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APP > Potassium regulation > Flashcards

Potassium regulation Flashcards

1
Q

Extracellular K+ conc

A

3.5-5.0mM

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2
Q

Intracellular K+ conc

A

140mM

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3
Q

Describe short-term and long-term control of K+

A

Short term - movement of K+ into and out of cells

Long term - kidney

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4
Q

What do many of. the short-term mechanisms involve?

A

Na+/K+-ATPase

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5
Q

What factors affect short-term control?

A
  1. insulin
  2. catecholamines
  3. aldosterone
  4. acid base balance
  5. plasma tonicity
  6. cell lysis
  7. strenuous exercise
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6
Q

Describe how insulin affects K+

A
  • short term rises may occur after a meal
  • Insulin → binds to its receptor leads to phosphorylation of the insulin receptor substrate protein (IRS-1) → this binds to PI3K → this interaction leads to the activation of a kinase, known as PDK1 → aPKC activation then leads to Na+/K+-ATPase insertion
    Loss of the insulin signalling pathway in diabetes mellitus results in hyperkalemia
    This can be corrected via insulin injections
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7
Q

Describe how catecholamines may affect K+

A

β2 also acts via Na+/K+-ATPase → cAMP and PKA-dependent pathway

In contrast, α receptors impair cellular entry

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8
Q

Describe aldosterone in short term control

A

Serves functions modulating NA+/K+-ATPase but its actions are mainly involved in mediating renal excretion

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9
Q

Describe how acid base balance may have an effect?

A
  • acidosis = hyperkalemia through mechanisms that are not well-understood
  • Causes K+ loss from cells
  • acidosis → increased rate of Na+/H+ exchange (NHE1_ and inward Na+-3HCO3- cotransport
    Consequently, the intracellular Na+ concentration drops, and so Na+-K+-ATPase activity drops, causing a net reduction in cellular K+.
    Furthermore, the decrease in extracellular HCO3- concentration favours Cl–HCO3- exchange, increasing the intracellular Cl- concentration. This provokes an increase in K+ efflux by K+-Cl- cotransport.
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10
Q

Describe effects of plasma tonicity

A

If hyperglycemia occurs, water moves out of the cell, down its water potential gradient, and this movement also causes K+ to exit the cell via solvent drag.
Alternatively, in cell shrinkage, the intracellular K+ concentration rises, favouring K+ efflux.

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11
Q

Describe the role the colon plays in long-term control

A

GI tract plays minor role in K+ excretion –colon can adjust its K+ excretion in response to certain stimuli (e.g. adrenal hormones, changes in dietary K+, and decreased capacity of the kidneys to excrete K+), but the colon isn’t capable of increasing K+ secretion sufficiently to maintain external K+ balance.

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12
Q

Describe effects of catecholamine agonists and antagonists on K+ levels

A

Agonists, including adrenaline, salbutamol and insulin, increase uptake of K+ by cells
Beta-antagonists (beta blockers, such as atenolol) prevent this and cause hyperkalaemia in overdose

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13
Q

Describe K+ reabsorption in the PCT

A

Mainly passive and occurs paracellularly in relation to Na+ and water reabsorption

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14
Q

Describe K+ reabsorption in the LOH

A

Additional transcellular pathway → NKCC2

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15
Q

Where does K+ secretion begin?

A

Early DCT and increases along the distal nephron, most occurs in the principal cells of the PD

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16
Q

Describe the process of K+ secretion

A

Firstly, the K+ is taken up from the interstitium by a sodium-potassium ATPase basolaterally into the epithelial cell
This maintains a favourable gradient for K+ efflux and therefore K+ diffuses out of the cell luminally (and basolaterally)

17
Q

What is apical K+ permeability in the distal nephron maintained by?

A

Presence of renal outer medullary potassium channels (ROMK) and big potassium (BK) channels, as well as K+-Cl- cotransporter

18
Q

What channel can also contribute to K+ rebasorption in the CD in conditions of K+ depletion

A

apical H+-K+-ATPase on alpha intercalated cells

19
Q

What are the two key determinants of K+ secretion?

A
  • mineralocorticoid activity

- distal delivery of Na+ and water

20
Q

What is the body’s major mineralocorticoid?

A

Aldosterone

21
Q

Where is aldosterone release from?

A

Zone glomerulsa of adrenal cortex

22
Q

What state of K+ triggers aldosterone synthesis? What does aldosterone do to K+ levels?

