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Physiology 1 Semester 2 > Potassium Balance > Flashcards

Potassium Balance Flashcards

1
Q

State the sources of potassium intake and output and the relative amounts

A

Intake -
Diet - 50 to 100 mmol/day

Output -
Urine - 45 to 112 mmols
Stools - 5 to 10 mmols
Sweat - 5mmols

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2
Q

Describe the intra and extra cellular distrbution of K+ and what determines this

A

Intracellular distribution of K+ = 150 mmol/L average but some cells have higher [ ] such as muscle, liver, bone RBC and other cells
Extracellular distribution of K+ = 4.5 mmol/L
The distribution can be changed by insulin, adrenaline, pH and aldosterone (internal balance)

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3
Q

State what acute and chronic potassium regulation is

A
  • Acute regulation -
    Distribution of K+ between intra and extracellular fluid compartments
  • Chronic regulation -
    Achieved by the kidney adjusting K+ excretion and reabsorption
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4
Q

State the 3 main functions of potassium

A
  1. Determines intracellular fluid osmolality - changes cell volume via osmosis
  2. Determines resting membrane potential - very important for normal functioning of excitable cells
  3. Affects vascular resistance
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5
Q

Describe how the Na+/K+ pump works

A
  • Na+/K+ ATPase pumps 3Na+ out of the cell and 2K+ ions into the cell
  • This maintains the fact that more than 95% of bodily K+ is located intracellularly and only 2.5% in ECF - high intracellular [K+] and low intracellular [Na+]
  • Energy to drive the pump is released by ATP hydrolysis
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6
Q

Describe the internal balance/acute regulation of K+

A
  • Extracellular fluid pool will change more dramatically with changes in body K+ distribution e.g. after a meal there is a slight increase in plasma [K+] which is shifted into the intracellular fluid compartment
  • Shift is mainly subject to hormonal control- insulin, adrenaline, aldosterone and pH changes
  • It is key that plasma [K+] remains in the right range
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7
Q

What determines whether a person is hyper or hypo kalaemic?

A

Hyperkalaemia - plasma [K+] is above 5.5 mM

Hypokalaemia - plasma [K+] is below 3.5 mM

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8
Q

Describe how resting potential is normally maintained

A

Membrane potential formed by creation of ionic gradients - combination of chemical and electrical gradients

Normal resting membrane potential is maintained by a dynamic balance between Na+ and K+ concentrations

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9
Q

Describe how hypokalaemia and hyperkalaemia affect potential difference in a cell and what the significance is

A
  • When [K+] outside the cell increases and the [K+] inside the cell is constant the nernst equilibrium potential increases and potential becomes more positive
  • When [K+] outside the cell decreases and the [K+] inside the cell is constant the nernst equilibrium potential decreases and potential becomes more negative
  • Relatively small changes in the [K+] extracellularly are enough to drastically change the potential difference in a cell so can severely affect cardiomyocyte membrane potential which causes changes in ECG
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10
Q

Describe how ECG changes during hypokalaemia and hyperkalaemia

A

Hypokalaemia - decreased amplitude of T wave, prolonged QU interval and prolonged P wave

Hyperkalaemia - increased QRS complex, increased amplitude of T wave and loss of P wave

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11
Q

Describe how hypokalaemia and hyperkalaemia affect action potentials

A

Lower (more negative) - low [K+] = hyperpolarisation - the cell is more negative than the resting potential so it takes more for it to reach the threshold potential for an action potential to propagate

Higher (less negative) - high [K+] = depolarisation - the cell is less negative than the resting potential so it takes less for the threshold potential to be reached and an action potential to propagate

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12
Q

Describe what causes hypokalaemia

A

Caused by renal or extra renal loss of K+ or by restricted intake

E.g.
- Long standing use of diuretics without KCl compensation
- Hyperaldosteronism/conn’s syndrome which increase aldosterone secretion
- Prolonged vomiting = Na+ loss = increased aldosterone secretion = K+ excretion in kidneys
- Profuse diarrhoea

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13
Q

State what hypokalaemia results in

A
  • Decreased resting membrane potential
  • Decreased release of adrenaline aldosterone and insulin
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14
Q

Describe what causes hyperkalaemia

A
  • Acute hyperkalaemia is normal during prolonged exercise
  • Disease states -
  • Insufficient renal excretion
  • Increased release from damaged body cells e.g. during chemotherapy, long lasting hunger, prolonged exercise or severe burns
  • Long term use of potassium sparing diuretics
  • Addison’s disease - adrenal insufficiency
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15
Q

What happens when plasma [K+] is above 7mM?

A

It is life threatening - asystolic cardiac arrest

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16
Q

What is the treatment for hyperkalaemia?

A
  • Insulin/glucose infusion used to drive K+ back into cells
  • Insulin is extremely important - mechanism is unclear - may stipulate Na+/K+ pump
  • Other hormones (aldosterone and adrenaline) stimulate Na+/K+ pump - increases cellular K+ influx
17
Q

In a healthy person what determines most of K+ balance?

