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
Q

L-lactic acidosis DDx

A

(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
Q

Pathophysiology of D-lactic acidosis

A

short bowel syndrome: ↓ carbohydrate absorption –> ↑ metabolism into D-lactate by gut bacteria

27
Q

Ketones (which is the one detected by dipstick?)

A

acetoacetate (this), β-hydroxybutyrate

28
Q

DDx of ketoacidosis (4)

A

DKA (↓ insulin –> ↑ lipolysis & FA oxidation)
Ethanol toxicity (↑ NADH –> inhibit gluconeogenesis –> ↑ FA oxidation)
Starvation
IEM

29
Q

DDx of normal anion gap metabolic acidosis (4)

A

GI loss (diarrhoea)
Renal loss
Ingestion of HCl / NH4Cl
Urine diversion

30
Q

urine anion gap

A

Na+ + K+ - Cl-
RR: 20~90
Positive indicates high H+ in urine, like RTA 1,4, CKD

31
Q

Saline responsive metabolic alkalosis DDx (3)

A

hypovolaemia
vomiting, nasogastric suction
previous chronic use of diuretics

32
Q

Saline resistant metabolic alkalosis DDx (4)

A

Mineralocorticoid excess
Glucocorticoid excess
Base excess
severe hypoK (transcellular shift)

33
Q

Symptoms for hypoNa and hyperNa (4+4)

A

hypoNa: malaise, nausea, headache, confusion
hyperNa: thirst, lethargy, weakness, seizures