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Flashcards in Urinary Session 4 Deck (196):
1

Describe the osmotic status of sweat.

Hyposmotic

2

What must happen in order to change plasma volume?

Isosmotic solution must be added or removed so osmolarity remains constant

3

How is isosmotic volume added or removed from the plasma volume?

Movement of osmoles which water follows

4

What method of reabsorption does sodium mainly undergo?

Transcellular active driven by 3Na-2K-ATPase on basolateral membrane

5

In which part of the nephron is movement of water and sodium separated?

Descending thin limb and ascending thin and thick limbs of Henle's loop

6

What percentage of sodium in the filtered load is reabsorbed in the PCT?

67

7

How does the percentage of water and sodium reabsorption from the filtered load in the PCT compare and why?

Approximately equal due to isosmotic reabsorption

8

What percentage of water in the filtered load is reabsorbed in the ascending limbs of Henle's loop and the DCT?

0%

9

What is renal sodium excretion altered by?

Changes in osmotic and hydrostatic pressure in peritubular capillaries

10

What does an increase in oncotic or hydrostatic pressure in the peritubular capillaries cause?

Inhibition of sodium reabsorption leading to decreased water reabsorption

11

What is PCT sodium reabsorption stimulated by?

RAAS

12

What are the target cells for aldosterone?

Principal cells of DCT and CD

13

What does chloride absorption depend on?

Sodium reabsorption

14

Why is chloride reabsorption important?

To maintain electroneutrality

15

What must a finite volume of filtrate contain in terms of ions?

Anions=cations

16

What main method of reabsorption is used for chloride ions?

Transcellular active coupled to 3Na-2K-ATPase

17

Is paracellular reabsorption possible with chloride ions?

Yes

18

Which sodium transporters are found in the PCT tubular cells?

Na-H antiporter
Na-glucose symporter
Na-a.a. cotransporter
Na-Pi PTH transporter

19

Can the proportions of salts in the filtrate of the PCT vary as long as the osmolarity is constant?

Yes

20

Why does the proportion of chloride in the filtrate of the PCT increase?

Chloride reabsorption lagers behind so as everything else is removed its relative proportion increases

21

Why are glucose, a.a. and lactate transporters not needed in the distal PCT?

Fast, preferential reabsorption means that almost 100% is absorbed very quickly

22

What compensates for loss of glucose in S1 of the PCT to keep osmolarity constant?

Increasing urea and chloride concentration down the segment

23

What does the compensation of loss of glucose provide for S2-3 of the PCT?

Provide chloride concentration gradient for reabsorption

24

What type of sodium transporters are seen in S1 of the PCT?

Co transporters

25

Which sodium transporter is found in the apical membrane along the length of the PCT?

Na-H exchanger

26

Describe the permeability of the PCT to water.

Very permeable

27

How is chloride reabsorbed in S2-3 of the PCT?

Intra- and paracellularly

28

What favours water uptake from the lumen in S2-3 of the PCT?

Presence of oncotic proteins in the peritubular capillaries

29

What increases uptake into the capillaries surrounding the PCT?

Increased osmolarity of the interstitial spaces
Increased hydrostatic forces in the interstitium
Increased oncotic force from cells and proteins in peritubular capillaries

30

What is the first line of defence in autoregulation of GFR?

Myogenic action and tubulo-glomerular feedback

31

Why is the first line of defence in autoregulation of GFR not always sufficient?

Not instantaneous
Not always able to mount a big enough response

32

What is the second line of defence in maintaining constant GFR via autoregulation?

Glomerulotubular balance to ensure 67% of filtered sodium is reabsorbed regardless of the amount of filtration

33

What is the benefit of using glomerulotubular balance when GFR has varied widely?

Blunts extreme sodium excretion as a response to GFR changes that have not been corrected so the rest of the tubule can function

34

What is found between tubular cells of the thick and thin descending limbs of Henle's loop?

Loose junctions

35

What is the purpose of increasing intracellular sodium concentration in the thick and thin ascending limbs of Henle's loop?

Allow paracellular reabsorption of water

36

What is the purpose of allowing paracellular absorption of water in the thick and thin descending limb of Henle's loop?

Concentrates sodium and chloride in lumen ready for active transportin the ascending limb

37

What is found between tubular cells of the thin ascending limb of Henle's loop?

Tight junctions

38

What type of sodium reabsorption occurs in the thin ascending limb of Henle's loop?

Passive paracellular

39

What is the purpose of ROMK in the apical membrane of thick ascending limb tubular cells?

