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1B Urology and Renal Medicine > Sodium and potassium balance: > Flashcards

Sodium and potassium balance: Flashcards

1
Q

what is osmolarity?

A

measure of the solute (particle) concentration in a solution

osmoles/L

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2
Q

what does osmolarity depend on?

A

number of dissolved particles

greater number of dissolved particles, greater the osmolarity

the osmolarity is kept constant under changing salt and water concentrations

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3
Q

what is normal plasma osmolarity?

A

285-295 mosmol/L

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4
Q

what is the most prevalent and important solute in ECF?

A

sodium

more sodium= higher ECF volume

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5
Q

what is the effect of increased dietary sodium?

A

increased total body sodium

increased osmolarity (but this cant happen)

increased water intake and retention

increased ECF volume

increased blood volume and pressure

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6
Q

what is the effect of decreased dietary sodium?

A

decreased total body sodium

decreased osmolarity (but this cant happen)

decreased water intake and retention

decreased ECF volume

decreased blood volume and pressure

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7
Q

what are the regulation mechanisms of sodium intake?

A

Central Mechanism:

  • Normally suppressing sodium intake via lateral parabrachial nucleus
    • Cells that respond to serotonin and glutamate suppress basal sodium intake
  • Under sodium deprivation:
    • Increased appetite for Na+ via GABA and opioids

Peripheral:

  • Salt in food is appetitive at low concentrations in food and aversive at high levels
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8
Q

where is the bulk of filtered sodium reabsorbed and how?

A

proximal convoluted tubule (67%)

use of sodium as a co or counter transported ion facilitating reabsorption of other things (glucose,amino acids, bicarbonate)

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9
Q

where other than the PCT is sodium reabsorbed?

A

thick ascending limb (25%)

DCT (5%)

CD (3%)

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10
Q

what transporter is used for sodium in the thick ascending limb?

A

counter current mechanism through Na+/K+/Cl- triple transpoter

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11
Q

what transporter is used in the DCT for sodium reabsorption?

A

Na+/Cl- transporter

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12
Q

what transporter is used in the CD for sodium reabsorption?

A

Na+ channel ENAC

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13
Q

what percentage of Na is excreted?

A

<1%

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14
Q

how does GRF affect sodium excretion?

A
  • Renal plasma flow rate is proportional to blood pressure
  • GFR is proportional to RPF
  • Increase RPF= increase GFR = proportional to BP
  • BP can increase in exercise and so if this was maintained= inappropriate sodium and fluid loss
  • Once reach 100mmHg RPF does not increase with BP preventing this loss
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15
Q

how is GFR calculated?

A

RPF * 0.2

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16
Q

what are the effects of GFR increase in kidney sodium reabsorption?

A

flow rate in PCT and LOH increases

sodium reabsorption increases but will be maximum rate dependant on transporters and flow

as GFR increases = increased delivery of sodium/ chloride reaching distal nephron

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17
Q

what is the connection between DCT and glomerulus?

A

DCT separated from glomerulus by extraglomerular mesangial cells and juxtaglomerular cells

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18
Q

what occurs when there is high tubular sodium?

A
  • Increased sodium/chloride uptake via triple transporter
  • Macular densa cells release adenosine once threshold transport reached (and ATP)
  • This is detected by extraglomerular mesangial cells
  • EMC stimulate contraction of smooth muscle of afferent arteriole
  • causes reduction in RPF and perfusion pressure
  • tubular flow rate lowers preventing loss sodium and fluid
  • EMC stimulate reduction of renin production (long term response)
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19
Q

what occurs in the kidney when need to retain sodium and water?

A
  1. reduce glomerular filtration
    1. reduction filtration pressure across bowman’s capsule
    2. sympathetic activity
      1. constricting afferent arteriole more than efferent
      2. stim sodium uptake by cells of PCT
      3. stim JGA to produce renin= production angiotensin 2 production
      4. angiotensin 2= increased aldosterone
    3. or relaxing efferent arteriole more than afferent arteriole
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20
Q

what can oppose the effects of uptake of Na and cause a decrease in uptake sodium

A

Atrial Naturietic peptide

promotes dilation of afferent arteriole and inhibits renin release

therefore reduces uptake sodium in PCT, DCT and CT

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21
Q

what are the effects of low sodium on volume expansion and contraction?

