Brainscape's Knowledge GenomeTM

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


See full index

BRS 1b > Sodium and Potassium Balance > Flashcards

Sodium and Potassium Balance Flashcards

1
Q

What is osmolarity?

A

Osmolarity is a measure of the 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

Which ion is the most prevalent in plasma?

A

Sodium

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

What is the average osmolarity of sodium in plasma?

A

140mmol/L

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

What the normal plasma osmolarity?

A

285-295

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

What is the effect of an increase in dietary sodium?

A

The increase in the amount of sodium within the extracellular fluid will result in an increase in water retention –> Weight increase

There is a plateau in body weight gain

A reduction in dietary sodium causes a negative balance

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

What is the physiological response to an increase in total body sodium?

A

Increased water intake and retention in response to an increase in osmolarity (Must be maintained within a homeostatic end point)
This increases the ECF volume and subsequently blood pressure

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

Which nucleus within the brainstem regulates sodium intake?

A

Lateral parabrachial nucleus

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

What is the definition of euvolemia?

A

Inhibition of sodium intake (Activity of serotonin and glutamate)

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

Which hormones are involved with the inhibition of sodium intake?

A

Serotonin and glutamate

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

Which neurotransmitters are responsible for increasing the appetite for sodium?

A

GABA and opioids

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

Describe how dietary sodium intake is influenced at lower levels?

A

Enhances the taste of food

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

Describe the peripheral mechanism for regulating dietary intake?

A

Bimodal

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

At high concentrations of meal sodium, what is the impact?

A

Aversive

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

In euvolaemia, what is the response to sodium intake?

A

Inhibition of sodium intake

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

Where is the majority of sodium ions reabsorbed within the nephron?

A

Proximal convoluted tubule (67%)

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

What proportion of sodium ions are reabsorbed in the proximal convoluted tubule?

A

67%

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

What proportion of sodium is reabsorbed in the thick ascending limb of the loop of Henle?

A

25%

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

Which transporter is responsible for sodium reabsorption within the thick ascending limb?

A

Na-K-Cl triple transporter

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

How is sodium reabsorbed within the distal convoluted tubule (transporter)?

A

Na-Cl transporter

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

Which transporter is concerned with the reabsorption of sodium within the collecting ducts?

A

Sodium channel ENAC

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

If the GFR increases, what happens to the proportion of sodium that is filtered?

A

Remains the same (amount increases)

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

What approximate proportion of renal plasma enters the tubular system?

A

20%

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

What happens to renal perfusion flow with increasing blood pressure?

A

• 100mgHG RPF does not increase with increasing blood pressure –> There is a plateau effect to minimise electrolyte and water loss.

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

Where is the macula densa located?

A

Within the proximal part of the distal convoluted tubule separated from the glomerulus by extraglomerular mesangial cells and JG cells

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

Which two cells are concerned with the macula densa?

A

Extralglomerular mesangial cells

JG cells

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

Above a sodium tubular threshold, what happens in terms of the macula densa?

A

The macula densa releases adenosine and ATP,

activating receptors in the extraglomerular mesangial cells

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

Above a tubular sodium threshold what is released by the macula densa?

A

Adenosine

ATP

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

What are the consequences in response to a high tubular sodium?

A

In the long term - reduces renin production
Stimulates the contraction of the smooth muscles of the afferent arteriole - to reduce renal plasma flow and a reduction in perfusion pressure- this prevents the loss of sodium and fluid

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

Which cells secrete renin?

A

Juxtaglomerular cells (JG)

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

What effect does sympathetic stimulation have on tubular sodium regulation?

A

Increases uptake of sodium by the cells of the proximal convoluted tubule
Promotes the contraction of smooth muscle in the afferent arteriole to reduce GFR
Increased renin secretion

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

How is an increase in renin promoted by the sympathetic system?

