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3 - Urinary > deck_1650074 > Flashcards

deck_1650074 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 ECFBody 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 volumeRegulating intracellular pH Controlling cell-enzyme functionDNA/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 pancreasInsulin 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 ICFK+ moves down conc grad out of cell

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25
Q

What does acidosis do to K+ conc in cell?

A

• Shift of H+ into cells • Reciprocal K+ shift• Out of the cells • Causes hyperkalaemia

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26
Q

What does akalosis do to K+ concentration in cell?

A

• Shift of H+ out of cells• Reciprocal K+ shift • Move into cells causes hypokalaemia

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27
Q

How is potassium balanced?

A

• External balance• Internal balance

28
Q

What is external balance?

A

• Regulates total body K+ content• Depends on dietary intake, and excretion • Responsible for the long-term control of K+

29
Q

How is external balance controlled?

A

• Controlled by renal excretion

30
Q

What is internal balance?

A

• 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
Q

Give three hormones which cause movement of K+ from ECF to ICF?

A

• Insulin• Catecholamines• Aldosterone

32
Q

What does insulin do to promote movement of K+ from ECF to ICF?

A

• 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
Q

How do catecholamines promote movement of K+ from ECF to ICF?

A

• 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
Q

What happens to K+ in kidney?

A

• K+ reabsorbed• K+ secreted

35
Q

Where is K+ reabsorbed in the kidney?

A

• Proximal tubule• Thick ascending limb of loop of henle• Distal tubule/Cortical collecting duct (intercalated cell)• Medullary collecting duct - intercalated cells

36
Q

Where is K+ secreted in the kidney?

A

• Distal tubule and cortical collecting duct • principle cells

37
Q

How is K+ reabsorbed in proximal convoluted tubule and in what quantities?

A

• Passive process• By paracellular diffusion ○ 67% reabsorbed regardless of diet

38
Q

How is K+ reabsorbed in thick ascending limb of loop on henle, and it what quantities?

A

• Active process (Driven by Na-K-ATPase pumps in basolateral membrane)• Na-K-2Cl transporter in apical membrane ○ 20% reabsorbed regardless of diet

39
Q

What occurs in the principle cells of the DCT and cortical collecting duct in a high K+ diet?

A

• Substantial secretion (15-20%)

40
Q

What occurs in the principle cells of the DCT and cortical collecting duct in a low K+ diet?

A

• Little secretion

41
Q

What occurs in the intercalated cells of DCT and cortical collecting duct and medullary collecting duct?

A

• 10-12% K+ reabsorbed regardless of diet

42
Q

How is K+ secreted from principal cells in the DCT and cortical CD

A

• 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
Q

What are the two main factors which affect K+ secretion by principal cells?

A

• Tubular factors• Luminal factors

44
Q

What are three tubular factors affecting K+ secretion

A

• Aldosterone• K+ in ECF• Acid base status

45
Q

What are two luminal factors affecting K+ secretion?

A

• Increase distal tubular flow rate• Na delivary to distal tubule results in more K+ loss

46
Q

How does high K+ in ECF effect K+ secretion in principal cell?

A

• Stimulates NaKATPase and increases permeability of apical K+ secretion• Stimulates aldosterone secretion

47
Q

How does aldosterone affect secretion by principal cells?

A

• Increase transcription of relevant proteins, such as ○ Na/K/ATPase ○ K+ channels & ENAC in apical membrane Gives increased K+ excretion

48
Q

How does acid base status affect secretion of K+ ions from principle cells?

A

• Acidosis decreases K+ secretion - Inhibits Na/K+/ATPase, decreases K+ channel permeability• Alkalosis Increase K+ secretion - Stimulates KaKATPase, increase K+ channel permeability

49
Q

How is K+ reabsorbed in the DCT and cortical CD

A

• Intercalated cells • Active process • Mediated by H+-K+-ATPase (2H+ into lumen, K+ out )

50
Q

What does hypokalaemia do to an ECG and resting membrane potential?

A

• Hypokalemia hyperpolarises cardiac cells ○ More fast Na+ channels available in active formHeart more excitable

51
Q

What does hyperkalaemia do to ECG and resting potential?

A

• More fast Na+ channels remain in inactive form• Heart less excitable • Hyperkalaemia depolarises cardiac cells More fast Na+ channels

52
Q

What is hypokalaemia?

A

• K+

53
Q

What two things can cause hypokalaemia?

A

• Problems of external balance ○ Excessive loss• Problems of internal balance ○ Shifts of potassium into ICF

54
Q

Outline some causes of excessive loss of K+

A

• GI - diarrhoea/vomiting• Kidney ○ Diuretic drugs § Osmotic diuresis (diabetes)High aldosterone

55
Q

Outline a problem of internal balance of K+ causing hypokalaemia

A

• Shift of potassium into ICF• Metabolic alkalosis

56
Q

What are the general effects of hypokalaemia on cardiac cells?

A

• Hyperpolarises - Faster• Na+ channels available in active form -> heart more excitable

57
Q

Give four clinical features of hypokalaemia

A

• 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
Q

What ECG changes occur in hypokalaemia?

A

• Increased amplitude and width of the P wave• Prolongation of the PR interval• T wave flattening and inversion• ST depression• ProminentU waves(best seen in the precordial leads)

59
Q

Outline treatment for hypokalaemia?

A

• 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
Q

What is hyperkalaemia caused by?

A

Ø >5nmol/l K+Ø External balance problemsØ Internal balance problems

61
Q

Outline the external balance problems which can cause hyperkalaemia

A

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
Q

Outline internal balance problems which can cause hyperkalaemia

A

o Shifts of K+ from ICF à ECF • Acidaemia (Ketoacidosis / Metabolic Acidosis) • Cell Lysis

63
Q

Give three clinical features of hyperkalaemia

A

• Heart• GI ○ Neuromuscular dysfunction -> Parlytic ileusAcidosis

64
Q

Outline the ECG changes you will see with high serum K+

A

8 mmol/LProlonged P-R IntervalTall T wavesST Segment depression9 mmol/LWidened QRS Interval10 mmol/LVentricular fibrillation

65
Q

What is the emergency treatment for hyperkalaemia?

A

o Reduce K+ effect on heart • IV Calcium Gluconateo Shift K+ into ICF via glucose and insulin IV • Remove excess K+Dialysis

66
Q

Give some of the longer term treatments for hyperkalaemia

A

• Remove excess K+ ○ Dialysis ○ Oral K+ binding resinds to bind K in the gut• Reduce intake• Treat cause

67
Q

Give some of the longer term treatments for hypokalaemia

A

• Treat cause • Potassium replacement - IV/oral • If due to increased mineralocorticoid activity ○ Potassium sparing diuretics which block action of aldosterone on principal cells

3 - Urinary (39 decks)

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