A
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22
Q

what are the effects of high sodium on volume expansion and contraction?

A
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23
Q

what is aldosterone?

A

steroid hormone

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24
Q

where is aldosterone synthesised and released?

A

adrenal cortex (zona glomerulosa)

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25
what is aldosterone released in response to?
* Angiotensin II * Promotes synthesis of aldosterone synthase: (in zona glomerulosa) * Causes increased production aldosterone from cholesterol * Increased aldosterone * Decrease in blood pressure (via baroreceptors)
26
what does aldosterone stimulate?
* Increased Sodium reabsorption * (controls reabsorption of 35g Na/day) * Increased Potassium secretion * Increased hydrogen ion secretion
27
what does aldosterone excess cause?
hypokalaemia alkalosis
28
how does aldosterone work?
* steroid hormone so crosses cell membrane and binds to mineralocorticoid receptor * in absence of aldosterone, this receptor is a monomer bound to HSP90 and kept in the cytoplasm * on binding the steroid, the MR loses its association with HSP90 and dimerizes * it translocated into nucleus where binds DNA in promoter region of target genes and stimulates their expression
29
what are the important aldosterone target genes in CCD?
ENaC (epithelial sodium channel) sodium-potassium ATPase this coordinates an increase in number of sodium transporters and their activity and thereby increasing sodium reabsorption
30
what is hypoaldosteroinism?
1. Reabsorption of sodium in distal nephron is reduced 2. Increased urinary loss of sodium 3. ECF volume falls 4. Increased renin, ang II and ADH 5. Dizziness, low blood pressure, salt craving, palpitations
31
what are the effects of hyperaldosteronism?
1. Reabsorption of sodium in distal nephron is increased 2. Reduce urinary loss sodium 3. ECF volume increases (hypertension) 4. Reduced renin, AngII and ADH 5. Increased ANP and BNP 6. High blood pressure, muscle weakness, thurst & polyuria 7. Treat with spironolactone (lower aldosterone)
32
what part of the nephron is permeable to Na
33
what is Liddle's syndrome?
inherited disease of high blood pressure mutation in aldosterone activated sodium channel (ENaC) the channel is always activated results in sodium retention, leading to hypertenion number of mutations but main one alters re-internalization and degradation of the channel
34
what is the difference in hyperaldosteronism and Liddle's syndrome?
Liddle's is same phenotype as hyperaldosteronism but with normal to low levels of aldosterone
35
where are the baroreceptors located?
* heart * atria * right ventricle * vascular system * pulmonary vasculature * carotid sinus * aortic arch * JGA
36
what is the difference between the baroreceptors?
atria, right ventricle and pulmonary vasculature respond to low pressures carotid sinus, aortic arch and JGA respond to high pressure
37
how do the low-pressure baroreceptors respond to pressure changes?
38
how do high pressure baroreceptors respond to low pressure?
39
where is atrial natriuretic peptide (ANP) made? where does ANP circulate?
made in atria (also make BNP) circulates in blood and binds to its receptors
40
what is ANP released in response to?
atrial stretch (i.e high blood pressure)
41
what are the actions of ANP?
* Vasodilatation of renal (and other systemic) blood vessels (decreases GFR) * Inhibition of Sodium reabsorption in proximal tubule and in the collecting ducts * Inhibits release of renin and aldosterone * Reduces blood pressure
42
what does ANP stimulate the produciton of?
cGMP and activated protein kinase G= vasodilation to reduce BP
43
what is the response to volume expansion?
1. increased GFR (increased water and sodium excretion) 2. Afferent vasodilation and reduction sodium uptake in PCT 3. Reduced renin-angiotensin and aldosterone levels in PCT, DCT and CT 4. Reduced sodium reabsorption= reduced water reabsorption= increased excretion 5. ANP release compliments these effects suppressing renin increasing GFR and inhibiting sodium reuptake in the CT. It was also suppress release ADH. 6. Overall reduction in volume
44
what does water reabsorption require?
osmotic gradient
45
what occurs during volume contraction?
46
how is an interstitial osmolarity generated?
generate interstitial osmolarity through renal medulla
47
what happens if the osmolarity of fluid in tubule is same as interstitium?
no net movement of water into interstitium
