Brainscape's Knowledge GenomeTM

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


See full index

Aneesha Flashcards BRS 2 > Sodium and potassium balance > Flashcards

Sodium and potassium balance Flashcards

1
Q

Define osmolarity

A

The measure of a solute (particle) concentration in a solution (osmoles/litre)
1 osmole= 1 mole of dissolved particles per litre
(1 mole of NaCl=2 moles of particles in solution)

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

What is osmolarity dictated by?

A

The number (NOT THE SIZE) of dissolved particles- the greater the number, the greater the osmolarity)

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

How does our osmolarity remain constant?

A

By water moving around through semi-permeable membranes

If there’s increased salt concentration in an area, osmolarity of that area will go up, so there’s increased water moving into that area to increase the volume to bring osmolarity back down to normal

If there’s decreased salt concentration in an area, osmolarity of that area will decrease, so there’s water moving out of that area to decrease the volume and bring osmolarity back up to norma;

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

What is normal plasma osmolarity?

A

285-295mOsm/L

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

What particles make up normal plasma osmolarity in the body?

A

Na+ 140mmol/L
Cl- 105mmol/L
HCO3- 24mmol/L
K+ 4mmol/L
Glucose 3-8mmol/L
Ca2+ 2mmol/L
Protein 1mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does an increased dietary sodium intake affect weight and blood pressure?

A

Increased dietary sodium–> increase in total body sodium–> increased osmolarity (but our body won’t allow this to happen)–> increased water intake and retention–>increased ECF volume–> increased blood volume and blood pressure and total body weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does an decreased dietary sodium intake affect weight and blood pressure?

A

Decrease in dietary sodium–> decrease in total body sodium–> decreased osmolarity (but our body does not allow this to happen)–>decreased water intake and retention → decreased ECF volume → decreased blood volume and pressure and decreased body weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What part of the brain centrally controls regulation of sodium intake?

A

Lateral parabrachial nucleus at the junction of the midbrain and pons

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

What happens at the lateral parabrachial nucleus under normal conditions of euvolemia (normal sodium levels)?

A

We are suppressing our desire to intake sodium
A set of cells in the parabrachial nucleus that respond to serotonin glutamate suppress basal Na+ intake

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

What happens at the lateral parabrachial nucleus under conditions of Na+ deprivation?

A

There is an increased appetite for Na+
This is driven by GABA and opioids

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

What is the peripheral mechanism for regulating sodium intake?

A
  • Taste
  • If you have food with no salt it tastes unpleasant
  • When salt is present in low concs in food it makes it appetising so we want to eat it
  • As Na+ conc increases, it becomes more aversive for us so we don’t want to eat it
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How much (in %) sodium is reabsorbed in different parts of the nephron and how much is excreted?

A

67% in the PCT (which causes 67% of water to be reabsorbed too)
25% in the thick ascending limb of the loop of Henle
5% in the DCT
3% in the collecting duct
<1% is excreted

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

What happens to sodium excretion if we increase GFR?

A

Increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is GFR linked to renal plasma flow rate and blood pressure?

A

Renal plasma flow rate is proportional to mean arterial pressure

Approx. 20% of renal plasma enters tubular system and therefore GFR= RPF*0.2 and GFR is also proportional to mean arterial pressure

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

What happens at a certain threshold of high blood pressure to GFR and RPF? When and why?

A

RPF and GFR both plateau at high blood pressures e.g. when exercising, we don’t want to excrete more sodium than is needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the nephron’s system to limit sodium loss through kidney excretion

A

If there’s high sodium in filtrate, there’s higher than normal sodium passing through the distal convoluted tubule
The DCT is in close association with glomerulus and JGA has macula densa cells which can detect increase in sodium concentration
This leads to increased Na+Cl- uptake via triple transporters
Macula densa cells release adenosine which is detected by extraglomerular mesangial cells which interact with smooth muscle cells in afferent arteriole
This reduces flow of blood into glomerulus, thus reducing perfusion pressure and thus GFR
This adenosine release also leads to reduction in renin production (however this is for a short period of time so doesn’t affect overall renin production over long time period)

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

What are the various systems in the nephron to increase Na+ reabsorption/retention?

