Basics Flashcards

1
Q

What will happen if there is a rapid rise / drop of tonicity in Na correction?

A

Rise: central pontine myelinolysis
Drop: cerebral oedema

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2
Q

DDx of hypoNa

A
  1. Spurious (drip arm, dead space)
  2. Hyperosmolar (hyperglycaemia, mannitol)
  3. Isoosmolar (hyperproteinaemia, hyperlipidaemia)
  4. 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
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3
Q

What is pseudohyponatraemia and pseudohypernatraemia?

A

hypoNa caused by hyperglycaemia or mannitol electrolyte exclusion effect

hyperNa caused by severe hypoproteinaemia

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4
Q

Mechanism that causes effective hypoNa

A

(hypervolemic hypoNa, non renal causes)
water shifts from ECF to ICF –> ↓ effective circulating volume –> activate RAAS and ADH to ↑ Na reabsorption –> ↑ hypervolaemia

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5
Q

DDx of hyperNa

A
  1. Spurious hyperNa
  2. Isoosmolar: severe hypoproteinaemia
  3. 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
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6
Q

Signs for abnormal hydration status

A

Hypervolemic: ↑ JVP, oedema, ascites…
Hypovolemic: ↓ capillary refill, ↓ skin turgor, mucousal dryness…

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7
Q

Dx of SIADH (6)

A
  • hypoosmolar hypoNa with inappropriately concentrated urine (Uosmo > Sosmo)
  • clinically euvolemic
  • UNa >40
  • ⨉ renal, cardiac or endocrine causes
  • ⨉ diuretics
  • improvement after fluid restriction
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8
Q

DDx of hyperK

A
  1. PseudohyperK (blood taking contamination, IV contamination, ex vivo release from cells)
  2. ↑ intake
  3. Transcellular shift
    a. mineral acidosis, hypertonicity
    b. ↓ insulin, ↓ sympathetic, drugs
    c. exercise
    d. tumour lysis syndrome, rhabdomyolysis, trauma
  4. ↓ excretion
    a. CKD, AKI (oliguric)
    b. Mineralocorticoid deficiency
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9
Q

DDx of hypoK

A
  1. PseudohypoK (drip arm, leukocytosis)
  2. ↓ intake
  3. Transcellular shift
    a. alkalosis
    b. ↑ insulin, ↑ sympathetic
  4. ↑ excretion
    a. non renal loss (sweating, GI)
    b. renal loss (metabolic acidosis, metabolic alkalosis, hypoMg)
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10
Q

Presentations of tumour lysis syndrome

A
  1. hyperK –> arrhythmia
  2. hyperP –> hypoCa –> seizures
  3. hyperuricaemia –> gout, acute kidney injury
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11
Q

What is TTKG?

A

trans-tubular potassium gradient
= U[K] / P[K] ➗ U[osm] / P[osm]
RR: 6~8

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12
Q

Acute management of hyperK (3)

A

calcium gluconate
dextrose-insulin drip
resonium C

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13
Q

Typical presentation of hypoK periodic paralysis

A

cannot stand up after a big meal / heavy exercise

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14
Q

Why is there hypoMg and what are its effects?

A

cisplatin
↑ K excretion –> hypoK
↓ secretion & action of PTH –> hypoCa

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15
Q

How to treat hypoK?

A

treat underlying causes
correct dehydration
replace K (PO / IV)

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16
Q

DDx of hyperCa

A

hyperPTH
malignancy (local osteolysis, HHM)
TB (↑ calcitriol by activated macrophages)

17
Q

Examples of cancers with HHM (what is HHM?) (5)

A

humoral hyperCa of malignancy
- CA lung
- RCC
- ATLL
- CA breast
- CA oesophagus

18
Q

Presentations of hyperCa

A

bone pain, stones, abdominal groans (ileus, peptic ulcer, panceratitis), psychic moans (lethargy, depression)

19
Q

Chovostek’s sign

A

tapping –> twitching of facial muscles
==> hypoCa

20
Q

Trousseau sign

A

pressurise the arm by a sphygmomanometer –> muscle contraction of wrist & fingers
==> hypoCa

21
Q

Typical example of metabolic acidosis + respiratory alkalosis

A

aspirin overdose

22
Q

Typical example of metabolic alkalosis + respiratory acidosis

A

COPD on diuretics

23
Q

Common unmeasured osmoles that lead to ↑ osmolar gap

A

ethanol, methanol, isopropyl alcohol, mannitol

24
Q

DDx of high anion gap metabolic acidosis

A

Glycols
Oxoproline (paracetamol)
L-lactate
D-lactate
Methanol
Aspirin
Renal disease
Ketones

25
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)
26
Pathophysiology of D-lactic acidosis
short bowel syndrome: ↓ carbohydrate absorption --> ↑ metabolism into D-lactate by gut bacteria
27
Ketones (which is the one detected by dipstick?)
acetoacetate (this), β-hydroxybutyrate
28
DDx of ketoacidosis (4)
DKA (↓ insulin --> ↑ lipolysis & FA oxidation) Ethanol toxicity (↑ NADH --> inhibit gluconeogenesis --> ↑ FA oxidation) Starvation IEM
29
DDx of normal anion gap metabolic acidosis (4)
GI loss (diarrhoea) Renal loss Ingestion of HCl / NH4Cl Urine diversion
30
urine anion gap
Na+ + K+ - Cl- RR: 20~90 Positive indicates high H+ in urine, like RTA 1,4, CKD
31
Saline responsive metabolic alkalosis DDx (3)
hypovolaemia vomiting, nasogastric suction previous chronic use of diuretics
32
Saline resistant metabolic alkalosis DDx (4)
Mineralocorticoid excess Glucocorticoid excess Base excess severe hypoK (transcellular shift)
33
Symptoms for hypoNa and hyperNa (4+4)
hypoNa: malaise, nausea, headache, confusion hyperNa: thirst, lethargy, weakness, seizures