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Urology > Renal Physiology > Flashcards

Renal Physiology Flashcards

1
Q

What are the 3 basic renal processes?

A

Filtration
Reabsorption
Secretion

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2
Q

What is the GFR?

A

Glomerular filtration rate

180l/day

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3
Q

What % of fluid is reabsorped back into the body?

A

99%

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4
Q

Where are alot of drugs metabolised?

A

Liver

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5
Q

How long does it take for a volume equal to BV to pass through the kidneys?

A

5 minutes

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6
Q

Are red BC filtered in the kidney?

A

No

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7
Q

What factors determine the filterability of solutes across the glomerular filtration barrier?

A

Molecular size
Electrical charge
Molecular shape

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8
Q

What does the first layer of membrane in the glomerulus filter out?

A

Everything except blood cells

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9
Q

What does the second layer in glomerulus prevent the filtration of?

A

Larger proteins

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10
Q

What does third layer in the glomerulus

prevent the filtration of?

A

prevent filtration of medium sized proteins

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11
Q

Which membrane layer of the glomerulus prevents the filtration of larger proteins?

A

Basal lamina

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12
Q

Which membrane of the glomerulus prevents the filtration of medium sized proteins?

A

Silt membrane

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13
Q

Which membrane in the glomerulus prevents the filtration of blood cells but allows components of plasma to get through?

A

Fenestration (pore) of glomerular endothelial cell

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14
Q

Which is glomerular pressure higher than most capillaries in the body?

A

Because afferent arterioles are short and wide offering little resistance to flow

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15
Q

Describe the unique arrangement of efferent arterioles

A

Long and narrow

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16
Q

What is the overall effect of having little resistance in the afferent arteriole and high resistance in the efferent arteriole?

A

High hydrostatic pressure

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17
Q

How does hydrostatic pressure at the glomerular capillaries compare to oncotic pressure?

A

Exceeds oncotic pressure

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18
Q

Which process occurs at the glomerular capillaries?

A

Only filtration

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19
Q

Which is the major factor in determining GFR?

A

Afferent and efferent arteriolar diameter

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20
Q

Which extrinsic factors control afferent and efferent arteriolar diameter?

A

Sympathetic VC nerves
Circulating catecholamines
Angiotensin II

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21
Q

How do sympathetic nerves affect afferent and efferent diameters?

A

Give afferent and efferent constriction

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22
Q

If you have high resistance how does this affect hydrostatic pressure upstream?

A

Increases it

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23
Q

If you have high resistance how does this affect hydrostatic pressure downstream?

A

Decreases it

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24
Q

How do circulating catecholamines affect afferent and efferent arterioles?

A

Constriction of only afferent

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25
Q

How does angiotensin II affect afferent and efferent arteriole?

A

Constriction of efferent at low

Both afferent and efferent at high

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26
Q

Which major factor is crucial in determining GFR?

A

Diameter of afferent and efferent arterioles

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27
Q

What is the minimum pressure needed to drive filtration?

A

50 mmHg

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28
Q

If mean arterial pressure what is the effect on afferent arteriolar constriction?

A

There is an increase in constriction to slow down GFR

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29
Q

What is meant by autoregulation of GFR?

A

There is a zone of atuoregulation where GFR will alter and autoregulate over a range of BP

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30
Q

What happens to kidney blood flow during haemorrhage?

A

It reduces to flow to immediately important organs

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31
Q

What happens in prolonged reduction in renal BF?

A

Can lead to irreparable damage and can lead to death due to disruption of the kidney’s role in homeostasis

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32
Q

What % of plasma is filtered though the glomerulus?

A

20%

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33
Q

What % of filtered fluid is reabsorbed along the remaining nephron?

A

19%

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34
Q

What % of plasma entering the kidneys return back to the systemic circulation?

A

> 99%

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35
Q

What is the volume excreted to the external environment known as?

A

Urine

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36
Q

Where does filtration only occur?

A

At the glomerular capillaries

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37
Q

Describe the concentration of plasma proteins in the blood remaining in the efferent arteriole compared to the proximal tube

A

Higher concentration of plasma proteins in efferent

Due to only 20% being filtered into Bowman’s capsule

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38
Q

What is the consequence of the low Ppc and high oncotic pressure in the peritubular capillaries?

A

Balance of Starling’s forces in the peritubular capillaries is entirely in favour of reabsorption

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39
Q

Where are molecules mainly reabsorbed in the nephron?