A

Sympathetic activity
Angiotensin II
Low sodium in DCT will stimulate renin production from JGA and thus angiotensin II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does sympathetic activity affect sodium retention?

A

Contracts smooth muscle cells of afferent arteriole
Increases Na+ uptake of PCT cells
Stimulates renin production at JGA cells which leads to Ang II production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does Ang II affect sodium retention?

A

Vasoconstriction
Increased Na+ uptake of PCT cells
Stimulates adrenal gland to produce aldosterone which stimulates Na+ uptake in the distal part of DCT and collecting duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the function of atrial natriuretic peptide?

A

Decreases Na+ reabsorption by:

Vasodilation
Decreasing Na+ reabsorption at PCT, DCT and collecting duct
Suppressing renin production at JGA

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

How does the body react when we have low sodium levels?

A

1) Low sodium means lower blood pressure and low fluid volume

2) This increases beta1-sympathetic activity which stimulates afferent arteriole SMC to contract and reduce glomerular filtration pressure

3) Stimulates renin production which cleaves angiotensinogen into Ang I which is cleaved by ACE into Ang II

4) Ang II stimulates zona glomerulosa of adrenal gland to release aldosterone which increases Na+ reabsorption

5) Ang II also promotes vasoconstriction and Na+ reabsorption

6) This all reabsorbs more Na+ and reduces water output

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

How does the body react when we have high sodium levels?

A

1) High sodium means higher fluid volume meaning higher blood pressure

2) This suppresses beta1-sympathetic activity and causes production of ANP

3) This reduces renin which reduces Ang I which reduces Ang II which reduces aldosterone

4) This promotes vasodilation and decreases Na+ and water reabsorption

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

What factors stimulate aldosterone synthesis?

A

Angiotensin II- Ang II stimulates the production of aldosterone synthase which causes the last 2 enzymatic steps in the production of aldosterone from cholesterol

Also released when there’s a decrease in blood pressure via baroreceptors

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

What does aldosterone do in the kidney?

A
  • Stimulates Na+ reabsorption (35g per day)
    • Increased K+ secretion
    • Increased H+ secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What can happen if there’s aldosterone excess?

A

Hypokalaemic alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does aldosterone work at a cellular level in collecting duct cells?

A

1) It’s a steroid hormone which are lipid soluble so passes through cell membrane
2) It binds to a mineralocorticoid receptor sitting in cytoplasm bound to a protein called HSP90
3) Once aldosterone is bound, HSP90 gets removed and the mineralocorticoid receptor dimerises
4) It now translocates into nucleus where it binds to DNA and stimulates production of mRNA for genes for epithelial Na+ channel (ENaC) and Na+ K+ ATPase which go to their respective membranes (apical and basolateral respectively)
5) It also increases transcription of regulatory proteins that stimulate activity of those 2 transporters- so you get both more sodium channels and more active sodium channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What happens in hypoaldosteronism?

A

Reabsorption of sodium in the distal nephron is reduced
Increased urinary loss of sodium
Reduced ECF volume as water moves out with sodium

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

What does the body do to try and compensate in hypoaldosteronism?

A

Increases renin, angiotensin II and ADH (other sodium absorption mechanisms) to try and increase reabsorption

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

What symptoms does hypoaldosteronism cause?

A

Low blood pressure
Dizziness- caused by low bp
Salt craving
Palpitations-due to change in membrane potential

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

What happens in hyperaldosteronism?

