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Y2 Urology And Renal > Sodium And Potassium Balance > Flashcards

Sodium And Potassium Balance Flashcards

1
Q

Which part of the brain is central to alter appetite for salt?

A

Lateral Parabrachial nucleus. This region takes information from other areas as well as from neurotransmitters including serotonin and glutamate and in euvolemia the main outcome is inhibition of sodium intake

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2
Q

Salt is often added to food to improve the flavour. Why does salt improve the flavour, but too much salt make food taste bad, and how do we sense this?

A

Salt is one of the 5 basic taste sensations, it is sensed by a specific sense of cells located on the tongue. At low salt concentrations the sensation is positive but as the concentration increases the sensation becomes aversive.

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3
Q

What proportion of filtered sodium load is taken up by
Distal convoluted tubule
Thick ascending limb of the loop of Henle
Proximal convoluted tubule

A

Distal convoluted tubule
About 5%

Thick ascending limb of the loop of Henle
About 25%

Proximal convoluted tubule
About 65%

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4
Q

What proportion of renal blood flow is filtered into the nephrons

A

20%

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5
Q

What is the effect of increased tubular sodium concentration on the juxtaglomerular cells of the macular densa

A

Increased sodium uptake through the Na/K/Cl triple transporter, leading to release of adenosine and ATP

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6
Q

Which cells respond to the adenosine by reducing renin production

A

Extraglomerular mesangial cells

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7
Q

Why does the release of adenosine lead to a reduction in GFR in the short term

A

It causes the afferent SMCs to contract reducing renal plasma flow and therefore GFR

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8
Q

What is the effect of low tubular sodium at the macular densa on the production of Angiotensin II

A

It increases it because it stimulates the production of renin leading to angiotensinogen conversion to AI and finally to AII

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9
Q

Where in the tubular system does aldosterone work?

A

Distal DCT collecting duct

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10
Q

From where is aldosterone released?

A

Adrenal cortex

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11
Q

What is the effect of angiotensin2 on aldosterone release?

A

Increases it

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12
Q

how does aldosterone affect potassium balance?

A

Increases potassium secretion by stimulating sodium uptake: increased Na/K+ ATPase expression will increase the rate of K+ uptake and combined with the increase in Na reabsorption from the lumen (and excretion in to the blood) this will lead to increased K+ excretion

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13
Q

What is the effect og hypoaldosteronism on plasma renin?

A

It causes and increase in plasma renin because of the reduction in sodium reabsorption and the consequent loss of water reducing ECF and therefore BP. This leads to low sodium in the nephron and therefore the release of renin

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14
Q

What are the six major locations of baroreceptors?

A

Atria, right ventricle, pulmonary vasculature, carotid sinus, aortic arch, JGA

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15
Q

What are the effects of atrial natriuretic peptide (ANP) on sodium reabsorption in the PCT?

A

Reduces sodium reabsorption

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16
Q

What proportion of filtered potassium load is reabsorbed by:
Distal convoluted tubule
Thick ascending limb of the loop of Henle
Proximal convoluted tubule

A

Distal convoluted tubule
Variable depending on potassium status ranges from 3% reabsorbed to secretion of 50%

Thick ascending limb of the loop of Henle
About 20%

Proximal convoluted tubule
About 65%

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17
Q

What happens to plasma potasssium after a meal?

A

Initially increases then taken up into cells by Na/K ATPase

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18
Q

Calculate the osmolarity of a solution containing 120mM NaCl, 5mM KCl, 10mM Na2HPO4, 5mM glucose at physiological pH

A

Na = (120 + 20) mM =140 mM
Cl = (120 +5) mM = 125 mM
K = 5 mM
HPO4 = 10mM
Glucose = 5mM

Total = 285mM of ‘particles’ = 285 mosmoles/L

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19
Q

A salmon swims from the sea into its home river. It is covered in small parasitic lice, why do the lice die?

A

The fish moves from a high salt to a low salt region. The sea lice are adapted to a high salt environment but are suddenly exposed to the low salt environment. Their cell membranes are semi-permeable and their extracellular and intracellular osmolarity is normally set to that of sea water. In the low salt environment, they take up water and their extracellular osmolarity drops. Now because their intracellular osmolarity is higher than the external osmolarity their cells take up water and swell. As they cannot regulate their osmolarity well, cell swelling leads to cell death and eventually to death of the parasite.

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20
Q

You are developing a new diuretic drug that targets a specific transporter protein
The effects of the drug in whole animals are as follows
Reduced renin production
Increased sodium excretion to 8% of filtered load
An early reduction in GFR that is prevented by co-treatment with furosemide

Which part of the nephron does this drug work in?
PCT
DCT
Thick Ascending limb of the Loop of Henle
Juxtaglomerular apparatus
Collecting duct

A

The drug acts in the PCT.

