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Y2 - BRS - Uro > Sodium and Potassium Balance > Flashcards

Sodium and Potassium Balance Flashcards

1
Q

What is osmolarity?

A

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

Depends on the number of dissolved particles

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2
Q

So what is 1 Osmole?

A

1 Osmole = 1 mole of dissolved particles per litre (e.g. 1 mol of NaCl = 2 mol of particles in solution)

The greater the number of dissolved particles, the greater the osmolarity

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3
Q

How is osmolality different?

A

Osmolarity = number of particles of solute per liter of solution

Osmolality = number of particles of solute per kilogram of solvent

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4
Q

What is normal plasma osmolarity?

A

285-295 mosmol/L

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5
Q

What is the most prevalent solute in the plasma?

What else makes up plasma?

A

Sodium - 140 mmol/L (most important and dictates ECF volume)

Chloride - 105 mmol/L
Bicarbonate - 24 mmol/L
Potassium - 4 mmol/L
Glucose - 3-8 mmol/L
Calcium - 2 mmol/L
Protein - 1 mmol/L
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6
Q

What happens when you increase sodium dietary intake?

A

Increase total body sodium
Increased osmolarity (but this can’t happen due to semi-permeability of membranes)
So leads to increased water intake and retention
Increased ECF volume - until plateau reached
Increased blood volume and pressure

Then if you reduce sodium in your diet - you lose the water as you lose sodium from the system

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7
Q

What happens when you decrease sodium dietary intake?

A

Decrease total body sodium
Decreased osmolarity (but this can’t happen due to semi-permeability of membranes)
So leads to decreased water intake and retention
Decreased ECF volume - until plateau reached
Decreased blood volume and pressure

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8
Q

What happens under normal conditions of euvolemia?

A

Euvolemia has normal sodium levels = inhibition of Na+ intake

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9
Q

What controls sodium intake?

A

Lateral parabrachial nucleus - a set of cells that respond to serotonin and glutamate as transmitters to suppress basal sodium intake

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10
Q

What happens at the lateral parabrachial nucleus during Na+ deprivation VS euvolemia?

A

Na+ deprivation = increased appetite for Na+ driven by GABA and opioids

Euvolemia = inhibit Na+ intake

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11
Q

What is salt when present in low quantities in food?

What is salt when present in high quantities in food?

A

Appetitive = low sodium content in food

Aversive = high sodium content in food

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12
Q

Where is sodium reabsorbed in the nephron?

So how much sodium is actually excreted?

A

60-70% reabsorbed in PCT

As the tubular fluid travels down the descending limb of the loop of Henle, no sodium is reabsorbed

However, in the thick ascending limb a further 25% is reabsorbed

A further 5 % is reabsorbed in the DCT

A further 3% in the collecting duct

So less than 1% of the sodium that enters the tubular fluid is excreted

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13
Q

How would you increase the amount of sodium excreted?

A 
Increase GFR (glomerular filtration rate)
Increase sodium excretion
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14
Q

What affects GFR?

Is it desirable that changes in GFR are proportional to sodium lost?

A

Renal plasma flow
Mean arterial pressure
Proportional up to a threshold then plateaus

Not really

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15
Q

How does sodium affect GFR?

A

The DCT is in contact with cells around the glomerulus - so the DCT contains macula densa cells, which are in contact with the extraglomerular mesangial cells (found between the glomerulus and DCT), which are in contact with the juxtaglomerular cells (on the glomerulus)

High tubular sodium

Macula densa cells are found on the DCT and respond to high sodium levels by increasing sodium/chloride uptake via triple transporter

Causes Macula Densa cells to release adenosine

Detected by extraglomerular mesangial cells - which interacts with the juxtuglomerular cells to release renin

This causes smooth muscle cells of the glomerulus to contract = reduced blood flow

Reduces perfusion pressure and so GFR

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16
Q

Why is the macula densa production of renin in response to high sodium less important?

A

Over a short period of time = short term regulation system

So does not affect overall renin production long term

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17
Q

What is the best way to retain sodium and water?

A

Filter less

Reduction of pressure gradient at Bowman’s capsule

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18
Q

What factors allow for less filtration?

A

Sympathetic activity:

Contracts SMC of afferent arteriole

Stimulates sodium uptake of cells of PCT

Stimulates JGA (juxtaglomerular apparatus) to produce renin

Renin cleaves angiotensinogen to form angiotensin I, ACE cleaves angiotensin I to Angiotensin II

Angiotensin II promotes vasconstriction and reabsorption of sodium in PCT

Angiotensin II stimulates adrenal glands to produce aldosterone

Aldosterone promotes reabsorption in collecting duct

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19
Q

What factors allow for greater filtration?

A

ANP (atrial naturietic peptide) - acts as a vasodilator

Reduces reabsorption of sodium throughout nephron - PCT, DCT and CD

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20
Q

What is aldosterone and where is it synthesised?