A
  • Increased reabsorption of sodium in distal nephron is increased → reduced urinary loss of sodium → increase in total body sodium → ECF volume increases as we’re absorbing lots of water (hypertension)
  • This reduces renin, Ang II and ADH production and increases ANP and BNP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Symptoms of hyperaldosteronism

A

High bp
Polyuria- since we have more water we try to get rid of more
Thirst- since our body thinks there’s insufficient water in system
Muscle weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is Liddle’s syndrome and what causes it?

A

An inherited disease of high blood pressure
Caused by a mutation in the aldosterone activated sodium channel so it’s always on
This leads to increased sodium reabsorption and therefore hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What other condition does Liddle’s syndrome resemble? How does it differ from it?

A

Like hyperaldosteronism but with normal or low aldosterone levels

34
Q

Where do we have low pressure baroreceptors?

A

Heart- atria, right ventricle
Vascular system- pulmonary vasculature

35
Q

What is the response to low pressure from the low pressure baroreceptors?

A

low pressure–>low baroreceptor firing–> signal through afferent fibres to the brainstem–>sympathetic activity and ADH secretion for water retention

36
Q

What is the response to high pressure from the low pressure baroreceptors?

A

High pressure–> atrial stretch–>ANP and BNP released for greater water loss

37
Q

Where is ANP and BNP made?

A

Both in atria

38
Q

Describe the mechanism of ANP working after it’s released (on a molecular level)

A

1)Released in response to atrial stretch
2)Binds to a receptor which is guanylyl cyclase
3)This converts GTP to cyclic GMP (cGMP)
4)This activates protein kinase G
5)This leads to cellular responses

39
Q

What are the cellular responses of ANP?

A
  • Vasodilation of renal (and other systemic) blood vessels
  • Inhibition of Na+ reabsorption in proximal tubule and in collecting duct
  • Inhibits release of renin and aldosterone
40
Q

What high pressure baroreceptors do we have?

A

Carotid sinus, aortic arch, JGA (all in vascular system)

41
Q

How do high pressure baroreceptors respond to low pressure?

A

Low pressure–> low baroreceptor firing–> signal through afferent fibres to brainstem–> increased sympathetic activity and ADH secretion for water retention

reduced baroreceptor firing also → JGA cells → renin released

42
Q

How does the body react in response to volume expansion?

A

Reduction in sympathetic activity which leads to reduced Na+ reabsorption in PCT

Reduced renin production which leads to reduced Ang II and aldosterone production which reduces Na+ reabsorption and promotes excretion

Increased ANP and BNP which affects GFR and Na+ reabsorption leading to increased sodium excretion

43
Q

How does the body react in response to volume contraction?

A

Increased sympathetic activity leading to increased Na+ reabsorption in PCT

Increased renin production which leads to increased angiotensin II and aldosterone synthesis, which increases sodium and consequently water reabsorption in collecting duct

Reduced ANP and BNP

More AVP production in brain to promote water reabsorption by inserting aquaporins in collecting duct cells

44
Q

What is the effect of increased sodium levels on water secretion in nephron?

A
  • Water is reabsorbed in nephron because medulla has gradient of osmolarity throughout it which we match with the osmolarity in the tubular fluid
  • If there’s increased Na+ in tubular fluid, there’s a reduced gradient from tubular fluid to medulla because tubular fluid osmolarity is higher now so water won’t move into medulla so won’t be reabsorbed
  • So the more solute arriving in later part of nephron, the less water we can absorb
45
Q

What is the effect of reducing Na+ reabsorption on Na+ levels, ECF volume and BP?

A
  • Reducing Na+ reabsorption reduces total Na+ levels, ECF volume and BP
  • This is because Na+ levels determine ECF volume and reducing ECF volume reduces BP
46
Q

What types of diuretics are there

A

ACE inhibitors
Osmotic diuretics
Carbonic anhydrase inhibitors
Loop diuretics
Thiazide diuretics
K+ sparing diuretics

47
Q

What do ACE inhibitors primarily do?

