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BRS UROLOGY & RENAL > 1b// Sodium and Potassium Balance > Flashcards

1b// Sodium and Potassium Balance Flashcards

1
Q

What is osmolarity?

A

measure of the solute (particle) concentration in a solution (osmoles/liter)

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2
Q

What is 1 osmole equal to?

A

1 Osmole = 1 mole of dissolved particles per liter (1 mole of NaCl = 2 moles of particles in solution)

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3
Q

What does osmolarity depend on?

A

Depends on the number of dissolved particles

The greater the number of dissolved particles, the greater the osmolarity

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4
Q

Is our plasma or urine osmolarity constant?

A

our plasma
urine changes a lot

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5
Q

What does water cross?

A

semi permeable cell membrane

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6
Q

How is constant osmolarity kept?

A

if volume increases, both salt and water increase

and vice versa is decreased volume

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7
Q

What happens to osmolarity of volume of ECF changes?

A
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8
Q

What is the most common ion in our plasma?

A

sodium

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9
Q

What is the most common ion in our cells?

A

potassium

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10
Q

What is our normal plasma osmolarity?

A

285-295 mosmol/L

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11
Q

What happens to your body weight if you increase or decrease your sodium intake?

A

positive balance (body weight increases to retain water)

negative balance once you return to normal sodium intake

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12
Q

What happens to your bp when you increase/ decrease sodium intake?

A

(but this can’t happen is due to semi-permeable membranes)

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13
Q

What are the main mechanism to control sodium intake?

A

central mechanism

peripheral mechanism

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14
Q

What is the central mechanism to control sodium intake?

A
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15
Q

What is the peripheral mechanism to control sodium intake?

A

aka taste

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16
Q

Where is sodium reabsorbed in the nephron?

A

*not desirable

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17
Q

How does GFR and RPF change with increasing blood pressure?

A

GFR= glomerular filtration rate
RPF= renal plasma flow

They both increase, and then plateau

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18
Q

How much of the renal plasma enters the tubular system?

A

approx 20%

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19
Q

How do you calculate GFR from RPF?

A

GFR= PRF * 0.2

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20
Q

How much sodium do you excrete?

A

less than 1%

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21
Q

What happens at the macula densa when there is increased tubular sodium?

A

High tubular sodium

Increased sodium/chloride uptake via triple transporter

Adenosine release from Macula Densa cells

Detected by extraglomerular mesangial cells

Reduces renin production from juxtaglomerular cells

Promotes afferent smooth muscle contraction

Reduces perfusion pressure and so GFR

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22
Q

What is perfusion pressure?

A

The renal perfusion pressure is defined as the difference between the mean arterial pressure, which is the average pressure in a person’s arteries during one cardiac cycle, and the pressure within the renal tubular system.

MAP- renal tubular system pressure

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23
Q

What is the best way to retain sodium? (simple answer)

A

filter less

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24
Q

What increases GFR?

A

increased blood pressure and volume

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25
Q

What difference between the afferent and efferent arteriole cause a decrease in GFR?

A

Constriction in the afferent arterioles going into the glomerulus and dilation of the efferent arterioles coming out of the glomerulus will decrease GFR
- aka less sodium will be filtered

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26
Q

How is there increased Na reabsorption/ retention? (4)

A

Increased sympathetic activity

Angiotensin II

Low tubular Na

Aldosterone

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27
Q

How does increasing sympathetic activity increase Na reabsorption?

A

Increases blood pressure at afferent arteriole (contracts)

Stimulates increased uptake of Na at the PCT

stimulates renin secretion from the juxtaglomerulosa apparatus (specifically juxtaglomerular cells)

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28
Q

How does low tubular Na cause increased Na reabsorption?

A

acts on JGA to make renin–> angiotensin I and II and then aldosterone

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29
Q

What does angiotensin and aldosterone do to increase Na reabsorption/ retention?aka what does aldosterone act on?

A

angiotensin II makes aldosterone

aldosterone acts on DCT and CT to stimulate reabsorption of sodium

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30
Q

What decreases Na reabsorption and what does it act on?

A

atrial natriuretic peptide

act os PCT, LOH, JGA, DCT, DCT, CT

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31
Q

Describe volume expansion and contraction depending on high or low sodium.

A
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32
Q

What is aldosterone and how and where is it synthesised and released?

