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Semester 3 > Urinary Session 5 > Flashcards

Urinary Session 5 Flashcards

1
Q

How are sodium concentration changes seen?

A

Change in ECF volume

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2
Q

What volume do most people urinate on average?

A

1-1.5l per day

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3
Q

What is the normal range of urine osmolarity?

A

500-700 mOsm per litre

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4
Q

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

A

Volume excreted in

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5
Q

Where are osmoreceptors found?

A

OVLT of hypothalamus, anterior and central to third ventricle

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6
Q

How do osmoreceptors detect plasma osmolarity?

A

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

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7
Q

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

A

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

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8
Q

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

A

ADH and thirst

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9
Q

Where is ADH released from?

A

Posterior pituitary

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10
Q

What is the action of ADH on the collecting duct?

A

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

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11
Q

What is ADH release coordinated with?

A

Degree of stimulation

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12
Q

Which areas of the nephron relatively unaffected by ADH release?

A

Glomerulus, PCT and loop of Henle

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13
Q

Describe the control of ADH release.

A

-ve feedback loop constantly responding to small stimuli

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14
Q

What stimulates the thirst pathway?

A

> /= 10% increase in plasma osmolarity

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15
Q

What causes feelings of thirst to stop?

A

Sufficient fluid ingestion despite no change yet in plasma osmolarity

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16
Q

What is meant by our hedonistic appetite for salt?

A

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

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17
Q

Describe the distribution of AQP2 in the absence of ADH.

A

None

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18
Q

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

A

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

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19
Q

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

A

So any water that enters can move into the peritubular blood

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20
Q

What happens to AQP2 in the absence of ADH?

A

Endocytosed

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21
Q

Is volume or osmolarity more important for ECF?

A

Volume

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22
Q

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

A

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

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23
Q

Is there always a basal level of ADH release?

A

Yes

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24
Q

What causes diabetes incipidus?

A

Lack of ADH from posterior pituitary

Acquired insensitivity of kidney to ADH

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25
Q

What does diabetes incipidus cause?

A

Inadequate water reabsorption in collecting leading to polyuria

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26
Q

How is diabetes incipidus treated?

A

ADH nasal spray/injections

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27
Q

What is syndrome of inappropriate ADH secretion (SIADH)?

A

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

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28
Q

What is an ineffective osmole?

A

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

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29
Q

What is reflection coefficient?

A

How effectively an osmotic gradient can be maintained

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30
Q

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

A

Passes through lipid bilayers via transporters

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31
Q

What do osmolarity changes in ECF indicate?

A

Disorders of water balance

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32
Q

What is an effective osmole?

A

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

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33
Q

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

A

1

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34
Q

Where does urea become an effective osmole?

A

Kidney

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35
Q

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?

A

Corticopapillary osmotic gradient

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36
Q

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

A

Cortico-medullary border: isotonic

Medullary intersticium: hyper osmotic up to 1000 mOsm per litre at papilla

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37
Q

What happens in countercurrent multiplication in the Loop of Henle?

A

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

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38
Q

What limits the final gradient in establishing countercurrent multiplication?

A

Diffusional processes

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39
Q

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

A

Block NaKCC transporters so medullary intersticium becomes isosmotic

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40
Q

What happens to urea in the PCT?

A

~45% of filtered urea is reabsorbed into peritubular capillaries

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41
Q

Describe the permeability of cortical CD cells to urea.

A

Impermeable

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42
Q

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

A

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

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43
Q

How is recycling of urea affected by ADH?

A

Increases to promote water reabsorption and decreases fractional excretion of urea

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44
Q

Why is urea recycling described as an ‘active process’?

A

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

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45
Q

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

A

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

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46
Q

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

A

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

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47
Q

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

A

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

48
Q

Can the vasa recta carry out active transport?

A

No

49
Q

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

A

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

50
Q

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

A

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

51
Q

Why is bloodflow in the vasa recta low?

A

Compromise delivery of nutrients and maintenance of medullary hypertonicity

52
Q

What forms does plasma calcium take?

A

48% ionised
46% protein bound
7% complexed

53
Q

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

A

Albumin

54
Q

What is plasma calcium complexed with?

A

Citrates, phosphates etc

55
Q

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

A

To negate effects of abnormal albumin values

56
Q

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

A

Investigate albumin levels

57
Q

What percentage of dietary calcium is absorbed in the intestine?

A

20-40%

58
Q

How does absorption of calcium change?

A

Increases in growth, pregnancy and lactation

Decreases in advancing age

59
Q

What is calcium absorption in the gut under control by?

A

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

60
Q

What can decrease intestinal absorption of calcium?

A

Completing with phytates, oxalates etc

61
Q

What action does the kidney have on calcium?