A

Proximal convoluted tubule

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40
Q

Why is hydrostatic pressure in the peritubular capillaries very low?

A

Because of hydrostatic pressure having to overcome the frictional resistance in the efferent arterioles

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41
Q

Why is the plasma protein concentration higher in the efferent capillary than it was in the afferent?

A

Due to the loss of 20% of proteins in the glomerular concentrating that in in remaining plasma

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42
Q

What is the function of Bowman’s Capsule?

A

To collect the filtrate that is filtered out at the glomerulus

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43
Q

What is the effect of increased afferent diameter on GFR?

A

it increases

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44
Q

What is the effect of increased efferent diameter on GFR?

A

It decreases

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45
Q

What is the effect of decreased afferent diameter on GFR?

A

It decreases

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46
Q

What is the effect of decreased efferent diameter on GFR?

A

It increases

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47
Q

What is meant by Tm?

A

Maximum transport capacit

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48
Q

What happens to a substrate when Tm is exceeded?

A

It is passed out int he urine

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49
Q

Why does Tm exist?

A

Because there are only so many transporters to reabsorb substances

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50
Q

What is the effect of transport molecules bonding to their carrier?

A

A conformational change

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51
Q

What is capacity of transportation limited by?

A

The number of carriers

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52
Q

What is the effect on transportation once maximum saturation has been reached?

A

Transportation levels out

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53
Q

What is renal threshold?

A

Plasma threshold at which saturation occurs

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54
Q

What is the renal threshold for glucose?

A

10mmol/l

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55
Q

What happens to glucose beyond 10mmol/l?

A

Excess is excreted in the urine

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56
Q

If 5 mmol/l of glucose is present how much do we reabsorb?

A

5mmol/l

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57
Q

If 10mmol/l of glucose is present how much do we reabsorb?

A

10mmol/l

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58
Q

If 15mmol/l of glucose is present how much do we reabsorb?

A

10mmol/l other 5mmol/l is excreted in the urine

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59
Q

Do the kidneys regulate glucose?

A

No

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60
Q

What is responsible for regulating glucose in the body?

A

Insulin and other counter regulatory hormones

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61
Q

What is glycosuria due to the failure of?

A

Insulin NOT the kidney

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62
Q

Why is Tm for glucose set way above any possible level of diabetes?

A

To ensure all variants of glucose are normally reabsorbed

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63
Q

How does Tm mechanism achieve plasma regulation for substrates such as sulphate and phosphate?

A

Tm is set at a level whereby the normal plasma conc. causes saturation
So any level above normal will be excreted
Therefore achieving its plasma regulation

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64
Q

Where are sodium ions most abundant?

A

In the ECF

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65
Q

What % of sodium is reabsorbed by the kidneys?

A

99.5%

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66
Q

Where does most Na reabsorption occur?

A

In the proximal tubule

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67
Q

How is sodium reabsorbed?

A

By active transport

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68
Q

Explain the active transport of sodium?

A

Active Na+ pumps are located on the basolateral membrane pumping sodium into the ISF and K+ into the proximal tubule cell
This passively drives Na+ from the tubule lumen into the proximal tubule cell
To then be actively pumped out by the pump

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69
Q

Describe the permeability of the proximal tubule cells to Na+ ions?

A

Higher permeability than most other membranes of the body

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70
Q

What does sodium also drive the transport of?

A

Glucose

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71
Q

How is Cl- reabsorbed?

A

Passively crosses across the proximal tubular membrane down the electrical gradient established and maintained by the active transport of Na+

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72
Q

What is the effect of the active transport of Na+ out of the tubule followed by Cl- on water?

A

Creates an osmotic force drawing H2O out of the tubules

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73
Q

What is the effect of H2O removed by osmosis from the proximal tubule?

A

Concentrates all the substances left in the tubule creating outgoing concentration gradients

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74
Q

What does the rate of reabsorption of non-actively reabsorbed solutes depend on?

A

Amount of H2O removed - determining concentration gradient

Permeability of the membrane to any particular solute

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75
Q

Describe the tubules membrane permeability to urea?

A

Moderately permeable to that 50% is reabsorbed and 50% remains in the tubule

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76
Q

Describe the permeability of the tubular membrane to insulin and mannitol?

A

The membrane is impermeable

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77
Q

What happens to mannitol with a concentration gradient favouring reabsorption?

