6.2 K balance renal control Flashcards

1
Q

Interactions between acid-base status and plasma [K+]

A
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2
Q

Explain how K handling occurs in the various segments of the nephron

A
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3
Q
  1. Majority (approx 98%) of the 3500 mEq of k+ within body is located within where ?
  2. only 2% found where ?
A
  1. cells
  2. extracellular fluid
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4
Q
  1. Intracellular [k+] = ~ … mmol/L
  2. extracellular [k+] = ~… mmol/L
A
  1. 150
  2. 4
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5
Q

Why is most K+ found intracellularly ?

A
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6
Q

What is role of potassium [k+] in the body ?

A

major determinant of intracellular osmolarity
ratio of [k+] ECF: ICF influences cell membrane polarisation

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7
Q

why is it important to maintain normokalaemia ?

A

small changes in plasma [k+] can have significant clinical implications
e.g. conduction of nerve impulses to skeletal muscle (muscle weakness) , cardiac action potentials (arrhythmias)

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8
Q

What factors affect ECF [K+] ? medium to long-term …

A

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9
Q

What factors affect ECF [K+] ?short term …

A
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10
Q

What is K+ concentration in the extracellular fluid (ECF) is affected by ?

A
  • dietary intake
  • exchange with the intracellular fluid (ICF)
  • urinary excretion
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11
Q

values of ECF [K+] in the following:
1. hyperkalaemia
2. normokalaemia
3. hypokalaemia

A
  1. > 5.0 mmol/L
  2. 3.5-5.0 mmol/L
  3. < 3.5 mmol/L
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12
Q

Effects of hyperkalaemia & hypokalaemia on excitable tissues ….

A

slide 9/22

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13
Q

Movement of K+ between the cells and the ECF depends on factors including what ?

A
  • insulin concentration
  • Beta 2 - adrenergic activity
  • acid-base status
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14
Q

K+ moved from ECF into cells following what ?

A

insulin/adrenaline-stimulated activation of Na+/K+-ATPase

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15
Q

Give examples of how the release of small amounts of k+ from cells can INC [k+] ?

A
  • insulin deficiency
  • cell lysis
  • severe exercise
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16
Q

INC [H+] ions causes what in cells ?

A

Uptake of H+ into cells and intracellular buffering, to some extent, in exchange for K+

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17
Q

Effect of [K+] in ECF in acidosis and alkalosis happens why ?

A

acidosis = INC [k+]
alkolosis DEC [k+]

  • INC [H+] ions causes uptake of H+ into cells , where to some extent in exchange for K+
18
Q

Potassium handling in the nephron ?

A
19
Q

what can elevated plasma [K+] directly induce ?

A

aldosterone release

20
Q
  1. INC aldosterone stimulates what ?
  2. INC aldosterone facilitates what ?
A
  1. Na/K- ATPase expression (and therefore ↑ K+ uptake into cells)
  2. K+ secretion via ROMK channels following Na+ uptake (via ENaC channels)
21
Q

Action of aldosterone on principle tubular cells of the cortical collecting duct ?

A
  • ROMK
  • ENaC
  • MR
22
Q

Interaction between pH and K+ ???

A
23
Q

What does acute metabolic acidosis cause K+ to do ?

A

move out of cells

24
Q

What does acute metabolic alkalosis cause K+ to do ?

A

move into cells

25
Q

What in ECF may be more important than changes in pH ?

A

[HCO3-]

26
Q

Why does the hyperkalaemia common in diabetic ketoacidosis result more from insulin deficiency than from acidosis ? [I DON’T GET HTIS !!!!!]

A

non-anion gap (hyperchloraemic) metabolic acidosis causes INC K+

In contrast, metabolic acidosis organic acids (INC anion gap acidosis) does NOT cause hyperkalaemia

27
Q

What affects serum potassium concentraiton less than metabolic acidosis and alkalosis ?

A

acute respiratory acidosis and respiratory alkalosis

28
Q

Insulin stiumlates cellular uptake of K+ …

A
29
Q

Apart from insulin what else can also induce cellular uptake of K+

A

thyroxine and beta-adrenergic stimulation

30
Q

What happens to potassium in the distal tubule ?

A
  • secreted by principal cells
  • reabsorbed by type-A-intercalated cells

which balance between the 2 determines ECF [K+]

31
Q

Movement of what is dependent on maintaining a low [K+] in the filtrate (concentration gradient) ?

A
  • Na/K-ATPase drives K+ secretion from principal cells into the tubular filtrate via ROMK channels.
32
Q

Na/K-ATPase drives K+ secretion from principal cells into the tubular filtrate via ROMK channels

what is this movement sitmulated by ?

A
  • High ECF [K+]
  • Aldosterone
  • High ECF pH
  • High GFR (high flow quickly removes secreted K+ and ‘steepens’ the K+ concentration gradient).
33
Q

What is K+ reabsorption via alpha-intercalated cells driven by ?

A

H+/K+ ATPase exchanger
* driven by pH of ECF
* low ECF pH more K+ absorbed
* high ECF pH less K+ absorbed
* K+ exits the cell via basolateral K+ channels

34
Q

Causes of hypokalaemia can include ?

A
  • diuretics (e.g. K+ sparing ? , aldosterone antagonists)
  • hypokalaemia associated with vomiting
  • renal tubular acidoses
  • some antibiotics (e.g. penicillins and aminoglycosides)
  • insulin excess or overdose
  • mutations in the NK2Cl transporter
35
Q

causes of hyperkalaemia can include ?

A
  • rhabdomyolysis
  • insulin deficiency
  • metabolic acidosis
  • hypoaldosteronism
  • ACE inhibitors
  • pseudohypoaldosteronism
36
Q

Why could rhabdomyolysis cause hyperkalaemia ?

A
37
Q

Hypoaldosteronism can cause hyperkalaemia as a result of what ? why ?

A

potassium-sparing diuretics …

38
Q

Can you think why ACE inhibitors could cause hyperkalaemia ?

A
39
Q

Why can pseudohypoaldosteronism cause hyperkalaemia ?

A

an inactivating mutation in ENaC channels

40
Q

clinical features of hypokalaemia

A
41
Q

clinical features of hyperkalaemia

A