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Kidneys and Renal functions > Potassium Balance > Flashcards

Potassium Balance Flashcards

1
Q

What are the most prevalent cations in the body?

A

Na+ and K+ are the most prevalent cations in body fluids

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2
Q

What is the typical daily intake of potassium in the UK?

A

A typical daily intake in the UK is 50-125 mmol.

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3
Q

How should potasium in the diet be regulated?

A

Unlike sodium, potassium intake should not be restricted routinely – only in cases of renal impairment with a low GFR. This is because potassium-containing foods include many healthy foods.

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4
Q

Describe the [K] in and around the cells of the body

A

[K] is high within cells and low outside of cells

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5
Q

What maintains the [K] gradient ?

A

Maintained by Na-K-ATPase
Maintenance of low ECF [K] is crucial
[K] is maintained mainly by internal balance, which shifts K+ between ECF & ICF compartments

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6
Q

What are the outputs of Potassium?

A

Urine‡: 45-112 mmols - ‡increased retention /loss
Stools: 5-10 mmols
Sweat: 5 mmols

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7
Q

What is the effect of diarrhoea/vomiting on potassium balance?

A

increased losses through stools and sweat due to intense heat or diarrhoea/vomiting (i.e skin/GI)

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8
Q

How do the kidneys control K balance via urine?

A

with renal K balance can get both increased loss OR increased retention

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9
Q

Describe acute regulation of K+ homeostasis

A

Distribution of K+ through ICF and ECF compartments

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10
Q

What is chronic regulation of K+ homeostasis?

A

Achieved by the kidney adjusting K+ excretion & reabsorption

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11
Q

What are the functions of potassium?

A
  1. Determines ICF osmolality → cell volume
  2. Determines resting membrane potential→v. important
    for normal functioning of excitable cells
    i.e. repolarisation of cell
    ⇒ myocardial, skeletal muscle & nerve cells

3.Affects vascular resistance

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12
Q

How does Na/K/ATPase pump maintain Na/K balance?

A

Pumps Na+ out of cell and K+ into cell driven by energy provided by ATP

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13
Q

What is the role of the Na/K/ATPase pump?

A

Na+-K+-ATPase pump maintains HIGH [K+]i and LOW [Na+]i

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14
Q

What is the effec of changing the distribution of K within the body?

A

ECF pool will change more dramatically with changes in body K distribution e.g. after a meal, get slight increase in plasma [K+], which is shifted into ICF compartment

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15
Q

What causes shifts in K distribution around the body?

A 
Shift mainly subject to hormonal control:
Insulin
Adrenaline
Aldosterone
pH changes
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16
Q

What is the maximum healthy level of [K+]?

A

VERY IMPORTANT that plasma [K+] does not rise beyond 6.5 mmol

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17
Q

What is hyperkalaemia?

A

Hyperkalaemia = plasma [K+] > 5.5mM

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18
Q

What is hypokalaemia?

A

Hypokalaemia = plasma [K+] < 3.5mM

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19
Q

How is the membrane potential formed?

A

Membrane potential formed by creation of ionic gradients (i.e. combination of chemical & electrical gradients)

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20
Q

What determines the resting membrane potential ?

A

Dynamic balance between membrane conductance to Na+ and K+ determines RMP normally

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21
Q

What are the consequences of developing hyper/hypo-kalaemia?

A

Can severely affect the heart - cardiac cell membrane potential (depolarisations / hyperporlarisations) producing characteristic changes in ECG

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22
Q

What is cell membrane hyperpolarisation?

A

increased negativity of voltage across membrane, hence decreased excitability of neurones & muscle cells

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23
Q

What is cell membrane depolarisation?

A

Decreased negativity of voltage, hence threshold approached quicker, increased excitability & muscle contractions

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24
Q

Describe what you would see on an ECG of a hyperkalemic patient

A

↑QRS complex, ↑amplitude T-wave, eventual loss P-wave

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25
Q

Describe the ECG pattern oh a hypokalaemic patient

A

↓amplitude T-wave, prolong Q-U interval, prolong P-wave

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26
Q

What causes Hypokalaemia?

A

caused by renal or extra-renal loss of K+ or by restricted intake

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27
Q

What factors contribute to hypokalaemia?

A
  • Long-standing use of diuretics w/out KCl compensation
  • Hyperaldosteronism/Conn’s Syndrome
    (↑↑ aldosterone secretion)
  • Prolonged vomiting → Na+ loss → ↑aldosterone secretion
    → K+ excretion in kidneys
  • Profuse diarrhoea (diarrhoea fluid contains 50mM K+)
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28
Q

What effect does Hypokalaemia have on hormones?

