Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What % K+ is in the ECF?

A
  • 2%

* 3.5 - 5 mmol/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the difference between ICF & ECF maintained by?

A

Na+/K+ ATPase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does K+ establish the resting membrane potential?

A
  • Diffusion out of ICF into ECF

* Gives resting cell membrane potential of -90mv

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does an increase in ECF K+ cause?

A

• Depolarisation of cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What do a decrease in ECF K+ cause?

A

Hyperpolarization of the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is potassium regulated?

A
  • Internal balance, maintaining ECF K+

* External balance, adjusts K+ excretion to intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is average K+ intake in diet?

A

40 - 100 mmol/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A
  • K+ moves into cells

* Kidneys begin to excrete K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What factor can stimulate aldosterone secretion?

A

• Hyperkalaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do catecholamines increase uptake of K+ in ECF?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

• By increasing K+ uptake to other cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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 form

Heart 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+ <3.5 nmol/L

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 problems
Ø 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 ileus

Acidosis

64
Q

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

A

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
Q

What is the emergency treatment for hyperkalaemia?

A

o Reduce K+ effect on heart
• IV Calcium Gluconate
o 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

Semester 3 - Urinary (33 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions