclusion
so NO adrenal/ thyroid / renal dysfunction, AND:
TRUE
hyponatraemia (< 135) + LOW
plasma osmolality + HIGH
urine sodium (>20) + HIGH
urine osmolality (>100)
SIADH = syndrome of inappropriate ADH secretion (not in response to a stimulus), which results in less water excreted in the urine
Ix require normal 9am cortisol, short synATCHen test and TFTs (as this is a diagnosis of exclusion)
2. Causes = L
ung, B
rain, D
rugs:
- Malignancy (ectopic ADH secretion): SCLC, pancreas, prostate, lymphoma
- CNS disorders: infection, haemorrhage
- Lungs: TB, pneumonia
- Drugs: opiates, SSRIs, TCAs, carbamazepine, PPIs
3. Mx = acute vs chronic:
-
Acute: fluid restriction, if severe
IV hypertonic saline +/- furosemide
-
Chronic: fluid restrict to 1L per day,
demecocycline
(check renal function first as it can cause NDI) ortolvaptan
SUMMARY CARD:
Why does cirrhosis cause hypervolaemic hyponatraemia?
BONUS: why does HF cause hypervolaemic hyponatraemia?
Due
Due to poor breakdown of vasodilators e.g. nitric oxide in the liver = ↓ BP
= subsequent ↑ ADH release
= ↑ water retention
BONUS: similar reason to cirrhosis –> ↓ cardiac output
= subsequent ↑ ADH release
= ↑ water retention
SUMMARY CARD:
What happens if Na+ is corrected too quickly (+Sx)?
What is the ideal rate of Na+ correction?
Central pontine myelinolysis
RF = malnourished alcoholic
- Pseudobulbar palsy =
indistinct speech, drooling, dysphagia
, spastic tongue, brisk jaw jerk, dysarthria - Paraperesis = partial inability to move
- Locked-in syndrome = body paralysis but consciousness and ability to move eyes are preserved
Ideally: do NOT increase Na+ by more than 8-10 mmol/L per 24hrs
DISEASE:
A patient is getting IV NaCl rehydration in their R arm following a night of binge drinking
They are currently asymptomatic
Their blood test shows Na+ of 123 mmol/L but high osmolality
Identify a possible cause of this result?
hint: nurse took blood from R arm
Low Na+ and ↑ osmolality = PSEUDO
hyponatraemia
Sample was taken from drip arm
–> caused dilution of the Na+
DISEASE:
28F - abdo pain + confusion + kussmaul breathing
PMH = T1DM
Ix = incidental hyponatraemia finding
What is a possible cause of this?
Pt is presenting w/ DKA = ↑ ketones –> lowers water potential of blood = high osmolality
, therefore it appears they have hyponatraemia (AKA pseudohyponatraemia
)
DISEASE:
Post-surgical pt complains of N&V + cramping in his legs
He was given IV fluids during his surgery
Ix = Na+ of 122 mmol/L
Identify a possible cause of this result?
(BONUS: Mx?)
(Hypervolaemic) hyponatraemia
(AKA pseudohypoatraemia) can occur post surgery due to overhydration with IV fluid during the surgery
As the pt is symptomatic with severe hyponatraemia (< 125), Mx = IV 3% NaCl (hypertonic
) + furosemide
DISEASE:
35M = extensive burns following a workplace accident
He complains of weakness and confusion
Ix = hyponatremia w/ Na+ 125 mmol/L
What type of hyponatraemia is this?
(Bonus: Mx for ↓Na+?)
Hypovolaemic hyponatraemia
due to fluid loss via burns
Mx = fluid replacement w/ IV NaCl
DISEASE:
65M - underwent transurethral resection of the prostate for BPH
Post-op, he develops hyponatremia (Na+ 128 mmol/L)
What is this syndrome called and why does it occur?
TURP
(transurethral resection of the prostate) syndrome
Fluids absorbed during irrigation in TURP through damaged prostate = hyponatraemia
DISEASE:
26F - 5kg weight loss, muscle weakness, hyperpigmented palms of hands
Does not appear clinically dehydrated
U&Es = ↓Na+, ↑K+
- Diagnosis?
- Ix?
- Mx?
- BONUS: how is an addisonian crisis managed?
