Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is normal plasma osmolarity?

A

285-295 mosmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the most prevalent and important solute in ECF?

A

sodium

more sodium= higher ECF volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

where other than the PCT is sodium reabsorbed?

A

thick ascending limb (25%)

DCT (5%)

CD (3%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what transporter is used in the DCT for sodium reabsorption?

A

Na+/Cl- transporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what transporter is used in the CD for sodium reabsorption?

A

Na+ channel ENAC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what percentage of Na is excreted?

A

<1%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how is GFR calculated?

A

RPF * 0.2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the connection between DCT and glomerulus?

A

DCT separated from glomerulus by extraglomerular mesangial cells and juxtaglomerular cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is aldosterone?

A

steroid hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

where is aldosterone synthesised and released?

A

adrenal cortex (zona glomerulosa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is aldosterone released in response to?

A
  • Angiotensin II
    • Promotes synthesis of aldosterone synthase: (in zona glomerulosa)
      • Causes increased production aldosterone from cholesterol
      • Increased aldosterone
  • Decrease in blood pressure (via baroreceptors)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what does aldosterone stimulate?

A
  • Increased Sodium reabsorption
    • (controls reabsorption of 35g Na/day)
  • Increased Potassium secretion
  • Increased hydrogen ion secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what does aldosterone excess cause?

A

hypokalaemia alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

how does aldosterone work?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are the important aldosterone target genes in CCD?

A

ENaC (epithelial sodium channel)

sodium-potassium ATPase

this coordinates an increase in number of sodium transporters and their activity and thereby increasing sodium reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is hypoaldosteroinism?

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what are the effects of hyperaldosteronism?

A
  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
Q

what part of the nephron is permeable to Na

A
33
Q

what is Liddle’s syndrome?

A

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
Q

what is the difference in hyperaldosteronism and Liddle’s syndrome?

A

Liddle’s is same phenotype as hyperaldosteronism but with normal to low levels of aldosterone

35
Q

where are the baroreceptors located?

A
  • heart
    • atria
    • right ventricle
  • vascular system
    • pulmonary vasculature
    • carotid sinus
    • aortic arch
    • JGA
36
Q

what is the difference between the baroreceptors?

A

atria, right ventricle and pulmonary vasculature respond to low pressures

carotid sinus, aortic arch and JGA respond to high pressure

37
Q

how do the low-pressure baroreceptors respond to pressure changes?

A
38
Q

how do high pressure baroreceptors respond to low pressure?

A
39
Q

where is atrial natriuretic peptide (ANP) made?

where does ANP circulate?

A

made in atria (also make BNP)

circulates in blood and binds to its receptors

40
Q

what is ANP released in response to?

A

atrial stretch (i.e high blood pressure)

41
Q

what are the actions of ANP?

A
  • 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
Q

what does ANP stimulate the produciton of?

A

cGMP and activated protein kinase G= vasodilation to reduce BP

43
Q

what is the response to volume expansion?

A
  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
Q

what does water reabsorption require?

A

osmotic gradient

45
Q

what occurs during volume contraction?

A
46
Q

how is an interstitial osmolarity generated?

A

generate interstitial osmolarity through renal medulla

47
Q

what happens if the osmolarity of fluid in tubule is same as interstitium?

A

no net movement of water into interstitium

48
Q

what happens on a reduction in osmolarity in the interstitium to water reabsorption?

A

reduce water reabsorption

49
Q

what happens to water reabsorption if tubular fluid osmolarity increases?

A

reduce gradient between tubular fluid and interstitium

reduce water reabsorption

50
Q

what ion levels determine the ECF volume?

A

Na+

51
Q

what is the effect of ECF volume on BP?

A

proportional

reduction ECF volume reduces BP

52
Q

what effect does reducing Na+ reabsorption have on ECF vol and BP?

A

reduces total Na+

reduces ECF volume

reduces BP

53
Q

what are the different types of diuretics?

A

ACEi

osmotic diuretics

carbonic anhydrase inhibitors

loop diuretics

thiazide diuretics

potassium-sparing diuretics

54
Q

how do ACEi work?

A
  • 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
Q

what are the effects of reducing Ang II production?

A

vascular effects (vasodilating) increasing volume of the vascular tree

so reducing blood pressure

56
Q

what is angiotenin II produced from?

A
57
Q

where do the different diuretics work in nephron?

A
58
Q

how do osmotic diuretics work?

A

put something in that doesn’t get reabsorbed

increases osmolarity of tubular fluid so reduces water reabsorption

59
Q

how do carbonic anhydrase inhibitors work?

A

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
Q

how do loop diuretics work?

A

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
Q

how do thiazide diuretics work?

A

block Na+Cl- transporter

reduced Na+ reuptake in DCT

increased Na+ in distal nephron

62
Q

what are the side effects of thiazide diuretics?

A

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
Q

how do potassium-sparing diuretics work?

A
  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
Q

what is the normal intracellular and extracellular potassium conc?

A

intracellular -150 mmol/L

extracellular- 3-5mmol/L

65
Q

what are the effects of extracellular K+?

A

effects on excitable membranes of nerve and muscle

66
Q

what is the main intracellular ion?

A

potassium

67
Q

what are the effects of high K+?

A

depolarises membranes- action potentials, heart arrhythmias

68
Q

what are the effects of low K+

A

heart arrhythmias (asystole)

69
Q

what is the level of potassium in ECF?

A

low

70
Q

what affect does a meal have on potassium?

A

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
Q

where is potassium reabsorbed?

A

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
Q

what are the effects of increased K+ on reabsorption?

A

increases activity Na+ ATPase and reduces return on potassium into plasma by principal cells

73
Q

how does tubular flow regulate potassium?

A

activates cilia that activate PDK1

this increases CA2+ in cell

this stimulates opening of potassium channels on apical membrane

74
Q

what electrolyte imbalance is seen most commonly?

A

hypokalemia

up to 20% hospitalised patients

75
Q

what are the causes of hyperkalemia?

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)
76
Q

how common is hyperkalaemia?

A

common

1-10% hospitalised patients

77
Q

what are the causes of hyperkalaemia?

A
  • ACEi
  • Elderly
  • Severe diabetes (insulin resistance)
  • Kidney disease
  • Response to K+ sparing diuretics

1B Urology and Renal Medicine (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions