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brs (phase 1b) > (uro) sodium potassium balance > Flashcards

(uro) sodium potassium balance Flashcards

1
Q

define osmolarity

A

a measure of the number of particles of a solute per litre of solution

= measured in osmoles/litre (osm/L)

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2
Q

what is one osmole?

A

used to describe when there is one mole of dissolved particles per litre of solution

(depends on the number of dissolved particles)

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3
Q

what is the osmolarity of a 1M NaCl solution?

(explain why)

A

1M = 1 mol/L

and 1 mol/L of NaCl = 2 Osm/L

as 1 mole of NaCl, will in solution, dissociate fully and become two separate particles and give 2 osmoles (1 mole of Na+, 1 mole of Cl-)

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4
Q

what is the expected molarity of 1 Osm/L NaCl solution?

A

NaCl
= in 1 mole of NaCl, there are 2 dissociated particles so 2 Osm/L

so if the osmolarity is 1 Osm/L, molarity must be 0.5 mol/L

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5
Q

differentiate between molarity and osmolarity

A

molarity = number of moles of solute per litre of solution (mol/L)

osmolarity = number of dissolved particles per litre of solution (osm/L)

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6
Q

what is the relationship between number of dissolved particles and osmolarity?

A

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

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7
Q

our blood has a ‘constant osmolarity’

what is the significance of this statement?

A

water is the major component of our body fluids

= when the amount of salt changes, the amount of water also changes appropriately

(increase in salt = increase in water & vice versa)

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8
Q

what does an ECF osmolarity of 290mOsm/L mean?

A

for every change of 290 mosmols, the volume will changes by 1L as well

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9
Q

what is the normal plasma osmolarity?

A

285-295 mosmol/L

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10
Q

what is the most important solute in determining ECF volume?

A

sodium
(most prevalent, and most

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11
Q

what is the concentration of sodium in the plasma?

A

approx 140 mmol/L

= the more sodium you have in the plasme, the greater the ECF volume will be

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12
Q

how does increased dietary sodium affect body weight and why?

A

increased dietary sodium
= increased plasma sodium concentration
= increased subsequent water retention + more thirst (so more water drank)
= increased body weight

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13
Q

explain how an increase in dietary sodium affects blood pressure

A

increased dietary sodium

= increased plasma sodium concentration

= increased osmolarity (but this cannot happen as osmolarity is constant)

= compensatory increased water retention and increased water intake

= increased ECF volume

= increased blood pressure

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14
Q

explain how an decrease in dietary sodium affects blood pressure

A

decrease in dietary sodium

= decrease in plasma sodium concentration

= decreased osmolarity (but this cannot happen as osmolarity is constant)

= compensatory reduction in water intake and retention

= reduced ECF volume

= reduced blood pressure

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15
Q

when sodium levels are altered, why is the osmolarity not appropriately altered too?

A

the osmolarity remains constant always

= to ensure this, the only alterable feature, the water content, is changed accordingly

= so when sodium levels change, to keep osmolarity constant, water levels change

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16
Q

when sodium levels are altered, what happens to blood volume and blood pressure?

A

sodium levels increase/decrease

= blood volume increases/decreases subsequently to maintain osmolarity
= however, as there is a relatively FIXED blood volume, volume cannot change significantly
= so blood pressure increases/decreases accordingly

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17
Q

what are the two mechanisms by which sodium is regulated?

A

central = lateral parabrachial nucleus

peripheral = taste

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18
Q

describe the CENTRAL mechanism of sodium regulation

A

controlled by the lateral parabrachial nucleus

1) in euvolemic state
= cells that respond to glutamate and serotonin act to inhibit Na+ uptake

2) in the sodium deprived state = cells that respond to GABA and opioids act to increase Na+ uptake

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19
Q

describe the PERIPHERAL mechanism of sodium regulation

A

based on taste (bimodal)

1) in small amounts, salt enhances the taste of food = appetitive

2) at high concentrations, make food taste bad = aversive

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20
Q

how does the lateral parabrachial nucleus respond to euvolemia?

A

in the euvolemic state, inhibition of Na+ uptake is promoted by the neurotransmitters, glutamate & serotonin

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21
Q

how does the lateral parabrachial nucleus respond to sodium deprivation?

A

in the sodium deprived state, stimulation of Na+ uptake is promoted by the neurotransmitters, GABA and opioids

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22
Q

why is taste described as ‘bimodal’ when it comes to salt?

A

in low concentrations = enhances the taste of food (appetitive)

in high concentrations = makes food taste bad (aversive)

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23
Q

which neurotransmitter control the inhibition of sodium uptake?