A

Despite a concentration gradient favouring reabsorption they cannot gain access through the tubular membrane so that ALL is filtered and stays in the tubule to be passed out in the urine

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78
Q

Give examples of substances which share the same carrier molecule as sodium?

A

Glucose

Amino acids

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79
Q

What is the effect of high sodium conc. on the tubule on glucose transport?

A

It facilitates it

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80
Q

What is the effect os low sodium conc. on the tubule transport of glucose?

A

It inhibits it

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81
Q

Can sodium pump transport glucose across its concentration gradient

A

Yes

Indirectly it can

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82
Q

Where does the energy to drive glucose against its concentration gradient come from?

A

The energy used in the ATP pump to transport sodium

Na/ATP ase

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83
Q

What is the secondary route from the peritubular capillaries into the tubule lumen?

A

Secretory mechanisms

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84
Q

How are protein bound substances usually excreted?

A

Their filtration at the glomerulus is restricted

So they can be secreted form the peritubular capillaries into the tubule lumen

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85
Q

Where are substances secreted?

A

At the proximal tube

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86
Q

Why are secretory mechanisms not very specific?

A

So that they can be used for a wide range of endogenous or exogenous substances

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87
Q

What do organic acid secretory mechanisms secrete?

A

Lactic acid and uric acid

But can also be used for things like penicillin, aspirin

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88
Q

What are organic base secretory mechanisms used to secrete?

A

Choline and creatine ect

But can be used for morphine and atrophine

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89
Q

What is normal ECF potassium conc.?

A

4mmoles/l

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90
Q

What mmol/l is classed as hyperkalaemia?

A

> 5.5 mmoles/l

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91
Q

What mmol/l is classed as hypokalaemia?

A

<3.5 mmol/l

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92
Q

What can be the result of hyperkalaemia?

A

Decrease in resting membrane potential

Eventually VF and death

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93
Q

What can be the result of hypokalaemia?

A

Increase in resting potential

Can cause cardiac arrhythmias and eventually death

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94
Q

What is the effect of increased renal tubule cell potassium concentration?

A

Increase in K+ secretion

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95
Q

What is the effect of decreased renal tubule cell potassium concentration?

A

Decrease in K+ secretion

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96
Q

What are changes in K+ excretion due to?

A

Changes in its secretion in the distal parts of the tubule

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97
Q

Which adrenal cortical hormone regulates potassium?

A

Aldosterone

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98
Q

What is the role of aldosterone in increased K+ conc. in ECF?

A

Increase in K+ in ECF
Stimulates aldosterone release
Stimulates increase in renal tubule K+ secretion

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99
Q

What is the effect of increased aldosterone on potassium?

A

Increases renal tubule cell K+ secretion

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100
Q

How are proteins reabsorbed in the proximal tubule?

A

Tm carrier mechanism

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101
Q

What does the liver do to drugs and pollutants?

A

Metabolises it to polar compounds
That can not be reabsorbed
Facilitating their excretion

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102
Q

What is the loop of henle important for?

A

Reabsorbing only

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103
Q

Why is all fluid leaving the proximal tubule isosmotic?

A

Because all the solute movements are accompanied by osmosis so that osmotic equilibrium is maintained

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104
Q

Where do all nephrons have their proximal and distal tubes located?

A

In the cortex

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105
Q

Where is the location of the loop of henle in the kidney?

A

Medulla of the kidney

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106
Q

What is the minimum obligatory loss of H2O?

A

500mls

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107
Q

What is the effect of no H2O intake on urintation?

A

Still excrete 500ml a day

Can urinate to death

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108
Q

Why are the kidneys able to produce urine of varying concentration?

A

Because the loops of henle of juxtamedullary nephrons act as counter-current multipliers

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109
Q

What is the main function of the loop of henle?

A

To create a concentration gradient in the medulla

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110
Q

What is meant by isosmotic?

A

That the concentration on one side is the same as on the other side

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111
Q

Why does the medulla interstitial space need to become more concentrated with ions?

A

To allow water to move out at the collecting ducts oft he nephron

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112
Q

What are the 2 critical characteristics of the loop of henle that make then counter-current multipliers?

A

The ascending limb transports Na+ and Cl- out of the tubule into the lumen being impermeable to water
The descending limb is freely permeably to H2O but relatively impermeable to NaCl

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113
Q

What is the osmolarity of fluid as it enters the loop of henle?