A

Sympathetic stimulation increases the uptake of sodium by the cells in the proximal convoluted tubule.
• Activity of the sodium proton exchanger increases (relies on RAAS).
• Production of renin by the juxtaglomerular cells
• Reduce sodium reaching the distal tube (measured at the JGA). This reduces the production of adenosine from the Macula densa, thus there is reduced inhibition of renin release from the JG cells.

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

What effect does the sympathetic system have on extraglomerular cells?

A

: Sympathetic activity overrides the effect of extraglomerular cells SMC relaxation of the afferent arteriole – There is an overall contraction of smooth muscle and reduced GFR.

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

What is the effect of renin?

A

Converted into angiotensin-II by RAAS, angiotensin-II is a potent vasoconstrictor that increases vascular resistance and stimulates sodium uptake in the PCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Where does angiontensin-II act within the nephron?

A

Promotes sodium reabsorption within the proximal convoluted tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What hormone is produced by the stimulation of angiontensin-II on the adrenal cortex?

A

Stimulates the synthesis of aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Where does aldosterone act on the nephron?

A

Stimulates sodium uptake in the DCT and collecting duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Which peptide opposes increased sodium retention/reabsorption?

A

Atrial natruiretic peptide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What does ANP do to the nephron?

A

Promotes dilation of the afferent arteriole, inhibits renin release and reduces sodium uptake in the PCT, DCT and CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

In response to low plasma sodium, what happens?

A
  • Upregulation in sympathetic activity – contraction of afferent arteriole SMC.
  • Reduced GFR  Reduced delivery of sodium and water to the nephron
  • Increased renin production  Angiotensin-II and aldosterone synthesis
  • Renal NaCl and water reabsorption to reduce volume loss
  • Vasoconstriction  Increase blood pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What type of hormone is aldosterone?

A

A steroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Where within the adrenal cortex is aldosterone produced?

A

Zona glomerulosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Which enzyme is activated by angiotensin-II, in order to synthesise aldosterone?

A

Aldosterone synthase

43
Q

What is the function of aldsoterone?

A

• Increased sodium reabsorption (Control’s reabsorption of 35g Na/day)
• Increased potassium secretion (A consequence of sodium reabsorption).
The change in voltage promotes an indirect stimulation of proton secretion, there are additional direct effects of aldosterone on the secretion of proton via alterations in the expression of anion exchanges as H+-ATPase.
• Increased hydrogen ion secretion

44
Q

in which cells does aldosterone have an impact on regarding sodium reabsorption?

A

Principal cells

45
Q

In which cells does aldosterone have an impact on regarding proton secretion?

A

Intercalated cells

46
Q

An excess of aldosterone can mediate as what?

A

Hypokalaemia alkalosis

47
Q

Which types of receptors does aldosterone bind onto?

A

Intracellular mineralocorticoid receptors

48
Q

Which protein dissociates from intracellular mineralocorticoid receptors upon aldosterone binding?

A

HSP90

49
Q

Upon HSP90 dissociation what happens to the aldosterone-MR complex?

A

Dimerises

50
Q

What function is performed by aldosterone-MR complexes?

A

Translocates to the nucleus, binding to promoter regions downstream to target genes, stimulating expression/transcription

51
Q

How does aldosterone increase sodium reabsorption within the cortical collecting duct?

A

Increases the transcription and ultimate synthesis of ENaC (epithelial sodium channel)

• Coordinates increase in the number of sodium transporters, and their activity thereby increasing sodium reabsorption.

52
Q

What pathologies or iatrogenic causes are linked with hypoaldosteronism?

A

NSAIDs, lead poisoning, diabetes and kidney disease

53
Q

What are the impacts of hypoaldosteronism?

A

Reabsorption of sodium in the distal nephron is reduced manifesting as hyponatremia

Increased urinary loss of sodium

ECF volume falls - incresed renin, angiotensin-II and ADH

Hyperkalaemia and alkalosis

54
Q

What are the symptoms associated with hypoaldosteronism?

A

Dizziness
Low blood pressure
Salt carving
Palpitations

55
Q

What is hyperaldosteronism?