A

The kidney

18
Q

What is the problem with K+ loss in stool?

A

K+ excretion in the stools is not under regulatory control e.g. large amounts can be lost by extra renal routes

19
Q

What is K+ homeostasis particularly important in now?

A

Increasingly important limiting factor in therapy for cardiovascular disease

20
Q

Which drugs increase serum [K+]?

A

Beta blockers, ACE inhibitors etc

21
Q

Describe overall what the kidneys do with Na+ and K+

A
  • The human kidneys have evolved to conserve Na+ and excrete K+
  • Na+ and K+ are filtered freely at the glomeruli
  • Plasma and glomerular filtrate have the same [Na+] and [K+]
  • In 24hr the glomerular filtrate contains 25 moles Na+ and 0.7 moles K+ but this depends on dietary intake
22
Q

Describe what happens to K+ in the proximal convoluted tubule including the mechanisms

A
  • In proximal convoluted tubule -
  • 60 to 70% Na+ and K+ reabsorbed in proximal convoluted tubule
  • Fraction that is reabsorbed in proximal convoluted tubule is constant
  • Absolute amount reabsorbed varies with glomerular filtration rate
  • How does K+ move in the proximal convoluted tubule? -
  • The Na+/K+ pump acts to pump Na+ ions out of the tubule epithelial cells into the ECF and pump K+ ions into it creating a low [Na+] intracellularly and a high [K+] intracellularly
  • While there is passive diffusion of K+ ions back into the ECF there is still a high [K+]
  • This creates a Na+ gradient which cause Na+ ions to enter the epithelial cells cotransporting amino acids, glucose and phosphates with them while another transporter (antiporter) transports H+ ions out of the epithelium into the tubular lumen
  • There is then passive/paracellular transport of Cl-, K+ and Na+ ions from the tubular lumen which are then reabsorbed
  • This occurs because removal of the other components from the tubular fluid (Na+, glucose, amino acids, phosphates) concentrates the K+ and Cl-
23
Q

Describe Na+/K+ movement in the loop of Henle including the mechanism

A

Na+/K+ movement in the loop of Henle -
- As the glomerular filtrate travels down the descending arm water freely diffuses out such that the filtrate becomes concentrated so it gets a much higher osmolarity
- As the filtrate ascends the ascending arm the NaCl initially diffuses out passively and then is pumped out which decreases osmolarity again to below the level it was when it entered the loop of Henle
- The transporter of Na+ and Cl- ions also transported K+ ions out of the loop of Henle’s ascending arm into the epithelial cells
- The movement of Na+ is again driven by the Na+/K+ ATPase which pumps 3Na+ ions out of the epithelial cells and into the ECF
- The K+ ions then diffuse from the epithelial cells into the ECF

24
Q

Describe K+ movement in the DCT and the mechanism

A

K+ movement in the distal convoluted tubule -
- More than 90% of filtered K+ is reabsorbed in the PCT and loop of Henle
- Excretion of K+ into urine by overload is controlled by K+ secretion by principal cells of late DCT and CD
- The Na+/K+ ATPase pumps 3Na+ ions out of the epithelial cells into the ECf and 2K+ ions into the epithelial cells from the ECF
- K+ ion would then usually diffuse from the epithelial cells into the ECF but they can enter the tubular lumen instead
- This occurs when ENaC channels (epithelial Na channels) also Na+ ions to move down the gradient from the tubular lumen into the epithelial cells
- There is also a second mechanism by which there is a symporter which transports both Cl- ions and K+ ions from the principal cells into the lumen

25
Q

Describe what determines K+ secretion in DCT and how it is achieved briefly

A
  • Determinants of K+ secretion in distal convoluted tubule -
  • Increased K+ intake
  • Changes in blood pH
  • Alkalosis - increased excretion of K+ which decreases serum [K+]
  • Acute acidosis - decreased excretion of K+ which increases serum [K+]
  • How is this achieved? -
  • Activity of Na+/K+ ATPase pump
  • Electrochemical gradient
  • Permeability of luminal membrane channel
26
Q

How does aldosterone increase secretion after increasing plasma [K+]? (3 ways)

A
  1. Slows exit from basolateral membrane which increases [K+] which produces a cell-lumen concentration gradient
  2. Increased activity of Na+/K+ ATPase which increases the [K+] inside the epithelial cells of the tubule which then increases movement of K+ into the tubular lumen
  3. Stimulates aldosterone secretion
27
Q

Describe how aldosterone has its effects

A
  1. There is an increased intake of potassium
  2. This increases the plasma [K+]
  3. This causes increased aldosterone secretion from the adrenal cortex
  4. This increases the plasma [aldosterone] which causes collecting ducts to increase K+ secretion
  5. The increased plasma K+ also directly causes the cortical collecting ducts to increase their K+ secretion
  6. Subsequently K+ excretion is increased
28
Q

What does aldosterone act to do?

