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Flashcards in Urinary Session 5 Deck (116):
1

How are sodium concentration changes seen?

Change in ECF volume

2

What volume do most people urinate on average?

1-1.5l per day

3

What is the normal range of urine osmolarity?

500-700 mOsm per litre

4

Does the number of osmoles or the volume they are excreted in vary in urine production?

Volume excreted in

5

Where are osmoreceptors found?

OVLT of hypothalamus, anterior and central to third ventricle

6

How do osmoreceptors detect plasma osmolarity?

Have fenestrated leaky endothelium therefore are in direct contact with the systemic circulation

7

What is the result of osmoreceptors detecting a change in plasma osmolarity?

Use two pathways to cause secondary responses to achieve two complimentary outcomes

8

Which two signalling pathways do the osmoreceptors use to cause secondary responses in changes of plasma osmolarity?

ADH and thirst

9

Where is ADH released from?

Posterior pituitary

10

What is the action of ADH on the collecting duct?

Acts on V2 ADH GPCRs --> cAMP --> PKA --> insertion of AQP2 in apical membrane and increased permeability to urea

11

What is ADH release coordinated with?

Degree of stimulation

12

Which areas of the nephron relatively unaffected by ADH release?

Glomerulus, PCT and loop of Henle

13

Describe the control of ADH release.

-ve feedback loop constantly responding to small stimuli

14

What stimulates the thirst pathway?

>/= 10% increase in plasma osmolarity

15

What causes feelings of thirst to stop?

Sufficient fluid ingestion despite no change yet in plasma osmolarity

16

What is meant by our hedonistic appetite for salt?

When plasma osmolarity is low we crave salt to counteract the deficiency

17

Describe the distribution of AQP2 in the absence of ADH.

None

18

How does the permeability of the apical and basolateral membranes of collecting duct cells to water compare?

Apical: variable with AQP2 due to ADH release
Basolateral: always permeable due to permanent AQP3&4 presence

19

Why are AQP3&4 channels always present in the basolateral membrane of collecting duct cells?

So any water that enters can move into the peritubular blood

20

What happens to AQP2 in the absence of ADH?

Endocytosed

21

Is volume or osmolarity more important for ECF?

Volume

22

What happens to the set-point of osmolarity if volume crashes?

Shifts down so kidney can conserve water and slope of plasma ADH level vs plasma osmolarity gets steeper

23

Is there always a basal level of ADH release?

Yes

24

What causes diabetes incipidus?

Lack of ADH from posterior pituitary
Acquired insensitivity of kidney to ADH

25

What does diabetes incipidus cause?

Inadequate water reabsorption in collecting leading to polyuria

26

How is diabetes incipidus treated?

ADH nasal spray/injections

27

What is syndrome of inappropriate ADH secretion (SIADH)?

Excessive ADH release from posterior pituitary or ectopically from tumour --> dilutional hyponatraemia --> low plasma sodium and high total body fluids

28

What is an ineffective osmole?

Solute that can move freely across a partially permeable membrane therefore cannot exert a osmotic effect as a gradient cannot be established

29

What is reflection coefficient?

How effectively an osmotic gradient can be maintained

30

Why is urea an ineffective osmole in most areas of the body?

Passes through lipid bilayers via transporters

31

What do osmolarity changes in ECF indicate?

Disorders of water balance

32

What is an effective osmole?

A solute that can be concentrated on one side of a partially permeable membrane so it can exert an osmotic effect due to its gradient

33

What does the reflection coefficient of an effective osmole tend towards?

1

34

Where does urea become an effective osmole?

Kidney

35

What is an essential mechanism caused by the active transport of NaCl in the TAL, recycling of urea and unusual arrangement of blood vessels in the medulla?

Corticopapillary osmotic gradient

36

Describe the osmotic state of the nephron surroundings at the cortico-medullary border in comparison to the medullary intersticium.

Cortico-medullary border: isotonic
Medullary intersticium: hyper osmotic up to 1000 mOsm per litre at papilla

37

What happens in countercurrent multiplication in the Loop of Henle?

Sodium pumped out to achieve maximum gradient --> water moves out of descending limb raising osmotic pressure in tubule --> fresh fluid enters glomerulus pushing concentrated fluid into ascending limb --> maximum sodium gradient created increasing external osmolarity further

38

What limits the final gradient in establishing countercurrent multiplication?

Diffusional processes

39

How can loop diuretics be used to prevent countercurrent multiplication and cause lots of dilute urine to be formed?

