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Semester 3 > Urinary Session 4 > Flashcards

Urinary Session 4 Flashcards

1
Q

Describe the osmotic status of sweat.

A

Hyposmotic

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2
Q

What must happen in order to change plasma volume?

A

Isosmotic solution must be added or removed so osmolarity remains constant

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3
Q

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

A

Movement of osmoles which water follows

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4
Q

What method of reabsorption does sodium mainly undergo?

A

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

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5
Q

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

A

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

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6
Q

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

A

67

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7
Q

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

A

Approximately equal due to isosmotic reabsorption

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8
Q

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

A

0%

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9
Q

What is renal sodium excretion altered by?

A

Changes in osmotic and hydrostatic pressure in peritubular capillaries

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10
Q

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

A

Inhibition of sodium reabsorption leading to decreased water reabsorption

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11
Q

What is PCT sodium reabsorption stimulated by?

A

RAAS

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12
Q

What are the target cells for aldosterone?

A

Principal cells of DCT and CD

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13
Q

What does chloride absorption depend on?

A

Sodium reabsorption

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14
Q

Why is chloride reabsorption important?

A

To maintain electroneutrality

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15
Q

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

A

Anions=cations

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16
Q

What main method of reabsorption is used for chloride ions?

A

Transcellular active coupled to 3Na-2K-ATPase

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17
Q

Is paracellular reabsorption possible with chloride ions?

A

Yes

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18
Q

Which sodium transporters are found in the PCT tubular cells?

A

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

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19
Q

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

A

Yes

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20
Q

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

A

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

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21
Q

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

A

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

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22
Q

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

A

Increasing urea and chloride concentration down the segment

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23
Q

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

A

Provide chloride concentration gradient for reabsorption

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24
Q

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

A

Co transporters

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25
Q

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

A

Na-H exchanger

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26
Q

Describe the permeability of the PCT to water.

A

Very permeable

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27
Q

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

A

Intra- and paracellularly

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28
Q

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

A

Presence of oncotic proteins in the peritubular capillaries

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29
Q

What increases uptake into the capillaries surrounding the PCT?

A

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

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30
Q

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

A

Myogenic action and tubulo-glomerular feedback

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31
Q

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

A

Not instantaneous

Not always able to mount a big enough response

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32
Q

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

A

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

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33
Q

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

A

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

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34
Q

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

A

Loose junctions

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35
Q

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

A

Allow paracellular reabsorption of water

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36
Q

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

A

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

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37
Q

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

A

Tight junctions

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38
Q

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

A

Passive paracellular

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39
Q

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

A

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

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40
Q

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

A

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

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41
Q

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

A

NaKCl2

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42
Q

What type of transporter is NaKCl2?

A

Symporter

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43
Q

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

A

Tight junctions

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44
Q

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

A

NaCl symporter

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45
Q

Describe the permeability of the early DCT to water.

A

Low

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46
Q

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

A

Hyposmotic

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47
Q

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

A

Calcium

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48
Q

How is sodium reabsorbed in the early DCT?

A

Active transport

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49
Q

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

A

~5-8%

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50
Q

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

A

More hyposmotic that when it entered

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51
Q

How can cortical and medullary CD cells be distinguished?

A

Have different transporters

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52
Q

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

A

ENaC

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53
Q

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

A

Late DCT and collecting duct

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54
Q

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

A

Principle cells

Type B intercalated cells

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55
Q

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

A

70% principal cells

30% type B intercalated cells

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56
Q

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

A

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

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57
Q

What effect does ADH have on principal cells?

A

Varies aquaporins for variable water uptake

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58
Q

What is the function of type B intercalated cells?

A

Active reabsorption of chloride

Secretion of H+/HCO3-

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59
Q

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

A

Darker staining nuclei

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60
Q

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

A

Pressure natriuresis and diuresis

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61
Q

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

A

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

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62
Q

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

A

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

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63
Q

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

A

Yes

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64
Q

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

A

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

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65
Q

What is the pressure natriuresis and diuresis system independent of?

A

Vasomotor activity

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66
Q

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

A

No

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67
Q

Why do pressure natriuresis and diuresis occur together?

A

Lack of independent control

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68
Q

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

A

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

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69
Q

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

A

Sodium

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70
Q

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

A

Carotid sinus

Aortic arch

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71
Q

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

A

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

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72
Q

How is BP regulated in the short term?

A

Adjustment of parasympathetic input to peripheral resistance vessels to alter TPR

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73
Q

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

A

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

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74
Q

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

A

RAAS
Sympathetic nervous system
ADH
Atrial natriuretic peptide

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75
Q

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

A

Acts to decreases plasma volume whereas others act to increase

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76
Q

Which fluid compartment is plasma part of?

A

Extra cellular fluid

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77
Q

How is the RAAS stimulated?

A

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

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78
Q

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

A

Local mediators

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79
Q

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

A

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

80
Q

Where is angiotensinogen synthesised?

A

Liver

81
Q

What is angiotensinogen cleaved by?

A

Renin

82
Q

What is angiotensinogen cleaved into?

