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Unit 10 > Week 1: Potassium homeostasis > Flashcards

Week 1: Potassium homeostasis Flashcards

1
Q

What is the function of the Na+ K+ ATPase?

A

3Na+ out and 2K+ into the cytoplasm
K+ generally higher in the cytoplasm so diffuses out down a conc gradient, cell membrane relatively permeable to k+ through open channels
Na+ higher in ECF but cell relatively impermeable to Na+ so no movement
This maintains the potential difference across the membrane (more negative inside) essential to function of excitable cells.

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2
Q

What is the normal range of plasma potassium?

A

3.5 - 5.0 millimoles per Litre

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3
Q

What is the normal regulated level of potassium in the ECF?

A

4.2 mmol per litre

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4
Q

What is the distribution of potassium across the body stores?

A

98% in the ICF
2% in the ECF

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5
Q

What are the average intakes of K+ into the human body?

A

About 50-200 mmol/L
Around 100 mmol per meal

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6
Q

Why is it difficult to regulate K+ levels in the body?

A

Failure to rapidly remove potassium from blood stream after a meal results in hyperkalemia

Small decrease in potassium in the blood stream results in hypokalemia

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7
Q

What are some consequences of hyperkalemia?

A

Cardiac arrhytmias
Cardiac arrest
Fibrillation

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8
Q

What structure is mainly responsible for regulating K+ levels?

A

The kidney - match urine output (90-95% of K+ excretion) to input

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9
Q

What is the role of cells in potassium regulation?

A

Contain 98% of K+ so can act as a source in hypokalemia or a store in hyperkalemia

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10
Q

What happens to potassium when it is consumed in a meal in order to regulate its levels?

A

Rapidly transferred into cells to prevent hyperkalemia
Then excreted by the kidneys when approproate

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11
Q

What is meant by internal K+ balance?

A

The regulation of K+ distribution between the ECF and the ICF.

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12
Q

What factors are the mainplayers causing cells to intake Potassium ions?

A

Insulin
Catecholamines (adrenaline)

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13
Q

How does insulin increase K+ absorption into the cell?

A

Insulin is released after a meal
Binds to IRS1 resulting in the activation of P13-K then PDPK1, this stimulates the GLUT4 transporter.
Also activates aPKC resulting in activation of the Na+/K+ ATPase
Causing K+ influx

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14
Q

How do catecholamines increase K+ absoprtion into the cell?

A

Adrenaline binds to Beta 2 adrenergic receptors on skeletal muscle.
This activates cAMP then PKA.
This results in activation of the Na+/K+ pump resulting in K+ absoprtion

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15
Q

What condition in relation to K+ levels are diabetics at risk of?

A

Hyperkalemia - unresponsive to insulin after a meal leading to decreased influx of K+ into cells

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16
Q

What is the physiological role of aldosterone in regulating K+ levels?

A

Inc K+ intake causes secretion of aldosterone
Aldosterone causes K+ intake into cells and K+ excretion

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17
Q

What conditions associated with aldosterone levels can have pathological K+ levels?

A

Conns syndrome - excess aldosterone leads to hypokalemia
Addisons disease - deficient aldoesterone leads to hyperkalemia

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18
Q

How can acid base abnormalities affect K+ distribution?

A

Metabolic alkalosis - decreased ECF K+ concentration
Metabolic acidosis - increased ECF K+ concentration

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19
Q

What factors increase K+ shift into cells?

A

Insulin
Catecholamines (adrenaline)
Aldosterone
Metabolic alkalosis

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20
Q

What factors decrease K+ shift into cells? Hyperkalemia causing

A

Diabetes mellitus (untreated)
Addison disease
Beta-adrenergic blockers
Metabolic acidosis
Cell lysis

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21
Q

How does the Na+ H+ exchanger affect the activity of the Na+ K+ ATPase?

A

Increased activity of Na+ H+exchanger results in H+ out and Na+ in.
This increases the activity of Na+ K+ ATPase
Leading to increased K+ influx into cells

22
Q

What is the difference between acidosis and acedmia?

A

Acidosis - increase in H+ conc
Acedmia - decrease in pH

23
Q

How does the Na+ HCO3- cotransporter effect the level of K+ in the ECF?