A

serotonin and glutamate

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24
Q

which neurotransmitter control the stimulation of sodium uptake?

A

GABA and opioids

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25
Q

why do we want to maximise sodium retention?

A

we want to retain as much sodium as possible to maintain our ECF osmolarity

= as sodium is the most prevalent ion that contributes to ECF

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26
Q

where is sodium reabsorbed in the nephron and how much?

A

1) PCT = approx 67%

2) thick ascending limb = approx 25%

3) DCT = approx 5%

4) collecting ducts = approx 3%

so overall, less than 1% of sodium is excreted int he urine

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27
Q

how is sodium reabsorbed in the PCT?

A

approx 67% of filtered sodium is reabsorbed in the PCT
(same as the amount of water reabsorbed in this region)

= usually via a co/counter-transported ion mechanism, facilitating the reabsorption of other things such as glucose, amino acids or bicarbonate

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28
Q

how is sodium reabsorbed in the thick ascending limb?

A

approx 25% is reabsorbed

= via counter-current mechanisms OR the triple transporter (Na+/K+/Cl-)

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29
Q

how is sodium reabsorbed in the DCT?

A

approx 5%

= via the Na+/Cl- transporter of this region

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30
Q

how is sodium reabsorbed in the collecting ducts?

A

approx 3%

= via the Na+ channel ENACs

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31
Q

how much of the filtered sodium is actually excreted in the urine?

A

< 1% of the filtered sodium

= as the body wants to keep as much sodium within the blood as possible to maintain ECF osmolarity

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32
Q

how will changes to GFR affect sodium excretion?

A

if GFR goes up, more sodium is filtered into the filtrate and so total sodium excreted would go up (= 1% of a larger amount of sodium filtered)

= increased sodium excretion
= increased water loss
= reduce blood volume

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33
Q

what is the relationship between RPF and GFR?

A

approx 20% of the RPF is filtered to make up the GFR

so GFR = 0.2 x RPF

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34
Q

how much of the RPF is filtered?

A

approx 20% of the renal plasma enters the tubular system

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35
Q

how does RPF affect the GFR?

A

RPF is proportional to GFR so if the renal plasma flow increases, the GFR will also increase

(kidneys will filter 20% of a greater starting amount so, greater finishing - tubular - amount)

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36
Q

what is the RPF proportional to?

A

besides GFR, RPF is also proportional to blood pressure

so as blood pressure increases, so does RPF (and therefore so does GFR)

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37
Q

explain the relationship between blood pressure, RPF and GFR

A

over a significant range of blood pressures (up to 100 mmHg), RPF is proportional to blood pressure

= so as the blood pressure increases, the RFP (and therefore the GFR) also increase

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38
Q

how does the RPF-GFR relationship change during exercise and WHY?

A

during exercise, blood pressure increases

if the proportionality bw RPF and blood pressure was maintained beyond 100 mmHg, then during the high blood pressures of exercise
= the RPF would be so high that
= significant amounts of fluid + sodium would be lost

SO beyond 100mmHg, the proportionality is no longer maintained between RPF and blood pressure

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39
Q

why is RPF not proportional to blood pressure beyond 100 mmHg?

A

to prevent large amounts of fluid and sodium loss

(especially during exercise)

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40
Q

what impact does an increase in GFR have on the tubular filtrate?

A

increased GFR
= more RPF has been filtered so
= increased sodium + chlorine delivery to the distal nephrone

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41
Q

which renal structure is closely associated with the DCT and why is this important?

A

a specific part of the DCT (macula densa)

= is closely associated with the the renal glomerulus

= essential for regulating sodium excretion

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42
Q

explain the mechanism of action by which sodium excretion is regulated

A

high blood pressure
= high RPF & high GFR
= high tubular sodium

= increased delivery of sodium to the macula densa (i.e. distal nephron)
= increased sodium-chlorine uptake via triple transport in the DCT
= increased activity of macula densa cells above a threshold value
= increased release of ATP and adenosine
= detected by extraglomerular mesangial cells causing two things

1) reduced renin release by juxtaglomerular cells (LONG-TERM response)
2) increase afferent SMC contraction (SHORT-TERM response)

= reduction in RPF + perfusion pressure
= reduction in GFR
= reduced sodium loss

43
Q

what does the juxtaglomerular apparatus consist of?

A
  • macula densa
  • afferent (and a few efferent) arteriole juxtaglomerular cells
  • extraglomerular mesangial cells
44
Q

what are juxtaglomerular cells and what is their function?