A

Angiotensin I

83
Q

What converts angiotensin I to angiotensin II?

A

Angiotensin converting enzyme

84
Q

Where is ACE found?

A

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

85
Q

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

A

Breaks down bradykinin into peptide fragments

86
Q

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

A

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

87
Q

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

A

AT1

88
Q

What type of receptor is AT1?

A

GPCR

89
Q

At what sites are angiotensin receptors found?

A 
Arterioles
Kidney
SNS
Adrenal cortex
Hypothalamus
90
Q

What does angiotensin II acting on receptors in arterioles cause?

A

Vasoconstriction

91
Q

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

A

Sodium reabsorption

92
Q

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

A

Increased noradrenaline release

93
Q

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

A

Adrenal cortex: increases aldosterone

Hypothalamus: increases thirst –> increases ADH release

94
Q

How does angiotensin II stimulate sodium reabsorption at the kidney?

A

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

95
Q

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

A

Activates apical ENaC and K+ channel

Increases basolateral sodium extrusion via 3Na-2K-ATPase

96
Q

Why does aldosterone increase receptor expression?

A

It is a steroid hormone

97
Q

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

A

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

98
Q

What is the affect of sympathetic stimulation on the PCT?

A

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

99
Q

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

A

Increases angiotensin II
Increases aldosterone
Increases sodium reabsorption

100
Q

What is the main role of ADH?

A

Control plasma osmolarity

101
Q

What stimulates ADH release?

A

1% increase in plasma osmolarity

10% decrease in blood volume

102
Q

What does ADH act on?

A

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

103
Q

What is the action of atrial natriuretic peptide?

A

Promote sodium excretion by inhibiting sodium reabsorption along nephron

104
Q

How is ANP stored and released?

A

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

105
Q

What are low pressure volume sensors?

A

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

106
Q

What are high pressure volume sensors?

A

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

107
Q

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

A

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

108
Q

What is the effect of ANP on the afferent arteriole?

A

Causes vasodilation to increase GFR

109
Q

What is the effect of prostaglandins in the kidney?

A

Locally enhance GFR and decrease sodium reabsorption by increasing blood flow

110
Q

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

A

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

111
Q

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

A

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

112
Q

How is dopamine formed locally in the kidney?

A

From L-DOPA

113
Q

What is the action of dopamine in the kidney?

A

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
Q

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

A

Inhibits NHE and Na/K/ATPase in principal cells

115
Q

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

A

Dopamine agonists are sometimes used as hypertensives

116
Q

What is the numerical classification of mild hypertension?

A

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

117
Q

What is the numerical classification of moderate hypertension?

A

160-179 over 100-109

118
Q

What is the numerical classification of severe hypertension?

A

> 180 over >110

119
Q

What is primary hypertension?

A

Cause unknown, may be due to genetic/environmental factors

120
Q

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

A

Dysfunction of dopamine agonist

121
Q

What are the causes of secondary hypertension?

A

Renalvascular disease
Renal parenchymal disease
Adrenal causes

122
Q

How does renalvascular disease cause secondary hypertension?

A

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

123
Q

How does renal parenchymal disease cause secondary hypertension?

A

Early stage causes loss of vasodilator substances

Later stage –> inadequate GFR –> sodium and water retention

124
Q

What is Conn’s syndrome?

A

Aldosterone secreting adenoma causing hypertension and hypokalaemia

125
Q

What are the adrenal causes of secondary hypertension?

A

Conn’s syndrome
Cushing’s syndrome
Phaeochromocytoma

126
Q

Why does Cushing’s syndrome cause secondary hypertension?

A

Excess cortisol acts on aldosterone receptors

127
Q

How does a phaeochromocytoma cause secondary hypertension?

A

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

128
Q

What can arterial damage caused by hypertension lead to?

A

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

129
Q

What is often the first visible damage due to hypertension?

A

Retinopathy

130
Q

What effects can increased afterload caused by hypertension have?

A

Left ventricular hypertrophy –> heart failure

Increased myocardial afterload –> myocardial ischaemia and MI

131
Q

How is secondary hypertension treated?

A

Identify and treat underlying cause

132
Q

What methods can be used to treat hypertension?

A 
Targeting RAAS
Diuretics
Vasodilators
Beta-blockers
Non-pharmacological approaches
133
Q

How can the RAAS be targeted to treat hypertension?

A

ACE inhibitors

Angiotensin II antagonists

134
Q

How do diuretics treat hypertension?

A

Reduce circulation and thus decease cardiac output

135
Q

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

A 
Thiazide
Aldosterone antagonists (Spironolactone)
136
Q

How do thiazide diuretics treat hypertension?

A

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

137
Q

Are aldosterone antagonists first line treatment for most hypertensive pts?

A

No

138
Q

How do vasodilators treat hypertension?

A

Decrease TPR

139
Q

How do L-type calcium channel blockers treat hypertension?

A

Decrease calcium entry into vascular smooth muscle and hence cause relaxation

140
Q

How do alpha-1-adrenocepetor blockers treat hypertension?