A

Released in response to increased plasma K+

Stimulates K+ secretion

23
Q

How does aldosterone stimulate K+ secretion?

A
  1. stimulate Na+/K+-ATPase synthesis and activity → increased intracellular K+
  2. Upregulating ENaC synthesis → increases NaC reabsorption and increases electronegativity of the lumen, increasing electrical gradient, which favours K+ secretion
  3. Directly increases K+ permeability of the luminal membrane, thought to be mediated by ROMK
24
Q

Describe effect of Conn’s on K+?

A

PRIMARY HYPERALDOSTERONISM → hypokalemia

25
Q

Describe effect of Addisons on K+?

A

HYPOALDOSTERONISM → decrease renal K+ secretion → hyperkalemia

26
Q

Describe effect rate of distal delivery of Na+ and water ha on K+ secretion

A
  • If distal Na+ delivery is increased, there is increased distal Na+ reabsorption, the lumen is made more electronegative which results in increased K+ secretion.
  • Increased flow rates also favour K+ secretion because at high flow rates, the K+ secreted into the lumen is diluted by the larger volume, reducing the luminal K+ concentration, creating a steeper K+ concentration gradient
27
Q

Which channels mediate the response to increase Na+ and water flow rate

A

Increased flow → increased intracellular Ca2+ concentrations of the principal cells, and Ca2+ activates the maxi-K+ channels, increasing K+ secretion.

It is thought that the increased flow is communicated to the central cilium of principal cells, and the cilium brings about an increase in intracellular Ca2+.

28
Q

What hormone, other than aldosterone, may also act on the kidney to have an effect on K+ secretion?

A

ADH

29
Q

How may ADH affect K+ secretion?

A

In times of antidiuresis, it would be expected that distal tubular K+ secretion would fall due to the decreased tubular flow rate.

However, ADH has a stimulatory effect on renal K+ secretion, because when ADH levels are increased, renal K+ secretion remains stable.

30
Q

What are the mechanisms by which ADH may stimulate K+ secretion?

A

It increases apical Na+ conductance (making the lumen more electronegative)

Increases apical K+ permeability.

31
Q

What is the level of K+ that defines hyperkalaemia?

A

> 5.0mM

32
Q

What may cause hyperkalemia?

A

Increased dietary intake of K+ (rare in patients with healthy kidneys)

Altered distribution of K+ (e.g. due to acidosis, β-adrenergic blockade, or massive cell breakdown which releases K+ into the extracellular space)

MAIN cause = impaired renal K+ excretion, e.g. due to hypoaldosteronism (e.g. in Addison’s disease) or more commonly advanced renal failure

33
Q

What does hyperkalaemia manifest as?

A

skeletal muscle fatigue and cardiac arrhythmias due to changes in membrane potentials and hyperaemia
Muscle fatigue due to depolarisation of myocyte and interference with excitation contraction coupling system → decrease in Ca2+ release from SR → contractile force possible decreases
Arrhythmias → increased rate of repolarisation and action potential duration

34
Q

Serum level of K+ for hypokalaemia

A

<3.5mM

35
Q

Causes of hypokalaemia

A

Renal losses often occur in patients with renal tubule disorders or alterations in the renin-angiotensin-aldosterone system (such as hyperaldosteronism in Conn’s syndrome).

GI losses may occur from vomiting and severe diarrhoea

K+ loss through skin may occur via sweat during intense exercise on a hot, humid day, or in the K+-containing fluid from severe burns.

Low plasma K+ can also be due to altered K+ distribution within the body. (e.g. due to alkalosis or excessive insulin administration) and inadequate dietary K+ intake.

36
Q

Symptoms of hypokalaemia

A
  • usually asymptomatic

- Leads to muscle weakness, paralysis, oedema, arrhythmias and orthostatic hypotension

37
Q

Normal roles of K in the body

A
  • cell-volume interactions (K draws water)
  • Intracellular pH regulation (K exchanges for H)
  • enzyme functions
  • DNA/protein synthesis and growth
  • resting membrane potential
  • neuromuscular activity
  • cardiac activity
  • vascular resistance (hypokalaemia = vasoconstriction)
38
Q

What is the largest source of K+ input into the body?

A

Dietary

But can also be released from IC stores under the correct conditions (necrosis)

APP (17 decks)

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