Leak K+ into the lumen where it is in low concentration in the filtrate so this does not become a limiting factor for reabsorption

40

Which part of the nephron is most sensitive to hypoxia and why?

Thick ascending limb of Henle's loop due to high energy demand

41

Which transporter facilitates sodium reabsorption in the thick ascending limb of the loop of Henle?

NaKCl2

42

What type of transporter is NaKCl2?

Symporter

43

What is found between cells of the thick ascending limb of Henle's loop?

Tight junctions

44

What type of sodium transporter is found in the apical membrane of the early DCT?

NaCl symporter

45

Describe the permeability of the early DCT to water.

Low

46

What is the osmotic state of fluid that enters the early DCT?

Hyposmotic

47

What is reabsorbed in the early DCT via PTH using an unknown mechanism?

Calcium

48

How is sodium reabsorbed in the early DCT?

Active transport

49

What percentage of filtered sodium is reabsorbed in the early DCT?

~5-8%

50

What is the osmotic state of fluid which exits the early DCT?

More hyposmotic that when it entered

51

How can cortical and medullary CD cells be distinguished?

Have different transporters

52

What apical sodium transporter is found in the late DCT and collecting duct tubular cells?

ENaC

53

Where is the filtrate in the nephron fine tuned in response to a variety of different stimulants?

Late DCT and collecting duct

54

Which two distinct cell types make up the late DCT and collecting duct?

Principle cells
Type B intercalated cells

55

What is the ratio of the two types of cells found in the late DCT and collecting duct?

70% principal cells
30% type B intercalated cells

56

What creates the -ve lumen charge in the late DCT and CD which drives paracellular chloride uptake?

Active Na+ uptake via a channel not cotransporter so no accompanying anion movement

57

What effect does ADH have on principal cells?

Varies aquaporins for variable water uptake

58

What is the function of type B intercalated cells?

Active reabsorption of chloride
Secretion of H+/HCO3-

59

How can type B intercalated cells be distinguished from principal cells on histological examination?

Darker staining nuclei

60

What system allows increased excretion of sodium and therefore water when increased circulating volume is exerting pressure on the filtration system?

Pressure natriuresis and diuresis

61

What does an increase in renal after BP cause to happen to transporters in the PCT?

Decreases expression of Na-H antiporter and Na-K-ATPase

62

What is the result of changes to transporters in the PCT caused by an increase in renal artery BP?

Decreased reabsorption of sodium and water in PCT:
Increased sodium excretion = pressure natriuresis
Increased water excretion = pressure diuresis

63

Do GFR autoregulation mechanisms still apply in pressure natriuresis and diuresis?

Yes

64

What in addition to pressure natriuresis and diuresis decreases fluid absorption in an increase of BP?

Increased BP --> increased peritubular capillary pressure --> increased fluid absorption

65

What is the pressure natriuresis and diuresis system independent of?

Vasomotor activity

66

Will urine always be isotonic when an isotonic volume is excreted to decrease blood volume?

No

67

Why do pressure natriuresis and diuresis occur together?

Lack of independent control

68

What does the degree of pressure natriuresis and diuresis depend on?

Volume status:
Increased ECF = high renal artery BP --> high pressure N&D
Decreased ECF = low renal artery BP --> low pressure N&D

69

What is the major osmotic ally effective solute in control of effective circulating volume?

Sodium

70

Where are nerve endings that are sensitive to stretch located which aid in acute regulation of BP?

Carotid sinus
Aortic arch

71

How do baroreceptors conduct signals to allow for acute regulation of BP?

Baroreceptors --> afferent pathways --> coordinating centre in the medulla --> efferent pathways

72

How is BP regulated in the short term?

Adjustment of parasympathetic input to peripheral resistance vessels to alter TPR

73

What happens to baroreceptors in the carotid sinus and aortic arch in long term raised BP?

Baroreceptor firing threshold resets so is still present but not constantly acting

74

What are the four medium/longer-term mechanisms of BP control?

RAAS
Sympathetic nervous system
ADH
Atrial natriuretic peptide

75

How does the action of atrial natriuretic peptide (ANP) act differently to the other systems of longer term BP control?

Acts to decreases plasma volume whereas others act to increase

76

Which fluid compartment is plasma part of?

Extra cellular fluid

77

How is the RAAS stimulated?

Decreased NaCl to distal tubule
Decreased BP in afferent arteriole
Sympathetic stimulation of beta-1-adrenoceptors

78

What is released by the macula densa and detected by baroreceptors in the RAAS?

Local mediators

79

What is the reaction to local mediator detection by baroreceptors in the RAAS?

Renin release from granular cells of the afferent arteriole in the juxtaglomerular apparatus

80

Where is angiotensinogen synthesised?