A

Steroid hormone

Synthesised and released from the adrenal cortex (zona glomerulosa)

Released in response to Angiotensin ll
Decrease in blood pressure (via baroreceptors)

angiotensin II (via aldosterone synthase)=> aldosterone

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33
Q

What is the function of aldosterone in the nephron?

A

Increased Sodium reabsorption
(controls reabsorption of 35g Na/day)

Increased Potassium secretion

Increased hydrogen ion secretion

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34
Q

What happens when there is an excess of aldosterone?

A

leads to hypokalaemic alkalosis

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35
Q

How does aldosterone work in a cell?

A
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36
Q

How does aldosterone work in the collecting duct?

A

ENaC= epithelial sodium channels

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37
Q

What happens during hypoaldosteronism? (disease of aldosterone synthesis/ secretion) (4)

A

Reabsorption of sodium in the distal nephron is reduced

Increased urinary loss of sodium

ECF volume falls

Increased renin, Ang II and ADH

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38
Q

What are the symptoms of hypoaldosteronism and why? (4)

A

Dizziness
Low blood pressure
Salt craving
Palpitations

due to ECF volume falling and increased renin and… etc.

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39
Q

What happens during hyperaldosteronism? (4)

A

Reabsorption of sodium in the distal nephron is increased

reduced urinary loss of sodium

ECF volume increases (hypertension) Reduced renin, Ang II and ADH
Increased ANP and BNP

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40
Q

What are the symptoms of hyperaldosteronism and why? (4)

A

High blood pressure
Muscle weakness
Polyuria
thirst

due to…
ECF volume increases (hypertension) Reduced renin, Ang II and ADH
Increased ANP and BNP (Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP))

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41
Q

What is the inherited disease of high blood pressure called?

A

Liddle’s Syndrome

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42
Q

What is Liddle’s syndrome?

A

An inherited disease of high blood pressure.
-mutation in the aldosterone activated sodium channel.
-channel is always ‘on’
-Results in sodium retention, leading to hypertension

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43
Q

What are the 2 types of baroreceptors and where are they found?

A

low and high pressure baroreceptors

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44
Q

What happens when low pressure baroreceptors detect a change in bp?

A
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45
Q

What happens when high pressure baroreceptors detect a change in bp?

A
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46
Q

What is ANP?

A

Arial Natriuretic Peptide (ANP)

Small peptide made in the atria (also make BNP)
Released in response to atrial stretch (i.e. high blood pressure)

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47
Q

What are the action of atrial natriuretic peptide? (4)

A

-Vasodilatation of renal (and other systemic) blood vessels

-Inhibition of Sodium reabsorption in proximal tubule and in the collecting ducts

-Inhibits release of renin and aldosterone

-Reduces blood pressure

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48
Q

What happens during volume expansion?

A

decreased symp activity
decreased renin
decreased aldosterone
increase Na and h2o excretion
increased ANP and BNP
decrease in AVP

49
Q

What happens during volume expansion?

A

increased symp activity
increased renin
increased aldosterone
decreased na and h2o excretion
decreased ANP and BNP
increased AVP

50
Q

What does water reabsorption require?

A

osmotic gradient

51
Q

What happens to ECF volume if there is increased sodium excretion?

A

reduced

52
Q

What determines ECF vol?

A

Na+ levels

53
Q

What happens if you reduce ECF?

A

reduces BP

54
Q

What happens in total if you reduce Na+ reabsorption?

A

reduced total NA
reduced ECF vol
and reduced BP

55
Q

Are ACE inhibitors anti-diuretic or diuretic?

A

diuretic

56
Q

What do ACE inhibitors do?

A

reduced angiotensin II

57
Q

What are the vascular effects of ACE ihibitors?

A

vasodilation

58
Q

What are the direct renal effects of ACE inhibitors?

A

decreased Na+ reuptake in the PCT

increased Na+ in the distal nephron

59
Q

What are the effects of ACE inhibitors on adrenals?

A

reduced aldosterone

60
Q

What are the indirect effects of ACE inhibitors on kidneys?

A

decreased Na+ uptake in the CCT

increased Na+ in the distal nephron

61
Q

How do ACE inhibitors affect blood pressure?

A

vasodilation= decreased bp

decreased water reabsorption= decreased bp

62
Q

How do ACE inhibitors work?