-
Addison's disease
(AKA adrenal insufficiency) –> causes hypo/eu volaemic hyponatraemia due to lack of aldosterone release - Ix:
- 9AM cortisol = low
- Short synACTHen test –> serum cortisol fails to double at 30 mins indicates adrenal failure (normal = sufficient increase in cortisol)
-
Long-term Mx = replacement of glucocorticoids with
hydrocortisone
(3x/day) and mineralocorticoids withfludrocortisone
BONUS:
-
Addisonian crisis
= hypotensive shock, usually precipitated by infection / surgery -
MEDICAL EMERGENCY
–> Mx = rapid IV fluid rehydration w/ 1l 0.9% normal saline over 1 hour + 50 mL of 5% dextrose to correct hypoglycaemia + IV/IM 200 mg hydrocortisone bolus + Tx of underlying cause
DISEASE:
60M - ascites + lower limb oedema
PMH - alcohol misuse
Bloods: ↑elevated liver enzymes, ↓Na+
What is this type of hyponatraemia?
BONUS: what is the cause?
Hypervolaemic hyponatraemia
due to cirrhosis
/ liver failure
Liver fails to break down vasodilators e.g. NO = ↓BP = ↑ ADH release = hypervolaemic hyponatraemia
DISEASE:
55M - severe D&V following street food/takeaway –> given IV NaCl
Now: quadriparesis, indistinct speech, dysphagia
PMH: poor diet + alcohol misuse
What is the diagnosis?
What are the RFs?
Central pontine myelinolysis
due to rapid correction of Na+
Sx = pseudobulbar palsy (indistinct speech, dysphagia), paresis, etc.
RFs = malnourished alcoholics
DISEASE:
70F - brought in by LAS from carehome following 2 hours of muscle weakness and confusion
No FLAWS
Ix = Na+ 126 mmol/L and plasma osmolality < 100
What is the diagnosis?
BONUS: Mx?
HINT: euvolaemic hyponatraemia
Psychogenic polydipsia
= euvolaemic hyponatraemia
RFs = carehome, elderly pt
Acute
Mx = IV 0.9% saline as pt is symptomaticChronic
MX = fluid restriction
DISEASE:
57M - cough + crackles in R lung bases
Tachycardic, temp 38.8°C
Ix = low Na+, normal urea
What is the cause of the low Na+?
SIADH - can be caused by pneumonia
SUMMARY CARD:
- What is mild vs clinically significant hypernatraemia?
- What are the Sx of hypernatraemia?
- Hypernatraemia is Na+ >145 mmol/L; it is clinically significant if
Na+ > 148
mmol/L - Sx = thirst, confusion, irritability, ataxia + seizures, coma
SUMMARY CARD:
What are the steps to identifying the cause of hypernatraemia?
Assess volume status
, then assess urinary Na+
-
HYPO
volaemic hypernatraemia +LOW
urinary Na+: GI losses (D&V if water>electrolytes lost), skin losses (sweating, burns) -
HYPO
volaemic hypernatraemia +HIGH
urinary Na+: loop diuretics, osmotic diuresis (e.g. uncontrolled DM, glucose, mannitol following initial hyponatraemia), DI -
EUVO
laemic hypernatraemia: tachypnoea, skin (sweating, fever), DI -
HYPER
volaemic hypernatraemia: Conn’s syndrome, inappropriate hypertonic saline
SUMMARY CARD:
- What are the TWO types of DI (+ Sx)?
- Ix?
- Mx?
Nephrogenic vs Cranial diabetes insipidus
Sx = lethargy, thirst, irritability, confusion, coma, fits –> due to ↑Na+
Clinically EUVOLAEMIC, but DILUTE urine
CDI
= lack of/ no ADH production
- Causes = surgery, trauma, craniopharyngioma, autoimmune hypophysitis (from CTLA-4 ipilimumab)
- Mx =
desmopressin
NDI
= receptor defect leads to insensitivity to ADH
- Causes = drugs (e.g. lithium, demecocycline)
- Mx =
thiazide diuretics
Ix:
- Check electrolytes to rule out other causes
- Plasma (normal / high) + urine osmolality (LOW)
8-hour water deprivation test:
* If urine to plasma (U:P) osmolality ratio > 2, then it’s normal (normal concentration ability)
* If urine osmolality increases after administration of desmopressin –> CDI
* If urine osmolality does not change after administration of desmopressin –> NDI
SUMMARY CARD:
What is the general management of hypernatraemia?