Liver

81

What is angiotensinogen cleaved by?

Renin

82

What is angiotensinogen cleaved into?

Angiotensin I

83

What converts angiotensin I to angiotensin II?

Angiotensin converting enzyme

84

Where is ACE found?

Endothelial cells in non-specific amounts (lots in the lungs)

85

What additional action does ACE have to its angiotensin converting function?

Breaks down bradykinin into peptide fragments

86

Why are angiotensin II antagonists sometimes used instead of ACE inhibitors?

To prevent the increase in bradykinin caused by the inhibition of ACE which leads to a dry cough

87

Which type of angiotensin II receptors carry out the main physiological actions identified with angiotensin II?

AT1

88

What type of receptor is AT1?

GPCR

89

At what sites are angiotensin receptors found?

Arterioles
Kidney
SNS
Adrenal cortex
Hypothalamus

90

What does angiotensin II acting on receptors in arterioles cause?

Vasoconstriction

91

What does angiotensin II acting on receptors in the kidney cause?

Sodium reabsorption

92

What does angiotensin II acting on receptors in the SNS stimulate?

Increased noradrenaline release

93

What effects does angiotensin II have on the adrenal cortex and hypothalamus?

Adrenal cortex: increases aldosterone
Hypothalamus: increases thirst --> increases ADH release

94

How does angiotensin II stimulate sodium reabsorption at the kidney?

Vasoconstriction of afferent and efferent arteriole to decrease GFR
Stimulates NHE3 in apical membrane of principle cell

95

What is the action of aldosterone release from the adrenal cortex?

Activates apical ENaC and K+ channel
Increases basolateral sodium extrusion via 3Na-2K-ATPase

96

Why does aldosterone increase receptor expression?

It is a steroid hormone

97

What effect does increased levels of sympathetic stimulation in the glomerulus have in longer term BP control?

Causes arteriole vasoconstriction --> decrease GFR --> decrease sodium excretion

98

What is the affect of sympathetic stimulation on the PCT?

Directly activates apical Na/H exchanger and basolateral Na/K-ATPase to increase sodium absorption

99

What are the effects of renin release stimulated by the sympathetic nervous system?

Increases angiotensin II
Increases aldosterone
Increases sodium reabsorption

100

What is the main role of ADH?

Control plasma osmolarity

101

What stimulates ADH release?

1% increase in plasma osmolarity
10% decrease in blood volume

102

What does ADH act on?

Thick ascending limb to stimulate apical Na/K/Cl co transporter and distal nephron for AQP2 insertion

103

What is the action of atrial natriuretic peptide?

Promote sodium excretion by inhibiting sodium reabsorption along nephron

104

How is ANP stored and released?

Synthesised and stored in atrial myocytes and released proportionally to stretch of these

105

What are low pressure volume sensors?

On low pressure side of circulation e.g. atrial myocytes

106

What are high pressure volume sensors?

Sensors on the atrial side of the circulation system e.g. baroreceptors

107

How does a decrease in effective circulation volume inhibit ANP release?

Decreases heart filling --> decreased stretch --> decreased ANP release

108

What is the effect of ANP on the afferent arteriole?

Causes vasodilation to increase GFR

109

What is the effect of prostaglandins in the kidney?

Locally enhance GFR and decrease sodium reabsorption by increasing blood flow

110

What do prostaglandins act as a buffer to to protect renal blood flow?

Excessive vasoconstriction produced by SNS and RAAS when levels of angiotensin II are raised

111

How can administration of NSAIDs to pts with compromised renal perfusion lead to acute renal failure?

NSAIDs inhibit cyclo-oxygenase pathway so prostaglandins are not synthesised and renal blood flow cannot be protected

112

How is dopamine formed locally in the kidney?

From L-DOPA

113

What is the action of dopamine in the kidney?

Acts on receptors on renal blood vessels, cells of PCT and TAL to cause vasodilation and decreased NaCl reabsorption to buffer against excessive vasoconstriction

114

What action does dopamine have on the transporters of the PCT and TAL?

Inhibits NHE and Na/K/ATPase in principal cells

115

Can the actions of dopamine in the kidney be used therapeutically?

Dopamine agonists are sometimes used as hypertensives

116

What is the numerical classification of mild hypertension?

140-159 (+/-) over 90-99

117

What is the numerical classification of moderate hypertension?

160-179 over 100-109

118

What is the numerical classification of severe hypertension?

>180 over >110

119

What is primary hypertension?

Cause unknown, may be due to genetic/environmental factors

120

What does recent research suggest is the pathogenesis of primary hypertension?