A

Reduced Ang II production

48
Q

What are the three types of effects of ACEi

A

Vascular effects
Direct renal effects
Adrenal effects

49
Q

What are the vascular effects of ACE inhibitors?

A

Reduced angiotensin II leads to vasodilation, which then leads to increased vascular volume and reduced blood pressure

50
Q

What direct renal effects do ACEi have?

A

Decreased Na+ reabsorption in the PCT
Increased Na+ in the distal nephron means there’s a reduced water potential gradient from tubular fluid into interstitium and therefore less water is reabsorbed
This leads to lower blood pressure

51
Q

What adrenal effects does reduced Ang II production have?

A
  • Reduced aldosterone
  • This leads to reduced Na+ uptake in cortical collecting duct
  • This also increases Na+ in distal nephron (the region of nephron with the highest osmolarity) which reduces water reabsorption because of reduction in osmotic gradient across tubular wall
  • Less water reabsorption means lower blood pressure
52
Q

How do osmotic diuretics work?

A

Put something that cannot be reabsorbed into the PCT
Since it cannot be reabsorbed it remains in PCT and lowers the osmolarity there
This means less water will get reabsorbed from PCT (which is usually where most water is reabsorbed so we will see the greatest effect here)

53
Q

Where do carbonic anhydrase inhibitors work and how do they function?

A

In PCT, which is where these enzymes are most active.
This drug
1) Block carbonic anhydrase which can’t convert bicarbonate into H2CO3 then H2O and CO2

2) so CO2 can’t go into cell to then be added to H2O to make H2CO3 using another carbonic anhydrase (which wouldn’t work either)

3) so no H2CO3 is split into H+ and HCO3- so H+ can’t be used to move Na+ into cell using Na+/H+ exchanger so net sodium uptake goes down and reduction in urinary acidity

so overall carbonic anhydrase inhibitors reduce Na+ reuptake in PCT, increase Na+ in distal nephron and reduce water reabsorption

54
Q

Where do loop diuretics work?

A

Thick ascending limb of loop of Henle

55
Q

Example of a loop diuretic?

A

Furosemide

56
Q

How do loop diuretics work?

A
  • Block the Na+/2Cl-/K+ triple transporter
  • This reduces Na+ reuptake in LOH
  • Increased Na+ in distal nephron
  • This decreases osmotic gradient across tubular wall into interstitium so reduced water reabsorption
57
Q

Where do thiazide diuretics work?

A

DCT

58
Q

What is the main function of thiazide diuretics?

A

Block NaCl transporter in DCT
Increase Na+ in DCT
Leads to increased Na+ in distal nephron, reduced osmotic gradient from tubular fluid into interstitium and reduced water reabsorption from distal nephron

59
Q

Secondary effect of thiazide diuretics?

A

They increase Ca2+ reabsorption

Na+/K+ ATPase isn’t affected by these drugs so Na+ is pumped from cell into blood
But the NaCl transporter in the DCT is blocked so Na+ can’t move into cell from tubular fluid
There’s a decrease of Na+ therefore in the cell so Na+ moves from blood into cell via Na+/Ca2+ antiporter so Ca2+ builds up in blood

60
Q

Where do K+ sparing diuretics work?

A

Collecting duct

61
Q

Give an example of a K+ sparing diuretic

A

Spironolactone

62
Q

How do K+sparing diuretics work?

A

Inhibit aldosterone function by binding to mineralocorticoid receptors
- Aldosterone usually increases production of Na+ channel and Na+/K+ ATPase to increase Na+ reuptake and also increases K+ secretion and H+ excretion so an excess of aldosterone can lead to hypokalaemic alkalosis
- So if this is blocked, activity of this uptake system reduces so Na+ reuptake in distal nephron reduces

63
Q

How are K+ diuretics K+ sparing?

