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Urology and renal medicine > sodium and potassium balance > Flashcards

sodium and potassium balance Flashcards

1
Q

What allows the homeostatic set point of plasma osmolarity?

A

Semi-permeable membranes allowing movement of H20

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2
Q

What is the normal plasma osmolarity?

A

285-295mosmol/L

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3
Q

What is the most prevalent and important solute in ECF?

A

Sodium, 140mmol/L

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4
Q

Is potassium concentration low or high in ECF?

A

Low 4mmol/L

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5
Q

What is euvolemia?

A

State of normal body fluid volume

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6
Q

At euvolemia, what effect is had on Na+ intake and through what nucleus does this occur in?

A

Inhibition of Na+ intake through the lateral parabrachial nucleus

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7
Q

What neurotransmitters does lateral parabrachial nucleus cells respond to when inhibiting Na+ intake

A

-Serotonin
-Glutamate

(SING) - Serotonin- inhibit- glutamate

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8
Q

What neurotransmitters does the lateral parabrachial nucleus respond to when increasing appetite for Na+?

A

-GABA
-Opioids

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9
Q

Other than the central lateral parabrachial nucleus control of Na+ intake, what peripheral level controls Na+ intake?

A

Taste, more Na+ → aversive (less tasty)

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10
Q

Where is most of the Na+ reabsorbed in the nephron?

A

PCT, 67%

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11
Q

How much Na+ is reabsorbed in the descending and and ascending limb of the nephron respectively?

A

-None in descending
-25 % in thick part of ascending

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12
Q

What percent of renal plasma enters the tubular system and therefore how do you calculate GFR from renal plasma flow?

A

20%

GFR = RPF x 0.2

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13
Q

What senses high tubular sodium?

A

Macula densa

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14
Q

What are 3 main physiological mechanisms that increase Na+ reabsorption and retention?

A

-Increased sympathetic activity
-Angiotensin II
-Low tubular Na+

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15
Q

How does an increase in sympathetic activity work to increase NA+ reabsorption and retention?

A

-Stimulates SMC of afferent arteriole so less is filtered
-Stimulates Sodium uptake from cells of the PCT
-Stimulates juxtaglomerular apparatus to release Renin which forms angiotensin II

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16
Q

How does angiotensin II work to increase Na+ reabsorption and retention?

A

-Stimulates sodium uptake from cells of PCT
-Stimulates aldosterone synthesis
-Stimulates Na+ reabsorption from the collecting duct

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17
Q

How does low tubular Na+ stimulate its own reabsorption/retention?

A

-Stimulates the release of Renin which is converted into angiotensin II.

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18
Q

What reduces Na+ reabsorption and retention and how does it do this?

A

Vasodilators - reduces afferent arteriolar pressure so more is filtered to be excreted

ANP (anti natriuretic peptide)- Decreases uptake of Na+ from PCT, DCT, CT

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19
Q

How does low sodium affect Beta1 sympathetic activity?

A

Decreased sodium → Decreased volume → Decreased BP → Increased Beta1 sympathetic activity

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20
Q

What does decreased Beta1 sympathetic activity due to high sodium induce?

A

Atrial natriuretic peptide

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21
Q

Where is aldosterone released from?

A

Zona glomerulosa in adrenal cortex

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22
Q

What 2 factors can aldosterone release be triggered by?

A

Angiotensin II
OR
Decrease in blood pressure via baroreceptors

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23
Q

How is aldosterone release triggered by increased sympathetic activity?

A

Increased sympathetic activity stimulates the cells of the juxtaglomerular apparatus to release renin.
-Renin cleaves angiotensinogen to angiotensin I
-Angiotensin I is converted to angiotensin II by ACE
-Angiotensin II stimulates aldosterone synthase

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24
Q

In the collecting duct and DCT, what does Aldosterone trigger the reabsorption of and what 2 effects will this have?

A

Increased Na+ reabsorption - 35g Na/day

Increased K+ secretion due to reabsorption of Na+ via basolateral Na+/K+ ATPase co-transporter and then secretion into lumen

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25
Q

If aldoesterone is in excess, what state is induced?

A

Hypokalaemic alkalosis

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26
Q

How does hypoaldosteronism lead to increased renin, angiotensin II and ADH?

A

Reabsorption of sodium in distal nephron is reduced → increased urinary loss of sodium → ECF volume falls → increased renin, angiotensin II and ADH

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27
Q

What symptoms does this lead to in hypoaldosteronism?

A

Low blood pressure

Dizziness

Salt cravings - due to reduction of salt

Palpitations - due to change in membrane potential as a result of decreased salt and so there is more norepinephrine release

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28
Q

What 2 proteins are increased as a result of hyperaldosteronism?

A

ANP and BNP secondary to the increased ECF volume as there is less urinary loss of sodium

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29
Q

What does BNP stand for what does it do?

A

Brain natriuretic peptide- Cardiac neurohormone biomarker that is secreted from ventricles when they are under increased pressure and stress.

30
Q

Liddle’s syndrome is an inherited disease of what?

A

(MUTATED EPITHELIAL SODIUM CHANNEL, ALWAYS ON- TOO MUCH SODIUM REABSORBED) High blood pressure

31
Q

What is the cause of Liddle’s syndrome?

A

Mutation in the aldosterone activated epithelial sodium channel

This means that the channel is always ‘on’

32
Q

When hypertension is resistant to diuretics, what is then used?

A

Spironolactone - a potassium sparing MR antagonist

33
Q

In the heart where are the baroreceptors that respond to low pressure?

A

Atria, Right Ventricle

34
Q

In the vascular system where are the baroreceptors that respond to low pressure?

A

Pulmonary vasculature

35
Q

In the vascular system where are the baroreceptors that respond to high pressure?

