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Urology > 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/liter)

1 Osmole = 1 mole of dissolved particles per liter (1 mole of NaCl = 2 moles of particles in solution)

Depends on the number of dissolved particles

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

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2
Q

What is normal plasma osmolarity?

What is the most prevalent, and important, solute in the ECF?

A

285-295mosmol/L

Sodium

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3
Q

How does an increase in sodium affect weight?

A

Increase in water and therefore increase in weight

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4
Q

What does an increased dietary sodium lead to?

A
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5
Q

Where are signals regarding sodium levels produced?

A

Lateral Parabrachial nucleus

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6
Q

What does a decrease in sodium lead to?

A

Increase appetite for Na+ via GABA and opiods

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7
Q

What does an increase in sodium lead to?

A

Inhibition of Na+ intake via seretonin glutamate

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8
Q

Where is sodium reabsorbed in the nephron

A

67% in the PCT
25% in the thick ascending limb
5% in the DCT
3% in the collecting duct
Rest excreted

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9
Q

What happens after a certain amount of blood pressure in terms of GFR and RPF?

A

It plateaus

Approx 20% of renal plasma enters the tubular system

GFR=RPF*2

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10
Q

What does an increase in tubular sodium lead to?

A
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11
Q

How does sympathetic activity affect sodium excretion?

A

Increases
-Contracts smooth muscle cells of afferent arteriole
-Stimulates sodium uptake via the PCT
-Stimulates JGA to produce renin
-Which leads to production of angiotensin II
-This stimulates cells of PCT to take up sodium and stimulates adrenal glands to produce aldosterone
-This stimulates uptake of sodium in DCT
Low tubular Na can stimulate renin production

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12
Q

How is sodium reabsorption decreased?

A

Using atrial naturietic peptide
Reduces uptake in PCT, DCT and CT
Suppresses renin production

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13
Q

What happens when there is low or high sodium in terms of volume expansion and contraction?

A
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14
Q

What is aldosterone and where is it synthesised?

A

Steroid hormone
Synthesised and released from the adrenal cortex (zona glomerulosa)
Released in response to
Angiotensin ll (which promotes release of aldosterone synthase), which produces aldosterone from cholesterol after 2 enzymatic steps
Decrease in blood pressure (via baroreceptors)

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15
Q

What does aldosterone stimulate?

What happens when there is excess aldosterone?

A
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16
Q

How does aldosterone work?

A

Is a steroid hormone so passes through membrane
Then binds to the mineralocorticoid receptor, which is inside the cytoplasm and binded to HSP19
Once aldosterone binds, the HSP19 is removed and the mineralocorticoid receptor, now a dimer, and is able to translocate to the nucleus and binds to the DNA. Stimulate mRNA genes under its control

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17
Q

What does the production of aldosterone lead to in terms of channels?

A

Important target genes include the ENaC (epithelial sodium channel) the sodium potassium ATPase and sets of regulatory proteins. This co-ordinates an increase in the number of sodium transporters and their activity thereby increasing sodium reabsorption

18
Q

What is hypoaldosteronism?

A
19
Q

What is hyperaldosteronism?

A
20
Q

What is Liddle’s syndrome?
What is it cause by?

A
21
Q

Where are baroreceptors found for low blood pressure?

A

Atria
Right ventricle
Pulmonary vasculature

21
Q

Where are baroreceptors found for high blood pressure?

A

Carotid sinus
Aortic arch
Juxtaglomerular apparatus

22
Q

What happens when the low pressure side detects low pressure?

What happens when the low pressure side detects high pressure?

A
23
Q

What happens when the high pressure side detects lower pressure?

A
24
Q

What is Atrial Natriuretic Peptide?
When is it released?

A

Small peptide made in the atria (also make BNP)
Released in response to atrial stretch (i.e. high blood pressure)
Binds to guanylyl cyclase and that causes conversion to cGMP and activation of PKG and PDE (therefore cellular responses)

25
Q

What are the actions of Atrial Natriuretic Peptide?

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

26
Q

What does an expansion in volume cause?

A

Reduction in sympathetic activity
Reduction in renin
Increase in sodium excretion

27
Q

How does increased sodium excretion affect ECF volume?

A

Reduces ECF volume and reduces BP
Reducing Na+ absorption reduced total Na+ levels, ECF volume and BP

28
Q

What is the effect of ACE inhibitors in the Renin Angiotensin System?

A
29
Q

What other diuretics have an effect?

A
30
Q

How do carbonic anhydrase inhibitors work?

A
31
Q

How do loop diuretics (furosemide) work?

A
32
Q

How do thiazides work?

A
33
Q

How to potassium sparing diuretics

A
34
Q

What is the main intracellular ion?

What are its extracellular effect?

What does high K+ do?

What does low K+ do?

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).

35
Q

How does dietary potassium work?

A

Meal results in an increase in K+ absorption
Then causes an increase in plasma K+
Then causes an increase in tissue uptake by insulin (also aldosterone and adrenaline)

36
Q

How does insulin increase uptake of K+ in tissues?

A

Increases rate of Na/H exchanger
Then increases rate of Na/K ATPase and K+ taken up

37
Q

What stimulates K+ secretion?

A

Increase in plasma K+
Increase in aldosterone
Increase in tubular flow rate
Increase in plasma pH

38
Q

What does tubular flow lead to in terms of potassium?

A

The primary cilium are activated and then PDK1 is activated
Causes an increase in Ca++ in cells and an increase in K+ secretion

39
Q

What is hypokalemia

A
40
Q

What is hyperkalaemia

A

Urology (5 decks)

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