Block NaKCC transporters so medullary intersticium becomes isosmotic

40

What happens to urea in the PCT?

~45% of filtered urea is reabsorbed into peritubular capillaries

41

Describe the permeability of cortical CD cells to urea.

Impermeable

42

What happens to urea when it comes into contact with medullary CD cells?

Cells are permeable so allow movement into the intersticium and subsequent diffusion back into the loop of Henle

43

How is recycling of urea affected by ADH?

Increases to promote water reabsorption and decreases fractional excretion of urea

44

Why is urea recycling described as an 'active process'?

Due to need for ADH secretion, not because of energy requirements

45

Why are osmoles not washed Out of the intersticium by movement of water out of the descending limb of the loop of Henle?

Opposing blood flow in vasa recta act as a counter-current exchanger

46

Describe the contents of blood in the vast recta as they move through the descending limb.

Isosmotic blood enters medulla --> sodium and chloride diffuse into lumen --> blood osmolarity increases as it reaches hairpin loop

47

Describe the contents of blood in the ascending limb of the vasa recta.

Blood starts off with higher solute content than surrounding intersticium --> water moves in from descending limb of the loop of Henle

48

Can the vasa recta carry out active transport?

No

49

What do the vasa recta use to carry out movement of substances?

NaCl gradient
Gradient of urea from cortex --> papilla
ADH presence

50

What can be said about the bloodflow in the vasa recta?

It is low (5-10% of total renal parenchymal flow)

51

Why is bloodflow in the vasa recta low?

Compromise delivery of nutrients and maintenance of medullary hypertonicity

52

What forms does plasma calcium take?

48% ionised
46% protein bound
7% complexed

53

What is 80% of protein-bound calcium bound to?

Albumin

54

What is plasma calcium complexed with?

Citrates, phosphates etc

55

Why does an adjusted calcium value need to be used to measure plasma calcium?

To negate effects of abnormal albumin values

56

What would you do if measured calcium level was within range when adjusted?

Investigate albumin levels

57

What percentage of dietary calcium is absorbed in the intestine?

20-40%

58

How does absorption of calcium change?

Increases in growth, pregnancy and lactation
Decreases in advancing age

59

What is calcium absorption in the gut under control by?

Calcitriol (1,25-(OH)2D)

60

What can decrease intestinal absorption of calcium?

Completing with phytates, oxalates etc

61

What action does the kidney have on calcium?

Filters 10 g of mainly ionised calcium per day, of which 98% is reabsorbed

62

What causes cellular and paracellular absorption of calcium in the ascending loop of Henle?

Calcitonin
PTH

63

Does paracellular reabsorption of calcium occur in the DCT?

No

64

What controls calcium reabsorption in the DCT?

PTH

65

How much calcium is excreted by the kidney?

~200 mg per day

66

Which three molecules regulate calcium homeostasis?

Vitamin D
PTH
Calcitonin

67

What is the mammalian form of vitamin D?

D3

68

Why is ergocalciferol, the fungal form of vitamin D, used for injections in the UK?

It is easier to synthesise than the mammalian form

69

What is the action of vitamin in calcium homeostasis?

Increases plasma concentration

70

Which type of vitamin D is usually given in deficiency?

Calciferol

71

What are the stages in vitamin D metabolism?

Calciferol --> calcidiol --> calcitriol or 24,25-(OH)2D

72

What determines the end product of vitamin D metabolism?

Circulating levels

73

What enzyme found in the liver needed for vitamin D activation?

25-hydroxylase

74

What enzyme is found in the kidney which is needed for vitamin D activation?

1-alpha-hydroxylase

75

Which form of vitamin D is given in renal failure or hypoparathyroidism?

Active form - calcitriol

76

What form of vitamin D is measured in laboratory tests?

Calcidiol

77

How is most of vitamin D need met?

Sunlight

78

What is the problem with vitamin D availability in Oct-Feb in the UK?

Isn't enough UVB so have to rely on tissue stores, supplements and diet

79

What tissues does calcitriol affect?

Bone and intestines

80

What action does PTH have in calcium homeostasis?

Increase plasma levels

81

What effect does PTH have on bone?

Stimulates osteoclasts and slowly stimulates osteoblasts

82

Why does treatment with PTH analogue have. Period of bone formation?

Due to slow stimulation of osteoblasts

83

What effect does PTH have on the kidney?

Increases calcium and magnesium reabsorption
Decreases Pi and HCO3- reabsorption
Stimulates 1-alpha-hydroxylase

84

What cation does calcitonin have on calcium homeostasis?

