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chem path > Sodium > Flashcards

Sodium Flashcards

1
Q

What is the normal serum sodium range?

A

135-145 mmol/L.

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2
Q

Describe the primary distribution of sodium in the body and the mechanism by which its concentration is largely maintained.

A

Sodium is predominantly an extracellular cation. Its concentration is largely maintained by active pumping from the intracellular fluid (ICF) to the extracellular fluid (ECF) via the Na+/K+ ATPase pump.

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3
Q

Define hyponatremia.

A

serum sodium concentration of less than 135 mmol/L.

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4
Q

how do you determine whether hyponatraemia is true or facticious?

A

measure serum osmolality.
true should have low serum osmolality
normal = spurious, drip arm sample, pseudohyponatraemia (high lipids, proteins)

high = high glucose, alcohol, mannitol

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5
Q

whats one other cause of pseudohyponatramia

A

TURP syndrome - irrigation absorbed through damaged postate (glycine 1.5) - hyponatraemia due to dilution

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6
Q

Step 1 of hyponatraemia patient

A

check serum osmolality to establish true hyponatraemia

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7
Q

step 2 of hyponatraemia patient

A

check volume status

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8
Q

presentation of hypovolaemic fluid status?

A

dry mucosa, reduced skin turgor, reduced urine output

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9
Q

how do you differentiate causes of hypovolaemic hyponatraemia?

A

check urinary sodium

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10
Q

causes of urinary sodium <20 mmol/L in hypovolaemic hyponatraemia?

A

<20 = kidneys working fine, trying to retain sodium
causes: extrarenal losses - vomiting, diarrhoea, sweat, burns

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11
Q

when does cerebral pontine myelinolysis happen?

A

too quick correction of hyponatraemia with fluids like saline
(water moves out to quickly from neurones causing myelin damage)

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11
Q

causes of urinary sodium >20 mmol/L in hypovolaemic hyponatraemia?

A

> 20 = kidney problem (renal loss)
causes: addisonian crisis (no aldosterone so increased Na+ secretion), renal failure, diuretics (thiazides), cerebral salt wasting

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12
Q

how do you treat hypovolaemic hyponatraemia? what is a caution?

A

1) treat underlying cause
2) IV 0.9% NaCl (in severe sometimes IV hypertonic 3% NaCl)
caution: cant correct more than 8-10 mmol/L over 24 hours -> can risk cerebral pontine myelinolysis

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13
Q

what do you do when euvolaemic hyponatraemia? what investigation first?

A

urinary sodium
<20 = psychogenic polydyspia, tea & toast
>20 = endo causes (hypothyroidism, addinsons/glucocorticoid insuffieincy, SIADH)

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14
Q

if euvolaemic hyponatraemia & urinary sodium >20 what investigations should you do?

A

1) check TFTs to exclude hypothyroidism
2) check cortisol levels (short synacthen) to exclude addisons/glucocorticoid insufficiency
3) check paired urine & serum osmolality to see if its SIADH

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15
Q

what happens in SIADH

A

-too much ADH (excess water reabsorption but no sodium)
-sodium low, osmolality low, urine sodium high (high urine osmolality)

(things are low in serum and high in urine)

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16
Q

how do we treat the causes of euvolaemic hyponatraemia?

A

treat underlying cause + fluid restrict
1) hypothyroidism - levothyroxine
2)addisons - hydrocortisone +/- fludrocortisone
3) SIADH - demeclocycline or tolvaptan

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17
Q

what are the causes of SIADH? + menominic

A

brain, lung, pills or 3 Cs
brain (CNS dysfunction)
lung - cancer (small cell lung cancer) or pneumonia, TB
pills - SSRIs, PPIs, TCA, carbamazepine

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18
Q

how is sodium regulated by the body

A

1) blood volume (sensed by carotid sinus) –> increase in blood volume causes atrial stretch and release of ANP –> decreases release of aldosterone (adrenals), ADH (hypothalamus) & renin (kindeys) –> reduce sodium concentration –> this gets rid of water & sodium and thus volume
2) blood osmolality (sensed by hypothalamus): high osmolality triggers thirst & ADH release (increases water reabsorption) to decrease sodium concentration

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19
Q

what happens if both blood volume & sodium concentration are low? (eg. haemorrhage)

A

volume is more important
-more ADH, renin & aldosterone to maintain blood volume

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20
Q

where is renin produced & when is it released?

