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REN > Potassium Regulation > Flashcards

Potassium Regulation Flashcards

1
Q

Give the Nernst Equation.

A

E = (-RT/F) * log ([K+in] / [K+out])

Where:

F = Faraday
R = Gas constant
E = Equilibrium potential
T = Temperature (kelvin)
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2
Q

What is the ratio of [K+in] / [K+out] in a normal cell?

A

140/4 = 35

*Intracellular / extracellular

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3
Q

What can be said about the movement of potassium ions across a membrane if [K+in] / [K+out] is constant?

A

Equilibrium potential has been reached.

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4
Q

Why, for acute loads, does K+ tend to accumulate in the extracellular space?

A

Because the equilibrium, which is greater intracellularly, takes time to develop.

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5
Q

List 6 causes of hyperkalaemia.

A

1 - End-stage renal failure.

2 - Crush injuries.

3 - Blood transfusion.

4 - Cytotoxic drugs.

5 - Insulin deficiency.

6 - Over-use of K+ sparing drugs.

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6
Q

What is the consequence of hyperkalaemia?

A

Cardiac dysrhythmias.

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7
Q

List 3 causes of hypokalaemia.

A

1 - Diarrhoea.

2 - Furosemide.

3 - Insulin overdose.

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8
Q

What is the consequence of hypokalaemia?

A

Cardiac dysrhythmias.

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9
Q

List the sites of renal K+ exchange.

For each site, give the transporter responsible for the exchange.

A

1 - Proximal tubules (passively and paracellularly with water).

2 - Thick ascending limb (NKCC cotransporters).

3 - Distal tubule principal cells (apical K+ channels under the control of aldosterone and Ca2+ activated K+ channels which are dependent on flow).

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10
Q

Why is absorption of potassium at the thick ascending limb negligible?

A

Because most of the potassium cycles back into the filtrate there.

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11
Q

What is the main hormone regulating K+?

A

Aldosterone.

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12
Q

Why is only 10% of the total blood Ca2+ filtered at the glomerulus?

A

Because 20% of free plasma Ca2+ is filtered at the glomerulus, and half of Ca2+ is bound to albumin and other carriers.

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13
Q

Describe the process of sulfate reabsorption in the proximal tubule.

A

1 - 3Na+ and 1 SO4 2- enter via the apical membrane with the NaS1 cotransporter.

2 - SO4 2- exits the cell on the basolateral membrane via the sat1 antiporter, where it is exchanged in reverse for anions.

3 - The Na+ gradient is maintained by the basolateral 3Na+/2K+ pump.

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14
Q

Via which protein can SO4 2- exit the cell via the apical membrane?

In exchange for which molecule does SO4 2- exchange occur here?

A
  • The cfex antiporter.

- In exchange for anions.

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15
Q

What is the limiting factor for SO4 2- transport?

Give an example of another molecule that is limited in the same way.

A
  • SO4 2- is Tm limited (transport maximum).

- The same is true for glucose.

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16
Q

What type of molecule is the erythropoietin hormone?

A

A glycoprotein.

17
Q

How many amino acids comprise erythropoietin?

What is the mass in Da?

A
  • 166.

- 34kDa.

18
Q

What is the normal concentration of erythropoietin in the blood?

A

10pM.

19
Q

Which cells synthesise erythropoietin?

A

Peritubular fibroblasts, sometimes called mesangial cells, in the renal cortex.

20
Q

What stimulates erythropoietin production and release?

A

Hypoxia.

21
Q

What are hypoxia-inducible factors?

What is the primary hypoxia-inducible factor?

A
  • Transcription factors which control the production and release of erythropoietin.
  • The primary hypoxia-inducible factor is HIF-2.
22
Q

Why does low blood Fe2+ lead to an increase in erythropoietin production?

A
  • HIF-alpha is a precursor to hypoxia-inducible factors.
  • Fe2+ is a cofactor in HIF-alpha dioxygenase, which catalyses the breakdown of HIF-alpha.
  • Hence, low blood Fe2+ leads to an increase in hypoxia-inducible factors and therefore an increase in erythropoietin production.
23
Q

List 3 factors, other than Fe2+, that control erythropoietin production.

A

1 - Prostaglandins.

2 - Beta-adrenoceptors.

3 - Angiotensin II.

24
Q

List 2 actions of erythropoietin.

A

1 - Acts as an anti-apoptotic agent for erythrocytic progenitors.

2 - Erythropoietin binds to erythropoietin receptors in the bone marrow to increase the production of proerythroblasts.

25
Q

Describe the process of erythropoietin clearance.

A
  • Erythropoietin binds to the EPOR receptor.
  • This activates the JAK2 tyrosine kinase.
  • This activates intracellular pathways including Ras/MAP kinase, phosphatidylinositol 3-kinase and STAT transcription factors.
  • The EPOR receptor clears the erythropoietin by binding and internalisation.
26
Q

Why might erythropoietin concentration be longer in some individuals?

A

Due to a low EPOR receptor expression or dysfunctional EPOR receptor.

27
Q

Why might renal failure cause anaemia?

A

Due to a decrease in erythropoietin production.

28
Q

In which form of renal failure will anaemia not occur?

A

Renal failure associated with polycystic kidney disease, in which sufficient renal parenchyma is present to prevent the loss of erythropoietin production.

29
Q

How is anaemia of renal failure treated?

A

By giving synthetic erythropoietin analogues.

30
Q

What type of anaemia occurs with anaemia of renal failure?

A

Normochromic normocytic anaemia.

31
Q

Give an example of a synthetic erythropoietin analogue.

A

Darbepoetin alfa.

32
Q

List 2 risks of erythropoietin abuse (e.g. for sport).

A

1 - Increased risk of thrombosis.

2 - Increased blood viscosity, which in turn decreases flow.

33
Q

Can erythropoietin be found in the urine?

A

Normally in small amounts, but it is particularly abundant with abuse.

34
Q

List the stages of processing of vitamin D.

For each stage, state the location in the body where that stage occurs.

A

1 - Vitamin D from the diet or skin is converted into 25-hydroxyvitamin D in the liver.

2 - 25-hydroxyvitamin D is converted into 1,25-dihydroxyvitamin D in the kidney.

35
Q

List 2 hormones that regulate the production of 1,25-dihydroxyvitamin D.

What are their roles in vitamin D regulation?

A

1 - Parathyroid hormone (stimulates).

2 - Calcitonin (inhibits).

36
Q

List the actions of 1,25-hydroxyvitamin D.

A

1 - To increase Ca2+ and phosphate absorption from the small intestine.

2 - To decrease Ca2+ and phosphate excretion.

37
Q

Why might patients with renal failure have low 25-hydroxyvitamin D?

What about 1,25-dihydroxyvitamin D?

A
  • Low 25-hydroxyvitamin D might be due to dietary restrictions.
  • Low 1,25-dihydroxyvitamin D ia due to the failure of the kidney to convert 25-hydroxyvitamin D into 1,25-dihydroxyvitamin D.
38
Q

Which enzyme is responsible for the conversion of 25-hydroxyvitamin D into 1,25-dihydroxyvitamin D?

A

1-alpha hydroxylase.

39
Q

What is the cutoff molecular mass for glomerular filtration?

A

70kDa.

REN (19 decks)

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