A
63
Q

What are other diuretics (apart from ACE) and where do they work? (6)

A

osmotic diuretics= PT
carbonic anhydrase inhibitors= PT

thiazides= DT

loop diuretics= TAL

k+ sparing diuretics= collecting duct and DT

aquarectics

64
Q

How do carbonic anhydrase inhibitors work?

A

Carbonic anhydrase activity leads to Na+ re-absorption and increased urinary acidity

therefore Carbonic anhydrase Inhibitors…
reduced Na+ reuptake in the PCT Increased Na+ in the distal nephron Reduced water reabsorption

65
Q

How do loop diuretics work?

A

Triple transporter Inhibitors
reduced Na+ reuptake in the LOH Increased Na+ in the distal nephron Reduced water reabsorption

66
Q

How do thiazides work?

A

idk about the extra black writing…

67
Q

How do potassium sparing diuretics work?

A

Inhibitors of aldosterone function (e.g. spironolactone)

inhibiting aldosterone receptors (spironolactone, eplerenone)
This prevents excessive excretion of K+ in urine and decreased retention of water, preventing hypokalemia

68
Q

What is the main intracellular ion?

A

Potassium is the main intracellular ion (150 mmol/L), extracellular [K+] = 3-5 mmol/L.

Extracellular K+ has effects on excitable membranes (of nerve and muscle).

69
Q

What happens if there is high k?

A

depolarises membranes - action potentials, heart arrhythmias.

70
Q

What happens if there is low k?

A

heart arrhythmias (asystole).

71
Q

Where is potassium present?

A

Potassium is the major intra-cellular ion but is low in the ECF

Potassium is present in most/all foods (especially unprocessed)

72
Q

What happens to k after a meal?

A

tissue uptake is stim by aldosterone, adrenaline and insulin

73
Q

What is the immediate response to dietary potassium?

A

insulin also inhibits potassium efflux

74
Q

What happens to k in the kidney during potassium depletion and normal/ increased potassium intake?

A

arrow out= reabsorption
in= secretion

75
Q

What is k+ secretion stimulated by? (4)

A

K+ secretion stimulated by…
increased Plasma [K+]
increased aldosterone
increased tubular flow rate
increased plasma pH

76
Q

Describe potassium secretion by the principal cells.

A

collecting duct

also membrane potential helps stimulate k secretion

Potassium secretion occurs in principal cells by active uptake across the basolateral membrane by Na-K-ATPase and passive diffusion across the apical membrane into the lumen

77
Q

Describe tubular flow and K+ excretion.

A

PDK1 on apical side

78
Q

What can cause hypokalemia? (5)

*Hypokalemia one of the most common electrolyte imbalances (seen in up to 20% of hospitalised patients)

A

Inadequate dietary intake (too much processed food)
Diuretics (due to increase tubular flow rates)
Surreptitious vomiting
Diarrhoea
Genetics (Gitelman’s syndrome; mutation in the Na/Cl transporter in the distal nephron)

79
Q

What can cause hyperkalemia? (5)

*Common electrolyte imbalance present in 1-10% of hospitalised patients

A

Seen in response to K+ sparing diuretics
ACE inhibitors
Elderly
Severe diabetes
Kidney disease

80
Q

Describe the pathway involving the kidney though which increased sympathetic stimulation increases aldosterone levels.

A

Increased sympathetic activity stimulates the cells of the juxtaglomerular apparatus (0.5 mark)
to release renin (0.5 mark).
Renin activity cleaves angiotensinogen to angiotensin I (0.5 mark).
Angiotensin I is cleaved by angiotensin converting enzyme (0.5 mark)
to produce angiotensin II (0.5 mark).
Angiotensin II stimulates the synthesis of aldosterone synthase (0.5 mark)
in the zona glomerulosa (0.5 mark)
to increase the synthesis (0.5 mark) of aldosterone.

81
Q

What would be the expected effect of spironolactone on the blood pressure of a person with the conditions below, and by what mechanism would it elicit this change (1 mark for effect on bp, 1 mark for the explanation).

a) Essential hypertension

A

A reduction in blood pressure (1 mark).
Spironolactone inhibits the effects of aldosterone on the mineralocorticoid receptor, causing an increase in sodium excretion and a leading to a reduction in water retention (1 mark).
Extra information: Though not the first line of use, spironolactone is used in hypertension especially that which is resistant to other diuretics (not required information)

82
Q

What would be the expected effect of spironolactone on the blood pressure of a person with the conditions below, and by what mechanism would it elicit this change (1 mark for effect on bp, 1 mark for the explanation).

b) Normal blood pressure

A

A reduction in blood pressure (1 mark) because of the increased sodium excretion leading to reduced water retention (1 mark). Even though the person has a normal blood pressure reducing their sodium content would cause a reduction in water and therefore a reduction in blood pressure.