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21
Q

Diuretics work by increasing the osmolarity of the tubular fluid. Carbonic anhydrase inhibitors, mannitol, furosemide, are all diuretics that act in nephron segments prior to the juxtaglomerular apparatus. Which of these diuretics would lead to an early reduction in GFR by activating tubulo-glomerular feedback? Carbonic anhydrase inhibitors reduce PCT sodium reabsorption, mannitol is an osmotic diuretic as it is not reabsorbed and furosemide is a loop diuretic.

Mannitol and carbonic anhydrase inhibitors
Furosemide only
Carbonic anhydrase inhibitors and furosemide
Carbonic anhydrase inhibitors only
All three of them

A

Mannitol and carbonic anhydrase inhibitors
Tubuloglomerular feedback requires increased Na load in the distal nephron and a functional NKCCT2

All three give increased Na load (mannitol because it increases flow a bit like an increase in GFR) in the distal nephron. BUT furosemide does this by inhibiting NKCCT2 so this increase can’t be detected by the JGA

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22
Q

T or F: ICF volume varies with osmolarity?

A

F, ECF volume varies with osmolarity - it increases or decreases to maintain constant osmolarity

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23
Q

Which is the most prevalent and important solute in the ECF?

A

Sodium

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24
Q

What does Plasma sodium concentration have an effect on?

A

ECF volume, body weight, blood pressure

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25
Q

Osmolarities of urine are more or less constant than plasma?

A

Less, plasma osmolality is very constant, urine osmolality varies widely

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26
Q

What term describes normal sodium levels?

A

Euvolemia

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27
Q

In euvolemia, what structures are involved in central sodium intake regulation?

A

Lateral parabrachial nucleus
Inhibits sodium intake via response to serotonin and glutamate

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28
Q

In sodium deprivation, what central structure regulates intake and how?

A

Lateral parabrachial nucleus increases appetite for sodium via response to GABA and opioids

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29
Q

As GFR increases what would hypothetically happen to sodium excretion and what mechanism stops this?

A

as GFR increases the amount of sodium excreted would also increase -not very desirable
• GFR is proportional to RPF (renal plasma flow)
• RPF is proportional to blood pressure over a large range (including normal MAP)
• however, blood pressure can increase at times of exercise - if this relationship was maintained you would get aninappropriate level of fluid and sodium loss
• once you reach about 100mmHg RPF does not increase with increasing bp - preventing this loss

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30
Q

What is the best way to retain sodium?

A

To reduce glomerular filtration

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31
Q

The best way to retain sodium is to reduce glomerular filtration, how is this achieved?

A

• by reducing filtration pressure across bowman’s capsule
• can constrict afferent arteriole more than efferent arteriole or relaxing efferent arteriole more than afferent
• leads to less Na+ and water lost

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32
Q

In what three ways is sodium reabsorption/ retention increased?

A

Increased sympathetic activity
Angiotensin2
Tubulo-glomerular feedback

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33
Q

How does increased sympathetic activity increase sodium reabsorption/ retention?

A

• promotes SMC contraction in afferent arteriole
• stimulates sodium uptake by PCT cells
• stimulates renin production from JGA → AT II

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34
Q

How does angiotensin2 act to increase sodium reabsorption/retention?

A

• stimulates sodium uptake by PCT cells
• stimulates aldosterone production → uptake of sodium in DCT and collecting duct

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35
Q

How does tubulo-glomerular feedback act to increase sodium reabsorption/retention?

A

• low tubular Na+ stimulates production of renin
• sympathetic activity overrides SMC relaxation

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36
Q

What mechanism acts to decrease sodium reabsorption?

A

Atrial naturietic peptide?

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37
Q

How does atrial naturietic peptide decrease sodium reabsorption?

A

Promotes dilation of afferent arteriole
Reduces Na uptake by PCT, DCT and collecting duct
Inhibits renin release from JGA

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38
Q

Aldosterone excess can lead to________

A

Hypokalaemic alkalosis

39
Q

How does increased sympathetic activity stimulating the JGA result in the increased synthesis of aldosterone?

A

• Increased sympathetic activity stimulates JGA to release renin
• Renin activity cleaves angiotensinogen to angiotensin I
• Angiotensin I is cleaved by angiotensin converting enzyme to produce angiotensin II
• Angiotensin II stimulates the synthesis of aldosterone synthase in the zona glomerulosa
• Increases the synthesis of aldosterone

40
Q

Aldosterone is what type of hormone?

