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Sodium and potassium balance Flashcards

1
Q

Osmolarity

A

Measure of solute concentration in a solution
(osmoles/litre)
Depends on the number of dissolves particles - as this increases so does osmolarity

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2
Q

What is the normal plasma osmolarity?

A

285-295 mOsm/L

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3
Q

Most common solute in ECF

A

Sodium

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4
Q

Impact of dietary sodium on body weight

A

incr diet Na -> incr body Na -> incr H20 retention and water intake -> incr bodyweight/ECF volume

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5
Q

Effects of increased ECF volume (due to ^ Na)

A

Incr blood volume/pressure

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6
Q

How does the body regulate sodium intake?

A

Two ways: Hypothalamus and Taste

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7
Q

How does the hypothalamus regulate sodium intake?
- central mechanism

A

Na+ deprivation, Lateral Parabrachial Nucleus increases appetite for Na+ via GABA/opioids.

In euvolemia (normal Na+), Lateral Parabrachial Nucleus decreases appetite for Na+ via serotonin glutamate

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8
Q

How does taste regulate sodium intake?

A

Low sodium diet increases appetite for Na+ vv

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9
Q

Where is sodium mostly reabsorbed from in the nephron?

A

67% in PCT
25% in thick Ascending Loop of Henle
8% in DCT/CD
Excrete < 1%

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10
Q

What part of the nephron is in tight association with the glomerulus?

A

Distal Convoluted Tubule

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11
Q

How does the DCT interact with the glomerulus in high tubular sodium?

A

High tubular sodium
Stimulates reuptake via triple transporter
Adenosine released from macula densa -> decr renin prod and afferent SMC contraction stimulated by extraglomerular mesangial cells
Results in reduced perfusion pressure .: decr EGFR

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12
Q

What is the best way to retain sodium?

A

Filter less into tubules

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13
Q

What are the different ways of decreasing sodium excretion?

A

Increased Sympathetic Activity,
Ang II Release
Low tubular Na stimulates renin prod in JGA

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14
Q

How does increased sympathetic activity decrease sodium excretion?

A

Contracts afferent arteries (less blood flow to glomerulus),
stimulates activity of PCT
stimulates renin production in the JGA -> incr AngII

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15
Q

How does the body increase sodium excretion?

A

Release of atrial naturietic peptide
Suppresses reabsorption at PCT/DCT/CD
suppresses renin prod by JGA

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15
Q

How does Ang II release decrease sodium excretion?

A

Increase PCT activity,
Stimulates aldosterone release (acts on DCT/CT for incr Na uptake)

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16
Q

Where is aldosterone synthesised?

A

Zona glomerulosa, adrenal cortex
steroid hormone

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17
Q

What aldosterone released in response to?

A

Angiotensin II,
Decrease in Blood Pressure (via baroreceptors)

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18
Q

What are the three functions of aldosterone?

A

Increased sodium reabsorption,
Increased potassium secretion, Na+/K+ pump
Increased H+ secretion

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19
Q

What condition occurs in hyperaldosteronism?

A

Hypokalaemic Alkalosis
Low K+/H+

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20
Q

Aldosterone mechanism

A

steroid hormone .: diffuses into cell
Binds to receptor which dimerises and travels to nucleus
stimulates transcription of Na+ channel proteins

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21
Q

What are the effects of hypoaldosteronism?

A

Reduced reabsorption of sodium in DCT/CD,
causes increased urinary loss of sodium, ECF volume falls

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22
Q

What is the body’s response to hypoaldosteronism?

A

Increased renin, Ang II, ADH

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23
Q

What are the symptoms of hypoaldosteronism?