A

Carotid sinus

Aortic arch

Juxtaglomerular apparatus

36
Q

In the low pressure side, how is low pressure dealt with?

A

Low pressure → Reduced baroreceptor firing → Signal through Afferent fibres to brainstem → Sympathetic activity & ADH Release

37
Q

How does the low pressure side deal with high pressure?

A

High pressure → Atrial stretch → ANP, BNP released

38
Q

In what 2 ways is low pressure dealt with in high pressure side?

A

Low pressure → Reduced baroreceptor firing → Signal through Afferent fibres to brainstem → Sympathetic activity and ADH Release

Low pressure → Reduced baroreceptor firing → JGA cells → Renin released

39
Q

Where is ANP anti natriuretic peptide made?

A

Atria

40
Q

What is ANP released in response to?

A

Atrial stretch

41
Q

Atrial Natriuretic Peptide leads to the activation of what protein?

A

Protein kinase G

42
Q

What are these cellular responses as a result of protein kinase G activation?

A

Vasodilatation of renal (and other systemic) blood vessels

Inhibition of Sodium reabsorption in PCT and in the CT

Inhibits release of renin and aldosterone

Reduces blood pressure

43
Q

What is the response to volume expansion within the nephron?

A
44
Q

What is the response to volume contraction within the nephron?

A
45
Q

What would be the effect on water reabsorption of increased sodium levels reaching the collecting duct and why?

A

Increased Na+ in the collecting duct means there is increased osmolarity and so it is more difficult to reabsorb water since water will migrate via osmosis into the collecting duct since there is a higher osmolarity here

46
Q

Through what 3 mechanisms do ACE inhibitors reduce blood pressure?

A
47
Q

Explain the mechanism of osmotic diuretics

A

Give something that will be filtered but not get reabsorbed

This means that the osmolarity of the nephron will increase

48
Q

Where do osmotic diuretics have the greatest effect?

A

In the PCT, (where most water reabsorption occurs)

49
Q

Where do carbonic anhydrase inhibitors act?

A

PCT as carbonic anhydrase is most active here

50
Q

How does carbonic anhydrase help to increase water reabsorption in the PCT

A

By generating bicarbonate ions, (HCO3-) carbonic anhydrase helps to create an electrochemical gradient that promotes the reabsorption of sodium and other ions from the tubular fluid back into the bloodstream.

51
Q

Where do loop diuretics work?

A

Thick, ascending limb of loop of Henle

52
Q

Where do thiazide diuretics work?

A

DCT

52
Q

Where do thiazide diuretics work?

A

DCT

53
Q

Where do K+ sparing diuretics work?

A

In the collecting duct

54
Q

What effect does carbonic anyhdrase have on Na+ re-absorption?

A

It increases sodium reabsorption

55
Q

How do carbonic anhydrase inhibitors work?

A

-They decrease the action of carbonic anhydrase in the PCT which means less CO2 and H2O gets absorbed into the tubule cell.

-The CO2 and water combine into carbonic acid then dissolve into H+ and Bicarbonate HCO3-

-H+ leaves the tubule into the urine/tubular fluid and a Na+ gets reabsorbed

-Carbonic anhydrase stops all this.

56
Q

How does carbonic anydrase inhibitor affect urinary pH?

A

Increases it as there is less H+ in the tubular fluid

57
Q

How do loop diuretics work?

A

Triple transporter inhibitors - prevent reabsorption of Na+, Cl-, K+

Reduced Na+ reuptake in Loop of Henle

Increased Na+ in the distal nephron

Reduced water reabsorption

58
Q

How do Thiazide diuretics work?

A

Inhibit Na+/Cl- symporter and this reduces Na+ reuptake in the DCT

Increased Na+ in the distal nephron

Reduced water reabsorption

59
Q

Where is the Na+/Cl- symporter found and what affects it?

A

In the DCT, thiazide diuretics affect it.

60
Q

What other effect do thiazide diuretics have?

A

Increases calcium reabsorption into the blood.

60
Q

How do thiazide diuretics increase calcium reabsorption into the blood

A

-The sodium potassium ATPase on the basal lateral membrane is unaffected by by the thiazide diuretics.

-To balance all the Sodium leaving the tubule, more sodium gets brought in into the tubule from the blood through the Na+/Ca+ antiporter on the bl membrane which pump Ca+ into the blood.

61
Q

How do K+ sparing diuretics work?

A

Inhibits aldosterone function (spironolactone)

This means there is less reuptake of Na+ in the DCT via the epithelial Na+ channels in the principal cells of the DCT.

The lack of sodium coming in means less K+ leaves as there is less need to balance charges

62
Q

What is the main intracellular ion?

A

K+

63
Q

What affects does low K+ have on the heart?

A

Heart arrythmias - asystole

64
Q

What is K+ uptake into tissue from plasma stimulated by?

A

Insulin mainly

Also aldosterone and adrenaline

65
Q

How does insulin stimulate K+ uptake after dietary intake?

A

Indirectly

66
Q

Where is most of the K+ reabsorbed from in the nephron?

A

PCT

67
Q

How much K+ is reabsorbed from the Thick Ascending Loop of Henle and what transporter allows this?

A

20%

Na+K+2Cl- triple transporter

68
Q

Where is K+ secreted from into the nephron tubule?

A

DCT - 10-50%

CCD - 5-30%

69
Q

What 4 factors stimulate K+ secretion from CCD and DCT?

A

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

70
Q

In K+ depletion, how does the reabsorption of K+ change?

A

Instead of being secreted, in the DCT and CCD, it is reabsorbed from the tubular fluid

This leads to less K+ being excreted

Urology and renal medicine (5 decks)

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