Drink more water
-
SLOW
IV fluids
as usually hypovolaemic cause (can use saline, dextrose or Hartmann’s) - Try IV dextrose if no improvement (1L/ 6hrs)
MEASURE urine output + plasma Na+ to guide Mx
DISEASE:
45F - severe D&V following BBQ
Ix = Na+ 150 mmol/L, low urinary Na+
What is the type of hypernatraemia?
BONUS: Mx?
Hypovolaemic hypernatraemia
due to water>electrolyte losses in D&V
Mx = encourage oral fluid intake (if not possible, slow IV fluids)
DISEASE:
60M - irritable + thirsty
PMH cirrhosis (on furosemide)
Ix = ↑Na+, ↑ urinary Na+
What type of hypernatraemia is this?
Hypovolaemic hypernatraemia
due to loop diuretic use
DISEASE:
40F - polyuria + polydipsia
no signs of dehydration or fluid overload
Ix = ↑Na+, low urinary Na+
water deprivation test shows U:P < 2
What to administer next + what the different results mean (+Mx)?
Administer desmopressin
CDI = responsive, concentrates urine –> Mx = desmopressin
NDI = unresponsive, urine conc remains the same –> Mx = thiazide diuretic
e.g. indapamide, bendroflumethiazide
DISEASE:
56M - confusion, irritability
PMH - poorly controlled hypertension despite trialing several different Tx
U&Es: ↑Na+, ↓ K+
Urinalysis: ↑K+
- What is the diagnosis?
- Ix?
- Mx?
-
Conn's syndrome
= primary hyperaldosteronism (most commonly caused by adrenal hyperplasia) - Ix =
aldosterone:renin ratio
(HIGH) - Mx =
spironolactone
(potassium-sparing diuretic - aldosterone antagonist) - Long-term Mx = laparoscopic adrenalectomy (if malignant or unresponsive to medical therapy)
SUMMARY CARD:
- What is the normal range for [K+]?
- Where is K+ normally found?
3.5-5.0 mmol/L
It is mostly only an intracellular cation (only 2% found extracellularly)
SUMMARY CARD:
- What is mild vs severe hypokalaemia and their
Mx
? - Sx of hypokalaemia (+ findings on ECG)?
Hypokalaemia, < 3.5mmol/L, is caused by either a depletion of K+
or due to a shift of K+ into cells
Moderate hypokalaemia = 3.0-3.5 mmol/L –> Mx is oral KCl
(2 SandoK tablets TDS for 48hrs) then recheck
serum K+
Severe hypokalaemia = < 3.0mmol/L (↑ risk of cardiac arrest) –> Mx = IV KCl
(max rate of 10 mmol/hr or else ↑ risk of arrhythmia)
Clinical features (everything is SLOW): hypo
tonia, hypo
reflexia, paralytic ileus, muscle weakness, cardiac arrhythmias
On ECG: flat/inverted t-waves
, prominent u-waves, prolonged PR interval + ST depression
SUMMARY CARD
What are some causes for hypokalaemia?
Hypokalaemia causes that result in ALKALOSIS:
-
GI
loss: D&V -
Renal
loss: hyperaldosteronism (suspect if ↑BP, ↑Na+, ↓K+), loop & thiazide diuretics
NOTE: loop diuretics block Na+/K+/Cl- transporter = reduced reabsorption of all 3
NOTE: Normally, in the CD, Na+ reabsorption is exchanges for K+ excretion –> thiazide diuretics block Na+ reabsorption earlier in the nephron so more Na+ reaches the CD, so more Na+ is reabsorbed as more K+ is excreted out
-
Redistribution
into cells e.g. insulin, salbubtamol, refeeding syndrome -
Mg2+ deficiency
(because Mg2+ deficiency can cause ↑K+ wasting) –> Mx = Mg2+ replacement alongside KCl
Hypokalaemia causes that result in ACIDOSIS:
-
Renal tubular acidosis
types 1 & 2 - Type
1
= most severe; distal failure of H+ excretion and subsequent acidosis + ↓K+ (failed H+/K+ pump) - Type
2
= milder, proximal failure to reabsorb bicarbonate –> leads to acidosis + ↓K+
SUMMARY CARD:
- What is hyperkalaemia?
