Brainscape's Knowledge GenomeTM

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


See full index

SGUL - Physiology 1 > Potassium Balance > Flashcards

Potassium Balance Flashcards

1
Q

Describe the intra- and extracellular concentrations of potassium.

A

~150 mmol/L within the cells
~4.5 mmol/L outside of the cells

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

What is the difference in potassium maintained by?

A

Na/K ATPase

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

What maintains the low ECF [K+]?

A
  • Internal balance
  • Shifts K+ between the ECF and ICF compartments.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the major factors that affect potassium balance?

A

Diet
Urine
Stools
Sweat

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

What does external balance refer to?

A

Balance between what is taken in via the diet and what is excreted out

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

What organs control external balance?

A

Kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does the regulation of K+ homeostasis imply?

A

ACUTE REGULATION
CHRONIC REGULATION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is acute regulation achieved?

A

Distribution of K+ through the ECF and ICF compartments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is chronic regulation achieved?

A

Kidney adjusting K+ excretion and reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

List some of the functions of potassium.

A
  • determines the ICF osmolality, and thus cell volume
  • determines the resting membrane potential (RMP)
  • affects vascular resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the significance of the Na+-K+ ATPase pump.

A
  • Establishes a net charge across the plasma membrane
  • Interior of the cell is negatively charged with respect to the exterior.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the importance of resting potential?

A
  • Prepares the nerve and muscle cells for the propagation of action potentials
  • For nerve impulses and muscle contraction.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does the accumulation of sodium ions outside of the cell allow?

A
  • Draws water out of the cell
  • Maintain osmotic balance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the importance of an osmotic balance?

A

Without it, cell would swell and burst from the inward diffusion of water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the boundary for hypokalaemia?

A

plasma [K+] < 3.5 mM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the boundary for hyperkalaemia?

A

plasma [K+] > 5.5 mM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the Nerst equation?

A

E = RT/zF ln[X]o/[X]i

E is the Nerst Equilibrium Potential, R is the ideal gas constant, T is the temperature in Kelvin, z is the charge of the ion (valance) and F is Faraday’s number.

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

How are membrane potentials formed?

A

Creation of ionic gradients (ie. the combination of chemical and electrical gradients).

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

What can be determined from the Nerst equation?

A

Determine at which point the chemical and electrical gradients balance each other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What happens the plasma [K+] is altered above or below normal?

A
  • Severely affect the heart (cardiac cell depolarisations and hyperpolarisations)
  • Produces changes in ECG.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How does [K+] affect action potentials?

A

low [K+] = hyperpolarisation
high [K+] = depolarisation

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

How does hyperkalaemia affect ECG readings?

A
  • increased QRS complex
  • increased amplitude of the t wave
  • eventual loss of the P wave
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does hypokalaemia affect ECG readings?

A
  • lowered amplitude of the T wave
  • prolonged Q-U interval
  • prolonged P wave
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe hypokalaemia.

A

Caused by a renal or extra-renal loss of K+ or by the restricted intake of K+.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What cases are linked to hypokalaemia? Briefly give a reason for each case. PART 1

A
  • long-standing use of diuretics without KCl compensation
  • hyperaldosteronism/ Conn’s Syndrome (increased aldosterone secretion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What cases are linked to hypokalaemia? Briefly give a reason for each case. PART 2

A
  • prolonged vomiting, which leads to Na+ loss, which leads to increased aldosterone secretion, which leads to K+ excretion by the kidneys
  • profuse diarrhoea (diarrhoea fluid contains 50 mM of K+)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What does hypokalaemia lead to?

A

Decreased release of adrenaline, aldosterone and insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Why is acute hyperkalaemia normal following exercise?

A

Kidneys will excrete the extra K+ easily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What cases are linked to diseased hyperkalaemia?

A
  • insufficient renal excretion
  • increased release of K+ from damaged body cells (eg. during chemotherapy, long-lasting hunger or prolonged exercise )
  • long-term use of potassium-sparing diuretics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is a life-threatening plasma [K+]? Give a reason why.

A

Plasma [K+] of > 7mM. Can lead to cardiac arrest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What can be used to drive K+ influx to reverse hyperkalemia?

A
  • Insulin/ glucose infusion
  • Hormones (such as aldosterone and adrenaline) by stimulating Na/K pump
32
Q

Describe the renal handling of Na+ and K+.

A
  • Kidneys are designed to conserve Na and excrete K.
  • Na+ and K+ are filtered freely at the glomeruli. Thus, the plasma and the GF have the same [Na+] and [K+].
33
Q

Which drugs can increase the risk of hyperkalemia?

A

Drugs like β-blockers and ACE inhibitors by raising serum [K+]

34
Q

Which drugs can enhance the risk of hypokalemia?

A

Loop diuretics - for heart failure

35
Q

Is K+ excretion in stools under regulatory control?