When is it released and why?

A

Aldosterone = steroid hormone

Synthesised and released from the adrenal cortex (zona glomerulosa)

Released in response to angiotensin II and a decrease in BP (detected via baroreceptors)

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21
Q

What does angiotensin II do to stimulate aldosterone production?

A

Promotes synthesis of aldosterone synthase (enzyme)

Aldosterone synthase causes the last 2 ezymatic steps in the production of aldosterone from cholesterol

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22
Q

What is the role of aldosterone in the kidney?

A 
Stimulates:
Increased Sodium reabsorption
(controls reabsorption of 35g Na/day)
Increased Potassium secretion
Increased hydrogen ion secretion
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23
Q

What does aldosterone excess lead to?

A

Hypokalaemic alkalosis

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24
Q

How does aldosterone work?

A

Steroid hormone - lipid soluble so will pass through the cell membrane

Once inside the cell, binds to mineralocorticoid receptor inside cytoplasm bound to protein HSP 90

HSP 90 is consequently removed and the receptor is dimerised (no longer a monomer, instead is a dimer)

Allows it to translocate to the nucleus - i.e. moves into nucleus

It binds to DNA, where it stimulates transcription of mRNA genes that are under its control

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25
Q

What proteins are produced in response to aldosterone?

A

Na/K ATPase
Epithelial sodium channel

These travel to their respective membranes

Regulatory proteins that stimulate the activity of the 2 transporters (Na+/K+ ATPase and epithelial sodium channel) so the channels are active

26
Q

What is hypoaldosteronism?

A

Reabsorption of sodium in the distal nephron is reduced

Increased urinary loss of sodium - leads to increased loss of water in the urine

ECF volume falls

Increased renin, Ang II and ADH

27
Q

What are signs and symptoms of hypoaldosteronism?

A

Dizziness
Low blood pressure - responsible for the dizziness
Salt craving
palpitations

28
Q

What is hyperaldosteronism?

A

Reabsorption of sodium in the distal nephron is increased

Reduced urinary loss of sodium = increase in total sodium

ECF volume increases (hypertension)

Reduced renin, Ang II and ADH

Increased ANP and BNP

29
Q

What are symptoms of hyperaldosteronism?

A

High blood pressure
Muscle weakness
Thirst - we think we have insufficient water in our system and so drink more water (but this is because of the high total sodium in the body)
Polyuria - trying to get rid of all the water being drunk

30
Q

What is Liddle’s syndrome?

A

Looks like hyperaldosteronism but with normal / low aldosterone levels

Inherited disease of high BP

Mutation in the aldosterone activated sodium channel

Channel is always in the ‘on’ state = sodium retention, leading to hypertension

31
Q

How is feedback from increased of decreased ECF detected?

A

Via baroreceptors (pressure receptors)

32
Q

Where are the low pressure baroreceptors found?

A

Atria
Right ventricle
Pulmonary vasculature

33
Q

Where are the high pressure baroreceptors found?

A

Carotid sinus
Aortic arch
Juxtaglomerular apparatus

34
Q

What happens in response to low pressure on the low pressure side of the baroreceptors?

A

Low BP

Reduced baroreceptor firing

Signal through afferent fibres to the brainstem

Leads to sympathetic activity

Leads to ADH release

35
Q

What happens in response to high pressure on the low pressure side of the baroreceptors?

A

High BP

Leads to atrial stretch

ANP, BNP released

36
Q

What happens in response to low pressure on the high pressure side of the baroreceptors?

A

Same as low pressure side (with reduced baroreceptor firing = sympathetic acitivy and ADH release) but also

Signals to JGA (juxtoglomerular apparatus) cells to suppress renin release

37
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)

38
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

39
Q

How does ANP work?

A

Binds to a receptor that is guanylyn cyclase

Guanylyn cyclase causes conversion of GTP to cyclic GMP

Leads to activation of protein kinase G

Cellular responses in response to that - e.g. vasodilation of the renal and systemic blood vessels, inhibition of sodium in PCT and CD and inhibition of renin + aldosterone production

40
Q

What happens in response to volume expansion of blood?

A

Reduced sympathetic activity leading to reduced sodium reuptake in the PCT, reduction in renin production (and so aldosterone)
Increase in ANP and BNP
Promotes sodium excretion

41
Q

What happens when there is contraction of the blood volume?

A

Increased sympathetic activity leading to increased sodium reuptake in the PCT, increase in renin production (and so aldosterone)
Decrease in ANP and BNP, increase ADH production
Promotes sodium reabsorption

42
Q

What would be the effect on water secretion of increased sodium levels reaching the collecting duct?

A

Increase osmolarity of tubular fluid by increasing sodium

Reduce gradient across membrane into the medulla (loop of henle)

Reduce amount of water that can be reabsorbed

So reduced ECF volume

43
Q

How are ACE inhibitors diuretics?

