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Sophie - Applied Physiology & Pharmacology Year 2 > 51.2 Regulation of Plasma Potassium > Flashcards

51.2 Regulation of Plasma Potassium Flashcards

1
Q

How abundant is K+?

A

It is the most abundant cation in the ICF

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2
Q

On average, how much K+ is in an average 70kg person?

A

3500 mM

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3
Q

What are the consequences of hyperkalaemia?

A
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4
Q

What are the consequences of hypokalaemia?

A
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5
Q

What are the different routes of excretion of potassium and how much is excreted by each per day?

A
  • Urine -> 88%
  • Stool -> 11%
  • Skin -> 1%
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6
Q

Draw a diagram to show potassium homeostasis.

A
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7
Q

Describe the dietary balance of potassium.

A
  • Around 100mEq are taken in per day
  • Around 90mEq are excreted in the urine
  • Around 10mEq are excreted in the stool
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8
Q

Describe the distribution of potassium in the body.

A
  • 98% stored intracellularly:
    • 80% in muscle -> 2700mEq
    • Liver -> 250mEq
    • Bone -> 300mEq
    • Erythrocytes -> 250mEq
  • 2% stored extracellularly -> 70mEq
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9
Q

What is the biggest intracellular store of potassium? How much does it typically store?

A
  • Muscle
  • Stores about 80% of total potassium -> 2700mEq
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10
Q

What is the extracellular concentration of potassium at rest?

A

4mmol/L

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11
Q

What is the normal range for plasma potassium concentration?

A

3.5 - 5.5mmol/L

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12
Q

What is the size of the potassium gradient between intracellular and extracellular fluid? What maintains this?

A
  • It is about 30 times greater intracellularly
  • This is maintained by a Na+/K+-ATPase on the cell membrane
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13
Q

What is responsible for short and long-term regulation of plasma potassium?

A
  • Short term -> Na+/K+-ATPase in cell membrane
  • Long term -> Kidneys
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14
Q

What things can cause low and high plasma potassium? (hypokalemia and hyperkalemia) [IMPORTANT]

A
  • Hypokalemia -> Diuretics + Diarrhoea
  • Hyperkalemia -> Kidney failure
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15
Q

Draw the relationship between total body potassium levels and plasma potassium levels. How is this affected by diuretics and renal failure?

A
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16
Q

What are the main consequences of hyperkalemia and hypokalemia?

A
  • Muscle weakness
  • Cardiac dysrhythmias
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17
Q

Why is it important to maintain potassium homeostasis (for example by moving extracellular potassium into cells)?

A
  • Marked changes in the ratio of extracellular/intracellular K+ can affect the excitability of cells.
  • This is particularly the case with cardiac myocytes.
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18
Q

What things can affect the extracellular concentration of potassium, [K+]o by changing the action of the cell-surface Na+/K+-ATPase?

A
  • Insulin
  • Catecholamines
  • Acid-base status
  • Hypoxia
  • Exercise
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19
Q

What effect do these have on extracellular potassium concentration:

  • Insulin
  • Catecholamines
  • Acid-base status
  • Hypoxia
  • Exercise
A
  • Insulin -> Decreases
  • Catecholamines -> Increase/Decrease (depending on whether they are alpha or beta agonists)
  • Acid-base status -> Increase/Decrease (acid leads to hyperkalemia)
  • Hypoxia -> Increase
  • Exercise -> Increase
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20
Q

Aside from the kidneys, which organs respond to high plasma potassium?

A
  • Pancreas -> Secretes insulin
  • Adrenal glands -> Secrete adrenaline and aldosterone
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21
Q

How is insulin involved in potassium homeostasis?

A

It decreases plasma potassium by moving potassium into cells:

  • When there is increased extracellular potassium, there is increased insulin secretion from beta cells of the pancreas
  • Stimulates Na+/K+-ATPase on cell membrane
  • This is due to second messenger which is not agreed upon, but it is probably a protein kinase that phosphorylates the ATPase
  • It also has an effect via stimulating Na+-glucose co-transport into the cell, which drives the ATPase
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22
Q

Compare the effects of α and β2 agonists on plasma potassium.

A
  • α agonists increase plasma potassium
  • β2 agonists decrease plasma potassium
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23
Q

What is the effect of β2 agonists (e.g. salbutamol) on plasma potassium?

A

It decreases plasma potassium by moving potassium into cells:

  • Stimulates Na+/K+-ATPase on cell membrane
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24
Q

What is the effect of aldosterone on the plasma potassium?

A

It decreases plasma potassium by moving potassium into cells:

  • Stimulates Na+/K+-ATPase on cell membrane
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25
Q

Draw a summary of the main hormones that affect the Na+/K+-ATPase on the surface of cells so as to reduce plasma potassium.

A
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26
Q

What is the effect of adrenaline on plasma potassium levels?

