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RENAL > 8 – Renal Regulation of K, Ca, and Mg > Flashcards

8 – Renal Regulation of K, Ca, and Mg Flashcards

1
Q

Normal plasma concentration of K is:

A

-4.2mEq/L

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2
Q

What systems depend on K a lot?

A

-neurons
-muscles

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3
Q

What can happen with increased plasma K concentration?

A

-more than 3-4mEq/L increases can cause cardiac arrest
*hyperkalemia

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4
Q

What happens with decreased plasma K concentration?

A

-very critical
*hypokalemia

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5
Q

Extracellular vs. intracellular K %:

A

-extracellular: 2%
-intracellular: 98%

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6
Q

What are the 2 ways the cells can adjust the changes in plasma K concentration?

A
  1. Fast response
  2. Slow response
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7
Q

What is the fast response of adjusting to changes in plasma K concentration?

A

-transport K between extra- and intracellular K stores

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8
Q

What is the slow response of adjusting to changes in plasma K concentration?

A

-renal excretion

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9
Q

What are the factors that shift K into cells (decrease EC K concentration)?

A

-insulin
-aldosterone
-beta-adrenergic stimulation (ex. E increase K uptake)
-alkalosis

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10
Q

What are the factors that shift K out of cells (increase EC K concentration)?

A

-insulin deficiency (diabetes mellitus)
-aldosterone deficiency
-beta-adrenergic blockage
-acidosis
-cell lysis
-strenuous exercise
-increased EC fluid osmolarity

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11
Q

Metabolic acidosis and K concentration:

A

-reduces N/K pump
>increases EC K

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12
Q

Cell lysis and K concentration:

A

-release of K into EC space
>increases EC K
Ex. severe muscle injury

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13
Q

Demanding exercise and K concentration:

A

-causes K release by skeletal muscle

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14
Q

Increased osmolarity of ECF

A

-cells are becoming dehydrated
>K inside is increasing, so they push it out into EC fluid to try and avoid damage from increased K in the cells

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15
Q

What are 3 factors affecting K+ excretion?

A
  1. Filtration rate
  2. Tubular reabsorption
  3. K+ secretion in late distal and collecting tubules
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16
Q

What will decreased GFR do to K concentration?

A

-hyperkalemia

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17
Q

K secretion in late distal and colleting tubules:

A

*very important for day to day adjustments (ex. 4%)
-principal cells
-if intake of K is high=secretion increases even more than the filtered amount

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18
Q

What are the steps of K secretion by principal cells?

A
  1. Uptake from interstitium into cells (Na/K pumps)=ACTIVE
  2. Diffusion of K into lumen (K channels)
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19
Q

What are the important factors for K secretion by principal cells?

A

-Na/K pumps
-concentration gradient
-permeability of luminal membrane

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20
Q

What happens to K secretion with increased EC K?

A

*important factor: works quickly when plasma concentration of K is increased
-3 mechanisms

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21
Q

What are the 3 mechanisms involved when EC K is increased?

A
  1. Stimulates Na/K pumps: moves K into epithelial cells and diffusion into tubules
  2. Reduces leakage of intracellular K to interstitium (since EC K concentration is high)
  3. Stimulates aldosterone secretion and K secretion
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22
Q

What happens to K secretion with increased aldosterone?

A

-enhances function of Na/K pumps
-increases permeability of apical cell membranes to K
*EC concentrations of K and aldosterone have a positive feedback loop

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23
Q

When does increased tubular flow rate occur?

A

-volume expansion
-high sodium intake
-treatment with diuretics

24
Q

What happens to K secretion with increased tubular flow rate?

A

-high tubular flow rate=secreted K is quickly flushed and net K secretion is stimulated

25
Q

What mechanism is important for K secretion with increased tubular flow rate (especially with high Na intake)?

A

-high Na intake causes LESS aldosterone release and LESS K secretion
*since tubular flow is increased=more K secretion is stimulated which helps to EXCRETE EXCESS K (happens in distal and collecting tubules)

26
Q

What happens to K secretion with acidosis: short term?