A

A disorder manifested by the hypersecretion of aldosterone from the adrenal gland

  • adrenal tumours
56
Q

What occurs due to hyperaldosteornism?

A 
Hyperaldosteronism increases the reabsorption of sodium in the distal nephron. 
•	Reduced urinary loss of sodium. 
•	ECF volume increases (Hypertension)
•	Reduced renin, Angiotensin-II, ADH
•	Increased ANP and BNP
57
Q

What the symptoms associated with hyperaldosteronism?

A
  • High blood pressure
  • Muscle weakness
  • Polyuria –> Consequence of thirst and increased drinking.
  • Thirst
58
Q

What is Liddle’s syndrome?

A

An inherited disorder characterised by chronic hypertension and exhibits the same phenotype of hyperaldosteronism (despite normal to low levels of aldosterone).
• Mutation in the aldosterone activated sodium channel (Alters re-internalisation and degradation of the channel, or opening time of the channel  Increasing likelihood of it being open).
• ENaC activity has overall increased (always ‘on’).
• Results in sodium retention  Leading to hypertension

59
Q

Which receptors detect pressure?

A

Baroreceptors

60
Q

Which protein channel is always on in Liddle’s syndrome?

A

ENaC

61
Q

What is the aldosterone level in Liddle’s syndrome?

A

Normal to low

62
Q

Which brainstem centre regulates blood pressure?

A

Cardio-regulatory centre

63
Q

What is the tonic frequency of baroreceptor firing rate?

A

baroreceptor firing of receptors which tonically suppress sympathetic activity

64
Q

What happens due to reduced baroreceptor firing?

A

There is an upregulation in sympathetic activity and ADH release

65
Q

What happens to the heart rate and stroke volume in response to reduced baroreceptor firing?

A

Increases (SAN and ventricular cardiomyocytes have sympathetic post-ganglionic neurones)

66
Q

Which peptides are released in response to high pressure?

A

ANP and BNP, synthesised in response to atrial stretch

67
Q

What is ANP?

A

A small peptide synthesised within the atria (In addition to BNP)

68
Q

When his ANP released?

A

In response to atrial stretch due to high blood pressure, and circulates in blood where it binds to complementary receptors

69
Q

Which enzyme is activated in response to ANP?

A

Protein kinase G

70
Q

What effect occurs by ANP stimulation?

A

Vasodilation to reduce blood pressure (renal and systemic vessels)

Inhibition sodium reabsorption in the distal nephron

Inhibits renin and aldosterone release

71
Q

What is the overall effect from ANP stimulation?

A

Reduces blood pressure

72
Q

What is volume expansion?

A

An increase in plasma sodium, increasing blood pressure and ECF volume

73
Q

What effect does reduced sympathetic activity have on GFR?

A

Afferent arteriole dilation increasing GFR (to increase sodium and water delivery)

  • Reduces sodium uptake in the PCT and reduce renin-angiotensin and aldosterone levels to reducing sodium reuptake in the distal nephron.
  • Reduced sodium reabsorption –> Reduced water reabsorption (excretion of both).
74
Q

What effect does ANP have on ADH?

A

Suppresses the release of ADH

75
Q

Which ion determines ECF volume?

A

Sodium

76
Q

What is the mechanism of action of ACE-inhibitors?

A

Reduce the conversion of angiotensin-I to angiotensin-II

77
Q

What are the vascular effects of ACEi?

A

Vasodilation - increasing the vascular volume to accommodate and reduce blood pressure

78
Q

What are the diuretic effects of ACEi?

A

Reduces sodium uptake in the PCT

79
Q

What effect does ACEi have on aldosterone?

A

Reduced aldosterone - reduced sodium reabsorption

80
Q

How does mannitol work?

A

• Add substrate that cannot be reabsorbed + increase tubular osmolarity to promote water retention in the filtrate.

81
Q

What is a carbonic anhydrase inhibitor?