A

300 mOsm/l

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114
Q

What happens in the ascending limb as the NaCl is pumped out?

A

Concentration in the tubule decreases

As the concentration in the interstitium increases

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115
Q

What is the limiting gradient different between the ascending limb and the interstitium?

A

200mOsm

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116
Q

Due to NaCl being removed in the ascending limb what is the effect in the descending limb?

A

Water is permeable

Will diffuse out to equate osmolarity between the descending limb and the interstitium

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117
Q

Does the H2O stay in the interstitium once pulled out of the descending limb?

A

No it is reabsorbed by the high oncotic pressure into the vasa recta

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118
Q

What happens to fluid as it moves down the descending limb?

A

It becomes more and more concentrated due to the loss of water

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119
Q

What happens to the fluid as it moves back up the ascending limb>

A

There is active NaCl removal

Further concentrating the interstitium

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120
Q

Describe the fluid as it moves down the descending limb and back up the ascending limb?

A

The fluid in the tubule is progressively concentrated as it moves down the descending limb and progressively diluted as it moves up the ascending limb

121
Q

Why is the fluid between the descending loop tubule fluid and interstitial fluid equal?

A

Because water moves freely to create isosmotic fluid

122
Q

Why is the fluid between the descending limb and interstitial fluid a difference of 200mOsmole?

A

Due to the pumping of active pumps in the ascending limb

123
Q

What is the key key step in the loop of henle?

A

The active transport of NaCl out of the ascending limb

124
Q

What mOsm does the fluid leave the loop of henle at?

A

100

125
Q

Why do we want to deliver hypotonic fluid to the distal tubule?

A

So we can regulate the osmolarity of the urine based on the needs of the body at the time

126
Q

What are the functions of the vasa recta?

A

To provide O2 for the medulla

Removed volume from the interstitium

127
Q

Why is the flow rate through the vasa recta very low?

A

So that there is plenty of time for equilibrium to occur with the interstitium

128
Q

Why is it important that the medullary capillaries follow the loop of Henle and don’t drain straight through?

A

If they were straight would carry away the NaCl removed from the loop of henle and disrupt the interestital gradient

129
Q

What is water regulation controlled by?

A

ADH

130
Q

What type of hormone is ADH?

A

Polypeptide

131
Q

Where is ADH synthesised?

A

In the supraoptic and paraventricular nuclei in the hypothalamus in the brain

132
Q

Where is ADH stored?

A

Posterior pituitary gland

133
Q

What is the half life of ADH?

A

10 minutes

134
Q

Where is the effect of increased cell osmolarity on ADH?

A

Increased osmolarity Drags water out of the cell
Cell shrinkage
So increase in neural discharge
And increase in ADH secretion

135
Q

What is the effect of decreased cell osmolarity on ADH?

A

Decreased osmolarity
Drags water into the cell
Decrease in neural discharge
Decrease in ADH secretion

136
Q

What is the effect of changes of volume of the osmoreceptors?

A

Changes in osmoreceptor discharge

137
Q

What is normal plasma osmolarity?

A

280-290mOsm/kg H20

138
Q

What is the effect of an increase in osmolarity that does not cause an increase in tonicity on ADH?

A

Ineffective at causing an increase in ADH

139
Q

What is tonicity?

A

A term that takes into account the total concentration of non-penetrating solutes only

140
Q

What is the maximum concentration of urine we can secrete?

A

1200-1400mOsm/l

141
Q

Why does ingestion of hypertonic solutions such as seawater cause more dehydration?

A

Because there is increase in solute to be excreted
Increase in urine flow
Leads to dehydration
Because more H20 is require to secrete the solute than was ingested with it

142
Q

What does urine osmolarity depend on?

A

Reabsorption in the collecting duct

143
Q

Where is the site of water regulation?

A

Collecting duct

144
Q

What is the permeability of the collecting duct under the control of?

A

ADH/Vasopressin

145
Q

What happens generally if there is more ADH?

A

More concentrated urine is secreted

As more water is reabsorbed in the body

146
Q

What does ADH mediate the change in permeability of?

A

The collecting duct

147
Q

Where is ADH produced?

A

In the posterior PG

148
Q

How does ADH increase water reabsorption?

A

By the recruitment of aquaporin 2 to the cell membrane of the collecting ducts

149
Q

What happens when more aquaporin 2 is recruited to the cell under the control of ADH?

A

The cortical collecting duct becomes equilibrated with that of the cortical interstitium

150
Q

What drives the movement of water in the collecting duct?