A

Dizziness, Low BP, Salt Craving, Palpitations

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24
What are the effects of hyperaldosteronism?
Increased reabsorption of sodium, Causes decreased urinary loss of sodium, ECF volume increases
25
What is the body's response to hyperaldosteronism?
Release of ANP (atrial) and BNP (brain)
26
What are the symptoms of hyperaldosteronism?
High BP, Muscle Weakness, Polyuria, Thirst
27
What is Liddle's syndrome
Inherited disease of HBP Low/normal aldosterone Mutation in aldosterone activated sodium channel -> greater Na retention and hypertension
28
Where are baroreceptors found on the 'Low Pressure Side'?
Atria, Right Ventricle, Pulmonary Vasculature (veins/deoxygenated)
29
Where are baroreceptors found on the 'High Pressure Side'?
Carotid Sinus, Aortic Arch, Juxtaglomerular Apparatus (all in vasculature) (arteries/oxygenated)
30
How does the 'Low Pressure Side' respond to low blood pressure?
Reduced baroreceptor firing, signals through afferent fibres to brainstem, increased sympathetic activity and ADH release (to increase blood pressure)
31
How does the 'Low Pressure Side' respond to high blood pressure?
Atrial stretch leads to ANP and BNP release (to decrease blood pressure)
32
How does the 'High Pressure Side' respond to low blood pressure?
Reduced baroreceptor firing. Two effects: 1. Signals through afferent fibres to brainstem, increased sympathetic activity and ADH release (same as low pressure side) 2. Juxtaglomerular apparatus releases renin (to increase blood pressure)
33
What is ANP- atrial natriuretic peptide
Small peptide made in the atria Released in response to atrial stretch
34
What are the actions of ANP?
Vasodilation of renal blood vessels, Inhibition of sodium reabsorption in PCT/CD, Inhibits renin & aldosterone release (leading to lower blood pressure)
35
What does blood volume expansion lead sodium to and how?
Na+ excretion // stimulates ANP release, inhibits renin, angiotensin and aldosterone release (decreased sympathetic activity)
36
What does blood volume contraction lead sodium to and how?
Na+ reabsorption // inhibits ANP release, stimulates renin, angiotensin and aldosterone release (increased sympathetic activity) Brain increased AVP production
37
What is urodilatin?
Hormone that increases renal blood flow - so for natriuresis (more sodium excretion)
38
Effect on water secretion if increased sodium reached collecting duct
Reduces osmotic gradient less water reabsorbed
39
What are ACE-inhib?
Diuretics Reduce Angiotensin 2 lvls
40
ACE-inhib effect on vasculature
vasodilation increases vascular volume results in decreased bp
41
ACE-inhib effect on renal system
Decreased Na+ reuptake in the PCT Increased osmolality of the distal nephron leads to decreased water reabsorption resulting in decreased bp
42
ACE-inhib effect on adrenal system
Reduced aldosterone which leads to less Na+ uptake in the CD Increased osmolality of the distal nephron decreased water absorption decreased bp
43
What are other examples of diuretics?
Carbonic-Anhydrase Inhibitors, Loop Diuretics (furosemide), Thiazide Diuretics, K+ Sparing Diuretics (spironolactone)
44
How do carbonic anhydrase inhibitors work?
Prevent action of the sodium/proton exchange as CO2 is no longer being used to form bicarbonate ions Results in decreased Na+ reuptake in PCT Reduction in urine acidity due to lack of H+ secretion
45
How do loop diuretics work?
E.g. Furosemide Block the triple transporter Na+.K+.2Cl- , reduced Na+ reuptake (in thick ascending LOH) increased osmolality of distal nephron -> less water reabsorption
46
How do thiazide diuretics work?
Block the Na+Cl- Symporter, reduced Na+ uptake (in DCT) Incr Ca2+ reabsorption due to change in gradient across membrane
47
What is the action of potassium sparing diuretics?
E.g. spironolactone Aldosterone inhibitors - block sodium reuptake but not potassium transporters (in principal cell of CD)
48
Extracellular enzyme released from the kidneys into the plasma
Renin Released by macula densa at the juxtaglomerular apparatus
49
Main intracellular ion
Potassium
50
What does hyperkalaemia lead to?
Action potentials, Heart Arrhythmias
51
What does hypokalaemia lead to?
Asystole heart arrhythmias
52
Potassium concentration in food
High especially in unprocessed food
53
Body response to dietary potassium
Increased uptake by tissues due to effects of insulin, aldosterone and adrenaline
54
Insulin effect on potassium uptake
Stimulates sodium/proton exchanger increased sodium gradient in the cell Na+/K+ ATPase activity increases to removes na+ from the cell
55
Where is the majority of potassium in the nephron reabsorbed?
2/3 in the PCT
56
What is potassium secretion stimulated by?
^ plasma K+, ^ aldosterone, ^ tubular flow rate, ^ plasma pH
57
Effect of tubular flow on potassium excretion
increased flow causes cilia to stimulate PDK1, results in greater calcium concentration in the cell and greater potassium channel sensitivity
58
What are some causes of hypokalaemia?
Inadequate dietary intake - lots of processed food diuretics - increased tubular flow vomiting&diarrhoea, genetics (Gitelman's syndrome - mutated Na/Cl channel in DCT)
59
What are some causes of hyperkalaemia?
K+ sparing diuretics, (spironolactone) ACE-i, Elderly patients, severe diabetes, CKD

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