Minor decrease in plasma levels

85

Does chronic excess of calcitonin lead to hypcalcaemia?

No

86

Does removal of parafollicular cells lead to hypercalcaemia?

No

87

What action does calcitonin take to decrease plasma calcium concentration?

Decreases bone resorption
Inhibits renal tubular calcium reabsorption

88

What is calcitonin used to treat?

Hypercalcaemia in malignancy

89

What are the actions of calcitriol?

Promotes receptors to increases availability of Ca2+ and Pi via intestinal uptake
Promotes osteoblasts activity and maturation of osteoclast precursors
Uses intestinal absorbed Pi to inhibit renal 1-alpha-hydroxylase
Promotes 24,25-(OH2)D synthesis
Exerts a small effect on renal Ca2+ and Pi reabsorption
Regulates cells differentiation and proliferation
Inhibits cellular growth
Stimulates insulin secretion
Modulation of immune and haemopoietic systems
Inhibit renin production

90

What are relatively common causes of hypercalcaemia?

Haematological and non-haematological malignancies
Primary hyperparathyroidism

91

What are the S/S of hypercalcaemia?

Stones, moans and groans:
Anorexia, diarrhoea, hypertension, polyuria, polysdipsia, gradual onset cognitive difficulties, apathy, depression

92

How do hypercalcaemic pts usually present?

AKI

93

What is the Tx for acute hypercalcaemia?

Normal saline to increase calcium loss in urine
Loop diuretics but not thiazide
Bisphosphonates to inhibit bone resorption
Calcitonin
Steroids if granulomas present to inhibit 1-alpha-hydroxylase action

94

Why can't thiazides be used to treat acute hypercalcaemia?

These retain calcium

95

How does hypercalcaemia of malignancy compare to primary hyperparathyroidism?

Higher serum calcium levels
Quicker onset
Renal calculi are rare
Plasma intact PTH is suppressed

96

What can cause hypercalcaemia in malignancy?

Extensive bone metastases
Local osteolysis
A.a. Homology of PTHiP with N-terminal of PTH
Ectopic PTH
Cytokines causing increased osteoclast activity

97

How can primary, secondary and tertiary hyperparathyroidism be distinguished from each other?

Primary: reduced calcium and raised PTH
Secondary: reduced/normal calcium with raised PTH
Tertiary: with autonomous PTH secretion

98

What usually causes tertiary hyperparathyroidism?

Complication of secondary hyperparathyroidism

99

By 70 y.o. what percentage of males and females will have developed a symptomatic kidney stone?

Males: 11.0%
Females: 5.6%

100

What population are renal stones most likely to form in?

Caucasian males

101

Which population are renal stones least likely to develop in?

Asian females

102

What are the S/S of renal stones?

Asymptomatic
Haematuria
Renal colic
Associated complications of obstructed renal tract

103

Where may renal colic pain be felt?

Loin
Testicle
Labia

104

What is the general treatment for renal stones?

Maintain hydration
Restrict oxalate and sodium in diet

105

What types of renal stones can form?

Calcium oxalate
Calcium
Struvite
Urate
Cysteine

106

What are rare forms of renal stones often due to?

Inborn error conditions

107

What is the general pathogensis of renal stone formation?

Supersaturation of the urine with solutes --> free ion activities of components --> stone formation

108

How does hyperoxaluria cause renal stone formation?

Decreased calcium intake leads to oxalate being bound to and absorbed with FA

109

How can hyperoxaluria be managed to prevent renal stone formation?

Encourage high calcium intake so oxalate can complex and be lost in faeces

110

What can cause hyperuricosuria which can lead to renal stone formation?

Commonly outline rich diet
High cell turnover in leukaemia, lesch-nyhon syndrome

111

How does acidaemia causing hypocitraturia lead to renal stone formation?

Citrate cannot bind with calcium to keep it soluble

112

What can cause acidaemia leading to hypocitraturia and eventual renal stone formation?

Hypokalaemia

113

How does urine pH favour renal stone formation?

Acidic urine favours uric acid and cystine crystal formation
Alkaline urine favours calcium phosphate and struvite stones

114

Why can hypomagnesemia lead to renal stone formation?

Reduction in magnesium available to bind to oxalate and prevent stone formation

115

What factors effect solubility of solutes in the urine?

Urine pH
Volume
Total excretion

116

How are renal stones managed?

Less than 5mm pass spontaneously
6-7 mm ESWL (shock waves) or more invasive is necessary