A
  • Increase the activity of the Na+/K+ pump which then -
  • Increases K+ influx
  • Increases [K+]
  • Produces a cell-lumen concentration gradient
  • Increases ENaC channels which then -
  • Increases Na+ reabsorption
  • This decreases cell negativity and increases lumen negativity
  • This then produces a voltage gradient

Redistributes ENaC from intracellular localisation to membrane

Also increases permeability of luminal membrane K+

29
Q

State and describe other factors that affect K+ secretion

A
  • Alkalosis and acidosis -
  • In a high pH environment (alkalosis) the activity of the Na+/K+ pump is elevated so there is an increase in the intracellular [K+] which favours its secretion to the tubular lumen
  • In a low pH environment (acidosis) the activity of the Na+/K+ pump is decreased so there is a decrease in the intracellular [K+] which decreases its secretion to the tubular lumen
  • Tubular flow rate and K+ secretion -
  • Increased flow rate can be caused by an increased glomerular filtration rate, an inhibition of reabsorption and K+ wasting diuretics
  • This essentially dilutes the potassium as it is being moved away from cells at a faster rate so the electrochemical gradient is favoured and more K+ ions enter the tubular lumen from the epithelial cells
  • ADH impacts K+ ion channels allowing more K+ to be secreted into the tubules
  • Reabsorption of K+ in severe hypokalaemia -
  • Intercalated cells of the late DCT and CD become active
  • This provides additional reabsorption of K+ to preserve its [ ]
  • Mechanism not well known by it activates a K+/H+ ATPase which pumps K+ ions into cells from the tubular lumen and pumps H+ ions into the lumen
  • This increases the intracellular [K+] so K+ is transported from the cells into the ECF
30
Q

Describe how Na+/K+ balance maintains K+ when ECF volume changes

A
  • There is a decrease in the ECF volume
  • This causes increases aldosterone secretion from the adrenal cortex
  • Aldosterone then promotes K+ secretion/excretion in the cortical collecting ducts
  • The decrease is ECF volume and aldosterone will also cause the proximal tubule to increase Na+ reabsorption so there is a reduced flow rate in the tubules
  • Such that there is an unchanged K+ excretion
31
Q

Describe the renin angiotensin aldosterone system and how it impacts Na+ and K+ when BP and Na+ decrease

A

E.g. If there was a decrease in BP (detected by juxtaglomerular apparatus) and decrease in Na+ (detected by macula densa)
- This would signal the release of renin which would release of angiotensin II which causes vasoconstriction to increase BP again
- The angiotensin II also acts on the adrenal cortex along with the high [K+] in the plasma to increase secretion of aldosterone
- In principal cells of the DCT and CD promotes H2O and Na+ reabsorption and K+ secretion
- In intercalated cells it promotes Na+ and K+ reabsorption and H+ secretion

32
Q

What hormones does the adrenal cortex produce?

A

Produces:
- Glucocorticoid hormones
- Sex hormones
- Mineralocorticoid hormones

33
Q

Describe Addisons disease (cause, what it leads to, treatment)

A
  • A primary adrenal insufficiency
  • Rare compared to secondary adrenal insufficiency
  • Damage to the cortex leads to reduced hormone production and numerous symptoms
  • Deficiency in aldosterone causes the body to secrete large amounts of Na+ which leads to low serum [Na+] so the body retains K+ and has hyperkalaemia
  • Treatment usually involves steroid replacement therapy for life
34
Q

Describe what happens in secondary adrenal insufficiency

A
  • The pituitary secretion of ACTH decreases
  • This reduces levels of cortisol
  • Causes the adrenal glands to shrink
35
Q

Describe what Conns syndrome is

A
  • Primary aldosteronism aka conn’s syndrome -
  • This is due to aldosterone producing adenoma of the adrenal gland zona glomerulosa
  • It is usually less than 3cm, unilateral and renin unresponsive - no control mechanism
  • Hyperaldosteronism (excess release of aldosterone) due to variety chronic disease
  • Most commonly (50-60%) due to conn’s syndrome remaining 40-50% due to bilateral adrenal hyperplasia
  • Aldosterone release in absence of stimulation by angiotensin II
36
Q

What is the mechanism behind the condition?

A
  • There is greatly increased plasma aldosterone which causes the kidneys to stimulate Na+ reabsorption and K+ excretion so the person develops hypertension and has increased fluid volume - causes hypokalaemia, hypernatremia and alkalosis (decreased K+, increased Na+ and increased pH)
  • There is increased BP and Na delivery to the macula densa which decreases the release of renin - renin independent hypertension
37
Q

What is the treatment for Conns disease?

A
  • Surgical removal of tumour containing adrenal gland
  • Hypertension and hypokalaemia controlled with K+ sparing agents e.g. spironolactone

Physiology 1 Semester 2 (50 decks)

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