A

Hypokalaemia results in ↓release of adrenaline, aldosterone & insulin

29
Q

Why is it possible to get hyperkalaemia if not in disease state?

A

Acute hyperkalaemia normal following prolonged exercise → normal kidneys excrete K+ easily

30
Q

When does hyperkalemia become a disease state?

A
  • Insufficient renal excretion
  • Increased release from damaged body cells eg. during chemotherapy, long-lasting hunger, prolonged exercise or severe burns
  • Long-term K+ sparing diuretics use
  • Addison’s disease (adrenal insufficiency)
31
Q

How can hyperkalaemia lead to cardiac arrest?

A

Plasma [K+] > 7mM life-threatening → asystolic cardiac arrest

32
Q

How can we treat hyperkalaemia?

A 
Insulin/Glucose infusion used to drive K+ back into cells 
Insulin extremely important – mechanism unclear, may stimulate Na-K-ATPase
Other hormones (aldosterone, adrenaline) stimulate Na+-K+ pump ⇒ ↑cellular K+ influx
33
Q

How i sthe external balane of K+ maintained?

A

In a healthy person, external balance is maintained almost entirely by the kidney

34
Q

Which drugs put you at risk of hyperkalaemia?

A

Drugs like β-blockers, ACE inhibitors etc raise serum [K] →risk of hyperkalaemia

35
Q

What drugs have the risk of developing hypokalemia?

A

Conversely loop diuretics, used to treat heart failure, enhance risk of hypokalaemia

36
Q

How do kidneys maintain a K+ balance?

A

Human kidneys designed to conserve Na & excrete K
Na+ & K+ filtered freely at glomeruli
So Plasma & GF have same [Na+] & [K+]

37
Q

How much of the Na+/K+ is reabsorbed in PCT?

A

Fraction that is reabsorbed in PCT is ~ constant at 60-70%

Although absolute amount reabsorbed varies with GFR

38
Q

How does K+ reabsorption occur in PCT?

A

In PCT K+ reabsorption is passive & paracellular through tight junctions.

39
Q

Describe the balance of ions maintained by the Na/K/ATPase pump

A

Na+/K+ pump in cell membranes maintain HIGH intracellular [K+] and LOW intracellular Na however - many K & Cl channels which ions leak out through

40
Q

By the end of the PCT, what has been reabsorbed?

A

By the end of the early proximal tubule essentially all glucose, aa and much of the bicarbonate has been reabsorbed

41
Q

How does reabsorption of substances allow K+ balance?

A

Establishes a Cl- & K+ conc. gradient from lumen to peritubular fluid
Na+ & K+ move passively along gradient with Cl- in a paracellular route
Gradient for Na+ entry across luminal membrane maintained by Na/K ATPase pump

42
Q

What is teh consequence of inhibiting the Cl- & K+ gradient?

A

Na gradient is dissipated, eventually loose primary Na transport and the associated secondary active solute transport and also NO osmotic gradient for water transport

43
Q

How is an osmotic gradient created in the LoH?

A

LoH creates a cortico-medullary osmotic conc. gradient in medulla,
descending limb = very permeable to water but ascending limb aren’t

44
Q

Why is the fluid more concentrated at the tip of the LoH?

A

Fluid enters descending limb
water moves out
Fluid gets more concentrated reaching 1200 mOsm at tip of LoH

45
Q

How do Na and Cl move out of the ascending limb?

A

Ascending limb is highly permeable to solutes so Na & Cl diffuse out

46
Q

How do Na and Cl move out of the thick ascending limb?

A

Active reabsorption/pumping of Na & Cl out of fluid, => more dilute
Via Na/2Cl/K symporter on luminal membrane
driven by the [Na] gradient from lumen-cell

47
Q

What is the fate of the solutes in the surrounding tubular cells?

A

Entry of Na from Na-H antiporter
Na/K ATPase pump on basolateral side and co-transport of Cl & K out of cell (especially in the thick ascending limb).
Some diffusion of K back into descending limb

48
Q

What are the 2 ways K+ is processed in the DCT?

A
  1. > 90% of filtered K reabsorbed in PCT & LoH
  2. Excretion of K into urine by overload,
    controlled by secretion in principal cells of
    late DCT & CD
49
Q

Explain how K+ is excreted due to the chemical gradient

A
  1. Excess K enters secreting cells from blood via Na-K-
    ATPase pump
  2. Diffuses down electrochemical gradient through K
    channels in luminal/apical membrane→ tubular fluid
  3. Electrical gradient across luminal membrane normally
    opposes K efflux from cell BUT gradient is reduced by
    Na flux through EnaC channel in membrane -
    aldosterone sensitive
  4. Chemical gradient dominates
50
Q

How does the amount of Na+ reabsorbed affect K+ secretion?