A

No

36
Q

Describe K+ movement in the PCT. PART 1

A
  • K+ reabsorption is passive and paracellular through tight junctions.
  • Na+/K+ pump in cell membranes maintains high intracellular [K+]
  • Many K+ channels through which ions leak out.
37
Q

Describe K+ movement in the PCT. PART 2

A
  • By the end of the early proximal tubule, essentially, all the glucose amino acids has been reabsorbed.
  • Establishes a Cl- and K+ concentration gradient from the lumen to the peritubular fluid. - Na+ and K+ move passively along this gradient with Cl- in a paracellular route.
38
Q

What can happen if the Na/K pump is inhibited?

A
  • Na gradient is dissipated
  • Loss of primary Na transport and the associated secondary active solute transport.
  • No osmotic gradient for water transport.
39
Q

What can inhibit the Na/K pump?

A

Dopamine

40
Q

Describe Na+/K+ movement in the Loop of Henle. PART 1

A
  • Loop of Henle creates a cortico-medullary osmotic concentration gradient
  • Hence, as the fluid enters the descending limb and water leaves, the fluids get more concentrated
  • As it enters the ascending limb, characteristic changes occur and it is now impermeable to H2O but highly permeable to solutes.
41
Q

Describe Na+/K+ movement in the Loop of Henle. PART 2

A
  • In the thin ascending limb, Na and Cl diffuse out.
  • In the thick ascending limb, active reabsorption/ pumping of Na and Cl out of the fluid occurs, thereby making it more dilute.
42
Q

Describe Na+/K+ movement in the Loop of Henle. PART 3

A
  • Thick ascending limb movement done via a Na/2Cl/K symporter on the luminal membrane, which is driven by the [Na] gradient.
  • Entry of Na from the Na-H antiporter.
  • On the basolateral side, we have Na/K ATPase pump and the cotransport of Cl and K out of the cell (especially in the thick ascending limb).
43
Q

Describe Na+/K+ movement in the Loop of Henle. PART 4

A
  • Some diffusion of K back into the descending limb.
  • No water movement, the fluid in the lumen is very diluted, when it reaches the distal tubule, it is very hyposmotic
44
Q

Describe K+ movement in the DCT. PART 1

A
  • Majority reabsorbed.
  • But, in order to balance the input and output, need to be able to excrete excess K into the tubule.
  • Most of this occurs mainly in the principal cells of the distal tubule and collecting duct.
  • Variation in K excretion not due to reabsorption in PCT and Loop of Henle
45
Q

Describe K+ movement in the DCT. PART 2

A
  • K would enter the secreting cells from the blood via the Na-K-ATPase pump.
  • Diffuses from the cell down the electrochemical gradient through K+ channels that exist in the luminal/ apical membrane into the tubular fluid.
  • Electric gradient across the luminal membrane normally opposes the exit of K from the cell
  • Gradient is reduced by the Na flux through the ENaC channel in that membrane (which, like the Na+/K+ transporter, is aldosterone-sensitive).
46
Q

Describe K+ movement in the DCT. PART 2

A
  • Chemical gradient dominates.
  • K+ secretion is coupled with Na+ reabsorption, ie. the more Na+ reabsorbed by the principle cell, the more K+ secreted.
  • K-Cl cotransporter (symporter) also exists in the apical membrane and transports both K and Cl from the cell into the lumen.
47
Q

What causes the switch between K secretion and reabsorption?

A
  • activity of the Na-K-ATPase pump
  • electrochemical gradient
  • permeability of the luminal membrane channel
48
Q

What determines K+ secretion in the DCT?

A
  • increased K+ intake
  • changes in blood pH (alkalosis and acidosis)
49
Q

How is aldosterone involved in K+ secretion? PART 1

A
  • Increase the activity of the Na+/K+ pump, which increases K+ influx, which increases intracellular [K+], which contributes to the cell-lumen concentration gradient
  • Increases ENaC channels, which increase Na+ reabsorption, which decrease cell negativity and increase lumen negativity, thus contributing to the voltage gradient
50
Q

How is aldosterone involved in K+ secretion? PART 2

A
  • Redistributes ENac from its intracellular localisation to the membrane
  • Increases the permeability of the luminal membrane to K+
51
Q

How does plasma [K] affect K+ secretion?

A
  • Slows k+ exit from the basolateral membrane, so increases intracellular [K+], so contributing to the cell-lumen concentration gradient
  • Increased activity of Na+/K+ ATPase, so increased [K+] within the cell
  • Increased plasma [K], so stimulated aldosterone secretion
52
Q

How does alkalosis affect K secretion?

A
  • Increased activity of the Na+/K+ pump
  • Increased [K+] in the cell - favours the concentration gradient for K secretion.
  • Increase in tubular fluid pH
  • Increases the permeability of the luminal membrane.
53
Q

Why does tubular pH increase during alkalosis?

A
  • Proximal tubule H+ secretion is decreased
  • Increases HCO3- in the tubular fluid
  • Greater tubule pH
54
Q

How does ACUTE acidosis affect K secretion?

A
  • Increase in [H+] of the ECF
  • Reduces the activity of the Na+/K+ pump
  • Decreases intracellular [K]
  • Reducing the passive diffusion and excretion of K.
55
Q

How does an increase in tubular flow rate affect K+ secretion?