A

juxtaglomerular cells
-in reponse to low BP, decreased renal perfusion pressure and SNS activation

21
Q

what is the role of renin (RAAS)

A

1)renin converts angiotensinogen to angiotenin I.
2)ACE converts angiotensin I to II.
3) angiotensin II stimulates aldosterone release from adrenal cortex.
4) aldosterone increases sodium reabsoprtion & potassium excretion in kidneys
5) water follows sodium to increase BP, blood volume & pressure

22
Q

what is the role of aldosterone

A

increased sodium reabsorption (and thus water retention) & K+ excretion in DCT and collecting duct

23
Q

mnemonic for aldosterone

A

sodium saviour, potassium pooper

24
Q

ADH mnemonic

A

anti - pee pee hormone

25
Q

what are some presentations of hypervolaemic hyponatraemia?

A

pulmonary oedema (bibasal crackles), bilateral pitting oedema, raised JVP,

26
Q

What happens in hypervolaemic hyponatraemia

A

high total body water but low effective arterial volume (volume of blood effectively perusing tissue is low)

27
Q

what do you do to determine cause of hypervolaemic hyponatraemia

A

urinary sodium

28
Q

hypervolaemic hyponatraemia urinary sodium >20 causes?

A

kidney not working to retain sodium
-kidney failure (CKD) (increased RAAS)

29
Q

hypervolaemic hyponatraemia urinary sodium <20 causes?

A

organ failures –> heart failure, cirrhosis, primary polydipsia, nephrotic syndrome
-decreased oncotic pressures (low albumin, protein loss)

30
Q

in one sentence, what are the causes of hypervolaemic hyponatraemia?

A

all the organ failures

31
Q

how do you manage hypervolaemic hyponatraemia?

A

1) treat cause
2) fluid restrict ( nothing more than 1L per day)

32
Q

why should diuretics be stopped before meausing urinary sodium?

A

they affect sodium excretion

33
Q

how does cirrhosis cause hyponatraemia?

A

low albumin –> low oncotic pressure
impaired breakdown of vasodilatorus like nitric oxide –> low BP –> ADH release
-ADH increases water reasoption

34
Q

why hyponatraemia in heart failure

A

low cardiac output triggers ADH release & water retention

35
Q

first step after establishing hypernatraemia?

A

assess volume status

36
Q

what is important to think about in hypernatraemia?

A

why they arent able to drink water

37
Q

causes of hypovolaemic hypernatraemia?

A

water is lost more than sodium
low urinary sodium –> fluid losses (GI loss diarrhoea & vomiting), skin loss (sweating, burns)

high urinary sodium –> osmotic diuresis followed by initial hyponatraemia (eg. DM), renal disease, DI

38
Q

causes of euvolaemic hypernatraemia

A

diabetes insipidus

39
Q

causes of hypervolaemic hypernatraemia

A

too much salt
-conns
-mineralocorticoid excess
-excess saline

40
Q

management of hypernatraemia?

A

drink more water if you can
1) correct water defit by slow IV 5% dextrose (1L/6hrs) guided by urine output
2)correct extracellular fluid volume depletion (0.9% saline)
3) serial Na+ measuremets

41
Q

what happens in DM regarding sodium

A

can go either way
-hypoNa+ as hyperglycaemia draws water out of cells causing Na+ dilution in water
-hyperNa+ as osmotic diuresis loses water so high blood Na+

42
Q

clinical features of diabetes inspidus?

A

hypernatraemia, polyuria/.polydypsia, urine:plasma osmolality of <2:1 (urine dilute despite concentrated plasma)

43
Q

what is diabetes inspidus called now

A

arginine vasopressin deficiency (cranial DI)
arginine vasopressin resistance (nephrogenic DI)

44
Q

what happens in cranial DI

A

lack of/no ADH produced

45
Q

what are the causes of cranial DI

A

surgery, trauma, tumours, autoimmune hypophysitis

46
Q

treatment for cranial DI

A

desmopressin (selective V2 agonist)

47
Q

causes of nephrogenic DI?

A

electrolyte disturbances (hypercalcaemia, hypokalameia), inherited channelopathies, lithium, demeclocycline

48
Q

treatment for nephrogenic DI?

A

thiazide diuretic

49
Q

investigations for suspected diabetes inspidus

A

1) serum glucose (exclude T2DM)
2) serum K+ & Ca2+ (exclude hypercalcemia, hypokalemia)
3) urine & plasma osmolality (EXCLUDED IF U:P ratio >2:1)
4) 8 -hour water deprivation test

50
Q

water deprivation results and meanings?

A

-if urine osmolality goes up (>600) (urine concentrates): normal or psychogenic polydypsia
-if urine osmolality goes up but not as much (>400 - 600) - primary polydypsia
-if urine osmolality goes up (>600) after desmopressin = cranial DI
-if it doesn’t go up after desmopressin = nephrogenic Di

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