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BRS Phase 1b > Sodium and Potassium Balance > Flashcards

Sodium and Potassium Balance Flashcards

1
Q

Define Osmolarity:

A

measure of the solute (particle) concentration in a solution.

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2
Q

Define 1 Osmole:

A

1 mole of dissolved particles per litre.

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3
Q

What is normal plasma osmolarity?

A

285-295 mosmol/L

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4
Q

What is normal Sodium osmolarity in the ECF?

A

140 mosmol/L

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5
Q

How does increased sodium intake lead to increased blood pressure?

A

Increased sodium intake leads to increased total body sodium and increased osmolarity (doesn’t happen though due to semipermeable membranes) which leads to increased water intake and retention and so increased ECF volume, and therefore increased blood volume and pressure.

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6
Q

Where is central sodium intake regulated?

A

Lateral parabrachial nucleus

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7
Q

What inhibits sodium intake?

A

Serotonin, Glutamate.

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8
Q

What increases appetite for sodium?

A

GABA, Opiods.

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9
Q

What is the peripheral regulation of Sodium?

A

Taste

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10
Q

Where is Sodium reabsorbed in the Kidney Nephron?

A 
67% - Proximal Convoluted tubule
25% - Thick ascending limb of loop of Henle
5% - Distal Convoluted tubule
3% - Collecting duct
1% - Excreted
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11
Q

What percentage of Renal Plasma enters the tubular system?

A

20%

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12
Q

What is the relationship between RPF, GFR and arterial blood pressure?

A

RPF & GFR are proportional to arterial blood pressure, however at a certain point they plateau, for example when blood pressure is raised when you are exercising
, this ensures that you don’t lose too much sodium.

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13
Q

What is the short term response to reduce GFR?

A

Macula densa cells detect high Na+ and increase Na+ & Cl- uptake via triple transporter. Adenosine released by macula densa causes extraglomerular mesangial cells to interact with smooth muscle cells and contract, reducing GFR. Adenosine also leads to a reduction in renin being reduced for a short time.

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14
Q

What is the short term response to retaining sodium?

A

Filter less. Increase pressure gradient in arteriole so that less is filtered via the nephron.

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15
Q

What are the mechanisms for longer term increased sodium retention?

A

Sympathetic activity - contracts smooth muscle of afferent arteriole, stimulates sodium re-uptake in PCT and juxtaglomerular apparatus to produce Renin. Renin will lead to production of Angiotensin 2.
Angiotensin 2 - Stimulates sodium re-uptake in PCT and adrenal glands to produce aldosterone, stimulating sodium re-uptake in DCT &CT.
Low tubular Na+ will also stimulate renin production.

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16
Q

What are the mechanisms for longer term decreased sodium retention?

A

Atrial naturietic peptide - Acts as a vasodilator, suppresses sodium re-uptake in PCT, DCT & CT. Suppresses renin production in juxtaglomerular apparatus.

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17
Q

What happens when sodium levels are low?

A

Increased - beta-sympathetic activity, renin, angiotensin 1&2, aldosterone, vasoconstriction, NaCl reabsorption.
Decreased - blood pressure, fluid volume.

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18
Q

What happens when sodium levels are high?

A

Increased - blood pressure, fluid volume.

Decreased -beta-sympathetic activity, renin, angiotensin 1&2, aldosterone, vasoconstriction, NaCl reabsorption.

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19
Q

What is Aldosterone?

A

Steroid hormone produced in response to Angiotensin 2 , increases blood pressure.

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20
Q

How does Angiotensin 2 stimulate aldosterone synthesis?

A

Promotes synthesis of aldosterone synthase, which is involved in the last 2 steps of aldosterone production.

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21
Q

What is the function of Aldosterone in the Kidney nephron?

A

Increase Sodium reabsorption.
Increase Potassium secretion.
Increase Hydrogen ion secretion.

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22
Q

What can excess Aldosterone lead to?

A

hypokalaemic alkalosis

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23
Q

How does Aldosterone work?

A

Lipid soluble, so it can pass through the semipermeable membrane. Once inside the cell it binds to a steroid hormone receptor within the cytoplasm, normally bound to HSP90 protein. Receptor will dimerise, allowing translocation into the nucleus, bind to DNA and stimulate production for mRNAs for genes that are under its control. e.g sodium channel, sodium potassium ATPase, as well as regulatory proteins that stimulate activity of these channels. not just more channels, but more active channels as well.

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24
Q

What happens in Hypoaldosteronism?

A

Reduced sodium reabsorption, increased urinary loss of sodium, ECF volume falls.
symptoms - low blood pressure, dizziness, salt cravings, palpitations.

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25
Q

What happens in Hyperaldosteronism?

A

Increased sodium reabsorption, reduced urinary loss of sodium, ECF volume increases.
symptoms - high blood pressure, muscle weakness, thirst, polyuria.

26
Q

What is Liddles syndrome?

A

looks like hyperaldosteronism, high blood pressure without high aldosterone levels. mutation in aldosterone activated sodium channel, increased sodium reabsorption, hypotension.

27
Q

Where are low pressure Baroreceptors found?

A

Atria, right ventricle, pulmonary vasculature.

28
Q

Where are high pressure Baroreceptors found?

A

Carotid sinus, aortic arch, juxtaglomerular apparatus.

29
Q

What is the low pressure Baroreceptor response to low blood pressure?

A

Reduced Baroreceptor firing, signal through Afferent fibres to the Brainstem, sympathetic activity & ADH release.

30
Q

What is the low pressure Baroreceptor response to high blood pressure?