A

(smooth muscle) cells of the juxtaglomerular apparatus that have two functions

1) secrete renin depending on sodium delivery to distal nephron

2) monitor the stretch of the afferent arteriole and contract/relax (depending on extraglomerular mesangial cells) to regulate RPF and perfusion pressure

45
Q

what are extraglomerular mesangial cells and what is their function?

A

cells of the juxtaglomerular apparatus that will detect the adenosine + ATP released by the macula densa cells and stimulate
1) reduced renin secretion
2) increased afferent SMC contraction

46
Q

where are juxtaglomerular cells found?

A

embedded mainly within the glomerular afferent arteriole, and adjacent to the extraglomerular mesangial cells

(w some in efferent)

47
Q

where are extraglomerular mesangial cells found?

A

found in the space bw the afferent and efferent arterioles, the glomerular capillaries and the macula densa cells

48
Q

what is the macula densa?

A

an area of specialised cells lining the distal convoluted tubule, where the DCT touches the glomerulus

= specifically the region where the thick ascending LOH meets the DCT

49
Q

where is the macula densa found?

A

region of specialised cells found specifically embedded in the DCT

= where the thick LOH meets the DCT, adjacent to the glomerulus

50
Q

what is the macula densa particularly close to physiologically?

A

glomerulus

51
Q

which transporter is involved with sodium uptake in the macula densa?

A

triple transporter

(Na+/Cl-/K+ transporter)

52
Q

what is released by macula densa cells to regulate sodium excretion and WHEN?

A

ATP and adenosine

= when a specific threshold value is exceeded (of sodium conc. in the DCT)

53
Q

where does the ATP and adenosine released by macula densa cells act and what is the effect of this?

A

acts on the extraglomerular mesangial cells to have two effects:

1) long-term = reduced renin secretion from the juxtaglomerular cells

2) short-term = increases afferent SMC contraction

= overall effect is to reduce RPF, perfusion pressure and therefore GFR

54
Q

when extraglomerular mesangial cells are activated, what two effects are achieved?

A

1) long-term = reduced renin secretion from the juxtaglomerular cells

2) short-term = increases afferent SMC contraction

55
Q

from where is renin secreted?

A

juxtaglomerular cells of the juxtaglomerular apparatus

56
Q

what is the implication of increased afferent SMC contraction and what triggers it?

A

reduces RPF and perfusion pressure
= reduces GFR
= reduces sodium excretion

triggered by extraglomerular mesangial cell activation

57
Q

what is the long-term response of the juxtaglomerular apparatus to increased sodium excretion?

A

reduced renin secretion

58
Q

what is the short-term response of the juxtaglomerular apparatus to increased sodium excretion?

A

increased afferent SMC contraction

59
Q

why is the reduction in perfusion pressure and RPF by the juxtaglomerular apparatus an important response?

A

results in a subsequent decrease in GFR
= so less sodium excretion
= so less sodium and fluid loss

60
Q

what is the best way to retain sodium within the plasma?

A

!! filter less !!

= reduce the GFR in order to reduce the volume of salt and water loss

61
Q

how is GFR most commonly reduced?

A

by reducing the filtration pressure across the Bowman’s capsule

= either
1) by increasing afferent SMC contraction
OR
2) by increasing efferent SMC contraction

62
Q

list three way in which increased sympathetic stimulation reduces sodium excretion

A

1) increases afferent arteriole SMC contraction so the AA pressure increases (increased filtration pressure = reduced GFR)

2) increased activation of the sodium-proton exchanger in the PCT so more sodium is reabsorbed into the plasma

3) increased activation of JGA cell apparatus to stimulate more renin production (to increase filtration pressure, and reduce sodium excretion)

63
Q

when the cells of the macula densa detect that there is low tubular sodium in the DCT, what is the response?

A

low tubular sodium
= less adenosine + ATP is released from the macula densa cells
= less activation of the extraglomerular mesangial cells
= less inhibition of renin production from the JGA
= so, more renin overall
= VASOCONSTRICTION in the afferent arteriole
= more sodium retention due to reduced RPF & GFR

64
Q

what does the production of renin automatically increase?

A

angiotensin II

65
Q

summarise the main actions of angiotensin II

A

1) increases vascular resistance (i.e. blood pressure)

2) increases sodium reabsorption from the PCT

3) increases aldosterone production in such a way that in turn, increases sodium reabsorption in the DCT and collecting duct

66
Q

if you want to INCREASE sodium reabsorption and retention, what are the four main ways to do so?

A

1) increased sympathetic activity (main)

2) low tubular sodium

3) increased angiotensin II production

4) increased aldosterone production

67
Q

if you want to DECREASE sodium reabsorption and retention, what is the main way to do so?