A

-reduces K secretion b/c it INHIBITS Na/K pumps
>more Na in urine

27
Q

What happens to K secretion with acidosis: chronic?

A

-increases K secretion
>b/c Na, Cl and water reabsorption is REDUCED and tubular flow increases

28
Q

EC K and aldosterone feedback loop:

A
  1. Increased EC K signals more aldosterone release
  2. More aldosterone increases K excretion
  3. More K excretion REDCUES EC K and that REDUCES aldosterone
29
Q

Calcium amount under normal conditions:

A

-2.4mEq/L
*tightly regulated
>kidneys help by adjusting reabsorption

30
Q

What does hypocalcaemia cause?

A

-reduces nerve and muscle excitability

31
Q

What does hypercalcaemia cause?

A

-suppress neuromuscular excitability
>may cause cardiac arrhythmia

32
Q

What are the 3 forms of Ca in plasma?

A
  1. Calcium ions: 50%, active form
  2. Protein-bound: 40%
  3. Non-ionized form: 10%
33
Q

Where is Ca stored?

A

-99% in bones
-1% inside cells
-0.1% in ECF

34
Q

How much of dietary Ca is excreted in the feces?

A

-90%

35
Q

How does acidosis effect Ca?

A

-reduces binding of Ca to plasma proteins

36
Q

What does PTH regulate in regards to Ca?

A

-bone uptake and/or release of Ca

37
Q

What are the 3 things that PTH does?

A
  1. Stimulates bone resorption (increase Ca release from bones)
  2. Activates Vit D which increases intestinal reabsorption of Ca
  3. Directly increases renal Ca reabsorption
38
Q

Is Ca excreted?

A

-NO
>therefore excretion rate=filtration-reabsorption

39
Q

What happens to ionized Ca in the nephron?

A

-99% is reabsorbed
>65% proximal
>25-30% loop of Henle
>4-9% distal and collecting tubules

40
Q

Proximal tubule reabsorption of Ca:

A

-80% paracellular (dissolved in water)
-20% transcellular
*independent of PTH

41
Q

Steps of transcellular reabsorption of Ca in proximal tubules:

A
  1. Diffusion at apical membrane due to electrochemical gradient (via Ca channels)
  2. Ca pumps at basolateral membrane
  3. Ca-Na cotransport at basolateral membrane
42
Q

Ca reabsorption at loop of Henle:

A

-only in THICK ascending limb
-50% paracellular
-50% transcellular

43
Q

Paracellular Ca reabsorption at loop of Henle:

A

-diffusion due to more positive charge of the lumen

44
Q

Transcellular Ca reabsorption at loop of Henle:

A

-regulated by PTH

45
Q

Ca reabsorption in distal tubules:

A

-mainly active transport
-mechanisms similar to proximal tubules
*affected by PTH and Vitamin D=both stimulate Ca reabsorption

46
Q

Mg location in the body:

A

-50% in bones
-49% within cells
-1% in ECF

47
Q

How much of Mg in plasma in bound to protein?

A

-more than half

48
Q

How much of filtered Mg is excreted?

A

-10-15%
*regulation is mainly by adjusting the reabsorption

49
Q

Where is Mg reabsorbed in the nephron?

A

-25% in proximal tubules
-65% Loop of Henle

50
Q

When is Mg excretion increased?

A

-increased EC Mg
-increased EC Ca
-increased EC volume

51
Q

What does phosphate excretion follow?

A

-an overflow pattern
-transport maximum is 0.1mM/min
>since there is usually more intake=continual urine P excretion

52
Q

P reabsorption in the nephron:

A

-75-80% in proximal tubules
-10% in distal tubules
-10% EXCRETED

53
Q

P reabsorption in proximal tubules:

A

-transcellular transfer
>co-transport with Na

54
Q

What does low P intake lead to?

A

-increased transport maximum over time

55
Q

What regulates P concentration?

A

-PTH

56
Q

What is the renal effect that PTH has on P concentration?

A

-decreases transport maximum of P=increase P excretion

RENAL (15 decks)

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