48
what happens on a reduction in osmolarity in the interstitium to water reabsorption?
reduce water reabsorption
49
what happens to water reabsorption if tubular fluid osmolarity increases?
reduce gradient between tubular fluid and interstitium reduce water reabsorption
50
what ion levels determine the ECF volume?
Na+
51
what is the effect of ECF volume on BP?
proportional reduction ECF volume reduces BP
52
what effect does reducing Na+ reabsorption have on ECF vol and BP?
reduces total Na+ reduces ECF volume reduces BP
53
what are the different types of diuretics?
ACEi osmotic diuretics carbonic anhydrase inhibitors loop diuretics thiazide diuretics potassium-sparing diuretics
54
how do ACEi work?
* Reducing production Ang II from Ang I * reduces sodium uptake in PCT * overall increases sodium in distal nephron so reducing osmotic difference between tubular fluid and interstitium so reducing water reabsorption and BP
55
what are the effects of reducing Ang II production?
vascular effects (vasodilating) increasing volume of the vascular tree so reducing blood pressure
56
what is angiotenin II produced from?
57
where do the different diuretics work in nephron?
58
how do osmotic diuretics work?
put something in that doesn't get reabsorbed increases osmolarity of tubular fluid so reduces water reabsorption
59
how do carbonic anhydrase inhibitors work?
inhibit carbonic anhydrase carbonic anhydrase converts H2O and CO2 to H2CO3- this leads to Na+ reabsorption and increased urinary acidity inhibiting CA inhibits sodium uptake in PCT= higher level sodium in distal nephron= reduced difference between tubular and interstitial osmolarity= reduce water reabsorption
60
how do loop diuretics work?
block triple transporter in ascending limb of LOH inhibit sodium uptake in LOH= higher sodium in distal nephron= reduction osmolarity interstitial fluid reduce difference between tubular fluid and interstitial osmolarity to reduce water reabsorption
61
how do thiazide diuretics work?
block Na+Cl- transporter reduced Na+ reuptake in DCT increased Na+ in distal nephron
62
what are the side effects of thiazide diuretics?
increased calcium reabsorption 1. In any nephron calcium is reabsorbed across lumen membrane down conc gradient created by activity of sodium calcium exchanger 2. Sodium potassium exchanger still functions so return sodium into cell via sodium calcium exchanger increased 3. Reduces calcium conc in cell so increases potential for calcium to e removed from tubular fluid
63
how do potassium-sparing diuretics work?
1. Inhibitors of aldosterone function (e.g spironolactone) 2. Aldosterone effects= increase sodium reabsorption & increases potassium secretion and proton secretion 3. Inhibiting activity of aldosterone reduces sodium reabsorption and excretion of potassium
64
what is the normal intracellular and extracellular potassium conc?
intracellular -150 mmol/L extracellular- 3-5mmol/L
65
what are the effects of extracellular K+?
effects on excitable membranes of nerve and muscle
66
what is the main intracellular ion?
potassium
67
what are the effects of high K+?
depolarises membranes- action potentials, heart arrhythmias
68
what are the effects of low K+
heart arrhythmias (asystole)
69
what is the level of potassium in ECF?
low
70
what affect does a meal have on potassium?
K+ absorption increase K+ conc tissue uptake stimulated by insulin (also aldosterone and adrenaline)- Na+ increases this causes Na/K ATPase to response to move Na+ out to bring K+ into the cell
71
where is potassium reabsorbed?
67% filtered potassium is reabsorbed in PCT 20% reabsorbed in LOH irrespective of plasma potassium (triple transporter) DCT and CCD depends on level of potassium
72
what are the effects of increased K+ on reabsorption?
increases activity Na+ ATPase and reduces return on potassium into plasma by principal cells
73
how does tubular flow regulate potassium?
activates cilia that activate PDK1 this increases CA2+ in cell this stimulates opening of potassium channels on apical membrane
74
what electrolyte imbalance is seen most commonly?
hypokalemia up to 20% hospitalised patients
75
what are the causes of hyperkalemia?
* 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)
76
how common is hyperkalaemia?
common 1-10% hospitalised patients
77
what are the causes of hyperkalaemia?
* ACEi * Elderly * Severe diabetes (insulin resistance) * Kidney disease * Response to K+ sparing diuretics

1B Urology and Renal Medicine (6 decks)

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