Dysfunction of dopamine agonist

121

What are the causes of secondary hypertension?

Renalvascular disease
Renal parenchymal disease
Adrenal causes

122

How does renalvascular disease cause secondary hypertension?

Renal artery stenosis --> decreased perfusion pressure --> RAAS --> vasoconstriction and sodium retention at the other kidney

123

How does renal parenchymal disease cause secondary hypertension?

Early stage causes loss of vasodilator substances
Later stage --> inadequate GFR --> sodium and water retention

124

What is Conn's syndrome?

Aldosterone secreting adenoma causing hypertension and hypokalaemia

125

What are the adrenal causes of secondary hypertension?

Conn's syndrome
Cushing's syndrome
Phaeochromocytoma

126

Why does Cushing's syndrome cause secondary hypertension?

Excess cortisol acts on aldosterone receptors

127

How does a phaeochromocytoma cause secondary hypertension?

Catecholamines act on beta-1 in kidney and alpha-1 in vasculature and heart

128

What can arterial damage caused by hypertension lead to?

Atherosclerosis and weakened vessels --> cerbrovascular disease, aneurysm, nephrosclerosis and renal failure, retinopathy

129

What is often the first visible damage due to hypertension?

Retinopathy

130

What effects can increased afterload caused by hypertension have?

Left ventricular hypertrophy --> heart failure
Increased myocardial afterload --> myocardial ischaemia and MI

131

How is secondary hypertension treated?

Identify and treat underlying cause

132

What methods can be used to treat hypertension?

Targeting RAAS
Diuretics
Vasodilators
Beta-blockers
Non-pharmacological approaches

133

How can the RAAS be targeted to treat hypertension?

ACE inhibitors
Angiotensin II antagonists

134

How do diuretics treat hypertension?

Reduce circulation and thus decease cardiac output

135

Give two examples of diuretics that can be used to treat hypertension.

Thiazide
Aldosterone antagonists (Spironolactone)

136

How do thiazide diuretics treat hypertension?

Act in DCT to inhibit Na/Cl co transporter on apical membrane

137

Are aldosterone antagonists first line treatment for most hypertensive pts?

No

138

How do vasodilators treat hypertension?

Decrease TPR

139

How do L-type calcium channel blockers treat hypertension?

Decrease calcium entry into vascular smooth muscle and hence cause relaxation

140

How do alpha-1-adrenocepetor blockers treat hypertension?

Decrease sympathetic tone thus relaxing vascular smooth muscle

141

How do beta-blockers treat hypertension?

Decrease cardiac output by decreasing HR and contractility

142

Are beta-blockers used as a first line hypertension Tx?

No, only if other indications e.g. previous MI or arrythmia

143

When are non-pharmacological approaches to treating hypertension used exclusively?

Mild hypertension

144

What non-pharmacological approaches can be used to treat hypertension?

Exercise
Diet
Decrease sodium intake
Decrease alcohol intake
Stop smoking

145

What can limit effectiveness of antihypertensive therapy and lead to more severe hypertension?

Failure to implement lifestyle changes

146

What is the action of aldosterone release from the adrenal cortex?

Activates apical ENaC and K+ channel
Increases basolateral sodium extrusion via 3Na-2K-ATPase

147

Why does aldosterone increase receptor expression?

It is a steroid hormone

148

What effect does increased levels of sympathetic stimulation in the glomerulus have in longer term BP control?

Causes arteriole vasoconstriction --> decrease GFR --> decrease sodium excretion

149

What is the affect of sympathetic stimulation on the PCT?

Directly activates apical Na/H exchanger and basolateral Na/K-ATPase to increase sodium absorption

150

What are the effects of renin release stimulated by the sympathetic nervous system?

Increases angiotensin II
Increases aldosterone
Increases sodium reabsorption

151

What is the main role of ADH?

Control plasma osmolarity

152

What stimulates ADH release?

1% increase in plasma osmolarity
10% decrease in blood volume

153

What does ADH act on?

Thick ascending limb to stimulate apical Na/K/Cl co transporter and distal nephron for AQP2 insertion

154

What is the action of atrial natriuretic peptide?

Promote sodium excretion by inhibiting sodium reabsorption along nephron

155

How is ANP stored and released?

Synthesised and stored in atrial myocytes and released proportionally to stretch of these

156

What are low pressure volume sensors?

On low pressure side of circulation e.g. atrial myocytes

157

What are high pressure volume sensors?

Sensors on the atrial side of the circulation system e.g. baroreceptors

158

How does a decrease in effective circulation volume inhibit ANP release?

