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Transition block > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

Normal concentration of sodium in a) the ICF b) the ECF

A

a) 4mmol/l

b) 140mmlol.l

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2
Q

Which steroids have mineralocorticoid activity?

A

aldosterone and cortisol

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3
Q

What does the term “mineralocorticoid activity” refer to?

A

Retain sodium in the kidney in exchange for potassium and/or hydrogen ions

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4
Q

How does the RAAS system work to retain sodium?

A

Falling blood pressure
Release of renin, which converts angiotensinogen to angiotenin I
AT1 converted to AT2
AT2 exerts effects on the adrenal cortex causing release of aldosterone, and retention of sodium (and hence water) at the kidneys

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5
Q

What is another name for ADH?

A

Arginine vasopressin

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6
Q

How does ADH release cause urine to be concentrated?

A

Causes reabsorption of water from the renal collecting tubules

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7
Q

Where is ADH released from?

A

Posterior pituitary

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8
Q

Main causes of hyponatraemia (2)

A

Too much water (mainly reduced excretion- SIAD)

Too little sodium (mainly increased gut/skin/kidney loss)

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9
Q

Why is clinical assessment of volume status important in assessing the cause of hyponatraemia?

A

Clinically dehydrated suggests a deficit of sodium and water as a consequence; unremarkable clinical volume status suggests too much water as a cause for the hyponatraemia

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10
Q

What does oedema in the presence of hyponatraemia suggest?

A

Suggests hyponatraemia as a consequence of fluid overload; heart failure and hypoalbuminaemia cause fluid retention

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11
Q 
Patient presentation:
tired
dizzy
pigmented skin
weight loss
low sodium
A

Addisons disease- adrenal insufficiency, hence loss of sodium + water

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12
Q

Reason for skin pigmentation in addisons disease

A

Increased ACTH from pituitary; ACTH bears the sequence for melanocyte-stimulating hormone (MSH) within it, so when ACTH increased there can be cross-stimulation of MSH receptors

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13
Q

What will the potassium be like in a patient with “acute” addisons disease?

A

High

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14
Q

Patient presentation:
in hospital with other illness
low sodium
clinical volume status unremarkable

A

Syndrome of inappropriate anti-diuresis- release of ADH in response to non-osmotic stimuli e.g. pain, nausea/vomiting, hypoglycaemia

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15
Q

Main causes of hypernatraemia (2)

A

Too little water (diabetes insipidus or reduced intake)

Too much sodium (rare)

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16
Q

Patient presentation:
head injury
high sodium
high urine output/IV fluid requirements

A

Diabetes insipidus (failure to produce ADH due to pituitary damage, hence excessive water loss)

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17
Q

How is diabetes insipidus managed?

A

Fluid replacement

Desmopressin (exogenous ADH)

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18
Q

What symptoms can be seen with either very high or very low sodium?

A

Altered consciousness
Confusion
Nausea

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19
Q

If adrenal insufficiency is suspected what should be measured?

A

serum cortisol (low) and ACTH (high)

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20
Q

Normal range of serum potassium

A

3.5-5.3mmol/l

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21
Q

ECG changes in hyperkalaemia (2)

A

Tall “tented” T-waves

Widening of the QRS complex

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22
Q

What is the main cause of hyperkalaemia?

A

Reduced GFR and hence reduced excretion of potassium

23
Q

What are the main causes of reduced GFR leading to hyperkalaemia? (2)

A

Renal failure
Hypoaldosteronism (usually due to use of ACE inhibitors/ARBs. These cause increased secretion of sodium with retention of potassium)

24
Q

In what situations can there be increased potassium release from cells?

A

Massive cellular damage e.g. rhabdomyolysis
Metabolic acidosis
Insulin deficiency

25
Q

How does metabolic acidosis cause hyperkalaemia?

A

As [H+] increases, potassium is displaced from the cell

26
Q

Why does insulin deficiency/resistance cause hyperkalaemia?