A

The hypertonic medullary intersitital gradient created by the countercurrent multiplier of the loop of henle

151
Q

When is maximum ADH present in terms of the medullary interstitium?

A

When the contents of the collecting duct equilibriate with that of the medullary interstitium via osmotic efflux of H2O

152
Q

Describe urine concentration when ADH is maximum?

A

Small volume of concentrated urine

153
Q

When is maximum ADH released?

A

When there is maximum water deficit

154
Q

Which forces drive the reabsorption of H2O from the medullary interstitium once moved out of the collecting duct?

A

H2O reabsorbed by oncotic pressure in vasa recta which will be even greater that usual due to H2O deficit

155
Q

What is the result of absent ADH?

A

Collecting duct impermeable to water
So the medullary interstitium gradient is ineffective in inducing H2O movements out of the CD
Compensating for H2O excess

156
Q

What is the consequence of H2O excess on ADH and the CD?

A

No ADH
CD impermeable to water
Medullary interstitial gradient is inneffective
so a large volume of dilute urine is excreted
Compensating for H2O excess

157
Q

Describe the permeability of CD membranes to urea

A

Relatively permeable particularly towards medullary tips

158
Q

What happens as urea approaches the medullary tipes?

A

there is an increasing tendency for it to move out down its concentration gradient.

159
Q

What is the permeability of the late medullary CD to urea enhanced by?

A

ADH

160
Q

Why is it important that urea is reabsorbed in the CD?

A

So that it can reinforce the intersitial gradient in the ascending loop of henle
and prevent water retention in the CD

161
Q

What would urea do if it all remained in the CD?

A

Would hold onto the water and reduce the potential for rehydration

162
Q

What is more important the conservation of H2O or urea?

A

H2O

163
Q

How does an increase in ECF volume affect ADH secretion?

A

Decreases it

164
Q

How does a decrease in ECF volume affect ADH secretion?

A

Increases it

165
Q

Where are low pressure receptors located?

A

In the L and R atria and great veins

166
Q

Where are high pressure receptors located?

A

At the carotid and aortic arch baroreceptors

167
Q

Which receptors does a moderate decrease in ECF volume affect?

A

Atrial receptors

168
Q

What is the effect when atrial receptors detect a moderate decrease in ECF vol.?

A

Decrease in ECF vol.
Decrease Atrial receptor discharge
Increase in ADH release

169
Q

Which receptors will also contribute to ADH change in secretion when volume changes enough to affect MPB?

A

Carotid and aortic baroreceptors

170
Q

What type of cells are ADH secreting cells?

A

Neurones

171
Q

Which OTHER stimuli increase ADH release?

A

Pain, emotion, stress, exercise, nicotine, morphine. Following traumatic surgery,

172
Q

Which OTHER stimuli decrease ADH release?

A

Alcohol

Suppresses ADH release

173
Q

Which receptors detect a decrease in atrial stretch due to low blood volume?

A

Atrial stretch receptors

174
Q

Which receptors detect a decrease in BP?

A

Carotid and aortic baroreceptors

175
Q

What is there a lack of in diabetes insipidus?

A

ADH deficiency

176
Q

What are the potential causes for central diabetes insipidus?

A

Hypothalamic area may become diseased due to tumours or meningitis
May be damaged during surgery

177
Q

What are the potential causes for peripheral diabetes insipidus?

A

The collecting duct may be insensitive to ADH

178
Q

What are the characteristic symptoms of diabetes insipidus?

A

Passage of very large volumes of very dilute urine - polyuria

179
Q

How can central diabetes insipidus be treated?

A

By giving ADH

180
Q

What determines how much fluid we have in out compartments?

A

Osmotically active particles in each compound

181
Q

What are the major ECF osmoles?

A

Na+ and Cl-

182
Q

What are the major ICF osmoles?

A

K+ salts

183
Q

What is the distribution of body water?

A

1/3 ECF

2/3 ICF

184
Q

How many L of water do we have in our bodies?

A

42l

185
Q

What is the main determinant in determining ECF volume?

A

Na+

186
Q

What are the cardiovascular effects of increased salt and water loss?

A

decrease in venous pressure, decrease in venous return, decrease in atrial pressure, decrease in EDV, decrease in SV, decrease in CO , decrease in BP

187
Q

What is the effect of increased sympathetic discharge on vessels?