83
Q

What would be the expected effect of spironolactone on the blood pressure of a person with the conditions below, and by what mechanism would it elicit this change (1 mark for effect on bp, 1 mark for the explanation).

c) Liddle’s syndrome

A

No effect (1 mark). The mutation in Liddle’s syndrome is in the aldosterone sensitive ENaC (epithelium sodium channels) sodium channel. This mutation means that the channel is always on so that there will be minimal effect on sodium reuptake (1 mark).

Detailed explanation: a) aldosterone levels are already low (so inhibiting them will have only a minor effect if any on ENaC expression), b) the channel is on and so will not respond to the regulatory proteins that are stimulated by aldosterone. Any change in the expression of these regulatory proteins (which would be minimal because of the low aldosterone levels) would have no effect.

84
Q

identify a.

A

ANP (or BNP).

85
Q

What is the effect of increased A on GFR?

A

It increases the GFR (by relaxing the SMCs in the afferent arteriole).

86
Q

What is B and how does it change in response to volume expansion?

A

Angiotensin I and it reduces.

87
Q

During volume expansion does renin increase or decrease?

A

Renin levels go down (because of the reduction in sympathetic activity).

88
Q

What is C and D?

A

C= ADH OR vasopressin.

D= aldosterone

89
Q

What proteins does C affect to alter water reabsorption and how does it affect these proteins?

A

C causes the aquaporins in the cells of the collecting duct to translocate from the cytoplasm to the cell wall increasing the permeability to water (in this context there is a reduction in C so a reduction in water permeability).

90
Q

How does Angiotensin II affect the production of D?

A

It causes an increase in the expression of aldosterone synthase (which is required for the last 2 steps of the conversion of cholesterol to aldosterone).

91
Q

How does D affect water reabsorption?

A

D increases water reabsorption by increasing the permeability of the principal cells to sodium (for information but not required for the answer it increases the expression of ENaC, the Na/KATPase and proteins that increase their activity so increases Na reabsorption).

92
Q

The excretion of which major ions/molecules is altered to correct the volume expansion and how is it affected?

A

Sodium and water and their reabsorption is reduced to correct the volume expansion.

93
Q

You are part of a team developing novel diuretic drugs. For each novel diuretic identify the region of the nephron that it is likely to work in.

  1. D1 inhibits a single transporter and inhibits the uptake of potassium, chloride and sodium.
A

Thick Ascending Limb (it inhibits the Na/K/Cl triple transporter).

94
Q

You are part of a team developing novel diuretic drugs. For each novel diuretic identify the region of the nephron that it is likely to work in.

  1. D2 inhibits the release of an extracellular enzyme from the kidney into the plasma.
A

The enzyme that is released into the plasma will be renin. Therefore, the drug is most likely to affect the juxtaglomerular apparatus. It could inhibit sympathetic activity so may have some wider effects it could affect the synthesis or renin or the export of renin.

95
Q

You are part of a team developing novel diuretic drugs. For each novel diuretic identify the region of the nephron that it is likely to work in.

  1. D3 inhibits the activity of an enzyme found in the cells of the nephron and in the tubular fluid.
A

D3 must be a carbonic anhydrase inhibitor, its primary site of action therefore is the Proximal Convoluted Tubule.

96
Q

You are part of a team developing novel diuretic drugs. For each novel diuretic identify the region of the nephron that it is likely to work in.

  1. D4 causes an increase in plasma calcium.
A

D4 will target the Na/Cl transporter in the Distal Convoluted Tubule.

97
Q

You are part of a team developing novel diuretic drugs. For each novel diuretic identify the region of the nephron that it is likely to work in.

  1. D5 is effective in most people but does not work in patients with a point mutation in the mineralocorticoid receptor.
A

D5 is an antagonist of the mineralocorticoid receptor, it therefore blocks the effects of aldosterone so will work in the cortical collecting duct.

98
Q

You are part of a team developing novel diuretic drugs. For each novel diuretic identify the region of the nephron that it is likely to work in.

