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BRS - Year 2 > 💧Urology💧 - Sodium & Potassium Balance > Flashcards

💧Urology💧 - Sodium & Potassium Balance Flashcards

1
Q

What is osmolality?

A

Measure of the solute (particle) concentration in a solution (osmoles/litre)

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2
Q

What is 1 osmole?

A

1 mole of dissolved particles per litre

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3
Q

How are salt and water levels connected?

A

Body fluids have a “constant osmolarity”
Therefore increased salt = increased water

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4
Q

What is the most prevalent ion in plasma and what does this tell us?

A

Sodium
This tells us that sodium is the most important solute in determining ECF volume

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5
Q

What is the connection between dietary sodium and body weight?

A

Increased dietary sodium leads to increased body weight
This is because increased sodium leads to increased water retention

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6
Q

What is the main physiological impact of increased sodium intake?

A

Increased blood volume and therefore pressure

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7
Q

What region of the brain does the mechanisms of sodium intake regulation depend on?

A

Lateral parabrachial nucleus

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8
Q

What occurs in the lateral parabrachial nucleus in the normal state (euvolemia)?

A

Inhibition of Na+ intake through the activity of neurotransmitters including serotonin and glutamate

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9
Q

What occurs in the lateral parabrachial nucleus in sodium deprives states?

A

The appetite for sodium is increased through a separate set of neurotransmitters including GABA and opioids

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10
Q

What is unique about salt as a taste?

A

It is bimodal
At lower levels salt enhances the taste of food but at high concentrations it can make things taste bad (aversive)

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11
Q

Where is sodium reabsorbed in the nephron?

A

67% PCT
25% thick ascending limb
5% DCT
3% is reabsorbed in the collecting ducts
(Less than 1% excreted)

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12
Q

What proportion of renal plasma enters the tubular system?

A

20%

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13
Q

How are GFR and RPF connected?

A

GFR = RPF x 0.2

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14
Q

What issue could arise from the GFR and RPF relationship, and how is this avoided?

A

Blood pressure can increase at times of exercise and if this relationship was maintained you would get an inappropriate level of fluid and sodium loss.
So once you reach about 100mmHg RPF does not increase with increasing BP, preventing this loss

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15
Q

How is high sodium detected?

A

High tubular sodium detected by the macula densa - specialized cells in the distal tubule

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16
Q

Outline the mechanism that occurs when high sodium is detected by the macula densa

A

High tubular sodium detected by the macula densa.
Increased sodium/chloride uptake via the triple transporter
Leads to adenosine release from macula densa cells
Effects on Extraglomerular Mesangial Cells - reduces renin production, promotes afferent SMC contraction
Reduces perfusion pressure and GFR

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17
Q

What is the best way for the body to retain sodium?

A

Filter less fluid through the kidneys

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18
Q

How does the body reduce glomerular filtration?

A

Reduce filtration pressure across the Bowman’s capsule

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19
Q

What is the effect of increased sympathetic activity on the filtration apparatus?

A

Increases retention
Contraction of the afferent arteriole
Increases the uptake of sodium by the cells in the proximal convoluted tubule - by increasing activity of sodium proton exchanger
Activates the production of renin by the juxtaglomerular cells - renin-angiotensin system

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20
Q

When would we see increased sympathetic activity in the kidneys?

A

Exercise
Blood volume/sodium levels are low - need to promote sodium retention

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21
Q

What is the overall impact of sympathetic stimulation on the kidneys?

A

Reduced GFR

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22
Q

What is aldosterone and where is it made?

A

Steroid hormone
Synthesized and released from the adrenal cortex - zona glomerulosa

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23
Q

What stimulates increased aldosterone synthesis?

A

Increased angiotensin II levels

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24
Q

How does increased angiotensin II lead to an increase in aldosterone synthesis?

A

Causes an increase in aldosterone synthase activity

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25
Q

How does aldosterone work?

A

Aldosterone crosses the cell membrane and binds to the mineralocorticoid receptor

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26
Q

What state is the mineralocorticoid receptor in while unbound to aldosterone?

A

A monomer bound to HSP90 and kept in the cytoplasm

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27
Q

What happens to the mineralocorticoid receptor upon binding with aldosterone?

A

MR loses its association with HSP90 and dimerises
Then translocates into the nucleus where it binds to DNA in the promoter region of target genes and stimulates their expression

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28
Q

Name some of the important target genes for aldosterone

A

ENaC (epithelial sodium channel) and Na/K ATPase and their regulatory proteins

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29
Q

What is the overall effect of aldosterone on sodium movement in the cortical collecting duct?

A

Increased movement of sodium into the cell from the tubular fluid
Increased exchange of sodium and potassium (with sodium moving out of the cell) past the basolateral membrane
Overall effect = removal of sodium from tubular fluid

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30
Q

What are the consequences of hypoaldosteronism on sodium?