A

Increased activity of Na+ HCO3- leads to more Na+ and HCO3- in the cell.
INcrease activity of Na+ K+ pump to remove Na+
Leads to increased influx of K+ into ICF

24
Q

Describe how the activity of the chloride bicarbonate antiporter affect K+ influx into the ICF?

A

Increased activity of chloride bicarbonate antiporter results in more Cl- in ICF and more HCO3- in ECF
Increases activity of Cl- K+ symporter to remove Cl- from the ICF in doing so moves K+ from the ICF to the ECF

25
Q

What is the effect of cell lysis on ECF K+ levels?

A

Can result in hyperkalemia
Large K+ stores are released from the cytoplasm as the cell is destroyed
Common in severe muscle injury or red blood cell lysis

26
Q

How does strenuous exercise affect ECF K+ levels?

A

Can result in hyperkalemia (mild)
Releases K+ from skeletal muscle
(cause fatigue from impaired membrane excitability)

27
Q

What is osmolarity?

A

The concentration of solutes in a solvent

28
Q

How does an increase in ECF osmolarity affect K+ levels?

A

Increased ECF osmolarity (increased solutes and lower water potential)
Water moves into ECF by osmosis from the cells
This increases the conc K+ in cells, more likely to diffuse out increasing ECF K+ levels

29
Q

What three processes determine renal K+ excretion?

A
  1. Rate of K+ filtration
  2. Rate of K+ reabsorption
  3. Rate of K+ secretion by the tubules
30
Q

How do you calcuate the ranel rate of K+ filtration?

A

Glomerular filtration rate x plasma K+ concentration

31
Q

What is the normal renal rate of K+ filtration?

A

756 mEq per day

32
Q

In the nephron where is K+ mainly reabsorbed or secreted?

A

Reabsorbed - 65% in PCT, 27% in Thick AL, 4% in collecting duct

Secreted - 8% in collecting tubule and duct (and DCT)

Overall 12% of K+ filtration is excreted in urine

33
Q

How does potassium excretion / reabsorption in the nephron vary dependent on the body needs?

A

Stable reabsorption in PCT and LOH
Variation in excretion occurs due to changes in the amount secreted into the urine in the DCT, CT and CD.

34
Q

Describe how potassium is handled in the proximal tubule cell?

A
  1. Active sodium reabsoprtion (SGLT2 and Na+k+ATPase) drives net fluid reabsorption from the lumen into the blood
  2. K+ is reabsorbed paracellularly with H2O be solvent drag
  3. Increased luminal voltage providing a stronger drive for K+ movement by paracellular diffusion
  4. K+ uptake by the Na+K+ ATPase can exit the basolateral membrane by K+ channels or co-transport with Cl-, (small amount may go back into lumen by K+ channels)
35
Q

What is the handling of K+ like in the thick ascending limb cells?

A
  1. Na+ K+ pump on basoloateral membrane creates conc gradient for NKCC2
  2. NKCC2 (Na+ K+ and 2Cl-)from lumen into cytoplasm
  3. K+ may enter lumen again by ROMPK channel down conc to ensure plenty supplied for NKCC2
  4. ROMK creates a lumen positive voltage allows some K+ reaborption by paracellular diffusion
  5. Alternativly K+ in the cytoplasm exts basolateral membrane by a voltage gated channel along with Cl-
36
Q

How is potassium secreted in the principle cells of the Late DCT and CT?

A
  1. Na+ K+ ATPase - on basolateral membrane increases K+ in the cytoplasm
  2. Creates a concentration gradient for K+ to diffuse out by BK and ROMK channels into renal lumen
  3. The permeability of the membrane by these channels increases during high K+ intake
  4. Na+ enters by ENaC channels on the luminal side to continue fuelling Na+K+ ATPase
37
Q

What are the different cell types with different roles in regards to K+ in the CT?

A

Principle cell - majority - secrete into lumen
Intercalated cells - type A reabsorbed K and type B can secrete K+

38
Q

How do type A intercalated cells in the CT handle K+ reabsoprtion?

A

Active in severe hypokalaemia
Action of principle cells decreases and intercalated cell activity increases
CO2 diffuses from blood/ITF into cytoplasm, dissociates to HCO3- and H+
H+ leaves the lumen side by H+ K+ ATPase antiporter, increasing K+ cytoplasm concentration
Then leaves the basolateral side by co transport with cli- maintained by cl- hco3- antiporter

39
Q

How do intercalated cells in the CT of nephron secrete K+?