A

Atrial stretch, ANP & BNP released.

31
Q

What is the high pressure Baroreceptor response to low blood pressure?

A

Reduced Baroreceptor firing, signal through Afferent fibres to the Brainstem, sympathetic activity & ADH release.
Juxtaglomerular cell apparatus activity induced, renin released.

32
Q

What is Atrial Natiuretic peptide ANP?

A

small peptide made in the atria, released in response to atrial stretch (high blood pressure).

33
Q

What is the mechanism of action for ANP?

A

ANP binds to Guanylyl cyclase receptor which converts GTP to cGMP, this activates protein kinase G which activates cellular responses.

34
Q

What are the actions of ANP?

A

Vasodilation of renal and other systemic blood vessels.
Inhibition of sodium reabsorption in the PCT and CT.
Inhibits renin and aldosterone release.
Reduces blood pressure.

35
Q

What effect does increased sodium excretion have on ECF volume and blood pressure?

A

Reduces both.

36
Q

What do ACE inhibitors do?

A

Reduce Angiotensin 2 by inhibition of angiotensin converting enzyme which converts angiotensin 1 to 2.

37
Q

What are the vascular effects of ACE inhibitors?

A

Vasodilation, increase vascular volume therefore decreasing blood pressure.

38
Q

What are the direct renal effects of ACE inhibitors?

A

Reduce Sodium re-uptake in the PCT increasing sodium in the distal nephron, this decreases water reabsorption and therefore blood pressure.

39
Q

What are the indirect renal effects of ACE Inhibitors?

A

Reduces aldosterone, reduced Sodium re-uptake in the CCT increasing sodium in the distal nephron, this decreases water reabsorption and therefore blood pressure.

40
Q

Give some examples of diuretics that do not interfere with sodium re-uptake?

A

Osmotic diuretics - effect PCT, increases osmolarity, less water reabsorption.
Carbonic anhydrase inhibitors, Loop diuretics, thiazide diuretics, K+ sparing diuretics.

41
Q

What is the effect of Carbonic anhydrase inhibitors?

A

Reduced NA+ re-uptake in PCT,
Increased Na+ in distal nephron,
Less Water reabsorbed & less acidic urine.

42
Q

What is the effect of Loop diuretics (furosemide)?

A

Block Na+Cl-K+triple transporter,
Reduced NA+ re-uptake in LOH,
Increased Na+ in distal nephron,
Less Water reabsorbed.

43
Q

What is the effect of thiazide diuretics?

A

Block Na+Cl- co-transporter in the DCT,
Reduced NA+ re-uptake in DCT,
Increased Na+ in distal nephron,
Less Water reabsorbed.

44
Q

What is the effect of thiazide diuretics on Ca2+ re-absorption?

A

Increased Ca2+ re-absorption due to greater Na+ externally so greater gradient, so Ca2+Na+ co-transporter moves Ca2+ out of cell, leading to Cl2+ gradient , bringing Ca2+ into the cell via Ca2+ channel.

45
Q

What is the effect of Potassium sparing diuretics?

A

Inhibitors of aldosterone function e.g spironolactone. K+ is spared as less Na2+ is taken into the cell so less K+ leaves.

46
Q

What is the main intracellular ion?

A

K+, 150mmol/L

47
Q

What is the intracellular concentration of K+?

A

3-5 mmol/L

48
Q

What does extracellular potassium have an effect on?

A

Excitable membranes e.g nerve and muscle fibres.

49
Q

What is the effect of high K+?

A

depolarises membranes - action potentials, heart arrhythmias.

50
Q

What is the effect of low K+?

A

heart arrhythmias - asystole.

51
Q

What stimulates K+ uptake into tissue cells after a meal?

A

Insulin

aldosterone & adrenaline also but not mainly

52
Q

How does insulin indirectly cause K+ increased uptake by tissue cells?

A

stimulates Na+H+ exchanger, increasing intracellular Na+ concentration, Na+K+-ATPase is activated bringing more K+ into the cell.

53
Q

Where is K+ reabsorbed in the Kidney nephron?

A

PT - 67%

Thick ascending limb - 20%

54
Q

Where is the Na+K+Cl- triple transporter found?

A

Thick ascending limb.

55
Q

Where is K+ secreted?

A

DT - 10-50%

CCD - 5-30%

56
Q

What 4 factors stimulate increased K+ secretion?

A

Increased Aldosterone
Increased Plasma pH
Increased Tubular flow rate
Increased Plasma [K+]

57
Q

How does Increased Plasma [K+] lead to increased K+ secretion?

A

More K+ enters cell via Na+K+ co-transporter, more K+ leaves cell via K+ channel due to increased concentration gradient. effect on membrane potential also helps K+ secretion.

58
Q

How does increased tubular flow effect K+ secretion?

A

primary cilia on cells stimulates PDK1 which increases [Ca2+] in the cell, which stimulate opening of K+ channel allowing K+ to leave the cell.

59
Q

What is Hypokalaemia?

A

One of the most common electrolyte imbalances, seen in up to 20% of hospitalised patients. Caused by; Inadequate dietary intake (too much processed food), Diuretics ( increased tubular flow rates), Surreptitious vomiting, Diarrhoea, Genetics, e.g. Gitelman’s syndrome; mutation of the Na/Cl transporter in the distal nephron.

60
Q

What is Hyperkalemia?

A

Common electrolyte imbalance in 1-10% of hospitalised patients. Caused by; K+ sparing diuretics, ACE inhibitors, Elderly, Severe diabetes, Kidney disease.

BRS Phase 1b (80 decks)

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