A

Insulin stimulates the uptake of potassium into the cell

27
Q

Emergency treatment of hyperkalaemia (4)

A

Calcium gluconate
Insulin + glucose
Nebulised salbutamol
Potentially dialysis

28
Q

Signs and symptoms of hyperkalaemia (3)

A

Fast irregular pulse + palpitations
Chest pain
Light-headadness

29
Q

What should be given in non-emergency treatment of hyperkalaemia?

A

Calcium resonium binds potassium in the gut

30
Q

What is pseudohyperkalaemia?

A

Artefactual high [K+]

31
Q

Common causes of hypokalaemia (2)

A

Diarrhoea and vomiting

Loop and thiazide diuretics

32
Q

Symptoms of hypokalaemia (4)

A

Muscle hypotonia
Hyporeflexia
Palpitations and light-headedness
Muscle cramps and tetany

33
Q

Redistributive causes of hypokalaemia (i.e. cause potassium to move into cells) (4)

A

Metabolic alkalosis
Insulin treatment
Catecholamines e.g. salbutamol
Treatment of megaloblastic anaemia (causes increased K uptake into the new cells)

34
Q

If a patient is on diuretics, what is the best indication that the hypokalaemia is long-standing?

A

Bicarb will be high

35
Q

Main store of calcium in the body

A

In the bone

36
Q

PTH is released in response to..?

A

Low unbound (i.e. not bound to albumin) serum calcium

37
Q

Actions of PTH (4)

A

Promotes bone resorption
Promotes resorption of calcium in the kidneys
Promotes absorption in the gut
Promotes 1,25 DHCC (calcitriol) synthesis

38
Q

Why should patients who have a low serum calcium with low albumin not be considered hypocalcaemic?

A

Only the unbound calcium is physiologically active- their unbound calcium level is normal

39
Q

Causes of hypocalcaemia (4)

A

Vitamin D deficiency
Hypoparathyroidism
Renal disease
Magnesium deficiency

40
Q

How does renal disease lead to hypocalcaemia?

A

Failure to synthesize 1,25 DHCC

41
Q

Symptoms of hypercalcaemia

A

Moans (GI problems)
Psychic groans (lethargy, depression, confusion)
Stones (renal features such as calculi, thirst, polyuria)
Bones (pain, fractures)

42
Q

Commonest causes of hypercalcaemia (2)

A

Hypercalcaemia of malignancy

Hyperparathyroidism

43
Q

What is the most important investigation to detect the cause of hypercalcaemia?

A

PTH.
If inappropriately high- suspect primary hyperparathyroidism, usually an adenoma
If low/undetectable- malignancy or other rarer causes

44
Q

Drugs which reduce the rate of bone resorption

A

Bisphosphonates

45
Q

What effect does PTH have on the concentration of phosphate?

A

Decreases the renal re-absorption of phosphate

46
Q

Why is secondary failure to produce cortisol common?

A

Therapeutic administration of steroids suppresses the hypothalamic-pituitary-adrenal axis

47
Q

ACTH levels in a)primary adrenal insuffuciency b) secondary

A

a) very high

b) very low

48
Q

Test used to diagnose primary adrenal insufficency

A

Short synacthen test. Test is based on serum measurement of cortisol at 0, 30 and 60 minutes. In normal adrenal function Synacthen results in a rise in serum cortisol

49
Q

How can the integrity of the hypothalamic-pituitary-adrenal axis be assessed?

A

Insulin tolerance test. Induction of hypoglycaemia with insulin should cause a compensatory rise in growth hormone

50
Q

Causes of pseudohyponatraemia (2)

A

Myeloma

Severe hyperlipidaemia

51
Q

Why is hyponatraemia associated with water retention not always associated with clinical signs of fluid overload?

A

Water retention can be across any of the fluid compartments of the body

52
Q

Why is the sodium sometimes normal in Addisons?

A

In the early stages there is “equal” sodium and water loss; unless there is ADH secretion and pure water retention, the sodium will probably be normal

53
Q

How can central and nephrogenic diabetes insipidus be distinguished?

A

Give synthetic analogue of ADH; during water deprivation test it should increase the osmolality of the urine

54
Q

Why is a random cortisol difficult to interpret?

A

Shows marked diurnal variation

Transition block (7 decks)

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