A
  • Secreted K is sweeped away
  • Tubular fluid [K] low
  • Rapid rate of net secretion
  • Maintains the [K+] gradient favourable to secretion.
56
Q

How does ADH affect K+ secretion?

A
  • Increases the K conductance of the luminal membrane.
  • Stimulates secretion
  • Effect is not as great as that of aldosterone.
57
Q

Where does the reabsorption of K+ occur and what is its role?

A
  • Mainly in the intercalated cells (late DCT and CD)
  • Under normal conditions, it doesn’t play much of a role since most of the reabsorption occurs in the PCT and LoH.
  • Intercalated cells may have a H/K-ATPase pump with H excretion, resulting in K reabsorption - active in severe hypokalaemia.
58
Q

How are people with hypokalaemia affected by changes in K+ reabsorption activity?

A
  • Distal tubule, the connecting tubule, and the cortical collecting duct do not secrete K+, and may reabsorb some K+.
  • K+ which passes through the cortical collecting duct is reabsorbed in the medullary collecting duct
  • K+ excreted in the urine is minimal.
59
Q

How is K excretion maintained with a fall in ECFV?

A
  • Increased Na and fluid reabsorption in the PCT
  • Decreased distal K secretion because of reduced delivery of fluid and Na to the principal tubule cells.
  • Stimulates the release of aldosterone, which stimulates distal potassium secretion.
  • Change in potassium excretion is minimised.
60
Q

How does the RAAS system affect K secretion in a patient with low blood pressure? PART 1

A
  • JGA senses the fall in local BP
  • Macula densa detects the low sodium concentration in the DCT.
  • Release of renin, which leads indirectly to the formation of Angiotensin II.
  • Causes vasoconstriction and stimulates the adrenal cortex to produce aldosterone.
61
Q

How does the RAAS system affect K secretion in a patient with low blood pressure? PART 2

A
  • Aldosterone acts on the DCT to increase Na reabsorption by increasing insertion of Na/K ATPase pumps, and ENaC channels.
  • Incoming Na+ brings more water via osmosis, thus restoring fluid volume and pressure.
  • Greater K+ (or H+) secreted in exchange.
  • Aldosterone increases both the recovery of Na and the loss of K+ (or H+).
62
Q

How does the RAAS system affect K secretion in a patient with low blood pressure? PART 3

A
  • High plasma [K+] causes the release of aldosterone from the adrenal cortex.
  • Renin release is supressed by direct negative feedback from Angiotensin II.
  • Aldosterone also acts on the intercalated cells to increase the activity of the Na+/H+ antiporter
  • Influences the acid-base status by increasing H+ secretion - increase in serum pH.
63
Q

Describe Adisson’s Disease as a pathology related to Na and K balance.

A
  • Damage to adrenal cortex, so there is less hormone production
  • Deficiency in aldosterone, which leads to the body secreting large amounts of Na (leaving low serum Na levels) and the body retaining K (leading to hyperkalaemia).
64
Q

What is the treatment for Adissons’s Disease?

A

Corticosteroid (steroid) replacement therapy for life.

65
Q

What is Conn’s Syndrome?

A

Primary aldosteronism - due to an aldosterone-producing adenoma of the zona glomerulosa of the adrenal gland.

66
Q

How does Conn’s Syndrome cause hypokalaemia?

A
  • Increase in plasma aldosterone
  • Increase Na+ reabsorption and K+ excretion, so hypertension develops.
  • Increases the fluid volume, leading to hypokalaemia, hypernatremia (high serum sodium levels), and alkalosis.
67
Q

What is the treatment for Conn’s Syndrome?

A
  • Surgical removal of the tumor-containing adrenal gland
  • Hypertension and hypokalaemia are controlled with K+-sparing agents (eg. spironolactone).
68
Q

What does the adrenal cortex produce?

A

→ Glucocorticoid hormones
→Sex hormones

69
Q

What factors shift K+ out of cells?

A

→ Insulin deficiency
→ Aldosterone deficiency
→ Acidosis
→ Strenuous exercise
→ Increased ECF osmolarity

70
Q

What factors shift K+ into cells?

A

→ Insulin
→ Aldosterone
→ Alkalosis

71
Q

What does an increase in tubule fluid flow rate result from?

A

→ increased GFR or inhibition of reabsorption upstream or diuretics

72
Q

What inhibits eNAC channels?

A

Diuretics

73
Q

How is K+ maintained at high levels within the kidney cells?

A

→ Sodium travels from the tubular lumen to the ECF bringing glucose with it
→the Na+ and K+ pump maintains this on the basolateral side
→ Maintains K+ at high levels in the kidney cells

74
Q

What happens to the equilibrium potential when you have hyperkalaemia?

A

→ Less negative

75
Q

What happens to the equilibrium potential when you have hypokalaemia?

A

→ More negative

76
Q

What happens to K+ concentration after a meal?

A

→ Increase in plasma K+
→ shifted into ICF compartment

77
Q

What hormones is the ICF K+ shift due to?

A

→ insulin
→ adrenaline
→ aldosterone

SGUL - Physiology 1 (68 decks)

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