A

Carbonic anhydrase activity leads to sodium uptake and proton export in the PCT (urinary acidity)
• Inhibitors –> Inhibits sodium uptake into PCT cells, leading to a greater concentration of sodium in the distal nephron.
• Reduced difference between the tubular and interstitial osmolarity  Reduces water reabsorption.

82
Q

What is the mechanism of action of loop diuretics?

A

Loop diuretics target the triple transporter in the ascending limb of the loop of Henle.
• Inhibit sodium uptake – leading to higher levels of sodium in the distal nephron
• Reduction in the osmolarity of the interstitial fluid.
• Reduce the difference between the tubular and interstitial osmolarity – reduce water reabsorption.

83
Q

What type of diuretic is furosemide?

A

Loop diuretic

84
Q

What is the target and location of thiazides?

A

Sodium chloride transporter

Distal convoluted tubule

85
Q

What is the effect of thiazides?

A

Reduces sodium uptake and increases tubular sodium concentration

86
Q

What is the side effect concerned with thiazides?

A

increase in calcium reabsorption

87
Q

Why is there an increase in calcium reabsorption with using thiazides?

A

Calcium is reabsorbed across the lumen membrane down its concentration gradient that is generated by the activity of the sodium calcium exchanger

Blocking the entyr of sodium into the cell through the Na-Ca exchanger , whilst the Na-K still works means that the return of sodium into the cell via the Na-Ca is increased

This reduces sodium calcium concentration in the cell and therefore increases the potential for calcium to be removed from the tubular fluid

88
Q

How do potassium sparing diuretics work?

A

Inhibitors of aldosterone function (Spironolactone as a MR antagonist)

Decreases sodium reabsorption and subsequently water retention is impaired

89
Q

What risk is associated with Spironolactone?

A

Hyperkalaemic acidosis

90
Q

Which is the main ion intracellularly?

A

Potassium

91
Q

How is a high intracellular potassium ion maintained?

A

By the sodium potassium ATPase

92
Q

What effect does high K+ have?

A

Depolarises membrane, action potentials, heart arrhythmias (Tented T waves).

93
Q

What effect does a low K+ have?

A

Heart arrhythmias (asystole)

94
Q

What effect does insulin have on potassium?

A

Plasma insulin mediates the tissue uptake of potassium

95
Q

How does insulin mediate increased potassium uptake?

A

Stimulates the activity of the sodium proton exchanger which increases intracellular sodium

The increase in intracellular sodium activates sodium potassium ATPase, increasing potassium uptake

96
Q

What % of filtrate potassium is reabsorbed in the proximal convoluted tubule?

A

67%

97
Q

Which factors influence plasma secretion?

A

Plasma potassium, aldosterone, tubular flow rate , and plasma pH

98
Q

Which cells are responsible for plasma potassium?

A

Principal cells

99
Q

How do principal cells increase potassium excretion?

A

Increased activity of the sodium potassium ATPase, and reduce return of potassium into the plasma so increased potassium excretion

100
Q

What type of flow regulates potassium excretion?

A

Tubular flow

101
Q

How does tubular flow regulate potassium excretion ?

A

Activates cilia, activates PDK1

This increases calcium ions within the cell, stimulating the opening of potassium channels on the apical membrane

102
Q

What are the causes of hypokalaemia?

A

Common electrolyte imbalances (20% of hospitalised patients).
• Inadequate dietary intake (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).
 Increases aldosterone synthesis in response to low sodium – thus hypokalaemia.

103
Q

What is Gitelman’s syndrome?

A

• Genetics (Gitelman’s syndrome: Mutation in the Na/Cl transporter in the distal nephron).
 Increases aldosterone synthesis in response to low sodium – thus hypokalaemia.

104
Q

What are the common causes of hyperkalaemia?

A
  • Common electrolyte imbalance present in 1-10% of hospitalised patients.
  • Response to K+ sparing diuretics (spironolactone)
  • ACE-inhibitors
  • Elderly
  • Severe diabetes
  • Kidney disease

BRS 1b (62 decks)

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