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BPT Renal > Renal Physiology > Flashcards

Renal Physiology Flashcards

1
Q

Why does creatitine clearance exceed true GFR by 10 to 20%?

A

due to the tubular secretion of creatitine

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2
Q

What equation is most commonly used to calculate eGFR in Australia?

A

CKD-EPI

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3
Q

What percentage of an adult is water?

A

60%

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4
Q

What percentage of water is extracellular and intracellular?

A

33% extracellular 66% intracellular

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5
Q

How do you calculate plasma osmolality?

A

(2 x Na) + glucose + urea

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6
Q

What happens when there is an increase in plasma osmolality?

A

Triggers osmoreceptors in the hypothalamus to increase thirst and increase ADH

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7
Q

What is the role of ADH?

A

binds in the kidneys to V2 receptors which causes release of aquaporin (water channels from preformed vesicles) to allow free entry of water

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8
Q

How does ADH work as a volume regulator?

A

When there is a fall in arterial blood volume there is an increase in ADH and then it binds to V1 receptors to increase vascular resistance

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9
Q

What is the mechanism of action of tolvaptan?

A

blocks V2 receptors to prevent binding of vasopressin to promote water excretion

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10
Q

What is the result of a fall in extracellular volume?

A

acttivation of RAAS system and supression of natiuretic peptides, leads to fall in urinary sodium excretion

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11
Q

What happens in SIADH?

A

impaired water excretion leads to reduced urine output, water retention and low serum sodium

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12
Q

What type of hyponatraemia do you have in SIADH?

A

euvolaemic hypotonic hyponatraemia

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13
Q

What are the causes of SIADH?

A 
ectopic secretion of ADH (e.g. small cell lung cancer)
CNS disorders
drugs
recent surgery
pulmonary disease
hormone deficiency 
idiopathic
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14
Q

What are the non SIADH causes of euvolaemic hypotonic hyponatraemia?

A

psychiatric polydipsia
alcoholism (low dietary solute but high fluid intake)
advanced renal failure (impaired water excretion with increased solute excretion)
thiazides (impaired water excretion)

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15
Q

What causes hypovolaemic hyponatraemia?

A

excessive diuretic use
diarrhoea
vomiting

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16
Q

What is the urinary sodium with exessive diuretic use?

A

high

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17
Q

What is the urinary sodium in diarrhoea?

A

low

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18
Q

What is the urinary sodium in vomiting?

A

high due to metabolic alkalosis

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19
Q

What causes hypervolaemic hyponatraemia?

A

heart failure

cirrhosis

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20
Q

What causes hypertonic hyponatraemia?

A

hyperglycaemia
IVIG infusion
sorbitol/mannitol irrigation

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21
Q

What is the mainstay of treatment for hyponatraemia?

A

fluid restriction

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22
Q

How much should you correct sodium per day?

A

4 to 6 mmol

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23
Q

What is the mechanism of action of loop diuretics?

A

blocks the Na-K-2Cl transporter

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24
Q

Why is there an increased risk of renal stones with loop diuretics?

A

because there is increased calcium excretion because calcium normally gets reabsorped with sodium

25
Q

What is the mechanism of action of thiazide diuretics?

A

blocks the Na-Ck cotransporter in the distal convuluted tubules

26
Q

What is the mechanism of action of potassium sparing diuretics?

A

work in the collecting tubules to block the sodium transporters

27
Q

What is bartter’s syndrome?

A

a genetic disorder which impairs sodium reabsorption in the loop of henle (mimics loop diuretic therapy)
childhood onset, severe, can cause perinatal death

28
Q

What is Gitelman’s syndrome?

A

a genetic disorder which impairs sodium reabsorption in the distal tubule (mimics thiazide diuretic therapy)
occurs in adulthood

29
Q

Why do you also get hypokalaemia and metabolic alkalosis in bartter’s syndrome?

A

because there is preference for sodium reasborption in the distal tubule so potassium and hydrogen ions get secreted instead of reabsorbed
also because there is volume depletion which results in secondary hyperaldosteronism

30
Q

Why do you also get hypocalcaemia and hypomagnesaemia in barrter’s syndrome?

A

because they usually get reasbsorbed in the ascending loop with NaCl which doesn’t happen in barrter’s

31
Q

How can you tell the difference between barrter;s and gittleman’s syndrome?

A

in bartter’s calcium excretion is high whereas in gittleman’s it is reduced

32
Q

When should you suspect barrter’s/gittleman’s?

A

normal/low BP with low K and metabolic alkalosis

33
Q

What is the differential diagnosis for barrter’s/gittleman’s?

A

chronic vomiting
diuretic use
elevated renin

34
Q

How can you tell the difference between chronic vomiting and barrter’s/gittleman’s?

A

chronic vomiting will have low urinary chloride

35
Q

Where is renin released from?

A

the juxtaglomerular cells around the afferent arteriole

36
Q

What are the stimuli for renin release?

A

hypotension
volume depletion
increased sympathetic activity

37
Q

What is the role of renin?

A

to cleave angiotensiogen to angiotensin I

38
Q

What is the role of ACE?

A

to create angiotensin II from angiotenin II

39
Q

What is the role of angiotensin II?

A

arteriolar vasoconstriction and aldosterone release

40
Q

What is the difference between type I and type II angiotensin II receptors?

A

type I does classical effects, type II counteracts these classical effects by causing vasodilation and natriureisis

41
Q

What is the role of aldosterone?

A

works in the collecting tubules to increase sodium reasborption and increase potassium excretion

42
Q

What are the systemic effects of aldosterone?

A

inflammation
insulin resistance
cardiac fibrosis
involved in metabolic syndrome

43
Q

What are the causes of primary aldosteronism?

A 
bilateral hyperplasia of adrenals
unilateral adenoma (conn's syndrome)
adrenocortical carcinoma (rare)
44
Q

What is the classic presentation for Conn’s syndrome?

A

hypokalaemia and HTN

45
Q

What investigations are useful in Conn’s syndrome?

A

early morning renin/aldosterone ratio
CT adrenals
oral salt load test
adrenal vein sampling

46
Q

What is the treatment of conn’s syndrome?

A

spironolactone

47
Q

How do you calculate anion gap?

A

(Na + K) - (Cl + HCO3)

48
Q

What causes high anion gap metabolic acidosis?

A 
increased acid generation:
lactic acidosis
toxins (metanol, aspirin, paracetamol)
ketoacidosis
renal failure
rhabdomyolysis
49
Q

What causes normal anion gap metabolic acidosis?

A

loss of bicarbonate or diminished renal acid excretion:
severe diarrhoea
renal failure

50
Q

What is type 1 renal tubular acidosis?

A

due to a defect in the distal hydrogen ion excretion (distal)

51
Q

What is type 2 renal tubular acidosis?

A

a reduced capacity to reclaim filtered bicarbonate (proximal)

52
Q

What is type 4 renal tubular acidosis?

A

due to low aldosterone levels

53
Q

What is type 3 renal tubular acidosis?

A

a combination of type 1 and type 2

54
Q

What causes type 1 renal tubular acidosis?

A

autoimmune diseases

55
Q

When should you suspect type 1 RTA?

A

urine pH > 5.5 with normal anion gap metabolic acidosis

56
Q

Why is there hypokalaemia in type 1 RTA?

A

because there is increased K secretion

57
Q

What are the causes of type 2 RTA?

A

myeloma, fanconi’s syndrome, drugs, isolated

58
Q

In which type of RTA do you get renal stones?

A

type 1

59
Q

In which types of RTA do you get hypokalaemia?

A

type 1 and type 2

BPT Renal (9 decks)

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