A

Potent vasoconstriction
Increasing TPH
Increasing BP towards normal

188
Q

What may the release of only ADH to bring back up ECF volume cause?

A

Hypoosmolarity as no ions or substrates have been absorbed too

189
Q

What does renin allow the release of?

A

Angiotensin II

190
Q

What does angiotensin II do (generally)?

A

Increases sodium chloride and water absorption

191
Q

What is the effect of increased sympathetic discharge on the renal nerve activity?

A

Increases renal VC nerve activity

Increases renal arteriolar constriction and increases renin production

192
Q

What does renin allow the release of?

A

Angiotensin II

193
Q

Where is angiotensin II a strong vasoconstrictor in the kidney?

A

Afferent tubule

194
Q

What is the effect of angiotensin II being a strong vascoonstrictor of the afferent tubule on both the forces and sodium absorption?

A

Decreases peritubular capillary hydrostatic pressure and increased oncotic pressure in the peritutublar capillaries in the proximal tubule
Meaning more reabsorption of Na+

195
Q

What is the effect of renin and angiotensin on the distal tubule?

A

increase in renin increase in angiotensin II

increase in aldosterone increase in distal tubule Na+ reabsorption and less Na+ excreted.

196
Q

What pressure determines the uptake of sodium in the proximal tubules as determined by angiotensin II?

A

oncotic pressure

197
Q

What is the reabsorptive range for the proximal tubule under normal circumstances and when in volume deficit?

A

65% - normally

75% - vol. deficit

198
Q

When does GFR begin to be affected?

A

When BP drops below 60mmHg

199
Q

How is GFR maintained at different pressures?

A

Due to autoregulation

By means of vasconstriction of afferent and efferent arterioles

200
Q

Does angiotensin II work largely on the afferent or efferent tubule?

A

Efferent

201
Q

What is the regulation of distal tubule Na+ reabsorption under the control of?

A

hormone aldosterone

202
Q

What type of hormone is aldosterone?

A

Steroid

203
Q

Where is aldosterone released from?

A

Adrenal cortex

204
Q

What are the 2 components of the juxtaglomerular apparatus?

A

Macular densa

Juxtaglomerular cells

205
Q

Where are juxtaglomerular cells located?

A

Smooth muscle of the media of the afferent arteriole just before it enters the glomerulus

206
Q

What do JG cells produce?

A

Renin

207
Q

How does renin convert angiotensin to angiotensin II?

A

Renin splits off the decapeptide angiotensin I which is then converted by enzymes in the endothelium to the active octapeptide = angiotensin II

208
Q

Where is angiotensin produced?

A

In the liver

209
Q

Is angiotensin constantly produced?

A

Yes

210
Q

Which enzyme converts angiotensin I to II?

A

ACE enzyme

211
Q

What is the effect of ANG II on arteriole?

A

Vascoconstriction

Increasing BP

212
Q

What is the effect of angiotensin II on cardiovascular control centres in the medulla?

A

Increases cardiac response

Increasing BP

213
Q

What is the effect of angiotensin II on the hypothalamus?

A

Increase in ADH
and thirst
Increasing volume and maintaining osmolarity

214
Q

What is the effect of ANG II on the adrenal cortex?

A

Increases aldosterone
Increasing Na+ reabsorption
Increasing vol. and maintaining osmolarity

215
Q

What is the rate limiting step in the renin-angiotensin-aldosterone system?

A

Presence of renin

216
Q

What controls renin release?

A

Decrease in pressure in the afferent arterioles

Increase in sympathetic nerve activity

217
Q

What do JC cells act as?

A

Renal baroreceptors

218
Q

What is the rate of renin secretion inversely proportional to?

A

The rate of delivery of NaCL at the macula densa

Decrease in NaCl delivery increases renin

219
Q

What are the feedback controls of renin?

A
  1. Angiotensin II feeds back to inhibit renin.

2. ADH inhibits renin release (osmolarity control).

220
Q

How much more potent is angiotensin II than NE as a vasoconstrictor?

A

4-8 x

221
Q

What is the effect of angiotensin II on the hypothalamus?

A

Stimulated ADH secretion
Increasing water reabsorption from the CD
Also stimulates the thirst mechanism and salt apetite

222
Q

How is GFR regulated in the tubules when GFR increases?

