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Z Year 2 BRS URO > Sodium and Potassium Balance 2 > Flashcards

Sodium and Potassium Balance 2 Flashcards

1
Q

Where are the baroreceptors for low pressure side?

A
  1. Atria
  2. Right ventricle
  3. Pulmonary vasculature
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2
Q

Where are the baroreceptors for high pressure side?

A
  1. Carotid sinus
  2. Aortic arch
  3. Juxtaglomerular apparatus
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3
Q

What happens on the low pressure side when there is low pressure?

A
  1. Reduced baroreceptor firing
  2. Signal through afferent fibres to the brainstem
  3. Sympathetic activity + ADH release
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4
Q

What happens on the low pressure side when there is high pressure?

A
  1. Atrial stretch

2. ANP, BNP released (greater water loss)

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5
Q

What happens on the high pressure side when there is low pressure?

A
  1. Reduced baroreceptor firing
  2. Signal through afferent fibres to the brainstem
  3. Sympathetic activity + ADH release
    +
  4. JGA cells
  5. Renin released
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6
Q

What is atrial natriuretic peptide (ANP)?

A

Small peptide made in atria (also make BNP)

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7
Q

When is ANP released?

A

In response to atrial stretch (i.e. high BP)

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8
Q

What are the actions of ANP?

A
  1. Vasodilatation of renal (and other systemic) blood vessels
  2. Inhibition of Sodium reabsorption in proximal tubule and in the collecting ducts
  3. Inhibits release of renin and aldosterone
  4. Reduces blood pressure
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9
Q

How does the body respond to volume expansion?

A
  1. Reduction of sympathetic activity
  2. Reduced sodium uptake in pct
  3. Reduction in renin production (so decreased Ang II and aldosterone)
  4. Increase Na+. and H20. excretion
  5. Increase of ANP and BNP affecting GFR and inhibiting sodium reabsorption
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10
Q

How does the body respond to volume contraction?

A
  1. Increase of sympathetic activity
  2. Increase sodium uptake in pct
  3. Increase in renin production (so decreased Ang II and aldosterone)
  4. Decrease Na+ and H20 excretion
  5. Decrease of ANP and BNP affecting GFR and not inhibiting sodium reabsorption
  6. Brain increasing AVP production
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11
Q

What does water reabsorption require?

A

osmotic gradient

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12
Q

What happens the more solute/sodium that reaches the later part of the tubular system / ct?

A
  • If increase osmolarity of tubular fluid by increasing amount of sodium in it
  • reduces gradient
  • So less water can be reabsorbed
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13
Q

How is ECF volume affected by sodium excretion?

A
  • Increased sodium excretion reduces ECF volume
    1. Na+ levels determine the ECF volume
    2. Reducing ECF volume reduces BP
    3. Reducing Na+ reabsorption reduces total Na+ levels, ECF volume and BP
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14
Q

How do ACE inhibitors act?

A

Reduces conversion of Ag1 to Ag 2

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15
Q

What does reduced ang2 cause?

A

Vasodilation which increases vascular volume. which decreases DP

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16
Q

What are the direct renal effects of reduced ang2?

A
  1. Decrease Na+ reuptake in the PCT
  2. Increase Na+ in the distal nephron
    - leads to reduced water reabsorption
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17
Q

What are the adrenal effects of reduced ang2?

A

Reduced aldosterone

-leads to reduced water reabsorption

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18
Q

What are the indirect renal effects of reduced ang2?

A

1, Decrease Na+ uptake in the CCT

  1. Increase Na+ in the distal nephron
    - leads to reduced water reabsorption
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19
Q

What are osmotic diuretics?

A
  • Not get reabsorbed in pct

- Increase osmolarity in pct so less water reabsorption in pct

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20
Q

Where do carbonic anhydrase inhibitors work?

A

In pct

21
Q

Where do loop diuretics work?

A

thick ascending loop of henle

22
Q

Where do thiazides work?

A

dct

23
Q

Where do K+ sparing diuretics work?

A

cd

24
Q

What does carbonic anhydrase do?

A
  • Na+ re-absorption

- increased urinary acidity

25
Q

What do carbonic anhydrase inhibitors do?