A

Causes a transient hyperkalemia followed by hypokalemia:

  • This is due to the fact that it is a non-selective adrenergic agonist
  • The hyperkalemia is due to it acting on alpha receptors
  • The hypokalemia is due to it acting on beta-2 receptors
27
Q

Give some ways in which hyperkalemia may be treated clinically.

A
  • Insulin (+ Dextrose) -> Slower
  • Beta-2 agonist (e.g. salbutamol) -> Faster
28
Q

What are the effects of metabolic acidosis on plasma potassium?

A
  • Metabolic acidosis leads to hyperkalemia
  • However, this is only the case with mineral acid (HCl) and not organic acid (lactic)
29
Q

What is the effect of hypoxia on plasma potassium?

A

Hypoxia causes hyperkalemia.

30
Q

Explain the relationship between hypoxia and potassium.

A
  • Hypoxia leads to hyperkalemia
  • This is thought be due to low oxygen causing a drop in ATP levels, which leads to KATP channels remaining open, so that potassium can flow out of the cell.
31
Q

What is the effect of exercise on plasma potassium? What is the mechanism for this?

A

Exercise leads to hyperkalemia:

  • Potassium is lost from cells through delayed rectifier channels
  • Incomplete reuptake of the potassium by the Na+/K+-ATPase leads to hyperkalemia
32
Q

Exercise results in hyperkalemia. What things help the body recover from that?

A

Insulin and catecholamines increase the rate of potassium reuptake by the Na+/K+-ATPase.

33
Q

What are some of the functional consequences of hyperkalemia?

[IMPORTANT]

A
  • Skeletal muscle fatigue
  • Skeletal muscle hyperaemia (excess of blood in vessels supplying the muscle)
  • Blood pressure regulation
  • Hyperpnoea (increased breathing rate)
  • Myocardial stability
34
Q

How high can blood potassium get during exercise? [IMPORTANT]

A

8mM

35
Q

How does hyperkalemia during exercise affect blood flow? What is some evidence for this?

A
  • Potassium released by muscles during exercise leads to hyperpolarisation of arterial muscle, so that blood flow to that muscle increases (hyperaemia)
  • (Knochel, 1972):
    • Blood flow through a muscle was correlated with the potassium released during exercise
    • Causation was shown by depletion of potassium from the system, which resulted in no change in blood flow
36
Q

Draw how the hyperkalemia produced by this exercising muscle leads to the body’s response to exercise.

A
  • The potassium released by the muscle during exercise causing depolarisation and therefore activation of the C-type pain fibres in the muscle
  • This triggers the muscle-pressor reflex, mediated by the brain:
    • Vasoconstriction in non-exercising vascular beds
    • Sympathetic activation of the heart
  • Hyperkalemia is detected by arterial chemoreceptors, particularly in the carotid body
  • The carotid body feeds back to the cardiorespiratory integrating centre via the glossopharyngeal nerve (IX)
  • The response triggered involves stimulation of the diaphragm and intercostal muscles, so that the breathing rate is increased
37
Q

Draw the position of the carotid bodies and how they link to the nervous system.

A

This allows them to detect hyperkalemia and respond to it.

38
Q

At rest, the blood potassium levels that are reached during exercise would cause cardiac arrest. Why does this not happen during exercise?

A

The catecholamines and potassium cancel out each others deleterious effects (mutual antagonism). The angiotensin pathway is also involved.

The increased calcium entry due to catecholamines and angiotensin cancels out the negative inotropic effect of potassium.

39
Q

What are dangerously high levels of plasma potassium endogenously antagonised by?

A

Ca2+

40
Q

How is hyperkalemia treated clinically?

A
  • Insulin, dextrose and beta-2 agonists are used.
  • In renal failure, dialysis is used.
  • If a very fast response is required, calcium injection can antagonise the negative inotropic effect of hyperkalemia -> Allows time for clinical intervention
41
Q

What are some common causes of hypokalaemia and hyperkalaemia?

A
  • Hypokalemia -> Vomiting + Diarrhoea
  • Hyperkalemia -> Renal failure
42
Q

Describe the structure of alpha intercalated cells. How are does this aid in their role in potassium fine tuning?

A

REABSORPTION OF K+
Apical ATP driven H-K ATPase uptakes K+ and secretes H+
Basolateral K+ channel allows reabsorption

43
Q

Describe the structure of principal cells. How does this relate to their function in potassium handling?

A

ENaC channels on the apical membrane are driven by the Na/K ATPase
K+ accumulates inside the cell and flows down gradient into the lumen due to high apical permeability (KCC and K+ channels)

44
Q

Describe the type of potassium load that is presented to the kidneys?

A

Kidney presented a high potassium load
(filters 800mmol per day) so excretion is required

45
Q

How does the response to acidosis lead to a decrease in potassium excretion?