A

The more Na+ reabsorbed by the principle cell, the more K+ secreted

51
Q

What is K+ excretion into urine via the DCT determined by?

A

Increased K+ intake

Changes in blood pH

52
Q

How does alkalosis affect the k secretion?

A

Alkalosis ⇒ ↑excretion of K+ ⇒ ↓serum [K+]

53
Q

What is the effect of acute acidosis on K secretion ?

A

Acute Acidosis ⇒ ↓excretion of K+ ⇒ ↑serum [K+]

54
Q

How is acute acidosis caused?

A

Achieved by:

  1. activity of Na-K-ATPase pump
  2. electrochemical gradient
  3. permeability of luminal membrane channel
55
Q

How does aldosterone affect the Na/K/ATPase pump?

A

↑activity of Na+/K+ pump ⇒ ↑K+ influx ⇒ ↑[K+]i ⇒ cell-lumen concentration gradient

56
Q

What aeffect does aldosterone have on the ENaC channel?

A

↑ENaC channels ⇒ ↑Na+ reabsorption ⇒ ↓cell negativity and ↑lumen negativity ⇒ voltage gradient
Redistributes ENaC from intracellular localization to membrane

57
Q

Explain the effect of aldosterone on K permeability of luminal membrane

A

Causes ↑permeability of luminal membrane to K+

58
Q

How does increased plasma [K] increase K secretion into urine?

A

slows exit from basolateral membrane ⇒ ↑[K+]i ⇒ cell-lumen concentration gradient

↑activity of Na+/K+ ATPase ⇒ ↑[K+] within cell

↑Plasma [K] ⇒ stimulates aldosterone secretion

59
Q

What increases the tubule flow rate of fluid?

A

resulting from ↑GFR or inhibition of reabsorption upstream or diuretics (K+ wasting diuretics)

60
Q

What is the purpose of increasing the tubule fluid flow rate?

A

Sweeps away secreted K, making the tubular fluid [K] low allowing more rapid rate of net secretion & maintains [K+] gradient favourable to secretion

61
Q

How does ADH effect K secretion?

A

stimulates K secretion by increasing the K conductance of the luminal membrane
- Effect not as great as that of aldosterone

62
Q

Where does K reabsorption take place?

A

Occurs mainly in Intercalated cells (late DCT & CD)

under normal conditions most reabsorption occurs in PCT & LoH

63
Q

Explain why reabsorption of K occurs in disease states

A

The DCT, connecting tubule and the cortical CD don’t secrete K+ - may even reabsorb K+

The K+ which passes through cortical CD is reabsorbed in the medullary CD and K+ excreted in urine is minimal

64
Q

What disease states cause K reabsorption?

A

In people on a low K+ diet, or suffering from K+ loss e.g. diarrhea

65
Q

Explain how the RAAS system responds to low BP and/or vomiting

A
  1. JGA detects ↓BP
    Mac Den detects ↓[Na] in DCT
  2. Renin released from renin-containing JGA
    cells
  3. Indirectly forms Angiotensin II causing
    vasoconstriction and stimulation of adrenal
    cortex to produce aldosterone
  4. Aldosterone ↑Na reabsorption in DCT, by
    insertion of more Na/K-ATPase pumps and
    ENaC channels
  5. Na+ brings water in via osmosis, restoring
    fluid volume and pressure.
  6. More K+(or H+) secreted in exchange ∴
    aldosterone increases recovery of Na and
    loss of K+(or H+)

This is important because a high plasma [K+] itself causes release of aldosterone from adrenal cortex.

66
Q

What inhibits the effects of Aldosterone ?

A

Renin release is suppressed by direct negative feedback from Angiotensin II

67
Q

How does aldosterone affect pH of body?

A

Aldosterone acts on intercalated cells to ↑ activity of Na+, H+ antiporter - influences acid-base status of body by increasing H+ secretion – ↑serum pH

68
Q

Which factors cause K+ influx into cells?

A

Insulin
Aldosterone
Alkalosis
β-adrenergic stimulation

69
Q

Which factors cause an efflux of K+ out of cells into ECF?

A 
Diabetes Mellitus  (Insulin deficiency)
Addison's Disease (Aldosterone deficiency)
Acidosis
Cell lysis 
β-adrenergic blockade
Strenuous exercise
Increased ECF osmolarity

Kidneys and Renal functions (14 decks)

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