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Semester 3 - Urinary > Session 6 - Control of Potassium (OK+?) > Flashcards

Session 6 - Control of Potassium (OK+?) Flashcards

1
Q

What % of K+ is in the ICF?

A
  • 98%

* 120-150mmol

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2
Q

What % K+ is in the ECF?

A
  • 2%

* 3.5 - 5 mmol/l

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3
Q

What is the difference between ICF & ECF maintained by?

A

Na+/K+ ATPase

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4
Q

How does K+ establish the resting membrane potential?

A
  • Diffusion out of ICF into ECF

* Gives resting cell membrane potential of -90mv

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5
Q

What does an increase in ECF K+ cause?

A

• Depolarisation of cell membrane

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6
Q

What do a decrease in ECF K+ cause?

A

Hyperpolarization of the cell

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7
Q

Give a brief overview of K+ ions

A
  • K+ ions are the most abundant intra-cellular cation
  • 98% of total body K+ content is intracellular
  • 2% is in the ECF

Body tightly maintains plasma K+ in the range of 3.5 - 5.3 mmo

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8
Q

Why is high K+ inside cells and mitochondria necessary?

A 
Maintaining cell volume
Regulating intracellular pH 
Controlling cell-enzyme function
DNA/Protein synthesis 
Cell growth
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9
Q

What are the metabolic effects of extremely low extracellular K+?

A
  • Inability of the kidney to form concentrated urine
  • A tendency to develop metabolic alkalosis

Large enhancement of renal ammonium excretion

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10
Q

Why is low K+ necessary outside cells?

A
  • To maintain steep K+ ion gradient across cell membranes
  • Increase in ECF K+ depolarises cell membrane
  • Decrease in ECF K+ hyperpolarises the cell membrane
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11
Q

How is potassium regulated?

A
  • Internal balance, maintaining ECF K+

* External balance, adjusts K+ excretion to intake

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12
Q

What is average K+ intake in diet?

A

40 - 100 mmol/day

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13
Q

How does body prevent huge increase in ECF K+ after eating?

A
  • K+ moves into cells

* Kidneys begin to excrete K+

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14
Q

What is internal balance the net result of?

A
  • Movement of K+ from ECF -> into cells

* Movement of K+ out of cells into ECF

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15
Q

What factors promote the uptake of K+ into cells?

A 
• Hormones 
	○ Insulin 
	○ Aldosterone
	○ Catecholamines
• Alkalosis 
	○ Shift of H+ out of cells
	○ Reciprocal K+ shift into cells
• Increased K+ in ECF
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16
Q

How does insulin promote uptake of K+ in ECF?

A

• K+ in splanchnic blood stimulates insulin secretion by pancreas

Insulin stimulates K+ uptake by muscle cell and liver via an increase in Na+/K+ ATP-ase

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17
Q

How does aldosterone promote excretion of K+ into tubule lumen

A
  • Increases the transcription of Na/K/ATPase in basolateral membrane and ENaC/K+ channels in apical membrane
  • Increased channel number gives increases K+ excretion
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18
Q

What factor can stimulate aldosterone secretion?

A

• Hyperkalaemia

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19
Q

How do catecholamines increase uptake of K+ in ECF?

A

• Act via B2 adrenoreceptors which in turn stimulate Na-K+-ATPase

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20
Q

Outline 5 factors promoting K+ shift out of cell

A 
• Low ECF
• Exercise 
• Cell lysis
• Increase in ECF osmolality
• Acidosis - Increase ECF
	○ Acidosis, shift of H+ into cells, reciprocal K+ shift out of cells
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21
Q

How does exercise promote K+ shift of cells?

A
  • Skeletal muscle contraction -> Net release of K+ during recovery phase of action potential
  • Increase in plasma K+ which is proportional to the intensity of exercise
  • Uptake of K+ by non contracting tissues as a result of catecholamine release
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22
Q

How do catecholamines offset ECF rise in K+ during exercise?

A

• By increasing K+ uptake to other cells

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23
Q

How does cell lysis promote K+ shift out of cells

A
  • Cell lysis causes a release of K+ from ICF into the ECF

* Can be causes by skeletal muscle trauma, intravascular haemolysis and cancer chemotherapy

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24
Q

How does plasma tonicity cause K+ movement from ICF to ECF?