A
  1. reduced Na+ reuptake in the PCT
  2. Increased Na+ in the distal nephron
  3. Reduced water reabsorption
    - reduced urinary acidity
26
Q

What is an example of a loop diuretic?

A

furosemide

27
Q

What type of inhibitors are loop diuretics?

A

Triple transporter Inhibitors

28
Q

How do loop diuretics work?

A
  1. reduced Na+ reuptake in the LOH
  2. Increased Na+ in the distal nephron
  3. Reduced water reabsorption
29
Q

How do thiazides work?

A
  • Block Na+ Cl- transporter
    1. reduced Na+ reuptake in the DCT
    2. Increased Na+ in the distal nephron
    3. Reduced water reabsorption
    4. Increased calcium reabsorption
30
Q

What is an example of a potassium sparing diuretic?

A

spironolactone

31
Q

What do potassium sparing diuretics do?

A

inhibits aldosterone function

32
Q

What is intracellular potassium like?

A
  • Potassium is the major intracellular ion with an intracellular concentration of 150mmol/L
  • The extracellular concentration is much lower at 3-5mmol/L.
33
Q

What does extracellular K+ have an affect on?

A

on excitable membranes (of nerve and muscle)

34
Q

What does high K+ lead to?

A

depolarises membranes - action potentials, heart arrhythmias

35
Q

What does low K+ lead to?

A

heart arrhythmias (asystole)

36
Q

Is potassium high in ECF?

A

no

37
Q

Where is potassium present

A

in most/all foods

38
Q

What happens after we eat a meal?

A
  1. K+ absorption
  2. Increase in plasma K+
  3. Tissue uptake stimulated by insulin, aldosterone and adrenaline
39
Q

How does insulin respond to dietary k+?

A
  1. Insulin stimulates Na+ H+ exchanger which increases Na+ coming into cells
  2. Na+ conc has to be reduced by Na/K ATPase which brings more potassium into the cell
40
Q

What happens to potassium in the kidneys when there is normal/increased potassium intake?

A
  1. 67% reabsorbed in pct
  2. 20% reabsorbed in TAL (through K+Na+Cl- transporter)
  3. In dct and cd potassium secretion so up to 50% secreted into dct and up to 30% in ccd
  4. Therefore 15-80% of potassium (in glomerular filtrate) being excreted
41
Q

What happens to potassium in the kidneys when there is depleted potassium intake?

A
  1. 67% reabsorbed in pct
  2. 20% reabsorbed in TAL (through K+Na+Cl- transporter)
  3. 3% reabsorbed in dct
  4. 9% reabsorbed in ccd
  5. 1% excreted
42
Q

What is K+ secretion in dct/ccd stimulated by?

A
  1. Increase plasma K+ concentration
  2. Increase aldosterone
  3. Increase tubular flow rate
  4. Increase plasma pH
43
Q

Why does increase plasma K+ concentration lead to potassium secretion by the principal cells?

A
  • Increase plasma K+ conc means more K+ to come in via Na+K+ ATPase and more potassium inside the cells and more potassium going out
  • Also have an effect. on membrane potential which will help stimulate that potassium secretion
44
Q

Why does increase tubular flow cause K+ excretion?

A
  1. In response to tubular flow, the cells of the dct have primary cilia
  2. As we get increase in flow these cilia stimulate PDK1 which increases calcium concentrations in cell
  3. This stimulates the activity of the openness of the potassium channels allowing potassium to move out of the cell because its being pumped in by the sodium potassium ATPase and it will just come out of the cell in this direction
45
Q

What is hypokalemia?

A

-One of most common electrolyte imbalances (seen in up to 20% of hospitalised patients)

46
Q

What can hypokalemia be due to?

A
  1. inadequate dietary intake (too much processed food)
  2. Diuretics (due to increase tubular flow rates)
  3. surreptitious vomiting
  4. Diarrhoea
  5. Genetics (Gitelman’s syndrome; mutation in the Na/Cl transporter in the distal nephron)
47
Q

What is hyperkalemia?

A

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

48
Q

What can cause hyperkalemia?

A
  1. Seen in response to K+ sparing diuretics
  2. ACE inhibitors
  3. Elderly
  4. Severe diabetets
  5. Kidney disease

Z Year 2 BRS URO (5 decks)

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