A

Reabsorption of sodium in the distal nephron is reduced
Increased urinary loss of sodium

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31
Q

What can hypoaldosteronism lead to?

A

Decreased ECF volume
Increased renin, Ang II, ADH
Dizziness
Low BP
Salt cravings
Palpitations

32
Q

What are the consequences of hyperaldosteronism on sodium?

A

Reabsorption of sodium in the distal nephron is increased
Reduced urinary loss of sodium

33
Q

What can hyperaldosteronism lead to?

A

ECF volume increases (hypertension)
Reduced renin, Ang II and ADH
Increased ANP and BNP
High blood pressure
Muscle weakness
Polyuria
Thirst

34
Q

What is Liddle’s syndrome?

A

An inherited disease of high blood pressure.
mutation in the aldosterone activated sodium channel.
-channel is always ‘on’
-Results in sodium retention, leading to hypertension

35
Q

What causes Liddle’s syndrome?

A

A number of mutations can lead to it
A main one alters re-internalisation and degradation of the channel and others change the opening time of the channel

36
Q

How is Liddle’s syndrome different to hyperaldosteronism?

A

Liddle’s syndrome has normal/low aldosterone levels

37
Q

How is blood pressure monitored?

A

Baroreceptors in a range of systems in both the high and low pressure sides of the cardiovascular system

38
Q

Where are baroreceptors located in the low pressure side of the cardiovascular system?

A

Heart - atria and right ventricle
Vascular system - pulmonary vasculature

39
Q

Where are baroreceptors located in the high pressure side of the cardiovascular system?

A

Vascular system - carotid sinus, aortic arch, juxtaglomerular apparatus

40
Q

How does the low pressure side detect and deal with changes in blood pressure?

A
41
Q

How does the high pressure side detect and deal with changes in blood pressure?

A
42
Q

What is ANP?

A

Atrial Natriuretic Peptide
Small peptide made in the atria (also make BNP)
Released in response to atrial stretch (i.e. high blood pressure)

43
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

44
Q

What change occurs within sympathetic activity when the body detects volume expansion?

A

Volume expansion reduces sympathetic activity - afferent arteriolar dilation and increasing GFR
Greater water and sodium excretion

45
Q

What is the body’s overall response to volume expansion?

A

Decreased sympathetic activity
Reduced renin
Reduced sodium and water reabsorption
ANP release compliments these effects

46
Q

What is the body’s response to volume contraction?

A

Increased sympathetic activity
Increased renin
Reduced ANP and BNP
Increased ADH production

47
Q

What is the significance of an osmotic gradient in water reabsorption?

A

Water reabsorption requires an osmotic gradient as we have not evolved pumps for water
We generate a gradient of interstitial osmolarity through the renal medulla
So if you reduce the osmolarity of the interstitium you will reduce water reabsorption similarly if you increase the osmolarity of the tubular fluid you will reduce the difference between the tubular fluid and interstitium and so reduce water reabsorption

48
Q

What is the overall relationship between sodium and blood?

A

Na+ levels determine the ECF volume
Reducing ECF volume reduces BP
Reducing Na+ reabsorption reduces total Na+ levels, ECF volume and BP

49
Q

What are ACE inhibitors?

A

Inhibit angiotensin converting enzyme (ACE)
Reduced angiotensin II

50
Q

What effects will ACE inhibitors have?

A
51
Q

How do carbonic anhydrase inhibitors work?

A

They block the reaction of carbon dioxide/water, reducing production of H+ and HCO3-
Reduces activity of Na+/H+ antiporter, increased Na+ in the distal nephron
Reduced water reabsorption

52
Q

What are loop diuretics?

A

Triple transporter inhibitors
Inhibits Na+/Cl-/K+ transporter in ascending limb
Reduced Na+ reuptake in the LOH
Increased Na+ in the distal nephron
Reduced water reabsorption

53
Q

Give some examples of loop diuretics

A

Furosemide
Bumetanide
Ethacrynic acid

54
Q

What is the mechanism of action of thiazides?

A

Inhibit Na+/Cl- transporter in the early DCT
Reduced Na+ reuptake in the DCT
Increased Na+ in the distal nephron
Reduced water reabsorption
Increased Calcium reabsorption

55
Q

What are potassium sparing diuretics?

A

Inhibitors of aldosterone function
Reduces sodium reabsorption and potassium secretion
(Used to reduce potassium loss caused by loop diuretics)

56
Q

What are the physiological roles of potassium in the body?

