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)
DDx of hyperCa
hyperPTH
malignancy (local osteolysis, HHM)
TB (↑ calcitriol by activated macrophages)
Examples of cancers with HHM (what is HHM?) (5)
humoral hyperCa of malignancy
- CA lung
- RCC
- ATLL
- CA breast
- CA oesophagus
Presentations of hyperCa
bone pain, stones, abdominal groans (ileus, peptic ulcer, panceratitis), psychic moans (lethargy, depression)
Chovostek’s sign
tapping –> twitching of facial muscles
==> hypoCa
Trousseau sign
pressurise the arm by a sphygmomanometer –> muscle contraction of wrist & fingers
==> hypoCa
Typical example of metabolic acidosis + respiratory alkalosis
aspirin overdose
Typical example of metabolic alkalosis + respiratory acidosis
COPD on diuretics
Common unmeasured osmoles that lead to ↑ osmolar gap
ethanol, methanol, isopropyl alcohol, mannitol
DDx of high anion gap metabolic acidosis
Glycols
Oxoproline (paracetamol)
L-lactate
D-lactate
Methanol
Aspirin
Renal disease
Ketones
L-lactic acidosis DDx
(a) Type A: tissue hypoperfusion
(b) Type B
- DM (↑ anaerobic glycolysis in muscles)
- Ethanol / methanol toxicity (↑ NADH –> ↓ metabolism of lactate)
- Metformin
… (liver failure, malignancy, IEM)
Pathophysiology of D-lactic acidosis
short bowel syndrome: ↓ carbohydrate absorption –> ↑ metabolism into D-lactate by gut bacteria
Ketones (which is the one detected by dipstick?)
acetoacetate (this), β-hydroxybutyrate
DDx of ketoacidosis (4)
DKA (↓ insulin –> ↑ lipolysis & FA oxidation)
Ethanol toxicity (↑ NADH –> inhibit gluconeogenesis –> ↑ FA oxidation)
Starvation
IEM
DDx of normal anion gap metabolic acidosis (4)
GI loss (diarrhoea)
Renal loss
Ingestion of HCl / NH4Cl
Urine diversion
urine anion gap
Na+ + K+ - Cl-
RR: 20~90
Positive indicates high H+ in urine, like RTA 1,4, CKD
Saline responsive metabolic alkalosis DDx (3)
hypovolaemia
vomiting, nasogastric suction
previous chronic use of diuretics
Saline resistant metabolic alkalosis DDx (4)
Mineralocorticoid excess
Glucocorticoid excess
Base excess
severe hypoK (transcellular shift)
Symptoms for hypoNa and hyperNa (4+4)
hypoNa: malaise, nausea, headache, confusion
hyperNa: thirst, lethargy, weakness, seizures
