Basics Flashcards
What will happen if there is a rapid rise / drop of tonicity in Na correction?
Rise: central pontine myelinolysis
Drop: cerebral oedema
DDx of hypoNa
- Spurious (drip arm, dead space)
- Hyperosmolar (hyperglycaemia, mannitol)
- Isoosmolar (hyperproteinaemia, hyperlipidaemia)
- Hypoosmolar
a. Hypovolemic:
i. extra-renal Na loss: GI, skin, abdominal sequestration
ii. renal Na loss: diuretics, diuresis, Na+ wasting disease, mineralocorticoid deficiency
b. Hypervolemic
i. non-renal: CHF, cirrhosis, nephrotic syndrome
ii. renal: AKI (oliguric phase), CKD
c. Euvolemic
i. normal ADH: ↑ water intake
ii. ↑ ADH: hypothyroidism, hypocortisolism, SIADH
What is pseudohyponatraemia and pseudohypernatraemia?
hypoNa caused by hyperglycaemia or mannitol electrolyte exclusion effect
hyperNa caused by severe hypoproteinaemia
Mechanism that causes effective hypoNa
(hypervolemic hypoNa, non renal causes)
water shifts from ECF to ICF –> ↓ effective circulating volume –> activate RAAS and ADH to ↑ Na reabsorption –> ↑ hypervolaemia
DDx of hyperNa
- Spurious hyperNa
- Isoosmolar: severe hypoproteinaemia
- Hyperosmolar:
a. hypovolemic:
i. [Uosmo > 600] dehydration
ii. [Uosmo: 300~600] osmotic diuresis, diuretics, partial DI
iii. [Uosmo <300] complete DI
b. hypervolemic: excess Na load
Signs for abnormal hydration status
Hypervolemic: ↑ JVP, oedema, ascites…
Hypovolemic: ↓ capillary refill, ↓ skin turgor, mucousal dryness…
Dx of SIADH (6)
- hypoosmolar hypoNa with inappropriately concentrated urine (Uosmo > Sosmo)
- clinically euvolemic
- UNa >40
- ⨉ renal, cardiac or endocrine causes
- ⨉ diuretics
- improvement after fluid restriction
DDx of hyperK
- PseudohyperK (blood taking contamination, IV contamination, ex vivo release from cells)
- ↑ intake
- Transcellular shift
a. mineral acidosis, hypertonicity
b. ↓ insulin, ↓ sympathetic, drugs
c. exercise
d. tumour lysis syndrome, rhabdomyolysis, trauma - ↓ excretion
a. CKD, AKI (oliguric)
b. Mineralocorticoid deficiency
DDx of hypoK
- PseudohypoK (drip arm, leukocytosis)
- ↓ intake
- Transcellular shift
a. alkalosis
b. ↑ insulin, ↑ sympathetic - ↑ excretion
a. non renal loss (sweating, GI)
b. renal loss (metabolic acidosis, metabolic alkalosis, hypoMg)
Presentations of tumour lysis syndrome
- hyperK –> arrhythmia
- hyperP –> hypoCa –> seizures
- hyperuricaemia –> gout, acute kidney injury
What is TTKG?
trans-tubular potassium gradient
= U[K] / P[K] ➗ U[osm] / P[osm]
RR: 6~8
Acute management of hyperK (3)
calcium gluconate
dextrose-insulin drip
resonium C
Typical presentation of hypoK periodic paralysis
cannot stand up after a big meal / heavy exercise
Why is there hypoMg and what are its effects?
cisplatin
↑ K excretion –> hypoK
↓ secretion & action of PTH –> hypoCa
How to treat hypoK?
treat underlying causes
correct dehydration
replace K (PO / IV)