A

1) atrial naturietic peptide (ANP)

68
Q

describe how ANP (atrial naturietic peptide) works to decrease sodium retention

A

1) promotes the dilation of the afferent arteriole

2) inhibits renin release

3) reduces the uptake of sodium in the PCT, DCT and collecting duct

69
Q

when there is low tubular sodium, via the tubulo-glomerular feedback mechanism, why is there no afferent arteriole dilation/relaxation?

A

normally, via the tubulo-glomerular feedback mechanism, you would expect high tubular sodium to cause:

1) reduced renin production
2) increased afferent SMC contraction

BUT (!!!!) when increasing sodium retention with low tubular sodium, there is also increased sympathetic activity which overrides the INeffect of the extraglomrular mesangial cells and instead causes afferent SMC contraction + reduced GFR

70
Q

what are five main mechanisms of action of angiotensin II?

A

1) increases sodium reuptake in the PCT

2) increases adrenal cortex production of aldosterone (which in turn, increases DCT + CD sodium rebasoprtion)

3) increased sympathetic activity

4) increased vasoconstriction

5) increased pituitary ADH production (to increase water reabsorption)

71
Q

explain, in detail what happens if the blood pressure falls when there are low plasma sodium levels

A

low plasma sodium
= blood volume + blood pressure falls
+ increased activation of sympathetic nervous system
= increased afferent arteriolar vasoconstriction, increased renin release, increased PCT sodium reabsorption

increased renin
= increased conversion of angiotensinogen to angiotensin I
= increased ACE activity increases conversion of angiotensin I to angiotensin II
= increased angiotensin II has its normal five effects (more sympathetic activity, vasoconstriction, increased Na+ R in PCT, increased aldosterone to increase Na+ R in DCT, CD, increased ADH production to increase water reabsorption)

72
Q

explain, in detail what happens if the blood pressure rises when there are high plasma sodium levels

A

high plasma sodium levels
= high blood volume + pressure
+ reduced sympathetic activation
+ INCREASED ANP RELEASE

reduced renin
= reduced conversion of angiotensinogen to angiotensin I
= reduced subsequent production of angiotensin II
= reduced sympathetic activation, reduced vasoconstriction, reduced Na+ R in the PCT, reduced aldosterone production so less Na+ R in the DCT and CD, reduced ADH production so less water reabsorption

increased ANP
= increases afferent arteriole VASODILATION, reduces renin rpoduction, reduces PCT, DCT and CD Na+ R

73
Q

when is ANP released?

A

in situation where sodium retention needs to be decreased

i.e. high plasma sodium, increased blood pressure

74
Q

what type of hormone is aldosterone?

and what does this mean?

A

steroid hormone

i.e. the precursor molecule is cholesterol

75
Q

where is aldosterone synthesised?

A

zona glomerulosa of the adrenal cortex

76
Q

which substance stimulates aldosterone synthesis?

A

angiotensin II

77
Q

when is aldosterone actually released?

(i.e. in response to what)

A

1) increased aldosterone synthetase activity

2) decrease in blood pressure (detected by baroreceptors)

78
Q

which enzyme is essential for aldosterone production?

A

aldosterone synthetase

79
Q

what are the three main effects of aldosterone activity?

A

1) increases sodium reabsorption

2) increases potassium secretion

3) increases hydrogen ion secretion

80
Q

explain how aldosterone increases sodium reabsorption

A

aldosterone increases the activity of the apical ENaCs (sodium channels)

= increased sodium reabsorption from the lumen into the principal cells of the CD
= increased basolateral sodium-potassium exchange via the Na-K ATPases
= increased sodium reabsorption into the bloodstream

81
Q

explain how aldosterone increases potassium secretion

A

aldosterone increases sodium reabsorption via apical ENaCs and basolateral Na-K ATPases

= to enable more Na+ to reabsorbed into the bloodstream, more K+ must be secreted into the lumen
= more potassium secretion as a consequence of the increased Na+ reabsorption

82
Q

explain how aldosterone increases hydrogen secretion

A

in principal cells, more Na+ reabsorbed than K+ secreted

= gives rise to a lumen-negative transepithelial voltage (diff in voltages on either side)
= indirectly stimulates the secretion of H+ ions into the lumen from the adjacent, neighbouring alpha-intercalated cells

83
Q

what is the biggest risk associated with excess aldosterone?