A

GFR increases
Flow through tubule increases
Flow past macular densa increases
Paracrine from macula densa to afferent arteriole
Resistance in afferent arteriole increases
Hydrostatic pressure in glomerulus decreases
GFR decreases

223
Q

What 2 systems will oppose each other in a situation where a person has lost 3L of salt and water… then drinks 2 litres of pure water?

A

decrease in ECF osmolarity causes inhibition of ADH via osmoreceptors
decrease in ECF volume ADH via baroreceptors

224
Q

Which system would take over in a situation where there was low ECF volume yet hypoosmolarity in the system?

A

Volume considerations have primacy if ECV is compromised

225
Q

Why does low ECV take priority over hyposmolarity?

A

To save perfusion to the brain

226
Q

What should be the replacement if there are large losses of salt and water?

A

Infuse or drink saline

Replace water and salt

227
Q

What ion is the main determinant in maintaining ECF volume?

A

Na+

228
Q

How does aldosterone affect Na+?

A

Promotes its reabsorption

229
Q

What is the effect of ANP on Na+

A

Promotes Na+ excretion

230
Q

What is the effect of aldosterone on potassium?

A

Increases K+ secretion

231
Q

Why does aldosterone given to normal subject on an adequate Na+ diet cause weight gain?

A

Increase in weight

Due to increase retention of water with the sodium

232
Q

When does ANP override the effect of aldosterone?

A

AN overrides effects of Na+ eabsorption because of volume expansion

233
Q

Which system does ANP counteract?

A

Renin-angiotensin system

234
Q

What system will kick in if there is increased weight gain due to increased aldosterone?

A

ANP will be secreted in response to expansion of ECF volume and cause natriuresis

235
Q

What is natriuresis?

A

Loss of Na+ and H2O in the urine

236
Q

Does ANP affect K+?

A

No

237
Q

What is the effect ofK+ when the ANP system has kicked in to override the aldosterone system?

A

Na+ and H2O are excreted

However still K_ loss because still increase in K+ secretion

238
Q

Which cells secrete ANP?

A

Atrial cells

239
Q

What is the effect of ANP on the hypothalamus?

A

Less ADH secretion

240
Q

What is the effect of ANP on the kidneys?

A

Increased GFR

Decreased renin

241
Q

What is the effect of ANP on the adrenal cortex?

A

Less aldosterone

242
Q

In uncontrolled DM what is the effect of excess glucose remaining in the tubule on water?

A

Exerts an osmotic effect to retain H2O in the tubule

243
Q

What is the effect of increased glucose and water in the tubule on sodium?

A

Na+ concentration in the lumen is decreased because the Na+ is present in a larger volume of water

244
Q

What is the effect of decreased Na+ conc. in the proximal tubule on the reabsorption of Na+?

A

Since Na+ gains access to the proximal tubule cells by passive diffusion down a concentration gradient created by active transport
Na+ reabsorption will be decreased as the concentration gradient difference will no longer be as high

245
Q

Why does decreased Na+ reabsorption cause decrease glucose reabsorption?

A

Because they share a symport

246
Q

What is the effect of decreased Na+, chloride and glucose reabsorption on the descending loop of henle?

A

Movement of H2O out the tubule is reduced because the glucose and excess Na+ exert an osmotic effect to retain H2O.
Increased H2O retention
Fluid in the descending limb is not so concentrated

247
Q

What is the knock on effect of increased water retention in the descending loop on the ascending loop?

A

Fluid delivered to the ascending limb is less concentrated
NaCl pumps are gradient limited but the gradient is now much less
Considerable reduction in the NaCl reabsorbed from the ascending limb

248
Q

What is the effect of a considerable reduction in the volume of NaCl and H2O reabsorbed from the loops of Henle on the distal tubule and interstitial gradient?

A

Large volume of NaCl and H2O is delivered to the distal tubule
Interstitial gradient is gradually abolished

249
Q

What is the effect of increased NaCl delivery at the macula densa?

A

Rein secreton will be suppressed (will think the whole body has too much sodium)
Therefore Na+ reabsorption at the distal tubule will be decreased

250
Q

What is the effect of a large volume of nearly isotonic urine being excreted on PV?

A

Decrease in PV

251
Q

What will the decrease in PV stimulate the release of?

A

ADH

252
Q

Why can ADH not be effective when a large volume of nearly isotonic urine is delivered to the distal tubule?

A

Because the interstitial gradient driving the water reabsorption has run down

253
Q

What are 2 main signs of diabetes?