Decreases heart filling --> decreased stretch --> decreased ANP release

159

What is the effect of ANP on the afferent arteriole?

Causes vasodilation to increase GFR

160

What is the effect of prostaglandins in the kidney?

Locally enhance GFR and decrease sodium reabsorption by increasing blood flow

161

What do prostaglandins act as a buffer to to protect renal blood flow?

Excessive vasoconstriction produced by SNS and RAAS when levels of angiotensin II are raised

162

How can administration of NSAIDs to pts with compromised renal perfusion lead to acute renal failure?

NSAIDs inhibit cyclo-oxygenase pathway so prostaglandins are not synthesised and renal blood flow cannot be protected

163

How is dopamine formed locally in the kidney?

From L-DOPA

164

What is the action of dopamine in the kidney?

Acts on receptors on renal blood vessels, cells of PCT and TAL to cause vasodilation and decreased NaCl reabsorption to buffer against excessive vasoconstriction

165

What action does dopamine have on the transporters of the PCT and TAL?

Inhibits NHE and Na/K/ATPase in principal cells

166

Can the actions of dopamine in the kidney be used therapeutically?

Dopamine agonists are sometimes used as hypertensives

167

What is the numerical classification of mild hypertension?

140-159 (+/-) over 90-99

168

What is the numerical classification of moderate hypertension?

160-179 over 100-109

169

What is the numerical classification of severe hypertension?

>180 over >110

170

What is primary hypertension?

Cause unknown, may be due to genetic/environmental factors

171

What does recent research suggest is the pathogenesis of primary hypertension?

Dysfunction of dopamine agonist

172

What are the causes of secondary hypertension?

Renalvascular disease
Renal parenchymal disease
Adrenal causes

173

How does renalvascular disease cause secondary hypertension?

Renal artery stenosis --> decreased perfusion pressure --> RAAS --> vasoconstriction and sodium retention at the other kidney

174

How does renal parenchymal disease cause secondary hypertension?

Early stage causes loss of vasodilator substances
Later stage --> inadequate GFR --> sodium and water retention

175

What is Conn's syndrome?

Aldosterone secreting adenoma causing hypertension and hypokalaemia

176

What are the adrenal causes of secondary hypertension?

Conn's syndrome
Cushing's syndrome
Phaeochromocytoma

177

Why does Cushing's syndrome cause secondary hypertension?

Excess cortisol acts on aldosterone receptors

178

How does a phaeochromocytoma cause secondary hypertension?

Catecholamines act on beta-1 in kidney and alpha-1 in vasculature and heart

179

What can arterial damage caused by hypertension lead to?

Atherosclerosis and weakened vessels --> cerbrovascular disease, aneurysm, nephrosclerosis and renal failure, retinopathy

180

What is often the first visible damage due to hypertension?

Retinopathy

181

What effects can increased afterload caused by hypertension have?

Left ventricular hypertrophy --> heart failure
Increased myocardial afterload --> myocardial ischaemia and MI

182

How is secondary hypertension treated?

Identify and treat underlying cause

183

What methods can be used to treat hypertension?

Targeting RAAS
Diuretics
Vasodilators
Beta-blockers
Non-pharmacological approaches

184

How can the RAAS be targeted to treat hypertension?

ACE inhibitors
Angiotensin II antagonists

185

How do diuretics treat hypertension?

Reduce circulation and thus decease cardiac output

186

Give two examples of diuretics that can be used to treat hypertension.

Thiazide
Aldosterone antagonists (Spironolactone)

187

How do thiazide diuretics treat hypertension?

Act in DCT to inhibit Na/Cl co transporter on apical membrane

188

Are aldosterone antagonists first line treatment for most hypertensive pts?

No

189

How do vasodilators treat hypertension?

Decrease TPR

190

How do L-type calcium channel blockers treat hypertension?

Decrease calcium entry into vascular smooth muscle and hence cause relaxation

191

How do alpha-1-adrenocepetor blockers treat hypertension?

Decrease sympathetic tone thus relaxing vascular smooth muscle

192

How do beta-blockers treat hypertension?

Decrease cardiac output by decreasing HR and contractility

193

Are beta-blockers used as a first line hypertension Tx?

No, only if other indications e.g. previous MI or arrythmia

194

When are non-pharmacological approaches to treating hypertension used exclusively?

Mild hypertension

195

What non-pharmacological approaches can be used to treat hypertension?

Exercise
Diet
Decrease sodium intake
Decrease alcohol intake
Stop smoking

196

What can limit effectiveness of antihypertensive therapy and lead to more severe hypertension?

Failure to implement lifestyle changes