- What are some Sx of hyperkalaemia (+ ECG changes)?
- Mx?
- [K+] > 5.0 mmol/L, either caused by
reduced excretion
orrelease of intracellular K+
- Sx = weakness, paralysis, paraesthesia
- ECG changes: small / loss of p waves,
tall tented T waves
, widened QRS complex
Initiate Mx if
: K+ >5.5 w/ ECG changes OR K+ > 6.5 regardless of ECG changes
- 10mls 10% calcium gluconate over 10 minutes – cardioprotective (it doesn’t do anything to the K+)
- IV insulin w/ dextrose
- Nebulised salbutamol as an adjunct
- Consider calcium resonium (K+ binders - binds to K+ in the gut) 15g PO or 30g PR
- NOTE: cardiac monitoring for those on Digoxin as IV calcium can precipitate arrhythmias
NOTE: if K+ sample > 7 mmol/L and asymptomatic –> redo sample
(may be raised due to haemolysis in the sample)
SUMMARY CARD:
What are some causes of hyperkalaemia?
Hyperkalaemia can be caused by excessive intake, release of intracellular K+, OR decreased excretion
Excessive intake:
- Oral / parenteral
- Blood transfusion
Transcellular movement ICF>ECF:
- Acidosis (due to H+/K+ cotransporter)
- Insulin shortage (i.e.
DKA
) - Tissue damage e.g.
rhabdomyolysis
Decreased excretion:
- Acute
renal failure
- Drugs e.g.
spironolactone
(K+ sparing diuretic, NSAIDs, ACEi, ARBs -
Addison's
disease (↓Na+, ↑K+) - Type
4
renal tubular acidosis (aldosterone deficiency or resistance leads to ↓Na+, ↑K+)
OR may be due to artefact e.g. haemolysis
of the sample
DISEASE:
60M - muscle weakness, hypo
tonia, hypo
reflexia
ECG: flat t-waves
+ u-waves, PR prolongation
U&Es: K+ 3.2 mmol/L
PMH: recently started indapimide
- Cause of this electrolyte abnormality?
- Mx?
hypokalaemia due to thiazide diuretic (i.e. indapimide)
If K+ 3.0-3.5 mmol/L, Mx = oral KCl
(2 SandoK tablets TDS for 48hrs) then recheck
serum K+
DISEASE:
70F - muscle weakness
PMH: HF
currently on furosemide, dose recently increased
- What is the most likely electrolyte abnormality?
- Assuming it caused a severe electrolyte abnormality, what is the Mx?
Hypokalaemia due to loop diuretic
If severe hypokalaemia (< 3.0mmol/L) –> ↑ risk of cardiac arrest, therefore Mx = IV KCl
(max rate of 10 mmol/hr or else ↑ risk of arrhythmia)
DISEASE:
55M - muscle weakness + tingling
PMH: alcohol misuse and poor diet presents
K+ 3.2 mmol/L
What other electrolyte abnormality should be screened for?
Check for Mg2+ deficiency
DISEASE:
What is the difference in [K+] between type 1+2 RTA and Type 4 RTA?
Type 1
(failure of H+ excretion) + 2
(failure of bicarb reabsorption) = acidosis & hypokalaemia
Type 4
= hyperkalaemia (due to aldosterone deficiency / resistance)
DISEASE:
72M - found after a fall
complaints of severe muscle pain + dark urine
Ix = K+ 6.6 mmol/L, elevated Cr
- Cause of hyperkalaemia?
- Mx?
Rhabdomyolysis –> long lie = breakdown of muscle tissue = release of intracellular K+
Mx for [K+] >6.5 mmol/L:
* 10mls 10% calcium gluconate over 10 minutes – cardioprotective (it doesn’t do anything to the K+)
* IV insulin w/ dextrose
* Nebulised salbutamol as an adjunct
* Consider calcium resonium (K+ binders - binds to K+ in the gut) 15g PO or 30g PR
DISEASE:
65F - muscle weakness + tingling, nausea
PMH: HF –> treated with spironolactone
Ix = 5.7 mmol/L
- Reason for hyperkalaemia?
- Important Ix?
Spironolactone (K+ sparing diuretic
) can cause hyperkalaemia
Important to do ECG
–> may show tall t waves + absent p-waves (warrants immediate Mx)