A

Decrease sympathetic tone thus relaxing vascular smooth muscle

141
Q

How do beta-blockers treat hypertension?

A

Decrease cardiac output by decreasing HR and contractility

142
Q

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

A

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

143
Q

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

A

Mild hypertension

144
Q

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

A 
Exercise
Diet
Decrease sodium intake
Decrease alcohol intake
Stop smoking
145
Q

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

A

Failure to implement lifestyle changes

146
Q

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

A

Activates apical ENaC and K+ channel

Increases basolateral sodium extrusion via 3Na-2K-ATPase

147
Q

Why does aldosterone increase receptor expression?

A

It is a steroid hormone

148
Q

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

A

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

149
Q

What is the affect of sympathetic stimulation on the PCT?

A

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

150
Q

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

A

Increases angiotensin II
Increases aldosterone
Increases sodium reabsorption

151
Q

What is the main role of ADH?

A

Control plasma osmolarity

152
Q

What stimulates ADH release?

A

1% increase in plasma osmolarity

10% decrease in blood volume

153
Q

What does ADH act on?

A

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

154
Q

What is the action of atrial natriuretic peptide?

A

Promote sodium excretion by inhibiting sodium reabsorption along nephron

155
Q

How is ANP stored and released?

A

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

156
Q

What are low pressure volume sensors?

A

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

157
Q

What are high pressure volume sensors?

A

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

158
Q

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

A

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

159
Q

What is the effect of ANP on the afferent arteriole?

A

Causes vasodilation to increase GFR

160
Q

What is the effect of prostaglandins in the kidney?

A

Locally enhance GFR and decrease sodium reabsorption by increasing blood flow

161
Q

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

A

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

162
Q

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

A

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

163
Q

How is dopamine formed locally in the kidney?

A

From L-DOPA

164
Q

What is the action of dopamine in the kidney?

A

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
Q

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

A

Inhibits NHE and Na/K/ATPase in principal cells

166
Q

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

A

Dopamine agonists are sometimes used as hypertensives

167
Q

What is the numerical classification of mild hypertension?

A

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

168
Q

What is the numerical classification of moderate hypertension?

A

160-179 over 100-109

169
Q

What is the numerical classification of severe hypertension?

A

> 180 over >110

170
Q

What is primary hypertension?

A

Cause unknown, may be due to genetic/environmental factors

171
Q

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

A

Dysfunction of dopamine agonist

172
Q

What are the causes of secondary hypertension?

A

Renalvascular disease
Renal parenchymal disease
Adrenal causes

173
Q

How does renalvascular disease cause secondary hypertension?

A

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

174
Q

How does renal parenchymal disease cause secondary hypertension?

A

Early stage causes loss of vasodilator substances

Later stage –> inadequate GFR –> sodium and water retention

175
Q

What is Conn’s syndrome?

A

Aldosterone secreting adenoma causing hypertension and hypokalaemia

176
Q

What are the adrenal causes of secondary hypertension?

A

Conn’s syndrome
Cushing’s syndrome
Phaeochromocytoma

177
Q

Why does Cushing’s syndrome cause secondary hypertension?

A

Excess cortisol acts on aldosterone receptors

178
Q

How does a phaeochromocytoma cause secondary hypertension?

A

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

179
Q

What can arterial damage caused by hypertension lead to?

A

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

180
Q

What is often the first visible damage due to hypertension?

A

Retinopathy

181
Q

What effects can increased afterload caused by hypertension have?

A

Left ventricular hypertrophy –> heart failure

Increased myocardial afterload –> myocardial ischaemia and MI

182
Q

How is secondary hypertension treated?

A

Identify and treat underlying cause

183
Q

What methods can be used to treat hypertension?

A 
Targeting RAAS
Diuretics
Vasodilators
Beta-blockers
Non-pharmacological approaches
184
Q

How can the RAAS be targeted to treat hypertension?

A

ACE inhibitors

Angiotensin II antagonists

185
Q

How do diuretics treat hypertension?

A

Reduce circulation and thus decease cardiac output

186
Q

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

A 
Thiazide
Aldosterone antagonists (Spironolactone)
187
Q

How do thiazide diuretics treat hypertension?

A

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

188
Q

Are aldosterone antagonists first line treatment for most hypertensive pts?

A

No

189
Q

How do vasodilators treat hypertension?

A

Decrease TPR

190
Q

How do L-type calcium channel blockers treat hypertension?

A

Decrease calcium entry into vascular smooth muscle and hence cause relaxation

191
Q

How do alpha-1-adrenocepetor blockers treat hypertension?

A

Decrease sympathetic tone thus relaxing vascular smooth muscle

192
Q

How do beta-blockers treat hypertension?

A

Decrease cardiac output by decreasing HR and contractility

193
Q

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

A

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

194
Q

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

A

Mild hypertension

195
Q

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

A 
Exercise
Diet
Decrease sodium intake
Decrease alcohol intake
Stop smoking
196
Q

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

A

Failure to implement lifestyle changes

Semester 3 (50 decks)

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