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Transition Block > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

what controls sodium

A

mineralocorticoid activity

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2
Q

what controls water

A

ADH

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3
Q

how does mineralocorticoid control sodium

A

sodium retention in exchange for potassium and/or hydrogen ions

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4
Q

what happens if there is too much mineralocorticoid activity

A

sodium retention

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5
Q

what happens if there is too little mineralocorticoid activity

A

sodium loss

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6
Q

rule with sodium + water

A

water follows sodium

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7
Q

what happens to water if there is sodium loss

A

water is lost

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8
Q

main mineralocorticoid that influences sodium

A

aldosterone

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9
Q

what is released from the kidney when BP is low

A

renin

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10
Q

what cells release renin

A

juxtaglomerular cells

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11
Q

what cells sense sodium concentration

A

macula densa

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12
Q

what does renin act on

A

angiotensinogen

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13
Q

where is angiotensinogen released from

A

liver

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14
Q

what converts angiotensinogen to angiotensin 1

A

renin

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15
Q

what converts angiotensin 1 to angiotensin 2

A

ACE

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16
Q

where is ACE released from

A

lungs

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17
Q

what does angiotensin 2 act on

A

adrenals – aldosterone release

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18
Q

effect of aldosterone on kidneys

A

sodium + water retention - increased BP

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19
Q

effect of increased ADH

A

concentrated urine

- high osmolarity

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20
Q

effect of decreased ADH

A

dilute urine

- low osmolarity

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21
Q

how does ADH work

A

acts on renal tubules to cause water reabsorption

22
Q

what can cause decreased sodium

A

SIADH

Addisons disease

23
Q

what is SIADH

A

syndrome of inappropriate ADH release

- excessive ADH secretion causing water retention and decreased sodium by dilution

24
Q

causes of SIADH

A 
pneumonia
lung cancer
drugs- carbamazepine/ SSRI's 
subarachnoid haemorrhage 
hypothyroid
25
Q

what is Addison’s disease

A

autoimmune decreased production of cortisol + aldosterone

26
Q

symptoms of Addison’s disease

A

BRONZE SKIN
abdo pain
weakness
weight loss

27
Q

tx Addison’s

A

hydrocortisone as cortisol replacement

fludrocortisone as aldosterone replacement

28
Q

blood results in Addison’s

A

low sodium
high potassium
low cortisol

29
Q

what can cause increased sodium

A

diabetes insipidus - increased water loss

decreased water intake

30
Q

what non-osmotic stimuli can cause ADH release

A

hypovolaemia
hypotension
pain
N+V

31
Q

how can you get rid of excess sodium

A

diuretics

32
Q

2 most important factors in determining potassium concentration

A

GFR

plasma potassium concentration

33
Q

ECG hyperkalaemia

A

tall tented T waves

wide QRS

34
Q

symptoms of hyperkalaemia

A

cardiac arrest
muscle weakness
parasthesia

35
Q

causes of decreased potassium excretion

A

renal failure – decreased GFR

hypoaldosteronism – loss of sodium, decreased GFR, retention of potassium + hydrogen

36
Q

when do you see hyperkalaemia caused by hypoaldosteronism

A

ACE/ARB use

37
Q

causes of potassium redistribution

A

rhabdomyolysis – potassium released from damaged cells
metabolic acidosis – increased hydrogen ions so potassium ions increase as well
insulin deficiency– insulin stimulates uptake of potassium

38
Q

Tx of hyperkalaemia

A

calcium gluconate

insulin + glucose to redistribute potassium

39
Q

symptoms of hypercalcaemia

A 
stones 
- kidney stones
bones
- fractures
groans 
- constipation, abdo pain
moans
- fatigue, myalgia, proximal muscle weakness
physic overtones
- depression, confusion
40
Q

most common causes of hypercalcaemia

A

primary hyperparathyroidism

hypercalcaemia of malignancy

41
Q

difference between primary hyperparathyroidism and hypercalcaemia of malignancy

A

PTH is HIGH in primary

42
Q

tx hypercalcaemia

A

IV saline

biphosphonates

43
Q

familial hypocalciuric hypercalcaemia

A

high calcium – sensed by parathyroids as normal, so PTH is normal
low urinary calcium

44
Q

acute adrenal insufficiency crisis

A

hypotension
N+V
dehydration

45
Q

results of synatchen test in Addisons

A

ACTH is given and should stimulate cortisol production

- plasma cortisol will remain low in Addison’s as no cortisol is produced

46
Q

test for pituitary causes of adrenal insufficiency

A

insulin stress test

47
Q

where is most of sodium reabsorbed

A

proximal convoluted tubule

48
Q

where is 100% of glucose + amino acids reabsorbed

A

proximal convoluted tubule

49
Q

what is the descending limb permeable to

A

water

50
Q

what is used to distinguish between nephrogenic and central diabetes insipidus

A

Desmopressin

  • will retain salt + water in central when desmopressin is given
  • no change in nephrogenic as kidneys are not sensing ADH

Transition Block (8 decks)

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