A
  • Increase in plasma & ECF tonicity
  • Water moves from ICF into ECF
  • Increase in K+ in ICF

K+ moves down conc grad out of cell

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25
What does acidosis do to K+ conc in cell?
* Shift of H+ into cells * Reciprocal K+ shift * Out of the cells * Causes hyperkalaemia
26
What does akalosis do to K+ concentration in cell?
* Shift of H+ out of cells * Reciprocal K+ shift * Move into cells causes hypokalaemia
27
How is potassium balanced?
* External balance | * Internal balance
28
What is external balance?
* Regulates total body K+ content * Depends on dietary intake, and excretion * Responsible for the long-term control of K+
29
How is external balance controlled?
• Controlled by renal excretion
30
What is internal balance?
• Regulates K+ • Responsible for moment to moment control • If ECF/Plasma (K+) increases, K+ moves into cells ○ ECF -> ICF ○ Na/K/ATPase • If ECF/plasma K+ decreases, K+ moves out of cells ○ ICF -> ECF ○ K+ channels
31
Give three hormones which cause movement of K+ from ECF to ICF?
* Insulin * Catecholamines * Aldosterone
32
What does insulin do to promote movement of K+ from ECF to ICF?
* K+ in splanchnic blood stimulates insulin secretion from the pancreas * Insulin increases the amount of Na-K-ATPase as it provides the drive for the Na-glucose transporter * Increases K+ uptake
33
How do catecholamines promote movement of K+ from ECF to ICF?
* B2 adrenoreceptors stimulate Na/K+/ATPase * Exercise and trauma increases K+ exit from cells (ICF to ECF), but also increases catecholamines to help offset the ECF (K+) rise
34
What happens to K+ in kidney?
* K+ reabsorbed | * K+ secreted
35
Where is K+ reabsorbed in the kidney?
* Proximal tubule * Thick ascending limb of loop of henle * Distal tubule/Cortical collecting duct (intercalated cell) * Medullary collecting duct - intercalated cells
36
Where is K+ secreted in the kidney?
* Distal tubule and cortical collecting duct | * principle cells
37
How is K+ reabsorbed in proximal convoluted tubule and in what quantities?
• Passive process • By paracellular diffusion ○ 67% reabsorbed regardless of diet
38
How is K+ reabsorbed in thick ascending limb of loop on henle, and it what quantities?
• Active process (Driven by Na-K-ATPase pumps in basolateral membrane) • Na-K-2Cl transporter in apical membrane ○ 20% reabsorbed regardless of diet
39
What occurs in the principle cells of the DCT and cortical collecting duct in a high K+ diet?
• Substantial secretion (15-20%)
40
What occurs in the principle cells of the DCT and cortical collecting duct in a low K+ diet?
• Little secretion
41
What occurs in the intercalated cells of DCT and cortical collecting duct and medullary collecting duct?
• 10-12% K+ reabsorbed regardless of diet
42
How is K+ secreted from principal cells in the DCT and cortical CD
* Passive process driven by electro-chemical gradient * ENAC reabsorption of Na+ drives secretion of K+ through separate channel, creating a negative charge in the lumen * Process driven by Na+/K+ATPase, which created gradient for Na+ reabsorption
43
What are the two main factors which affect K+ secretion by principal cells?
* Tubular factors | * Luminal factors
44
What are three tubular factors affecting K+ secretion
* Aldosterone * K+ in ECF * Acid base status
45
What are two luminal factors affecting K+ secretion?
* Increase distal tubular flow rate | * Na delivary to distal tubule results in more K+ loss
46
How does high K+ in ECF effect K+ secretion in principal cell?
* Stimulates NaKATPase and increases permeability of apical K+ secretion * Stimulates aldosterone secretion
47
How does aldosterone affect secretion by principal cells?
• Increase transcription of relevant proteins, such as ○ Na/K/ATPase ○ K+ channels & ENAC in apical membrane Gives increased K+ excretion
48