A

Steroid hormone

41
Q

From where is aldosterone synthesized and released?

A

The zona glomerulosa of the adrenal cortex

42
Q

What stimulates the release of aldosterone?

A

Angiotensin2 (increases aldosterone synthase activity)
Decrease in BP (via baroreceptors)

43
Q

Outline the action of aldosterone

A

Increased sodium reabsorption
Increased potassium secretion
Increased hydrogen ion secretion

44
Q

How does aldosterone act to increase hydrogen ion secretion?

A

Indirectly due to change in voltage (changes in sodium and potassium)
Directly by changing expression of anion exchangers such as H+ATPase

45
Q

Increased potassium secretion through the action of aldosterone is the result of what?

A

Increased sodium absorption

46
Q

When aldosterone crosses the cell membrane, where does it bind to?

A

The mineralocorticoid receptor

47
Q

In the absence of aldosterone what is the mineralocorticoid receptor?

A

• in absence of aldosterone this receptor is a monomerbound to HSP90and kept in the cytoplasm

48
Q

On binding of aldosterone to the mineralocorticoid receptor once the hormone has crossed the cell membrane, what happens to the receptor?

A

on binding the steroid, the MRdissociates from HSP90and dimerises
• translocates into the nucleus
•binds to DNAin the promoter region of target genes
• stimulates their expression

49
Q

What are the three key target genes of aldosterone?

A

Key target genes of aldosterone
• ENaC (epithelial sodium channel)
• sodium potassium ATPase
• sets of regulatory proteins

50
Q

What are the effects of hypoaldosteronism?

A

• reduced reabsorption of sodium in the distal nephron
• increased urinary sodium loss
• reduces water retention
• ECF volume falls
• increased renin, ATII and AD

51
Q

What are the symptoms of hypoaldosteronism?

A

Dizziness, low BP, salt craving, palpitations

52
Q

What are the affects of hyperaldosteronism?

A

• increased reabsorption of sodium in the distal nephron
• reduced urinary sodium loss
• increased sodium and water retention
• ECF volume increases (hypertension
• reduced renin, ATII and ADH
• increased ANP and BNP

53
Q

What are the symptoms of hyperaldosteronism?

A

High BP
Muscle weakness
Polyuria
Thirst

54
Q

What is Liddles syndrome?

A

An inherited disease of high BP, the same phenotype as hyperaldosteronism but low to normal levels of aldosterone

55
Q

What is the underlying cause of Liddles syndrome?

A

Mutation in the aldosterone activated sodium channel meaning EnaC is always on
This results in sodium retention and thus HTN

56
Q

Low pressure side baroreceptors found in the?

A

Atria, right ventricle, pulmonary vasculature

57
Q

High pressure side baroreceptors found in the?

A

Carotid sinus, aortic arch, juxtaglomerular apparatus

58
Q

how do low pressure side baroreceptors respond to low pressure?

A

Reduced firing, signal through afferent fibres to brainstem, sympathetic activity and ADH release

59
Q

How do low pressure side baroreceptors respond to high BP?

A

Atrial stretch resulting in increased ANP and BNP

60
Q

What are ANP and BNP?

A

ANP = atrial natriuretic peptide
BNP = brain natriuretic peptide

61
Q

What is the function of ANP?

A

Causing reduction in ECF volume by increasing renal sodium excretion

62
Q

Where is ANP synthesised?

A

Synthesised and secreted via cardiac muscle cells in the walls of the atria of the heart

63
Q

What is the function of BNP?

A

Similiar to ANP but with lower affinity

64
Q

Where is BNP secreted from?

A

Cardiac muscle cells in the heart ventricles

65
Q

How do high pressure side baroreceptors respond to low BP?

A

Reduced baroreceptor firing, signal through afferent fibres to brainstem resulting in sympathetic activity and ADH release
Increased renin production from JGA

66
Q

What is ANP release in response to?

A

Atrial stretch

67
Q

Outline the mechanism of ANP

A

> binds to receptor> activates guanylyl cyclase> production of cyclic GMP> activates PKG> leads to many cellular responses

68
Q

What are the actions of ANP?

A

• Vasodilatation of renal (and other systemic) blood vessels• Inhibition of sodium reabsorption in proximal tubule and in the collecting ducts• Inhibits release of renin and aldosterone• Reduces blood pressure

69
Q

What is the response to volume expansion?

A

• reduced sympathetic activity• afferent arteriolar dilation• increased GFR• reduced RAAS• reduced sodium and water reabsorption• ANP release compliments these effects

70
Q

how does ANP release compliment the effects seen in the response to volume expansion?