A

H/K ATPase on alpha intercalacted cell (A for acid secretion) activity will increase to try and offset the acidosis by secreting more H+ ions
Means that more K+ ions are being absorbed

46
Q

What are the effects on the renal system during hyperkalaemia? How do the kidneys adjust?

A

High K+ load
Zona glomerulosa cells in the adrenal gland secrete aldosterone in response to depolarisation due to high K+
Aldosterone acts on principal cells to increase the transcription of Na/K ATPase in the basolateral memrbane
Leads to accumulation of K+ inside of prinicipal cells and increased secretion of K+

47
Q

What are the most common causes of hyperkalaemia?

A

Crush injury
Tumour lysis
Addisons disease (low aldosterone which usually increases K+ excretion)
Acidosis (K+ efflux in exchange for H+ ions)
Renal failure
ACE inhibitors (decreased aldosterone, -“-)

48
Q

What are the most common causes of hypokalaemia?

A

Alkalosis
Kidney failure
Loop diuretics
Diarrhoea
Vomiting
Conn’s syndrome (excess aldosterone)
Diabetic ketoacidosis (due to osmotic diuresis)

49
Q

What causes potassium reabsorption in the thick ascending limb?

A

Lumen positive voltage and high paracellular K+ permeability
Apical NKCC2 secondary active transporter

50
Q

What is a side effect of an overdose in salbutamol?

A

Hypokalaemia = light headed, arrhythmia
Due to shuttling of K+ out of plasma into cells

51
Q

What is the intracellular concentration of potassium?

A

140mM (120-150mM) per L

52
Q

What percentage of daily K+ intake is excreted by the kidneys and colon?

A

90-95% excreted by kidneys
5-10% excreted by the colon

53
Q

Where does fine tuning of potassium occur in the kidneys?

A

Distal convoluted tubule and collecting duct

54
Q

Where is most of potassium secreted?

A

Early DCT

55
Q

Where is most of the potassium stored?

A

INSIDE CELLS
-Lots in muscle (high faction of body mass)
-Smaller quantities in liver, bone and RBCs

56
Q

Where is the majority of potassium reabsorbed in the kidney? What is the importance of this?

A

Proximal convoluted tubule (80%)
Loop of Henle (10%)
Remaining 10% is presented to the DCT which performs the appropriate fine tuning

57
Q

Where is the potassium loss in loop diuretics?

A

With both loop diuretics and thiazides the potassium loss occurs in the distal nephron as sodium is reclaimed: the reabsorption of sodium creates a charge gradient across the epithelium, and potassium ions and protons move down this gradient into the urine

The sodium reabsorption in the distal tubule is augmented by the action of aldosterone, released when the renin axis is activated in response to the diuresis: this effect further increases the loss of potassium ions and protons from the distal nephron

58
Q

Which cell types in the nephron are responsible for fine tuning of potassium concentration?

A

Principal cells in the collecting duct and late DCT= SECRETE K+
Alpha intercalated cells in the collecting duct and DCT = ABSORB K+

59
Q

Which diuretics are potassium losing?

A

Loop diuretics
Thiazide diuretics

60
Q

Which diuretics are potassium sparing?

A

Antagonists of aldosterone
-Spironolactone (aldosterone antagonist)
-Amiloride (blocks apical ENaC) to stop Na reabsorption

61
Q

Why are thiazide diuretics potassium losing?

A

Thiazides inhibit the action of the sodium-chloride symporter (NCC) on the luminal (apical) surface of the epithelial cells = more Na in urine
increased sodium (and urine) flow in the distal nephron (caused by the diuretic drug) leads to increased sodium uptake by the epithelium of the distal convoluted tubule and collecting duct, through existing sodium channels and transporters in the luminal surface and existing Na/K-ATPase pumps on the basolateral surface: this is an immediate response, using channels and pumps that already exist and have spare capacity;
the result is that additional sodium is reabsorbed, and potassium ions and protons are lost into the urine;
the effects of the diuretic drug activate the juxtaglomerular apparatus, which responds by releasing renin: this hormone leads eventually to the production of angiotensin and so to the release of aldosterone = increase Na/K ATPase on basolateral membrane = increase K loss

62
Q

Why do loop diuretics cause hypokalaemia?

A

INHIBIT NKCC2 (Na/K/Cl)
Prevents active potassium reabsorption in the thick ascending limb, more stays in the tubule and is excreted

63
Q

Why does hypokalaemia cause muscle weakness?

A

increases the gradient across the sarcolemma to make it harder to depolarise the cells and cause contraction causing hypotonic weakness

64
Q

with which ion does K+ have reciprocity?

A

Hydrogen ions
*to maintain pH/ electrochemical balance.
*If ECF pH increases, H+ moves out of cells. K+ moves into cells to compensate.

Sophie - Applied Physiology & Pharmacology Year 2 (32 decks)

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