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Chemical Pathology > Fluid And Electrolytes > Flashcards

Fluid And Electrolytes Flashcards

1
Q

How is osmolality taken

A

Measured with osmometer using principle of freezing point depression

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2
Q

How is osmolarity taken

A

Calculated: 2Na + urea + glucose

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3
Q

Osmolal gap formula?

A

Osmolality - osmolarity
(Increases when other osmoles increase)

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4
Q

Normal osmolal gap?

A

<10

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5
Q

Name 3 physiological methods in which ECF osmolality is restored when water is lost

A

• Stimulation of vasopressin (adh) release → renal water retention
• stimulation hypothalamic thirst centre → increased intake
• redistribution of water from ICF

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6
Q

Define laboratory and clinical hyponatraemia

A

Lab <135 mmol/l
Clinical ≤ 125

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7
Q

Name 2 causes pseudo hypo Na

A

• Excess lipids
• excess protein
(Will have normal osmolality)

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8
Q

Normal sodium value?

A

135-145 mmol/l

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9
Q

Clinical consequence of acute hypona?

A

Cerebral oedema
Symptoms range from nausea and vomiting, confusion, coma death

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10
Q

Treatment hypervolaemic hyponatraemia?

A

Lasix and fluid restriction

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11
Q

Treatment euvolaemic hyponatraemia?

A

Fluid restriction

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12
Q

Treatment hypovolaemic hyponatraemia?

A

Saline rehydration
(True hypo Na )

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13
Q

Cause of hyper osmolar hypo na?

A

High glucose

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14
Q

Name 2 causes of hyponatraemia with urine sodium ≤ 30 mmol / L and decreased ECF volume

A

Sodium depletion:
• Gastrointestinal
• cutaneous

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15
Q

Name 3 causes of hyponatraemia with urine sodium ≤ 30 mmol / L and increased ECF volume

A

Sodium and water excess (oedema)
• heart failure
. Liver cirrhosis
• nephrotic syndrome

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16
Q

Name 2 causes of hyponatraemia with urine sodium > 30 mmol / L and decreased ECF volume

A

Sodium depletion
• adrenal failure
• renal salt wasting
• cerebral salt wasting
• diuretics

17
Q

Name 3 causes of hyponatraemia with urine sodium > 30 mmol / L and normal ECF volume

A

Water excess (no oedema)
• syndrome of inappropriate adh (diagnosis of exclusion)
• ckd
• excess iv fluid infusion

18
Q

Name 5 diagnostic criteria for syndrome of inappropriate adh

A

SIADH:

(Diagnosis of exclusion)

• serum euvolaemic: normal ECF volume

• > 100 urine osmolality: urine must not be maximally diluted (osmolality >100 mosm/kg)

• adrenal,thyroid function, kidney, normal

• drug not cause hypo Na

• hypo Na <135 and low serum osmolality <275

Continued natriunesis despite low plasma sodium, aldosterone secretion doesn’t increase

19
Q

Name 5 causes and diagnosis hypovolaemic hypernatraemia

A

Assess clinically: dehydrated

Water very low and sodium low, but high concentration

Do urine sodium

Urine Na >40: renal losses
• osmotic diuresis or diuretic use
• ATN polyuric disease
- AKI/CKD

Urine Na < 25: extra-renal losses
• GI LOSS: osmotic diarrhoea, git fistula
• DERM LOSS: sweating/burns

MOLE: Meds (diuretics), Osmotic diuresis, Excessive water loss, Low water intake

20
Q

Name 2 causes euvolaemic hypernatraemia

A

Clinically dehydrated.

Low water, normal sodium lab value but high concentration

Do urine:plasma osmolality

Urine osmolality <1:renal losses
• diabetes insipidus - central or nephrogenic (differentiate with desmopressin)

Urine osmolality >1: extra renal losses
• insensible losses

LED: Low water intake (extrarenal), Diabetes insipidus, Excess water loss

21
Q

Name 5 causes hypervolaemic hypernatraemia

A

Clinically oedema, overhydrated.

“Classic” because Na will be >145. And water high

• Hypertonic saline infusion
• iv naHco3 as emergency for severe metabolic acidosis
• overconcentrated formula milk
• hypertonic dialysis
• sea water ingestion
- hyperaldosteronism

22
Q

Name 4 trans cellular movement causes of hypo K

A

• alkalosis
• insulin administration
• refeeding syndrome
• increased k excretion

23
Q

Name 5 renal causes of hypo K

A

• Diuretics
• AKI: early diuretic phase
• renal tubular acidosis 1 and 2
• mineralocorticoid excess: primary and secondary aldosteronism, Cushing
• tubular (distal) disorders: batter syndrome, Liddle syndrome, Gitelman’s syndrome

24
Q

Name  2 extrarenal causes of hypo K

A

• diarrhea
• vomiting

25
Q

Treatment hypervolemic hyper na?

A

Furosemide (loop diuretic) and 5% dextrose (hypotonic fluid) iv

Possibly dialysis if severe

(Dextrose causes hyper osmolality so water moves intracellular to extra cellular, creating dilutional effect)

26
Q

Treatment euvolemic hyper na?

A

5% dextrose iv or water orally

27
Q

Treatment hypovolemic hyper na?

A

Isotonic saline slowly and 5% dextrose iv

28
Q

Name 6 factors that influence urinary potassium excretion

A

• Circulating aldosterone (cause hypo k in favour of sodium)
• amount of sodium arriving at distal tubules
• relative availability hydrogen and potassium of cells at distal tubules and collecting ducts
• capacity of cells to secrete hydrogen ions (h and K go together)
. Dietary K intake
• intravascular volume (reduction stimulate aldosterone)

29
Q

Name 4 causes spurious (“false”) hyperkalaemia

A

•Hamolysis
. EDTA contamination
• old sample
• abnormal blood cells: leukemia, thrombocytosis

30
Q

Name 7 causes transcellular movement hyperkalaemia

A

• Acidosis
• tissue damage (tumour lysis syndrome)
• vigorous exercise
. Decrease K excretion
• AKI and CKD
• K sparing diuretics
. Mineralocorticoid deficiency: Addison’s, aurenolectomy, hyporeninaemic hypoaldosteronism

31
Q

What is ADH, where produced and function

A
  • ADH = vasopressin
  • posterior pituitary
  • main function = water reabsorption by increase aquaporin 2 channels on DCT and CD
  • stimulated by increased plasma osmolarity (high na) and to lesser extent low blood volume
  • also vasoconstriction by increase vascular resistance
32
Q

What is aldosterone, where produced and function

A
  • Activated by RAAS (which is activated by low blood volume and pressure) and low Na or high K
  • adrenal cortex
  • activate eNAC channels and na/k ATP ase on DCT
  • reabsorb Na and water, excrete K
33
Q

What are natriuretic peptides, where produced and function

A
  • BNP, ANP
  • heart
  • stimulated by high blood pressure and volume
  • inhibit renin and therefore RAAS by
    A) decrease sympathetic response
    B) afferent arteriole vasodilation → increase GFR → naturesis
    Ultimately inhibit aldosterone → decrease Na and H2O
  • also vasodilation

Chemical Pathology (23 decks)

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