A

Type B intercalated cells Activated in hyperkalemia
CO2 diffuse in from blood and dissociates into H+ and HCO3-
H+ K+ antiporter on basolateral membrane (H+ out into intersitial and soidum in to cytoplasm)
Leaves cytoplasm down a conc gradient into renal lumen through K+ channels
Co with. Cl- maintained by cl- hco3- antiporter

40
Q

What factors increase K+ secretion by principal cells in the CT/CD?

A
  1. Hyperkalemia (ECF)
  2. Increased tubular flow rate
  3. Increased aldosterone
    These all affect the concentration gradient for K+ across the luminal membrane
41
Q

Descriibe how increased ECF K+ increases potassium secretion in the CD/CT?

A

More pronounced effect when ECF is above 4.2mmol?L K+
1. Increases supply for Na+K+ ATPase on basolateral membrane
leading to increase conc gradient for diffusion into the renal lumen
2. Increased conc in Interstitial fluid prevents backleakage from cytoplasm into ISF
3. Causes synthesis of BK and ROMK channels in luminal membrane
4. Stimulates aldosterone secretion

42
Q

How does a high tubular flow rate increase K+ secretion?

A

1.Rapidly clears lumen of high K+ conc filtrate - replaced by low conc - this maintains the conc gradient for K+ diffusion into lumen
2. Increases number of ROMK and BK channels in luminal membrane
3. Increases Na+ absorption so luminal voltage becomes more negative increasing K+ secretion

43
Q

How does aldosterone lead to increase K+ secretion in the collecting ducts?

A
  1. Increases activity of Na+ K+ pump leading to increased cytoplasm concentration of K+
  2. Stimulates absorption of Na+ by ENaC channels, creating more negative luminal voltage encouraging K+ secretion
  3. Increases the number of K+ channels on the luminal membrane
44
Q

What is the relationship between aldosterone and EC K+ conc?

A

Negative feedback mechanism

High plasma K+ cause aldosterone production
Aldosterone increases renal K+ secretion
Decreases plasma K+, leads to decreased aldosterone production

45
Q

How does sodium intake affect K+ secretion when soidum levels are high?

A
  1. High sodium and high renal perfusion decrease aldosterone release - decrease K+ secretion in CD
  2. High Sodium - high BP - increased tubular flow rate - increased K+ secretion
  3. Overall leads to unchanged K= secretion
46
Q

How does chronic vomitting effect K+ electrolyte levels?

A

Chronic vomiting - loss of electrolytes (particularly sodium = hypovolemia = RAAS activation = aldosterone release) leading to increased secretion of potassium

47
Q

How does diuretic use effect K+ levels?

A

Diuretics - increase GFR and tubular flow rate leading to increased K+ secretion
Leads to hypokalemia

48
Q

How do potassium levels affect cardiac function?

A

Cause arryhtmias by direct effects of K+ and changing effects on Na+K+ pump and Na+/Ca2+ exhcnager

49
Q

How does hypokalemia cause cardiac complications?

A

QT prolongation and prominent U waves
QT prolongation - due to slower rate of ventricular repolarisation
Due to
1. Faster inactivation of K+ channels (to preserve K+ store)
2. Enhanced Na+ dependent inhibition (K+ channels are slower to open)
3. Downregulation of the expression of the K+ channel in acute maintained hypokalaemia

50
Q

How can hypokalemia lead to ventricular fibrillation?

A
  1. Leads to delayed ventricular repolarisation
  2. Increased membrane potential can cause inappropriate reactivation of L-type Voltage gasted Ca2+ ion channels in model cells, creates a secondary action potential in the repolarisation phase
  3. Can cause abnormal re-excitation of ventricular myocytes resulting in ventricular fibrillation independent of the SAN
51
Q

Why does luminal voltage increase in the PCT?

A

Some K+ is passivly absorbed by solvent drag.
K+ are secreted due to conc gradient established by Na+K+ATPase.
More K+ secreted than reabsrobed in early PCT, combined with the voltage increases allowing more K+ to be reabsorbed later in the PCT by paracellular diffusion down an electrochemical gradient/

Unit 10 (37 decks)

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