A

Potassium is the main intracellular ion (150 mmol/L), extracellular [K+] = 3-5 mmol/L.
Extracellular K+ has effects on excitable membranes (of nerve and muscle).
High K+ : depolarises membranes - action potentials, heart arrhythmias.
Low K+ : heart arrhythmias (asystole)

57
Q

What maintains the high intracellular concentration of potassium?

A

Sodium potassium ATPase

58
Q

What occurs to potassium levels after a meal?

A

Plasma potassium will increase
Needs to be brought down

59
Q

How are plasma potassium levels reduced?

A

Insulin, aldosterone and adrenaline stimulate tissue uptake of potassium
Insulin stimulates activity of Na+/H+ pump, increasing intracellular sodium
Increase in sodium activates Na/K ATPase, increasing intracellular calcium

60
Q

Outline potassium reabsorption in the PCT

A

Proximal Convoluted Tubule (PCT)
Reabsorption: About 67% of filtered potassium is reabsorbed here
Key Point: This process is constant and does not depend on plasma potassium levels

61
Q

Outline potassium reabsorption in the LOH

A

An additional 20% of filtered potassium is reabsorbed, again independent of plasma potassium levels

62
Q

Outline potassium handling in the DCT and collecting duct

A

Highly variable depending on the body’s potassium status.
Potassium Reabsorption (during potassium depletion):
3% in the DCT
9% in the CT
Potassium Secretion (during normal or high potassium levels)

63
Q

What factors influence the amount of potassium secreted in the DCT and collecting duct?

A

Plasma potassium concentration: Higher levels stimulate secretion
Aldosterone: Increases secretion by stimulating potassium channels in the CT
Tubular flow rate: High flow rates enhance secretion
Plasma pH: Acidosis reduces secretion, while alkalosis increases it

64
Q

What are principal cells?

A

Cells in the collecting duct that secrete potassium, primarily in response to increased plasma potassium levels and aldosterone

65
Q

How do principal cells secrete potassium?

A

Increased plasma potassium levels - stimulates Na⁺/K⁺ ATPase activity, pumping K+ into the cell
Increased intracellular potassium causes it to be secreted into tubular lumen via potassium channels

66
Q

How does tubular flow effect K+ excretion?

A

By activating cilia that activate PDK1
This increases Ca2+ in the cell which stimulates the opening of potassium channels on the apical membrane

67
Q

Outline hypokalaemia

A

Hypokalemia one of the most common electrolyte imbalances (seen in up to 20% of hospitalised patients)
Causes:
Inadequate intake
Increased tubular flow rate due to the use of diuretics
Non-renal excretion via vomiting or diarrhoea
Genetics (Gitelman’s syndrome; mutation in the Na/Cl transporter in the distal nephron)

68
Q

Outline hyperkalaemia

A

Common electrolyte imbalance present in 1-10% of hospitalised patients
Causes:
Response to the use of potassium sparing diuretics
ACE inhibitors in the elderly
Severe diabetes (insulin resistance) Kidney disease

69
Q

Why do most diuretics cause an increase in potassium secretion?

A

Increased flow rate detected in the collecting duct - directly stimulates potassium excretion by activating cilia

70
Q

Which diuretic is the exception to those that cause potassium excretion due to increased flow rate?

A

Potassium sparing diuretics - they inhibit aldosterone, so the net effect vs potassium excretion due to tubular flow is a reduced in potassium loss

71
Q

Which diuretic causes a reduced uptake of K+ by the Na/K/Cl transporter?

A

Loop diuretics

72
Q

What effect does increased plasma urea have on ADH secretion?

A

No effect

73
Q

Why does urea have no effect on ADH secretion?

A

Ineffective osmole
Doesn’t cause movement of water, so won’t trigger a signal in the osmoreceptors

74
Q

Loss of function in the UT-B1 transporter will lead to what?

A

Lower osmolarity urine

75
Q

How does loss of function in the UT-B1 transporter lead to more dilute urine?

A

UT-B1 responsible for transporting urea from the medulla into the descending vasa recta, where urea will re-enter the medulla at the ascending vasa recta. This constant cycle ensures there is a constant increased concentration of urea in the medulla.
Without UT-B1, this cycle of urea recycling would stop, and so urea in the kidney would just diffuse away, and dissipate.
Therefore the UT-B1 makes sure there is a constant cycle of urea recycling so the urea does not simply dissipate, therefore loss of UT-B1 function would lead to lower osmolarity urine.

76
Q

How does liver cirrhosis lead to hyperosmotic urine?

A

Increased Vasopressin (ADH) Secretion - due to low effective circulating volume dure to systemic vasodilation - caused by portal hypertension and increased nitric oxide - perceived as hypovolemia
Increased ADH secretion also enhances urea recycling - promotes water reabsorption
Cirrhosis can cause secondary hyperaldosteronism - increases water reabsorption

77
Q
A

BRS - Year 2 (54 decks)

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