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

💧Urology💧- Sodium & Potassium Balance Flashcards

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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, RPF and BP 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
How does aldosterone work?
Aldosterone crosses the cell membrane and binds to the mineralocorticoid receptor
26
What state is the mineralocorticoid receptor in while unbound to aldosterone?
A monomer bound to HSP90 and kept in the cytoplasm
27
What happens to the mineralocorticoid receptor upon binding with aldosterone?
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
28
Name some of the important target genes for aldosterone
ENaC (epithelial sodium channel) and Na/K ATPase and their regulatory proteins
29
What is the overall effect of aldosterone on sodium movement in the cortical collecting duct?
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
30
What are the consequences of hypoaldosteronism on sodium?
Reabsorption of sodium in the distal nephron is reduced Increased urinary loss of sodium
31
What can hypoaldosteronism lead to?
Decreased ECF volume Increased renin, Ang II, ADH Dizziness Low BP Salt cravings Palpitations
32
What are the consequences of hyperaldosteronism on sodium?
Reabsorption of sodium in the distal nephron is increased Reduced urinary loss of sodium
33
What can hyperaldosteronism lead to?
ECF volume increases (hypertension) Reduced renin, Ang II and ADH Increased ANP and BNP High blood pressure Muscle weakness Polyuria Thirst
34
What is Liddle's syndrome?
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
What causes Liddle's syndrome?
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
How is Liddle's syndrome different to hyperaldosteronism?
Liddle's syndrome has normal/low aldosterone levels
37
How is blood pressure monitored?
Baroreceptors in a range of systems in both the high and low pressure sides of the cardiovascular system
38
Where are baroreceptors located in the low pressure side of the cardiovascular system?
Heart - atria and right ventricle Vascular system - pulmonary vasculature
39
Where are baroreceptors located in the high pressure side of the cardiovascular system?
Vascular system - carotid sinus, aortic arch, juxtaglomerular apparatus
40
How does the low pressure side detect and deal with changes in blood pressure?
41
How does the high pressure side detect and deal with changes in blood pressure?
42
What is ANP?
Atrial Natriuretic Peptide Small peptide made in the atria (also make BNP) Released in response to atrial stretch (i.e. high blood pressure)
43
What are the actions of ANP?
-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
What change occurs within sympathetic activity when the body detects volume expansion?
Volume expansion reduces sympathetic activity - afferent arteriolar dilation and increasing GFR Greater water and sodium excretion
45
What is the body's overall response to volume expansion?
Decreased sympathetic activity Reduced renin Reduced sodium and water reabsorption ANP release compliments these effects
46
What is the body's response to volume contraction?
Increased sympathetic activity Increased renin Reduced ANP and BNP Increased ADH production
47
What is the significance of an osmotic gradient in water reabsorption?
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
What is the overall relationship between sodium and blood?
Na+ levels determine the ECF volume Reducing ECF volume reduces BP Reducing Na+ reabsorption reduces total Na+ levels, ECF volume and BP
49
What are ACE inhibitors?
Inhibit angiotensin converting enzyme (ACE) Reduced angiotensin II
50
What effects will ACE inhibitors have?
51
How do carbonic anhydrase inhibitors work?
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
What are loop diuretics?
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
Give some examples of loop diuretics
**Furosemide** Bumetanide Ethacrynic acid
54
What is the mechanism of action of thiazides?
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
What are potassium sparing diuretics?
Inhibitors of aldosterone function Reduces sodium reabsorption and potassium secretion (Used to reduce potassium loss caused by loop diuretics)
56
What are the physiological roles of potassium in the body?
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
What maintains the high intracellular concentration of potassium?
Sodium potassium ATPase
58
What occurs to potassium levels after a meal?
Plasma potassium will increase Needs to be brought down
59
How are plasma potassium levels reduced?
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 potassium
60
Outline potassium reabsorption in the PCT
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
Outline potassium reabsorption in the LOH
An additional 20% of filtered potassium is reabsorbed, again independent of plasma potassium levels
62
Outline potassium handling in the DCT and collecting duct
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
What factors influence the amount of potassium secreted in the DCT and collecting duct?
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
What are principal cells?
Cells in the collecting duct that secrete potassium, primarily in response to increased plasma potassium levels and aldosterone
65
How do principal cells secrete potassium?
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
How does tubular flow effect K+ excretion?
By activating cilia that activate PDK1 This increases Ca2+ in the cell which stimulates the opening of potassium channels on the apical membrane
67
Outline hypokalaemia
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
Outline hyperkalaemia
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
Why do **most** diuretics cause an increase in potassium secretion?
Increased flow rate detected in the collecting duct - directly stimulates potassium excretion by activating cilia
70
Which diuretic is the exception to those that cause potassium excretion due to increased flow rate?
Potassium sparing diuretics - they inhibit aldosterone, so the net effect vs potassium excretion due to tubular flow is a reduction in potassium loss
71
Which diuretic causes a reduced uptake of K+ by the Na/K/Cl transporter?
Loop diuretics
72
What effect does increased plasma urea have on ADH secretion?
No effect
73
Why does urea have no effect on ADH secretion?
Ineffective osmole Doesn't cause movement of water, so won't trigger a signal in the osmoreceptors
74
Loss of function in the UT-B1 transporter will lead to what?
Lower osmolarity urine
75
How does loss of function in the UT-B1 transporter lead to more dilute urine?
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
How does liver cirrhosis lead to hyperosmotic urine?
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

BRS - Year 2 (75 decks)

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