A

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

62
Q

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

A

Calcitonin

PTH

63
Q

Does paracellular reabsorption of calcium occur in the DCT?

A

No

64
Q

What controls calcium reabsorption in the DCT?

A

PTH

65
Q

How much calcium is excreted by the kidney?

A

~200 mg per day

66
Q

Which three molecules regulate calcium homeostasis?

A

Vitamin D
PTH
Calcitonin

67
Q

What is the mammalian form of vitamin D?

A

D3

68
Q

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

A

It is easier to synthesise than the mammalian form

69
Q

What is the action of vitamin in calcium homeostasis?

A

Increases plasma concentration

70
Q

Which type of vitamin D is usually given in deficiency?

A

Calciferol

71
Q

What are the stages in vitamin D metabolism?

A

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

72
Q

What determines the end product of vitamin D metabolism?

A

Circulating levels

73
Q

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

A

25-hydroxylase

74
Q

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

A

1-alpha-hydroxylase

75
Q

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

A

Active form - calcitriol

76
Q

What form of vitamin D is measured in laboratory tests?

A

Calcidiol

77
Q

How is most of vitamin D need met?

A

Sunlight

78
Q

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

A

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

79
Q

What tissues does calcitriol affect?

A

Bone and intestines

80
Q

What action does PTH have in calcium homeostasis?

A

Increase plasma levels

81
Q

What effect does PTH have on bone?

A

Stimulates osteoclasts and slowly stimulates osteoblasts

82
Q

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

A

Due to slow stimulation of osteoblasts

83
Q

What effect does PTH have on the kidney?

A

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

84
Q

What cation does calcitonin have on calcium homeostasis?

A

Minor decrease in plasma levels

85
Q

Does chronic excess of calcitonin lead to hypcalcaemia?

A

No

86
Q

Does removal of parafollicular cells lead to hypercalcaemia?

A

No

87
Q

What action does calcitonin take to decrease plasma calcium concentration?

A

Decreases bone resorption

Inhibits renal tubular calcium reabsorption

88
Q

What is calcitonin used to treat?

A

Hypercalcaemia in malignancy

89
Q

What are the actions of calcitriol?

A

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
Q

What are relatively common causes of hypercalcaemia?

A

Haematological and non-haematological malignancies

Primary hyperparathyroidism

91
Q

What are the S/S of hypercalcaemia?

A

Stones, moans and groans:

Anorexia, diarrhoea, hypertension, polyuria, polysdipsia, gradual onset cognitive difficulties, apathy, depression

92
Q

How do hypercalcaemic pts usually present?

A

AKI

93
Q

What is the Tx for acute hypercalcaemia?

A

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
Q

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

A

These retain calcium

95
Q

How does hypercalcaemia of malignancy compare to primary hyperparathyroidism?

A

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

96
Q

What can cause hypercalcaemia in malignancy?

A

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

97
Q

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

A

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

98
Q

What usually causes tertiary hyperparathyroidism?

A

Complication of secondary hyperparathyroidism

99
Q

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

A

Males: 11.0%
Females: 5.6%

100
Q

What population are renal stones most likely to form in?

A

Caucasian males

101
Q

Which population are renal stones least likely to develop in?

A

Asian females

102
Q

What are the S/S of renal stones?

A

Asymptomatic
Haematuria
Renal colic
Associated complications of obstructed renal tract

103
Q

Where may renal colic pain be felt?

A

Loin
Testicle
Labia

104
Q

What is the general treatment for renal stones?

A

Maintain hydration

Restrict oxalate and sodium in diet

105
Q

What types of renal stones can form?

A 
Calcium oxalate
Calcium
Struvite
Urate
Cysteine
106
Q

What are rare forms of renal stones often due to?

A

Inborn error conditions

107
Q

What is the general pathogensis of renal stone formation?

A

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

108
Q

How does hyperoxaluria cause renal stone formation?

A

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

109
Q

How can hyperoxaluria be managed to prevent renal stone formation?

A

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

110
Q

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

A

Commonly outline rich diet

High cell turnover in leukaemia, lesch-nyhon syndrome

111
Q

How does acidaemia causing hypocitraturia lead to renal stone formation?

A

Citrate cannot bind with calcium to keep it soluble

112
Q

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

A

Hypokalaemia

113
Q

How does urine pH favour renal stone formation?

A

Acidic urine favours uric acid and cystine crystal formation

Alkaline urine favours calcium phosphate and struvite stones

114
Q

Why can hypomagnesemia lead to renal stone formation?

A

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

115
Q

What factors effect solubility of solutes in the urine?

A

Urine pH
Volume
Total excretion

116
Q

How are renal stones managed?

A

Less than 5mm pass spontaneously

6-7 mm ESWL (shock waves) or more invasive is necessary

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