A

Increase urination

Increased thirst

254
Q

How can DM cause a hyperglycaemic coma?

A

If ingestion of water is not adequate then hypotension may be so severe that there is lack of perfusion/BF to the brain

255
Q

How can DM cause a hypoglycaemic coma?

A

Inadequate glucose for the brain due to low glucose levels

256
Q

Why can we survive with one kidney?

A

Because one kidney has more nephrons than we need

257
Q

When is measuring GFR particularly useful in clinical situations?

A

In patients with renal disease

When prescribing drugs will have to take into consideration their renal function

258
Q

What tests are used to measure renal function?

A

Plasma clearance tests

259
Q

How is plasma clearance of X measured?

A

Cx = (Ux) V/(Px)

260
Q

Wha is Ux?

A

Urine concentration of X

261
Q

What is V?

A

Urine flow rate

262
Q

What is Px?

A

plasma concentration of X

263
Q

What is inulin clearance a measure of?

A

GFR

264
Q

Describe inulin at the nephron?

A

Inulin is freely filtered at the glomerulus and neither reabsorbed nor secreted
It is not metabolised by the kidney nor does it interfere with normal renal function

265
Q

What clearance is routinely used to estimate GFR?

A

Creatinine clearance

266
Q

Why will substances that are filtered and reabsorbed have a lower clearance than inulin?

A

Because (Ux) will be less than if only filtered

And (Px) will be higher

267
Q

Why will substances that are filtered and secreted have a higher clearance than inulin?

A

Because (Ux) will be higher and (Px) will be lower

268
Q

Why is inulin no longer used in clinical practice?

A

Because it is too cumbersome

269
Q

What is creatinine the breakdown product of?

A

Muscle creatine

270
Q

What is eGFR?

A

Estimated glomerular filtration rate

271
Q

What factors affect serum creatinine?

A

Muscle mass
Dietary intake
Drugs

272
Q

What is normal GFR approx?

A

100mls/min/1.73m squared

273
Q

Why does glucose have a clearance of 0?

A

Because all is normally rebsorbed

274
Q

Describe glucose clearance?

A

Glucose that is filtered is reabsorbed

Therefore clearance is 0

275
Q

Why is urea clearance less than that of inulin?

A

Because some urea is reabsorbed

276
Q

What is the clearance of urea?

A

50%

277
Q

What is PAH used to measure?

A

Renal plasma flow

278
Q

Describe PAH at the nephron?

A

Freely filtered at the glomerulus and then remaining PAH in plasma is actively secreted into tubule >90% of plasma is cleared of its PAH content in one transit of the kidney

279
Q

Why does penicillin have a greater clearance than inulin?

A

Because it is filtered then secreted

280
Q

How does urine flow from the kidneys to the ureters?

A

Via peristaltic contraction of the smooth muscle of the ureters

281
Q

How do the ureters enter the bladder?

A

At an oblique angle

282
Q

Why do the ureters enter the bladder at an oblique angle?

A

To prevent reflux

283
Q

Does the composition of urine change once left the kidneys?

A

No

284
Q

What is the external urethral sphincter made up of?

A

Skeleteal muscle

285
Q

Under what control is the external urethral sphincter?

A

Under voluntary somatic control

286
Q

Where does the bladder lie anatomically?

A

Midline posterior to pubic bones

Lies anterior to repro system and rectum

287
Q

What muscle is the bladder made up of?

A

Smooth muscle

Detrusor muscle

288
Q

What type of epithelium is found in the bladder?

A

Transitional epithelium

289
Q

What is the trigon of the bladder?

A

Smooth triangular region of the internal urinary bladder formed by the two ureteric orifices and the internal urethral orifice.

290
Q

What is the bladder overlain with?

A

Peritoneum

291
Q

What do urethral obstructions cause?

A

Bilateral renal problems

292
Q

What does a ureter obstruction cause?

A

Unilateral renal problems

293
Q

Hoe does urethral obstruction cause renal problems?

A

Increased renal pressure
Back flow will eventually cause acute renal failure
Will oppose filtration

294
Q

What is the normal daily variation of urine production?

A

750ml-2500ml

295
Q

What is the normal clearance of glucose?

A

0

296
Q

Normal pH

A

7.4 (7.37-7.43)

297
Q

Normal pCO2

A

40mmHg (36-44)

5.3kPa

298
Q

Normal HCO3-

A

24mmoles/L

(22-26)§

Urology (13 decks)

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