A

hypokalaemic alkalosis

84
Q

explain why excess aldosterone can lead to hypokalaemic alkalosis

A

aldosterone’s main purpose is to increase sodium reabsorption

to enable this, more potassium must be secreted (via Na-K ATPases) and more hydrogen must also be secreted (via H+ ATPases)

1) excess aldosterone = excess K+ secretion = hypokalaemia
2) excess aldosterone. = excess H+ secretion = alkalosis

85
Q

what are principal cells and what is the effect of aldosterone on them?

A

cells of the late DCT & CD

aldosterone acts on them to
1) increase sodium reabsorption
2) increase potassium secretion

86
Q

what are intercalated cells and what is the effect of aldosterone on them?

A

cells of the late DCT & CD

aldosterone acts on them to
1) increase apical H+ ATPase activity
= increase H+ secretion

87
Q

how does aldosterone affect intercalated cells both
a) directly and
b) indirectly?

A

directly = acts on intercalated cells to increase apical H+ ATPase activity and therefore H+ secretion

indirectly = acts on adjacent/neighbouring principal cells to increase Na+ R and K+ secretion so causes a lumen-negative TEPD, which in turn stimulates more H+ secretion

88
Q

what is the lumen-negative transepithelial voltage and how does it come about?

A

when 3+ Na ions are reabsorbed for every 2 K+ ions secreted, lumen becomes increasingly negative in comparison to the plasma

= happens when there is excess aldosterone acting on the principal cells of the CD

89
Q

what is the TEPD?

A

transepithelial potential difference

= voltage across an epithelium
(i.e. sum of the membrane potential for the outer and inner cell membranes)

90
Q

when aldosterone acts, why is a possible side effect increased chloride reabsorption?

A

aldosterone increases proton secretion from intercalated cells (both directly + indirectly)

= requires more carbonic acid dissociation so more HCO3- builds up in the cell
= increased reabsorption of HCO3- via the HCO3-C;- antiporter
= more Cl- ions are secreted

= maybe the increased chloride reabsorption is to tackle this subsequent increase in luminal chloride

91
Q

explain how aldosterone binds to its receptor and what the implications of this are

A
  • aldosterone is lipid-soluble and so can cross the cell membrane
  • binds to the mineralocorticoid receptor (MR)
  • MR is a monomoer bound to HSP90
  • when aldosterone binds, HSP90 dissociates and the monomers dimerise and become dimers
  • dimers enter the nucleus and bind to the DNA
  • the bind at the specific promotor region of the target genes and increase their expression

(i.e. ENaCs, Na-K ATPases)

92
Q

how does aldosterone reach its target receptor?

A

aldosterone is lipid-soluble and so can cross the cell membranes to reach the MR in the cytoplasm

93
Q

describe the structure of the mineralocorticoid receptor

A

a monomer bound to HSP90

(kept within the cytoplasm)

94
Q

how does the structure of the mineralocorticoid receptor change when aldosterone binds to it?

A

before aldosterone binds = monomer + HSP90

after aldosterone binds = dimer, w HSP90 dissociated

95
Q

upon dimerisation, where does the dimer bind to within the cell and why?

(aldosterone binding to MR)

A

translocates to within the nucleus AND binds to the DNA specifically in the promoter region of the target genes

96
Q

what are the important target genes for aldosterone?

A
  • ENaCs (epithelial sodium channels)
  • Na-K ATPases

+ sets of regulatory proteins (!!!!!)

97
Q

what effect does aldosterone have on ENaCs and Na-K ATPases?

A

increases the number of AND activity of
- ENaCs
- Na-K ATPases

= to increase sodium reabsorption

98
Q

what is the implication of aldosterone activity on the epithelial cells of the collecting duct?

A

increase BOTH the number and the activity of the sodium transporters (i.e. ENaCs, Na-K ATPases)

99
Q

explain why aldosterone increases sodium reabsorption

A

aldosterone acts to cause the binding of the dimer to the promoter region of the target genes

= target genes are that of the ENaCs + Na-K ATPases

= increases BOTH the number and the activity of the sodium transporters (i.e. ENaCs, Na-K ATPases)

= increased sodium reabsorption

100
Q

define hypoaldosteronism

A

a disease in which insufficient levels of aldosterone are secreted

101
Q

what occurs as a result of hypoaldosteronism?

A
  • low sodium reabsoprtion in the distal nephron
    = increased urinary loss of sodium
    = ECF volume falls
102
Q

summarise the body’s response to hypoaldosteronism

A

when ECF level falls
= same response as in volume contraction

= so overall, increased angiotensin II, renin and ADH

103
Q

what are the main symptoms of hypoaldosteronism?

A

due to low sodium:

  • low blood pressure
  • dizziness
  • palpitations
  • salt cravings

brs (phase 1b) (71 decks)

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