A

Reduces Angiotensin II production = vasodilation

Increases vascular volume = reduction in BP

Reduced Na+ reuptake in the PCT = reduced Na+ in the distal nephron

Reduces gradient across tubular fluid into interstitium at the loop of Henle = reduced water reabsorption

Reduced aldosterone = reduced uptake of sodium in the CD

Reduced ECF volume = reduced BP

44
Q

What are some other diuretics and where do they act on the nephron?

A 
Osmotic diuretics - PCT
Carbonic anhydrase inhbitors - PCT
Lymph diuretics - thin limb of loop of Henle
Thiazide diuretics - DCT
Potassium sparing - CD
45
Q

How do carbonic anhydrase inhibitors work?

A

Reduced Na+ reuptake in the PCT

Increased Na+ in the distal nephron = reduced gradient across tubular fluid into interstitium at the loop of Henle = reduced water reabsorption

Reduced acidity of urine as CA no longer converted H2CO3 into H2O and CO2

46
Q

How do loop diuretics work?

E.g. Furosemide

A

Block the triple transporter Inhibitors

Reduced Na+ reuptake in the loop of Henle

Increased Na+ in the distal nephron

Reduced water reabsorption

47
Q

How do thiazide diuretics work?

A

Block Na/Cl transporter

Reduced Na+ reuptake in the DCT

Increased Na+ in the distal nephron

Reduced water reabsorption

Also increases calcium reabsorption (via sodium calcium antiporters)

48
Q

How do potassium sparing diuretics work?

A

Inhibitors of aldosterone function (e.g. spironolactone)

Fewer sodium reuptake channels synthesised = reduced sodium reuptake in the distal nephron

49
Q

What is potassium?

A

Potassium = main intracellular ion at 150 mmol/L, extracellularly = 3-5 mmol/L

50
Q

What does extracellular postassium effect?

What does high extracellular K+ result in?

What does low extracellular K+ result in?

A

Excitable membranes

High K+ = depolarises membranes leading to more action potentials, heart arrhythmias

Low K+ = heart arrhythmias (asystole)

51
Q

What happens to dietary potassium?

A

K+ present in almost all foods, esp. unprocessed foods

After a meal –> K+ is absorbed

Increases plasma K+ conc.

Tissue uptake of K+ is stimulated by insulin, aldosterone, and adrenaline

52
Q

How does insulin stimulate uptake of K+ into tissues?

A

Stimulates Na+/H+ exchanger

Increases sodium entering cells

To reduce intracellular sodium Na+/K+ ATPase used

So Na+/K+ ATPase activity increases = brings in more K+

53
Q

Where in the nephron is potassium reabsorbed and secreted?

So how much potassium is excreted via the urine overall?

A

67% (or 2/3) reabsorbed in the PCT

Further 20% reabsorbed in thick ascending limb of loop of Henle - via Na+/K+/Cl- triple transporter

Potassium secretion in DCT and CD
Up to 50% of K+ secreted in DCT
Up to 30% secreted in CD

15-80% of K+ in glomerular filtrate is excreted

54
Q

Why can only 15% of the K+ in the filtrate be excreted?

A

Due to reabsorption in the DCT (3%) and CD (9%)

55
Q

Why is there a range of what percentage of K+ is reabsorbed?

A

Depends on plasma concentration

56
Q

What is K+ secretion stimulated by?

A

Increased plasma K+ concentration
Increased aldosterone
Increased tubular flow rate
Increased plasma pH

57
Q

How is potassium secreted by the principal cells in the DCT and CD?

A

Increase in activity of Na+/K+ ATPase - affects membrane potential to stimulate K+ secretion

More potassium inside the cell = more potassium secreted into DCT / CD

58
Q

How does K+ excretion respond to tubular flow?

A

Distal cells have primary cilia

Increase in flow detected by cilia = increase in PDK1

Increases Ca2+ conc in cell

Stimulates activity of opening K+ channels

K+ moves out of the cell as it is pumped by Na+/K+ ATPase

59
Q

What is hypokalemia?

A

Low K+ levels (in blood)

Hypokalemia one of the most common electrolyte imbalances (seen in up to 20% of hospitalised patients)

60
Q

What can cause hypokalemia?

Inadequate dietary intake (too much processed food)

A

Diuretics (due to increase tubular flow rates)

Surreptitious vomiting

Diarrhoea

Genetics (Gitelman’s syndrome; mutation in the Na/Cl transporter in the distal nephron)

61
Q

What is hyperkalemia?

A

High K+ levels (in blood)

Common electrolyte imbalance present in 1-10% of hospitalised patients

62
Q

What causes hyperkalemia?

A

Seen in response to K+ sparing diuretics

ACE inhibitors

Elderly

Severe diabetes

Kidney disesase

Y2 - BRS - Uro (8 decks)

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