How does acid base status affect secretion of K+ ions from principle cells?
* Acidosis decreases K+ secretion - Inhibits Na/K+/ATPase, decreases K+ channel permeability * Alkalosis Increase K+ secretion - Stimulates KaKATPase, increase K+ channel permeability
49
How is K+ reabsorbed in the DCT and cortical CD
* Intercalated cells * Active process * Mediated by H+-K+-ATPase (2H+ into lumen, K+ out )
50
What does hypokalaemia do to an ECG and resting membrane potential?
• Hypokalemia hyperpolarises cardiac cells ○ More fast Na+ channels available in active form Heart more excitable
51
What does hyperkalaemia do to ECG and resting potential?
* More fast Na+ channels remain in inactive form * Heart less excitable * Hyperkalaemia depolarises cardiac cells More fast Na+ channels
52
What is hypokalaemia?
• K+ <3.5 nmol/L
53
What two things can cause hypokalaemia?
• Problems of external balance ○ Excessive loss • Problems of internal balance ○ Shifts of potassium into ICF
54
Outline some causes of excessive loss of K+
• GI - diarrhoea/vomiting • Kidney ○ Diuretic drugs § Osmotic diuresis (diabetes) High aldosterone
55
Outline a problem of internal balance of K+ causing hypokalaemia
* Shift of potassium into ICF | * Metabolic alkalosis
56
What are the general effects of hypokalaemia on cardiac cells?
* Hyperpolarises - Faster | * Na+ channels available in active form -> heart more excitable
57
Give four clinical features of hypokalaemia
* Heart -> Altered excitability -> Arrhythmias * Gastro intestinal -> Neuromuscular dysfunction -> Paralytic ileus * Skeletal muscle -> Neuromuscular dysfunction -> Muscle weakness -> Conn's syndrome * Renal -> Dysfunction of collecting duct cells -> Unresponsive to ADH -> Nephrogenic diabetes insipidus
58
What ECG changes occur in hypokalaemia?
* Increased amplitude and width of the P wave * Prolongation of the PR interval * T wave flattening and inversion * ST depression * Prominent U waves (best seen in the precordial leads)
59
Outline treatment for hypokalaemia?
• Treat cause • K+ replacement - IV/oral • If due to high aldosterone ○ K+ sparing diuretics that block action of aldosterone on principal cells ○ K+ sparing - Amiloride ○ Aldosterone antagonist - Spironolactone
60
What is hyperkalaemia caused by?
Ø >5nmol/l K+ Ø External balance problems Ø Internal balance problems
61
Outline the external balance problems which can cause hyperkalaemia
``` Ø Inadequate renal excretion ○ (Increased intake only causes hyperkalaemia in the presence of renal dysfunction) o Acute kidney injury o Chronic kidney injury o Reduced mineralocorticoid effect ○ Drugs which reduce/block aldosterone action § K sparing diuretics § ACE Inhibitors • Adrenal insufficiency ```
62
Outline internal balance problems which can cause hyperkalaemia
o Shifts of K+ from ICF à ECF • Acidaemia (Ketoacidosis / Metabolic Acidosis) • Cell Lysis
63
Give three clinical features of hyperkalaemia
• Heart • GI ○ Neuromuscular dysfunction -> Parlytic ileus Acidosis
64
Outline the ECG changes you will see with high serum K+
8 mmol/L Prolonged P-R Interval Tall T waves ST Segment depression 9 mmol/L Widened QRS Interval 10 mmol/L Ventricular fibrillation
65
What is the emergency treatment for hyperkalaemia?
o Reduce K+ effect on heart • IV Calcium Gluconate o Shift K+ into ICF via glucose and insulin IV • Remove excess K+ Dialysis
66
Give some of the longer term treatments for hyperkalaemia
``` • Remove excess K+ ○ Dialysis ○ Oral K+ binding resinds to bind K in the gut • Reduce intake • Treat cause ```
67
Give some of the longer term treatments for hypokalaemia
• Treat cause • Potassium replacement - IV/oral • If due to increased mineralocorticoid activity ○ Potassium sparing diuretics which block action of aldosterone on principal cells

Semester 3 - Urinary (33 decks)

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