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Urology and renal medicine > sodium and potassium balance > Flashcards

sodium and potassium balance Flashcards

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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
If aldoesterone is in excess, what state is induced?
Hypokalaemic alkalosis
26
How does hypoaldosteronism lead to increased renin, angiotensin II and ADH?
Reabsorption of sodium in distal nephron is reduced → increased urinary loss of sodium → ECF volume falls → increased renin, angiotensin II and ADH
27
What symptoms does this lead to in hypoaldosteronism?
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
28
What 2 proteins are increased as a result of hyperaldosteronism?
ANP and BNP secondary to the increased ECF volume as there is less urinary loss of sodium
29
What does BNP stand for what does it do?
Brain natriuretic peptide- Cardiac neurohormone biomarker that is secreted from ventricles when they are under increased pressure and stress.
30
Liddle’s syndrome is an inherited disease of what?
(MUTATED EPITHELIAL SODIUM CHANNEL, ALWAYS ON- TOO MUCH SODIUM REABSORBED) High blood pressure
31
What is the cause of Liddle’s syndrome?
Mutation in the aldosterone activated epithelial sodium channel This means that the channel is always ‘on’
32
When hypertension is resistant to diuretics, what is then used?
Spironolactone - a potassium sparing MR antagonist
33
In the heart where are the baroreceptors that respond to low pressure?
Atria, Right Ventricle
34
In the vascular system where are the baroreceptors that respond to low pressure?
Pulmonary vasculature
35
In the vascular system where are the baroreceptors that respond to high pressure?
Carotid sinus Aortic arch Juxtaglomerular apparatus
36
In the low pressure side, how is low pressure dealt with?
Low pressure → Reduced baroreceptor firing → Signal through Afferent fibres to brainstem → Sympathetic activity & ADH Release
37
How does the low pressure side deal with high pressure?
High pressure → Atrial stretch → ANP, BNP released
38
In what 2 ways is low pressure dealt with in high pressure side?
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
Where is ANP anti natriuretic peptide made?
Atria
40
What is ANP released in response to?
Atrial stretch
41
Atrial Natriuretic Peptide leads to the activation of what protein?
Protein kinase G
42
What are these cellular responses as a result of protein kinase G activation?
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
What is the response to volume expansion within the nephron?
44
What is the response to volume contraction within the nephron?
45
What would be the effect on water reabsorption of increased sodium levels reaching the collecting duct and why?
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
Through what 3 mechanisms do ACE inhibitors reduce blood pressure?
47
Explain the mechanism of osmotic diuretics
Give something that will be filtered but not get reabsorbed This means that the osmolarity of the nephron will increase
48
Where do osmotic diuretics have the greatest effect?
In the PCT, (where most water reabsorption occurs)
49
Where do carbonic anhydrase inhibitors act?
PCT as carbonic anhydrase is most active here
50
How does carbonic anhydrase help to increase water reabsorption in the PCT
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
Where do loop diuretics work?
Thick, ascending limb of loop of Henle
52
Where do thiazide diuretics work?
DCT
52
Where do thiazide diuretics work?
DCT
53
Where do K+ sparing diuretics work?
In the collecting duct
54
What effect does carbonic anyhdrase have on Na+ re-absorption?
It increases sodium reabsorption
55
How do carbonic anhydrase inhibitors work?
-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
How does carbonic anydrase inhibitor affect urinary pH?
Increases it as there is less H+ in the tubular fluid
57
How do loop diuretics work?
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
How do Thiazide diuretics work?
Inhibit Na+/Cl- symporter and this reduces Na+ reuptake in the DCT Increased Na+ in the distal nephron Reduced water reabsorption
59
Where is the Na+/Cl- symporter found and what affects it?
In the DCT, thiazide diuretics affect it.
60
What other effect do thiazide diuretics have?
Increases calcium reabsorption into the blood.
60
How do thiazide diuretics increase calcium reabsorption into the blood
-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
How do K+ sparing diuretics work?
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
What is the main intracellular ion?
K+
63
What affects does low K+ have on the heart?
Heart arrythmias - asystole
64
What is K+ uptake into tissue from plasma stimulated by?
Insulin mainly Also aldosterone and adrenaline
65
How does insulin stimulate K+ uptake after dietary intake?
Indirectly
66
Where is most of the K+ reabsorbed from in the nephron?
PCT
67
How much K+ is reabsorbed from the Thick Ascending Loop of Henle and what transporter allows this?
20% Na+K+2Cl- triple transporter
68
Where is K+ secreted from into the nephron tubule?
DCT - 10-50% CCD - 5-30%
69
What 4 factors stimulate K+ secretion from CCD and DCT?
-Increased aldosterone -Increased tubular flow rate -Increased plasma pH -Increased plasma K+
70
In K+ depletion, how does the reabsorption of K+ change?
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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