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Uro > Sodium and potassium balance > Flashcards

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
Q

What are the effects of hyperaldosteronism?

A

Increased reabsorption of sodium,
Causes decreased urinary loss of sodium, ECF volume increases

25
Q

What is the body’s response to hyperaldosteronism?

A

Release of ANP (atrial) and BNP (brain)

26
Q

What are the symptoms of hyperaldosteronism?

A

High BP, Muscle Weakness, Polyuria, Thirst

27
Q

What is Liddle’s syndrome

A

Inherited disease of HBP
Low/normal aldosterone
Mutation in aldosterone activated sodium channel -> greater Na retention and hypertension

28
Q

Where are baroreceptors found on the ‘Low Pressure Side’?

A

Atria, Right Ventricle, Pulmonary Vasculature (veins/deoxygenated)

29
Q

Where are baroreceptors found on the ‘High Pressure Side’?

A

Carotid Sinus, Aortic Arch, Juxtaglomerular Apparatus (all in vasculature) (arteries/oxygenated)

30
Q

How does the ‘Low Pressure Side’ respond to low blood pressure?

A

Reduced baroreceptor firing,
signals through afferent fibres to brainstem,
increased sympathetic activity and ADH release (to increase blood pressure)

31
Q

How does the ‘Low Pressure Side’ respond to high blood pressure?

A

Atrial stretch leads to ANP and BNP release (to decrease blood pressure)

32
Q

How does the ‘High Pressure Side’ respond to low blood pressure?

A

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
Q

What is ANP- atrial natriuretic peptide

A

Small peptide made in the atria
Released in response to atrial stretch

34
Q

What are the actions of ANP?

A

Vasodilation of renal blood vessels,
Inhibition of sodium reabsorption in PCT/CD,
Inhibits renin & aldosterone release (leading to lower blood pressure)

35
Q

What does blood volume expansion lead sodium to and how?

A

Na+ excretion
// stimulates ANP release, inhibits renin, angiotensin and aldosterone release (decreased sympathetic activity)

36
Q

What does blood volume contraction lead sodium to and how?

A

Na+ reabsorption
// inhibits ANP release, stimulates renin, angiotensin and aldosterone release (increased sympathetic activity)
Brain increased AVP production

37
Q

What is urodilatin?

A

Hormone that increases renal blood flow - so for natriuresis (more sodium excretion)

38
Q

Effect on water secretion if increased sodium reached collecting duct

A

Reduces osmotic gradient
less water reabsorbed

39
Q

What are ACE-inhib?

A

Diuretics
Reduce Angiotensin 2 lvls

40
Q

ACE-inhib effect on vasculature

A

vasodilation
increases vascular volume
results in decreased bp

41
Q

ACE-inhib effect on renal system

A

Decreased Na+ reuptake in the PCT
Increased osmolality of the distal nephron
leads to decreased water reabsorption
resulting in decreased bp

42
Q

ACE-inhib effect on adrenal system

A

Reduced aldosterone which leads to less Na+ uptake in the CD
Increased osmolality of the distal nephron
decreased water absorption
decreased bp

43
Q

What are other examples of diuretics?

A

Carbonic-Anhydrase Inhibitors,
Loop Diuretics (furosemide),
Thiazide Diuretics,
K+ Sparing Diuretics (spironolactone)

44
Q

How do carbonic anhydrase inhibitors work?

A

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
Q

How do loop diuretics work?

A

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
Q

How do thiazide diuretics work?

A

Block the Na+Cl- Symporter, reduced Na+ uptake (in DCT)
Incr Ca2+ reabsorption due to change in gradient across membrane

47
Q

What is the action of potassium sparing diuretics?

A

E.g. spironolactone
Aldosterone inhibitors - block sodium reuptake but not potassium transporters (in principal cell of CD)

48
Q

Extracellular enzyme released from the kidneys into the plasma

A

Renin
Released by macula densa at the juxtaglomerular apparatus

49
Q

Main intracellular ion

A

Potassium

50
Q

What does hyperkalaemia lead to?

A

Action potentials, Heart Arrhythmias

51
Q

What does hypokalaemia lead to?

A

Asystole heart arrhythmias

52
Q

Potassium concentration in food

A

High especially in unprocessed food

53
Q

Body response to dietary potassium

A

Increased uptake by tissues due to effects of insulin, aldosterone and adrenaline

54
Q

Insulin effect on potassium uptake

A

Stimulates sodium/proton exchanger
increased sodium gradient in the cell
Na+/K+ ATPase activity increases to removes na+ from the cell

55
Q

Where is the majority of potassium in the nephron reabsorbed?

A

2/3 in the PCT

56
Q

What is potassium secretion stimulated by?

A

^ plasma K+,
^ aldosterone,
^ tubular flow rate,
^ plasma pH

57
Q

Effect of tubular flow on potassium excretion

A

increased flow causes cilia to stimulate PDK1, results in greater calcium concentration in the cell and greater potassium channel sensitivity

58
Q

What are some causes of hypokalaemia?

A

Inadequate dietary intake - lots of processed food
diuretics - increased tubular flow
vomiting&diarrhoea,
genetics (Gitelman’s syndrome - mutated Na/Cl channel in DCT)

59
Q

What are some causes of hyperkalaemia?

A

K+ sparing diuretics, (spironolactone)
ACE-i,
Elderly patients,
severe diabetes,
CKD

Uro (7 decks)

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