A

> suppressing renin> increasing GFR> inhibiting sodium reuptake in the CT> suppresses the release of ADH

71
Q

Outline the response to volume contraction

A

Increased sympathetic activity
Increased RAAS
Stimulates sodium and water reabsorption
Increased ADH production

72
Q

How does increased sodium excretion reduce BP?

A

> Na+ levels determine the ECF volume
Reducing ECF volume reduces BP
Reducing Na+ reabsorption reduces total Na+ levels, ECF volume and BP
* this has become a major method forBP reduction

73
Q

What are the six key diuretics?

A

ACE inhibitors
Osmotic diuretics
Carbonic anhydrase inhibitors
Loop diuretics
Thiazides
Potassium sparing diuretics

74
Q

What are the basic principles of diuretics?

A

Basic principle of diuretics
- increase osmolarity of tubular fluid in distal nephron
- reduced difference between the tubular and interstitial osmolarity
- reduces water absorption

75
Q

What are the vascular effects of ACE inhibitors?

A

Vasodilation via increased vascular volume and decreased blood pressure

76
Q

What are the direct renal effects of ACE inhibitors? what are the indirect effects following this?

A

Decreased sodium reuptake in PCT, increased sodium in the distal nephron.
Lowers water reabsorption and thus decreases BP

77
Q

What are the adrenal effects of ACE inhibitors?

A

Reduced aldosterone causing indirect renal effects such as reduced sodium uptake in the CCT and increased sodium in the distal nephron.
This acts to decrease water reabsorption and decrease BP

78
Q

How do carbonic anhydrase inhibitors work?

A

• reduced production of H+ and HCO3-• reduced activity of Na+/H+ antiporter• reduced Na+ reabsorption in PCT• increased Na+ in distal nephron• reduced water reabsorption• increased urinary acidity

79
Q

How do loop diuretics such as furosemide work?

A

•inhibits Na+/Cl-/K+ transporter in ascending limb of loop of Henle
• reduced Na+ reuptake in the LOH
• increased Na+ in the distal nephron
• reduced water reabsorption

80
Q

How do thiazides work?

A

• inhibit Na+/Cl- transporter in early DCT• reduced Na+ reuptake in the DCT• increased Na+ in the distal nephron• reduced water reabsorption• increased Ca2+ reabsorption

81
Q

How do potassium sparing diuretics work?

A

• Inhibitors of aldosterone function (e.g. spironolactone)
• reduces sodium reabsorption and potassium secretion

82
Q

What is the main intracellular cation?

A

Potassium

83
Q

What are the effects of high potassium on excitable membranes such as nerve and muscle?

A

Depolarises membranes, action potentials, heart arrhythmias

84
Q

What are the effects of low pottasium on excitable membranes such as nerves and muscles?

A

Heart arrhythmias - asystole

85
Q

How does potassium enter the body?

A

• Potassium is present in most/all foods (especially unprocessed)
• after a meal plasma potassium will increase
• needs to be brought down
• insulin, aldosterone and adrenaline stimulates tissue uptake of K+

86
Q

What affect does insulin have on both sodium and potassium?

A

• Insulinstimulatesthe activity of thesodium proton exchanger
• Increases intracellular sodium
• Increase in intracellular sodium activates thesodium potassium ATPase
• Increases potassium uptake

87
Q

How does potassium reabsorption vary along the nephron?

A

Normal and increased potassium intake• 67% in PCT• 20% in LOH• in DCT and collecting duct there is potassium secretion• 15-80% is secreted in totalPotassium depletion• potassium will be reabsorbed in DCT and collecting duct not secreted

88
Q

What is potassium secretion stimulated by?

A

Increased plasma potassium
Increased aldosterone
Increased tubular flow rate
Increased plasma pH

89
Q

What is the effect of increased plasma potassium in principal cells?

A

Leads to increased activity of the sodium/potassium ATPase
Results in reduced return of potassium into the plasma and increased potassium excretion
Change in membrane potential will also help to stimulate secretion

90
Q

How does tubular flow regulate K+ excretion?

A

• distal cells haveprimary cilia
• cilia stimulate PDK1
• increases Ca2+ in the cell
• stimulates opening of K+ channels in apical membrane

91
Q

What are the causes of hypokalaemia?

A

Inadequate dirty intake
Diuretics
Surreptitious vomiting
Diarrhoea
Genetics

92
Q

What genetics can cause hypokalaemia?

A

Gitelmans syndrome - mutation in the Na/Cl transporter in the distal nephron

93
Q

What are the causes of hyperkalaemia?

A

Seen in response to potassium sparing diuretics
ACE inhibitors
Elderly
Severe diabetes - insulin resistance
Kidney disease

Y2 Urology And Renal (7 decks)

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