  1. D6 inhibits the activity of an enzyme found predominantly in the endothelial cells of the lung.
A

D6 is an ACE inhibitor. It therefore has activity in the whole of the renal tubular system with the exception of the loop of Henle but these effects are indirect as they are through the production of AII and aldosterone.

99
Q

Define osmolarity.

A

Osmolarity is a measure of the solute (particle) concentration in a solution (osmoles/liter)

100
Q

What is the normal range of plasma osmolarity?

A

275-295 mosmoles/L

101
Q

Why does a high salt diet lead to an increase in blood pressure?

A

Increased salt in the diet leads to increased total body sodium so water is taken in to maintain osmolarity and this increases ECF fluid volume. This increases the pressure in the system i.e. increased blood pressure.

102
Q

Salt is often added to food to improve the flavour. Why does salt improve the flavour, but too much salt make food taste bad, and how do we sense this?

A

Salt is one of the 5 basic taste sensations, it is sensed by a specific sense of cells located on the tongue. At low salt concentrations the sensation is positive but as the concentration increases the sensation becomes aversive.

103
Q

Which part of the brain is central to alter appetite for salt?

A

Lateral Parabrachial nucleus. This region takes information from other areas as well as from neurotransmitters including serotonin and glutamate and in euvolemia the main outcome is inhibition of sodium intake

104
Q

What proportion of filtered sodium load is taken up by…
Distal convoluted tubule
Thick ascending limb of the loop of Henle
Proximal convoluted tubule

A

Distal convoluted tubule
About 5%

Thick ascending limb of the loop of Henle
About 25%

Proximal convoluted tubule
About 65%

105
Q

What proportion of renal blood flow is filtered into the nephrons

A

20%

106
Q

What is the effect of increased tubular sodium concentration on the juxtaglomerular cells of the macular densa

A

Increased sodium uptake through the Na/K/Cl triple transporter, leading to release of adenosine and ATP

107
Q

Which cells respond to the adenosine by reducing renin production

A

Extraglomerular mesangial cells

108
Q

Why does the release of adenosine lead to a reduction in GFR in the short term

A

It causes the afferent SMCs to contract reducing renal plasma flow and therefore GFR.

109
Q

What is the effect of low tubular sodium at the macular densa on the production of Angiotensin II

A

It increases it because it stimulates the production of renin leading to angiotensinogen conversion to AI and finally to AII

110
Q

Where in the tubular system does aldosterone work

A

DCT (distal end of the DCT) and CT

111
Q

Where is aldosterone released from?

A

Adrenal cortex

112
Q

How does aldosterone affect potassium balance?

A

It increases potassium secretion by stimulating sodium uptake: increased Na/K+ ATPase expression will increase the rate of K+ uptake and combined with the increase in Na reabsorption from the lumen (and excretion in to the blood) this will lead to increased K+ excretion

113
Q

What is the effect of hypoaldosteronism on plasma renin?

A

It causes and increase in plasma renin because of the reduction in sodium reabsorption and the consequent loss of water reducing ECF and therefore BP. This leads to low sodium in the nephron and therefore the release of renin

114
Q

What are the 6 major locations of baroreceptors?

A

Atria, right ventricle, pulmonary vasculature, carotid sinus, aortic arch, JGA

115
Q

What are the effects of ANP on sodium reabsorption in the PCT?

A

Reduced Na reabsorption

116
Q

What proportion of filtered potassium load is reabsorbed by
Distal convoluted tubule
Thick ascending limb of the loop of Henle
Proximal convoluted tubule

A

Distal convoluted tubule
Variable depending on potassium status ranges from 3% reabsorbed to secretion of 50%

Thick ascending limb of the loop of Henle
About 20%

Proximal convoluted tubule
About 65%

117
Q

What happens to plasma K+ after a meal

A

It initially increases then it is taken up into cells by the activity of the Na/K ATPase

118
Q

Why do diabetics have polyuria?

A

There is normally no glucose in the tubular fluid in the distal part of the nephron. If glucose is present it will increase the osmolarity of the tubular fluid. This will reduce the osmotic gradient between the tubule and plasma and lead to a reduction in water reabsorption. More water in the urine means more frequent urination. i.e. the glucose acts as an osmotic diuretic.

119
Q

Check Insendi for bigger Qs.

A

BRS UROLOGY & RENAL (10 decks)

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