A

Na+/K+ ATPase pumps K+ out of blood and cell from where it moves into lumen
If we block this K+ remains in blood (it is spared)

64
Q

How much K+ is present intracellularly vs extracellularly?

A

It’s the main intracellular ion (150mmol/L)
Extracellular K+ is much lower at 3-5 mmol/L

65
Q

Where does the main effect of extracellular K+ occur?

A

On excitable membranes of nerve and muscle

66
Q

What does high extracellular K+ do?

A

Depolarises membranes leading to action potential generation and heart arrhythmia

67
Q

What does low extracellular K+ do?

A

Makes depolarisation more difficult- also leading to heart arrhythmias and asystole (flatline with no ventricular depolarisation)

68
Q

What happens K+ wise when we eat a meal?

A
  • Eating a meal leads to K+ absorption (most foods contain some potassium)- especially unprocessed foods which have a lot of K+
  • This increases plasma K+ conc
  • This needs to be reduced which happens via tissue uptake
69
Q

What stimulates tissue uptake of K+?

A

Insulin
Aldosterone
Adrenaline

70
Q

How does insulin stimulate tissue uptake of K+?

A

Indirectly
Insulin stimulates Na+/H+ exchanger which increases Na+ coming into tissue cells
This increases intracellular Na+ concentration which needs to be reduced
This is done through Na+/K+ ATPase which moves Na+ back into blood out of cell and K+ into cell

71
Q

How is K+ excreted and reabsorbed through nephron in %s?

A

Like sodium and water about 67% of filtered potassium is reabsorbed in the PCT with a further 20% reabsorbed in the loop of Henle irrespective of plasma potassium. However, in the latter parts of the nephron the handling of potassium depends on a range of factors including plasma potassium such that the amount of potassium excreted is between 1 and 80% of the initial load. In conditions of potassium depletion further potassium reabsorption occurs in the DCT and CT with 3% in the DCT and 9% in the CT. In normal or high potassium levels potassium is secreted.

72
Q

What stimulates K+ secretion into tubular fluid?

A

Higher plasma K+
Increased plasma pH
Increased aldosterone
Increased tubular flow rate

73
Q

How does high plasma K+ lead to increased K+ secretion?

A
  • Increased activity of Na+/K+ exchanger meaning more K+ moves into cell
  • More K+ in the cell then means more K+ leaving the cell in tubular fluid
  • There is also an effect on membrane potential which helps stimulate K+ secretion
74
Q

How does increased tubular flow rate lead to increased K+ secretion?

A

Distal cells have primary cilia
When there’s increased tubular flow, primary cilia can stimulate PDK1
This leads to increased Ca++ in cell, which increases openness of K+ channels allowing K+ to leave cell into tubular fluid after being pumped into cell from blood via Na+/K+ ATPase

75
Q

How does K+ secretion in K+ depleted states differ from normal conditions?

A

Same as in normal conditions but instead of secretion at DCT and collecting duct, K+ is reabsorbed as well instead similar to the earlier parts of nephron - 3% reabsorbed in DCT and 9% reabsorbed in collecting duct

76
Q

How common is hypokalemia?

A

One of the most common electrolyte imbalances (seen in up to 20% of hospital patients)

77
Q

What causes hypokalaemia?

A
  • Inadequate dietary intake (too much processed food)
    • Diuretics which increases tubular flow rates
    • Surreptitious vomiting- reduced K+ intake
    • Diarrhoea- reduced K+ intake
78
Q

What genetic conditions can lead to hypokalaemia?

A

Gitelman’s syndrome (mutation in NaCl transporter in distal nephron) leads to increased K+ loss

79
Q

How common is hyperkalemia?

A

Common electrolyte imbalance seen in 1-10% of hospitalised patients

80
Q

What causes hyperkalemia?

A
  • K+ sparing diuretics
  • ACE inhibitors
  • Being old
  • Severe diabetes
  • Kidney disease

Aneesha Flashcards BRS 2 (47 decks)

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